Maximize22
03-08-2002, 05:55 PM
Hi - I'm male, 28, and just had my cholesterol checked for the first time (weighing in at a not so healthy 216). The doc told me I could try and get it under control with a better diet rather than going on any kind of drugs.
My question is how much can exercise impact these numbers - I haven't been able to find much on this. While I do plan on cutting back on certain foods, I love being able to grab a fast food burger or have cheese and crackers when I get home at night. Does anyone know how big of an impact aerobic exercise can have on cholesterol levels?
My question is how much can exercise impact these numbers - I haven't been able to find much on this. While I do plan on cutting back on certain foods, I love being able to grab a fast food burger or have cheese and crackers when I get home at night. Does anyone know how big of an impact aerobic exercise can have on cholesterol levels?
Sponsor
hunter44
03-09-2002, 01:35 PM
Excercise will greatly impact your cholesterol levels but it is hard to put a definite number on how much. It all depends on how much but even walking for an hour three times a week will benefit. Excercise will lower your overall numbers and increase your good HDL cholesterol. Diet is also very important. Recent info out is that a diet in low carbohydrates is more effective that one in low fat. You may want to investigate this further by doing a little reading. There are a quite a few excellent site if you search the web. Look at places like WebMD, low carb eating dot com, Weston Price Foundation, they all have links to specialty message boards.
Carreen
03-09-2002, 03:23 PM
This is a very good site (NIH National Institute of Health) for accurate info about your cholesterol.
http://www.nhlbi.nih.gov/health/public/heart/chol/wyntk.htm
http://www.nhlbi.nih.gov/health/public/heart/chol/wyntk.htm
vipergg22
03-09-2002, 08:01 PM
For a different point of view take a look at
this. http://www.ravnskov.nu/cholesterol.htm
this. http://www.ravnskov.nu/cholesterol.htm
LooneyJM
03-10-2002, 10:21 AM
216 could be an ideal number! What are your Tryglycerides and HDL's? Are you overweight? Recent studies are questioning the validity of cholesterol as an indicator of heart disease.
Excercise will help as will diet. Be cautious of a low-fat diet, replaced by carbs. This can make matters worse in some cases.
After charting my bloodwork for the past 2 years, my HDL's (good stuff) went up the most after adding fats in the form of walnuts and extra virgin olive oil.
Excercise will help as will diet. Be cautious of a low-fat diet, replaced by carbs. This can make matters worse in some cases.
After charting my bloodwork for the past 2 years, my HDL's (good stuff) went up the most after adding fats in the form of walnuts and extra virgin olive oil.
Magpiezoe
03-11-2002, 12:22 PM
Hello, The American Heart Association will send you free information on how to control cholesterol through diet and exercise. Their web site is http://216.185.112.5/presenter.jhtml?identifier=1518
I follow the guideline in the "Fabulous Fat-Free Cookbook" by Lynn fischer. She recommends 60 min. per day. You can break it up during the day if you want to. I walk 30 min. in the morning and alternate weight barring exercise and aerobics each day. I do the aerobics and weight barring exercises for 30-50min. at night. My night-time goal is 60min., which I just reached last night.
In addition to exercise I count my total fat and cal. intake. Since I am 115 lbs, I eat 16-39 grams fat and 1400 cal. per day. The diet and exercise really lower my cholesterol fast. I use light mayo, PAM, low-fat string cheese, and broil everything. I also only eat one serving of various foods, instead of a lot of one food. I will admit to kicking my diet off with going fish/vegetarian for one month. Good luck.
------------------
Magpie
I follow the guideline in the "Fabulous Fat-Free Cookbook" by Lynn fischer. She recommends 60 min. per day. You can break it up during the day if you want to. I walk 30 min. in the morning and alternate weight barring exercise and aerobics each day. I do the aerobics and weight barring exercises for 30-50min. at night. My night-time goal is 60min., which I just reached last night.
In addition to exercise I count my total fat and cal. intake. Since I am 115 lbs, I eat 16-39 grams fat and 1400 cal. per day. The diet and exercise really lower my cholesterol fast. I use light mayo, PAM, low-fat string cheese, and broil everything. I also only eat one serving of various foods, instead of a lot of one food. I will admit to kicking my diet off with going fish/vegetarian for one month. Good luck.
------------------
Magpie
arkie6
03-11-2002, 04:20 PM
Here is an excellent rebuttal to all of the anti-cholesterol and anti-saturated fat propaganda put out by the US government and various "health authorities":
http://www.second-opinions.co.uk/cholesterol_myth_1.html
Dietary cholesterol and saturated fat are not the demons they have been made out to be. The real bad guys are the highly refined carbohydrates and partially hydrogenated vegetable oils found in virtually every processed food product on your grocer's shelves and every fast food joint.
While moderate exercise will no doubt have a positive impact on your health, its ability to lower cholesterol levels without a change in diet is rather limited. One thing that exercise does is improve insulin sensitivity in the muscle cells which will allow insulin levels to drop some. This will have a small positive effect on cholesterol levels. But exercise alone is usually not the answer. The main focus should be on your diet with emphasis on whole natural foods and avoidance of all of the highly processed convienence foods.
Alan
http://www.second-opinions.co.uk/cholesterol_myth_1.html
Dietary cholesterol and saturated fat are not the demons they have been made out to be. The real bad guys are the highly refined carbohydrates and partially hydrogenated vegetable oils found in virtually every processed food product on your grocer's shelves and every fast food joint.
While moderate exercise will no doubt have a positive impact on your health, its ability to lower cholesterol levels without a change in diet is rather limited. One thing that exercise does is improve insulin sensitivity in the muscle cells which will allow insulin levels to drop some. This will have a small positive effect on cholesterol levels. But exercise alone is usually not the answer. The main focus should be on your diet with emphasis on whole natural foods and avoidance of all of the highly processed convienence foods.
Alan
Carreen
03-11-2002, 06:45 PM
I think that sticking with the guidelines researched, used and approved by the agencies below is more indicative of how cholesterol and heart disease occurs as compared to some extremists on the finge. Sure, a couple of people can come along with studies or websites to dispute this, but I'll put my eggs in the basket of these thousands and thousands of people.
The National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH) launched the National Cholesterol Education Program (NCEP) in November 1985. The goal of the NCEP is to contribute to reducing illness and death from coronary heart disease (CHD) in the United States by reducing the percentage of Americans with high blood cholesterol. Through educational efforts directed at health professionals and the public, the NCEP aims to raise awareness and understanding about high blood cholesterol as a risk factor for CHD and the benefits of lowering cholesterol levels as a means of preventing CHD.
Member Organizations of the NCEP Coordinating Committee:
American Academy of Family Physicians
American Academy of Pediatrics
American Association of Occupational Health Nurses
American College of Cardiology
American College of Chest Physicians
American College of Nutrition
American College of Obstetricians and Gynecologists
American College of Occupational Medicine
American College of Preventive Medicine
American Diabetes Association, Inc.
American Dietetic Association
American Heart Association
American Hospital Association
American Medical Association
American Nurses Association
American Osteopathic Association
American Pharmaceutical Association
American Public Health Association
American Red Cross
Association of Black Cardiologists
Association of Life Insurance Medical Directors of America
Association of State and Territorial Health Officials
Citizens for Pubic Action on Blood Pressure and Cholesterol, Inc.
National Black Nurses Association, Inc.
National Heart, Lung, and Blood Institute
National Medical Association
Society for Nutrition Education
Society for Public Health Education
Associate Member Organizations of the NCEP Coordinating Committee
American Association of Office Nurses
Federal Agencies
NHLBI Ad Hoc Committee on Minority Populations
Agency for Healthcare Research and Quality
Centers for Disease Control and Prevention
Coordinating Committee for the Community Demonstration Studies
Department of Agriculture
Department of Defense
Food and Drug Administration
Health Resources and Services Administration
National Cancer Institute
National Center for Health Statistics
Office of Disease Prevention and Health Promotion
Department of Veterans Affairs
The National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH) launched the National Cholesterol Education Program (NCEP) in November 1985. The goal of the NCEP is to contribute to reducing illness and death from coronary heart disease (CHD) in the United States by reducing the percentage of Americans with high blood cholesterol. Through educational efforts directed at health professionals and the public, the NCEP aims to raise awareness and understanding about high blood cholesterol as a risk factor for CHD and the benefits of lowering cholesterol levels as a means of preventing CHD.
Member Organizations of the NCEP Coordinating Committee:
American Academy of Family Physicians
American Academy of Pediatrics
American Association of Occupational Health Nurses
American College of Cardiology
American College of Chest Physicians
American College of Nutrition
American College of Obstetricians and Gynecologists
American College of Occupational Medicine
American College of Preventive Medicine
American Diabetes Association, Inc.
American Dietetic Association
American Heart Association
American Hospital Association
American Medical Association
American Nurses Association
American Osteopathic Association
American Pharmaceutical Association
American Public Health Association
American Red Cross
Association of Black Cardiologists
Association of Life Insurance Medical Directors of America
Association of State and Territorial Health Officials
Citizens for Pubic Action on Blood Pressure and Cholesterol, Inc.
National Black Nurses Association, Inc.
National Heart, Lung, and Blood Institute
National Medical Association
Society for Nutrition Education
Society for Public Health Education
Associate Member Organizations of the NCEP Coordinating Committee
American Association of Office Nurses
Federal Agencies
NHLBI Ad Hoc Committee on Minority Populations
Agency for Healthcare Research and Quality
Centers for Disease Control and Prevention
Coordinating Committee for the Community Demonstration Studies
Department of Agriculture
Department of Defense
Food and Drug Administration
Health Resources and Services Administration
National Cancer Institute
National Center for Health Statistics
Office of Disease Prevention and Health Promotion
Department of Veterans Affairs
hunter44
03-11-2002, 07:03 PM
"The National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH) launched the National Cholesterol Education Program (NCEP) in November 1985. The goal of the NCEP is to contribute to reducing illness and death from coronary heart disease (CHD) in the United States by reducing the percentage of Americans with high blood cholesterol. Through educational efforts directed at health professionals and the public, the NCEP aims to raise awareness and understanding about high blood cholesterol as a risk factor for CHD and the benefits of lowering cholesterol levels as a means of preventing CHD. "
In 1985 - shoot that's 15 years ago - read the recent research or for that matter the old research more clearly explained/exposed.
And how do they recommend getting the numbers down after diet and excercise(which most people don't do)? By prescibing statins like Lipitor. Well go to the Lipitor website and read their disclaimer.
www.lipitor (http://www.lipitor) dot com,
"LIPITOR has not been shown to prevent heart disease or heart attacks."
Now who are you going to beleive?
Question Authority
In 1985 - shoot that's 15 years ago - read the recent research or for that matter the old research more clearly explained/exposed.
And how do they recommend getting the numbers down after diet and excercise(which most people don't do)? By prescibing statins like Lipitor. Well go to the Lipitor website and read their disclaimer.
www.lipitor (http://www.lipitor) dot com,
"LIPITOR has not been shown to prevent heart disease or heart attacks."
Now who are you going to beleive?
Question Authority
Carreen
03-11-2002, 11:36 PM
The National Cholesterol Education Program was STARTED in 1985, not CONCLUDED. :) It continues today. Research continues, learning continues.
http://www.nhlbi.nih.gov/health/public/heart/chol/wyntk.htm
Lipitor(or other statin) don't claim to prevent heart disease or heart attacks. It's a synthetic lipid lowering agent not a heart attack preventer. There are several types of drugs available for cholesterol lowering including statins, bile acid sequestrants, nicotinic acid, and fibric acids. The statin drugs are very effective in lowering LDL levels and are safe for most people. Bile acid sequestrants also lower LDL and can be used alone or in combination with statin drugs. Nicotinic acid lowers LDL and triglycerides and raises HDL. Fibric acids lower LDL somewhat but are used mainly to treat high triglyceride and low HDL levels.
NOTHING you can do will GUARANTEE you won't have a heart attack. It's a matter of RISK. Excessive cholesterol contributes to atherosclerosis and subsequent heart disease. The RISK of developing heart disease or atherosclerosis increases as the level of blood cholesterol increases.
If you're overweight, smoke, eat high fat/high cholesterol, have a family history of heart disease, and don't exercise your RISK is greater, it's not a death sentence.
Conversely if you don't smoke, you eat healthy, don't have a family history of heart disease, and excercise your RISK is lower, it's not a guarantee.
People attempt to lower their cholesterol because they don't want to RISK an early death or coronary event.
People are perfectly able and willing to make their own health desisions. If someone doesn't want to do ANYTHING about their cholesterol, they can ignore it. Some feel an ounce of prevention is worth a pound of cure.
Eating a healthy low fat, low cholesterol diet, giving up smoking, taking up an excercise program and losing weight haven't been show in ANY study to contribute to coronary heart disease. EVERYONE should do this, not only to lower their risk of CHD but to lower risks of other diseases like cancer, diabetes, strokes, high blood pressure, etc.
A real good read is: http://www.nhlbi.nih.gov/guidelines/cholesterol/index.htm
http://www.nhlbi.nih.gov/health/public/heart/chol/wyntk.htm
Lipitor(or other statin) don't claim to prevent heart disease or heart attacks. It's a synthetic lipid lowering agent not a heart attack preventer. There are several types of drugs available for cholesterol lowering including statins, bile acid sequestrants, nicotinic acid, and fibric acids. The statin drugs are very effective in lowering LDL levels and are safe for most people. Bile acid sequestrants also lower LDL and can be used alone or in combination with statin drugs. Nicotinic acid lowers LDL and triglycerides and raises HDL. Fibric acids lower LDL somewhat but are used mainly to treat high triglyceride and low HDL levels.
NOTHING you can do will GUARANTEE you won't have a heart attack. It's a matter of RISK. Excessive cholesterol contributes to atherosclerosis and subsequent heart disease. The RISK of developing heart disease or atherosclerosis increases as the level of blood cholesterol increases.
If you're overweight, smoke, eat high fat/high cholesterol, have a family history of heart disease, and don't exercise your RISK is greater, it's not a death sentence.
Conversely if you don't smoke, you eat healthy, don't have a family history of heart disease, and excercise your RISK is lower, it's not a guarantee.
People attempt to lower their cholesterol because they don't want to RISK an early death or coronary event.
People are perfectly able and willing to make their own health desisions. If someone doesn't want to do ANYTHING about their cholesterol, they can ignore it. Some feel an ounce of prevention is worth a pound of cure.
Eating a healthy low fat, low cholesterol diet, giving up smoking, taking up an excercise program and losing weight haven't been show in ANY study to contribute to coronary heart disease. EVERYONE should do this, not only to lower their risk of CHD but to lower risks of other diseases like cancer, diabetes, strokes, high blood pressure, etc.
A real good read is: http://www.nhlbi.nih.gov/guidelines/cholesterol/index.htm
vipergg22
03-12-2002, 12:03 AM
Some interesting reading that really makes you think more and more about taking these potentially dangerous drugs for something that may not be a problem . We are treating for something that is a risk factor and a very real possibilty that nothing will ever happen . I'm not saying we should not watch what we eat but I had the extreme priviledge of taking 3 or 4 statins with all there nice side effects . I can count about a half dozen different symptoms that I had while I was on them . These things also affected your mood , I was a lot more impatient and irritable while taking these . I
ll do the best I can without drugs and I am not going to worry about it . I have had enough .
Originally posted by arkie6:
Here is an excellent rebuttal to all of the anti-cholesterol and anti-saturated fat propaganda put out by the US government and various "health authorities":
http://www.second-opinions.co.uk/cholesterol_myth_1.html
Dietary cholesterol and saturated fat are not the demons they have been made out to be. The real bad guys are the highly refined carbohydrates and partially hydrogenated vegetable oils found in virtually every processed food product on your grocer's shelves and every fast food joint.
While moderate exercise will no doubt have a positive impact on your health, its ability to lower cholesterol levels without a change in diet is rather limited. One thing that exercise does is improve insulin sensitivity in the muscle cells which will allow insulin levels to drop some. This will have a small positive effect on cholesterol levels. But exercise alone is usually not the answer. The main focus should be on your diet with emphasis on whole natural foods and avoidance of all of the highly processed convienence foods.
Alan
ll do the best I can without drugs and I am not going to worry about it . I have had enough .
Originally posted by arkie6:
Here is an excellent rebuttal to all of the anti-cholesterol and anti-saturated fat propaganda put out by the US government and various "health authorities":
http://www.second-opinions.co.uk/cholesterol_myth_1.html
Dietary cholesterol and saturated fat are not the demons they have been made out to be. The real bad guys are the highly refined carbohydrates and partially hydrogenated vegetable oils found in virtually every processed food product on your grocer's shelves and every fast food joint.
While moderate exercise will no doubt have a positive impact on your health, its ability to lower cholesterol levels without a change in diet is rather limited. One thing that exercise does is improve insulin sensitivity in the muscle cells which will allow insulin levels to drop some. This will have a small positive effect on cholesterol levels. But exercise alone is usually not the answer. The main focus should be on your diet with emphasis on whole natural foods and avoidance of all of the highly processed convienence foods.
Alan
arkie6
03-12-2002, 03:02 AM
Here is another article titled "The Cholesterol Myth" that is lengthy (it is a .pdf file) but well worth reading. It provides a review of the ongoing cholesterol studies. http://medicaltruth.com/cholesterol/myth.htm
This whole cholesterol/heart disease hypothesis is nothing more than a phoney issue to enrich the medical and pharmaceutical establishment. Here is some more reading along those lines: http://www.westonaprice.org/know_your_fats/fats_phony.html
Alan
This whole cholesterol/heart disease hypothesis is nothing more than a phoney issue to enrich the medical and pharmaceutical establishment. Here is some more reading along those lines: http://www.westonaprice.org/know_your_fats/fats_phony.html
Alan
arkie6
03-12-2002, 03:21 AM
Here is another must read article titled "The Soft Science of Dietary Fat" by Gary Taubes originally published in "Science"
http://people.bu.edu/sobieraj/nutrition/fat_science3_30_01.html
Alan
[This message has been edited by arkie6 (edited 03-12-2002).]
http://people.bu.edu/sobieraj/nutrition/fat_science3_30_01.html
Alan
[This message has been edited by arkie6 (edited 03-12-2002).]
Carreen
03-12-2002, 10:42 AM
The first link you give is an article by Thomas J Moore who is selling a book. On his site he describes himself as:
"If you need a medical title, the media often identifies me as a "policy analyst" or "health policy analyst." This identifies the kind of work I do and communicates that I do not approach medicine as a clinician or from a specialized medical background." (I'd classify him as a writer who is trying to SELL A BOOK)
The second link you give is ONE persons opinion. (And anything claiming to be scientific coming out of the weston price foundation is questionable)
The third link, Gary Taubes is a REPORTER for Science magazine. That's why his articles appear there, because he works there. Again, one REPORTERS opinion.
It's perfectly fine to agree with these people. You can eat and live any way you want :)
But these people are on the fringe. There are thousand and thousands of scientists, researchers, biologists, chemists, nutritionists, doctors and many agencies full of people who are not on the finge. There are hundreds and hundreds of clinical trials, past, present and continuing that show the RISK of developing heart disease or atherosclerosis increases as the level of blood cholesterol increases.
"If you need a medical title, the media often identifies me as a "policy analyst" or "health policy analyst." This identifies the kind of work I do and communicates that I do not approach medicine as a clinician or from a specialized medical background." (I'd classify him as a writer who is trying to SELL A BOOK)
The second link you give is ONE persons opinion. (And anything claiming to be scientific coming out of the weston price foundation is questionable)
The third link, Gary Taubes is a REPORTER for Science magazine. That's why his articles appear there, because he works there. Again, one REPORTERS opinion.
It's perfectly fine to agree with these people. You can eat and live any way you want :)
But these people are on the fringe. There are thousand and thousands of scientists, researchers, biologists, chemists, nutritionists, doctors and many agencies full of people who are not on the finge. There are hundreds and hundreds of clinical trials, past, present and continuing that show the RISK of developing heart disease or atherosclerosis increases as the level of blood cholesterol increases.
LooneyJM
03-12-2002, 11:17 AM
The sad fact is, most of us on these boards probably do more research than a general practitioner does. I will never trust the above mentioned organizations (trust - how about ENRON?)
There is plenty of evidence that a simple number (LDL) being below a certain level has nothing to do with coronary artery disease. Even LIPITOR claims it hasn't been proved on thier website. It's been proved that it causes cancer and many side effects.
Also, I posted this on another thread:
------------------------------------------
You MUST READ a bio on Dr. Michael Debakey, internationally recognized as an ingenious medical inventor and innovator, his credentials include:
- inventor of the roller pump for heart machine
- developed Dacron artificial grafts
- first carotid endarterectomy
- first graft replacement
- first patch-graft angioplasty
- first artery bypas
- first 12 heart transplants
In the section of the 1970s to 1980s it says:
"In 1983, Dr. Joseph Melnick and Dr. DeBakey and colleagues reported that evidence of cytomegalovirus (CMV), a common virus infecting a high percentage of people without causing symptoms, was present in the cells comprising the walls of 11 patients with atherosclerosis, or hardening of the arteries. Cytomegalovirus, which causes cells to multiply, often becomes dormant in the body for years after infection. The study suggested that early in life, cytomegalovirus may initiate the lesions that later cause atherosclerosis. In 1987, Dr. DeBakey and colleagues reported that patients with heart disease have higher-than-normal levels of antibodies to cytomegalovirus. The report supported their earlier finding that cytomegalovirus may play a major role in the development of atherosclerosis.
In another study in 1987, Dr. DeBakey reported that cholesterol levels in 15,000 patients were unrelated to how quickly blockage of major arteries progressed. In another 1 ,400 patients, all of whom had undergone coronary artery bypass operations, he found that patients with normal or below-normal cholesterol levels were just as prone to have clogging recur in their replacement arteries. Whereas smoking, a high-fat diet, and high blood pressure place persons at higher risk of developing heart disease, these studies imply that they do not, in themselves, cause atherosclerosis.
"
Link: http://www.mh-hannover.de/aktuelles/projekte/mmm/englishversion/fs_programme/cv/DeBakey.html
There is plenty of evidence that a simple number (LDL) being below a certain level has nothing to do with coronary artery disease. Even LIPITOR claims it hasn't been proved on thier website. It's been proved that it causes cancer and many side effects.
Also, I posted this on another thread:
------------------------------------------
You MUST READ a bio on Dr. Michael Debakey, internationally recognized as an ingenious medical inventor and innovator, his credentials include:
- inventor of the roller pump for heart machine
- developed Dacron artificial grafts
- first carotid endarterectomy
- first graft replacement
- first patch-graft angioplasty
- first artery bypas
- first 12 heart transplants
In the section of the 1970s to 1980s it says:
"In 1983, Dr. Joseph Melnick and Dr. DeBakey and colleagues reported that evidence of cytomegalovirus (CMV), a common virus infecting a high percentage of people without causing symptoms, was present in the cells comprising the walls of 11 patients with atherosclerosis, or hardening of the arteries. Cytomegalovirus, which causes cells to multiply, often becomes dormant in the body for years after infection. The study suggested that early in life, cytomegalovirus may initiate the lesions that later cause atherosclerosis. In 1987, Dr. DeBakey and colleagues reported that patients with heart disease have higher-than-normal levels of antibodies to cytomegalovirus. The report supported their earlier finding that cytomegalovirus may play a major role in the development of atherosclerosis.
In another study in 1987, Dr. DeBakey reported that cholesterol levels in 15,000 patients were unrelated to how quickly blockage of major arteries progressed. In another 1 ,400 patients, all of whom had undergone coronary artery bypass operations, he found that patients with normal or below-normal cholesterol levels were just as prone to have clogging recur in their replacement arteries. Whereas smoking, a high-fat diet, and high blood pressure place persons at higher risk of developing heart disease, these studies imply that they do not, in themselves, cause atherosclerosis.
"
Link: http://www.mh-hannover.de/aktuelles/projekte/mmm/englishversion/fs_programme/cv/DeBakey.html
hunter44
03-12-2002, 11:39 AM
Well - here is a quote directly from the famous "Framingham Study" that is used for the guidelines that all the doctors refer to:
Framingham Study Comments
The ongoing Framingham Study found that there was virtually no difference in coronary heart disease (CHD) "events" for individuals with cholesterol levels between 205 mg/dL and 294 mg/dL - the vast majority of the US population. Even for those with extremely high cholesterol levels - up to almost 1,200 mg/dL - the difference in CHD events compared to those in the normal range was trivial.29 This did not prevent Dr William Kannel, then Framingham Study Director, from making claims about the Framingham results. "Total plasma cholesterol," he said, "is a powerful predictor of death related to CHD." It was not until more than a decade later, in 1992, that the real findings at Framingham were published - without fanfare - in the Archives of Internal Medicine, an obscure journal. "In Framingham, Massachusetts," admitted Dr William Castelli, Kannel's successor, "the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people's serum cholesterol ... we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active."30
The NHLBI's Multiple Risk Factor Intervention Trial (MRFIT) studied the relationship between heart disease and serum cholesterol levels in 362,000 men, and found that annual deaths from CHD varied from slightly less than one per thousand, for serum cholesterol levels below 140 mg/dL, to about two per thousand, for serum cholesterol levels above 300 mg/dL - once again, a trivial difference. Dr John LaRosa, of the American Heart Association (AHA), claimed that the curve for CHD deaths began to "inflect" after 200 mg/dL, when in fact the "curve" was a very gradually sloping straight line that could not be used to predict whether serum cholesterol above certain levels posed a significantly greater risk for heart disease.
Framingham Study Comments
The ongoing Framingham Study found that there was virtually no difference in coronary heart disease (CHD) "events" for individuals with cholesterol levels between 205 mg/dL and 294 mg/dL - the vast majority of the US population. Even for those with extremely high cholesterol levels - up to almost 1,200 mg/dL - the difference in CHD events compared to those in the normal range was trivial.29 This did not prevent Dr William Kannel, then Framingham Study Director, from making claims about the Framingham results. "Total plasma cholesterol," he said, "is a powerful predictor of death related to CHD." It was not until more than a decade later, in 1992, that the real findings at Framingham were published - without fanfare - in the Archives of Internal Medicine, an obscure journal. "In Framingham, Massachusetts," admitted Dr William Castelli, Kannel's successor, "the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people's serum cholesterol ... we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active."30
The NHLBI's Multiple Risk Factor Intervention Trial (MRFIT) studied the relationship between heart disease and serum cholesterol levels in 362,000 men, and found that annual deaths from CHD varied from slightly less than one per thousand, for serum cholesterol levels below 140 mg/dL, to about two per thousand, for serum cholesterol levels above 300 mg/dL - once again, a trivial difference. Dr John LaRosa, of the American Heart Association (AHA), claimed that the curve for CHD deaths began to "inflect" after 200 mg/dL, when in fact the "curve" was a very gradually sloping straight line that could not be used to predict whether serum cholesterol above certain levels posed a significantly greater risk for heart disease.
arkie6
03-12-2002, 11:45 AM
Originally posted by Carreen:
And anything claiming to be scientific coming out of the weston price foundation is questionable.
I guess you totally ignored the scientific references they use to support their stance since the direction of the article didn't agree with your narrow view, that is, assuming you even read the article.
Carreen, you always defend the medical/pharmaceutical establishment and the status quo in medicine in your posts (in this forum and others). I sense that your financial well being is somehow tied to this profession. Is that correct? If you don't mind, how about telling the folks here what you do for a living.
There are hundreds and hundreds of clinical trials, past, present and continuing that show the RISK of developing heart disease or atherosclerosis increases as the level of blood cholesterol increases.
Ok, you've made the claim, now show me some sound scientific references to support that claim. I honestly can't find them, especially if you look deeper into the studies than just the conclusions reached. Maybe you have better resources at locating them than me.
Alan (Electrical Engineer with an interest in health issues)
And anything claiming to be scientific coming out of the weston price foundation is questionable.
I guess you totally ignored the scientific references they use to support their stance since the direction of the article didn't agree with your narrow view, that is, assuming you even read the article.
Carreen, you always defend the medical/pharmaceutical establishment and the status quo in medicine in your posts (in this forum and others). I sense that your financial well being is somehow tied to this profession. Is that correct? If you don't mind, how about telling the folks here what you do for a living.
There are hundreds and hundreds of clinical trials, past, present and continuing that show the RISK of developing heart disease or atherosclerosis increases as the level of blood cholesterol increases.
Ok, you've made the claim, now show me some sound scientific references to support that claim. I honestly can't find them, especially if you look deeper into the studies than just the conclusions reached. Maybe you have better resources at locating them than me.
Alan (Electrical Engineer with an interest in health issues)
Magpiezoe
03-12-2002, 01:02 PM
Hello Arkiao and hunter 44, Please correct me if I am wrong, but you both seem to believe in the low-carb. diet. I was wondering if you both have reduced your cholesterol, LDL, and triglyceride successfully through this type of diet? Also do you how much high fat foods do you really eat or do you balance your intake? I'm sticking to what works for me, but everyone is different and what works for one person may not work for another.
------------------
Magpie
------------------
Magpie
arkie6
03-12-2002, 08:35 PM
I never checked my cholesterol levels before I started low carbing. The first time I did check them after I started my total cholesterol was 199. I forget the other numbers, but nothing was abnormal. My last cholesterol check about a year ago and 3 years after starting this low carb diet, my total cholesterol was 187, HDL was 60, and triglycerides were 115. I forget what LDL was exactly, but it was somewhere in the low 100's. My bloodpressure tends to run 110-115/60-65. I'm 36 years old, 6'0" tall, and 185 lbs. with a 34" waist.
What do I eat? Lots of red meat including grass fed beef, venison, pork, and fish also. About 2 dozen eggs per week. I cook with lard, bacon grease, butter, olive oil, and unrefined coconut oil. I eat lots of green vegetables also. I eat virtualy no sugar or starchy foods (anything made from grain or potatoes).
Alan
What do I eat? Lots of red meat including grass fed beef, venison, pork, and fish also. About 2 dozen eggs per week. I cook with lard, bacon grease, butter, olive oil, and unrefined coconut oil. I eat lots of green vegetables also. I eat virtualy no sugar or starchy foods (anything made from grain or potatoes).
Alan
Carreen
03-12-2002, 10:54 PM
LooneyJM,
Debakey is a smart man. He continued to study cytomegalovirus and it's association with CHD since 1983. (For the sake of space I wrote the conclusions of most of these studies followed by the URL if you'd like to see the abstract.) There are many, many more that you can look up yourself of you so desire.
In 1993 Debakey wrote:
Eur Heart J 1993 Dec;14 Suppl K:30-8
Cytomegalovirus and atherosclerosis.
Melnick JL, Adam E, Debakey ME.
Division of Molecular Virology, Baylor College of Medicine, Houston, Texas 77030.
An avian herpesvirus is known to cause atherosclerosis in chickens. The same virus can induce a proliferative disease, malignant lymphoma, suggesting that this agent may also have transforming potential and thus stimulate the proliferation of arterial smooth muscle cells, a prominent feature of atherogenesis. The evidence for involvement of cytomegalovirus (CMV), a member of the human herpesvirus family, in atherosclerosis is much more circumstantial. The finding of CMV antigen and nucleic acid sequences in arterial smooth muscle cells of humans suggests that viral infection of the arterial wall may be common in the general population, including patients with severe atherosclerosis. In seroepidemiological studies, high levels of CMV antibodies were found to be associated with clinically manifest atherosclerotic disease, suggesting that a periodically activated latent infection or a continuously active infection is present in patients with atherosclerosis. Since the viral genome but not infectious virus is found in arterial cells, the artery itself may be the site of CMV latency. Of particular significance is the recent finding that heart transplant recipients, who are immunosuppressed, and who are also actively infected with CMV, are prone to develop accelerated atherosclerosis in the transplanted organ. Although suggestive, these observations by themselves do not demonstrate that viruses have a role in the pathogenesis of atherosclerosis, but they support a working hypothesis of the steps involved.
In 1997 he wrote:
Cent Eur J Public Health 1997 Sep;5(3):99-106
Cytomegalovirus infection and atherosclerosis.
Adam E, Melnick JL, DeBakey ME.
Division of Molecular Virology, Baylor College of Medicine, Houston, Texas 77030-3498, USA.
The biological properties of human cytomegalovirus are consistent with pathogenic involvement at several levels of the atherogenic process. Although the sites of latency of CMV have not been established, both smooth muscle cells and leukocytes are likely possibilities. The observations of viral antigens and nucleic acid sequences in arterial smooth muscle cells suggest that latent CMV infection of the arterial wall may be common in patients with atherosclerosis. The seroepidemiologic studies suggest that a periodically activated latent infection is present in patients with atherosclerosis. Important are the observations that in immunosuppressed heart transplant patients infected with CMV, atherosclerosis is prone to develop in the transplanted heart. This mainly circumstantial evidence of the involvement of CMV in human atherosclerosis provides an important basis for further investigation of the role of CMV in atherogenesis.
Note the last sentence. He indicated that his own conclusions were CIRCUMSTANTIAL, further investigation was necessary.
Below is some further investigation done in 1998.
J Infect Dis 1998 Jan;177(1):209-12
Prior infection with cytomegalovirus is not a major risk factor for angiographically demonstrated coronary artery atherosclerosis.
CONCLUSION: data suggest that CMV infection is not a major risk factor for the development of primary CAD in adults. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9419190&dopt=Abstract
Further investigation in 1999:
Circulation 1999 Mar 16;99(10):1290-4
Prior cytomegalovirus infection and the risk of restenosis after percutaneous transluminal coronary balloon angioplasty.
CONCLUSION: Data indicate that prior CMV infection, in contrast to optimal atherectomy, is not associated with chronic restenosis after conventional coronary balloon angioplasty. The results do not support a possible benefit from antiviral therapy. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10077511&dopt=Abstract
J Infect Dis 1999 Mar;179(3):690-2
Cytomegalovirus infection and coronary heart disease: results of a german case-control study.
CONCLUSION: serologic evidence of previous infection with CMV was not a major risk factor for CHD in this population. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9952378&dopt=Abstract
J Cardiovasc Risk 1999 Dec;6(6):387-90
Risk factors for coronary heart disease and persistent infection with Chlamydia pneumoniae or cytomegalovirus: a population-based study.
CONCLUSION: Serological evidence of persistent infection with C. pneumoniae or cytomegalovirus in this population was not strongly associated with most standard vascular risk factors and other characteristics. The main implication is that such risk factors are not likely to be important confounders or mediators of the reported associations between coronary heart disease and these agents. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10817084&dopt=Abstract
Further investigation in 2001:
Pol Arch Med Wewn 2001 Jan;105(1):39-44
[Influence of Chlamydia pneumoniae and cytomegalovirus infections on prevalence and the course of coronary artery disease]
CONCLUSION: We did not find a positive association of either infection markers with coronary atherosclerosis advancement. We did not find correlation of clinical restenosis after PCI with markers of CMV infection. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11505697&dopt=Abstract
Dr. DeBakey also wrote:
J Am Diet Assoc 1986 Jun;86(6):729-31 Related Articles, Books, LinkOut Diet, nutrition, and heart disease.
DeBakey ME, Gotto AM Jr, Scott LW, Foreyt JP.
Everyone should know his or her cholesterol level. The means are now available for lowering cholesterol in the general population. Such efforts should be coupled with identification of moderate- and high-risk individuals for whom special efforts should be made in cholesterol lowering. The dietary approach outlined by the American Heart Association, which is clearly described in The Living Heart Diet (6), provides the best overall strategy for reducing cholesterol and for battling the epidemic of cardiovascular deaths that represents the No. 1 health problem in our society. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3711556&dopt=Abstract
There is plenty of evidence that a simple number (LDL) being below a certain level has nothing to do with coronary artery disease. Where is this evidence?
Debakey is a smart man. He continued to study cytomegalovirus and it's association with CHD since 1983. (For the sake of space I wrote the conclusions of most of these studies followed by the URL if you'd like to see the abstract.) There are many, many more that you can look up yourself of you so desire.
In 1993 Debakey wrote:
Eur Heart J 1993 Dec;14 Suppl K:30-8
Cytomegalovirus and atherosclerosis.
Melnick JL, Adam E, Debakey ME.
Division of Molecular Virology, Baylor College of Medicine, Houston, Texas 77030.
An avian herpesvirus is known to cause atherosclerosis in chickens. The same virus can induce a proliferative disease, malignant lymphoma, suggesting that this agent may also have transforming potential and thus stimulate the proliferation of arterial smooth muscle cells, a prominent feature of atherogenesis. The evidence for involvement of cytomegalovirus (CMV), a member of the human herpesvirus family, in atherosclerosis is much more circumstantial. The finding of CMV antigen and nucleic acid sequences in arterial smooth muscle cells of humans suggests that viral infection of the arterial wall may be common in the general population, including patients with severe atherosclerosis. In seroepidemiological studies, high levels of CMV antibodies were found to be associated with clinically manifest atherosclerotic disease, suggesting that a periodically activated latent infection or a continuously active infection is present in patients with atherosclerosis. Since the viral genome but not infectious virus is found in arterial cells, the artery itself may be the site of CMV latency. Of particular significance is the recent finding that heart transplant recipients, who are immunosuppressed, and who are also actively infected with CMV, are prone to develop accelerated atherosclerosis in the transplanted organ. Although suggestive, these observations by themselves do not demonstrate that viruses have a role in the pathogenesis of atherosclerosis, but they support a working hypothesis of the steps involved.
In 1997 he wrote:
Cent Eur J Public Health 1997 Sep;5(3):99-106
Cytomegalovirus infection and atherosclerosis.
Adam E, Melnick JL, DeBakey ME.
Division of Molecular Virology, Baylor College of Medicine, Houston, Texas 77030-3498, USA.
The biological properties of human cytomegalovirus are consistent with pathogenic involvement at several levels of the atherogenic process. Although the sites of latency of CMV have not been established, both smooth muscle cells and leukocytes are likely possibilities. The observations of viral antigens and nucleic acid sequences in arterial smooth muscle cells suggest that latent CMV infection of the arterial wall may be common in patients with atherosclerosis. The seroepidemiologic studies suggest that a periodically activated latent infection is present in patients with atherosclerosis. Important are the observations that in immunosuppressed heart transplant patients infected with CMV, atherosclerosis is prone to develop in the transplanted heart. This mainly circumstantial evidence of the involvement of CMV in human atherosclerosis provides an important basis for further investigation of the role of CMV in atherogenesis.
Note the last sentence. He indicated that his own conclusions were CIRCUMSTANTIAL, further investigation was necessary.
Below is some further investigation done in 1998.
J Infect Dis 1998 Jan;177(1):209-12
Prior infection with cytomegalovirus is not a major risk factor for angiographically demonstrated coronary artery atherosclerosis.
CONCLUSION: data suggest that CMV infection is not a major risk factor for the development of primary CAD in adults. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9419190&dopt=Abstract
Further investigation in 1999:
Circulation 1999 Mar 16;99(10):1290-4
Prior cytomegalovirus infection and the risk of restenosis after percutaneous transluminal coronary balloon angioplasty.
CONCLUSION: Data indicate that prior CMV infection, in contrast to optimal atherectomy, is not associated with chronic restenosis after conventional coronary balloon angioplasty. The results do not support a possible benefit from antiviral therapy. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10077511&dopt=Abstract
J Infect Dis 1999 Mar;179(3):690-2
Cytomegalovirus infection and coronary heart disease: results of a german case-control study.
CONCLUSION: serologic evidence of previous infection with CMV was not a major risk factor for CHD in this population. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9952378&dopt=Abstract
J Cardiovasc Risk 1999 Dec;6(6):387-90
Risk factors for coronary heart disease and persistent infection with Chlamydia pneumoniae or cytomegalovirus: a population-based study.
CONCLUSION: Serological evidence of persistent infection with C. pneumoniae or cytomegalovirus in this population was not strongly associated with most standard vascular risk factors and other characteristics. The main implication is that such risk factors are not likely to be important confounders or mediators of the reported associations between coronary heart disease and these agents. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10817084&dopt=Abstract
Further investigation in 2001:
Pol Arch Med Wewn 2001 Jan;105(1):39-44
[Influence of Chlamydia pneumoniae and cytomegalovirus infections on prevalence and the course of coronary artery disease]
CONCLUSION: We did not find a positive association of either infection markers with coronary atherosclerosis advancement. We did not find correlation of clinical restenosis after PCI with markers of CMV infection. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11505697&dopt=Abstract
Dr. DeBakey also wrote:
J Am Diet Assoc 1986 Jun;86(6):729-31 Related Articles, Books, LinkOut Diet, nutrition, and heart disease.
DeBakey ME, Gotto AM Jr, Scott LW, Foreyt JP.
Everyone should know his or her cholesterol level. The means are now available for lowering cholesterol in the general population. Such efforts should be coupled with identification of moderate- and high-risk individuals for whom special efforts should be made in cholesterol lowering. The dietary approach outlined by the American Heart Association, which is clearly described in The Living Heart Diet (6), provides the best overall strategy for reducing cholesterol and for battling the epidemic of cardiovascular deaths that represents the No. 1 health problem in our society. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3711556&dopt=Abstract
There is plenty of evidence that a simple number (LDL) being below a certain level has nothing to do with coronary artery disease. Where is this evidence?
Carreen
03-12-2002, 11:01 PM
Hi Hunter,
Well - here is a quote directly from the famous "Framingham Study" that is used for the guidelines that all the doctors refer to:
That wasn't a quote from the Framingham study. It is a quote from Mary Enig's (for profit) paper called the "Oiling of America". It is her OPINION.
Well - here is a quote directly from the famous "Framingham Study" that is used for the guidelines that all the doctors refer to:
That wasn't a quote from the Framingham study. It is a quote from Mary Enig's (for profit) paper called the "Oiling of America". It is her OPINION.
Carreen
03-12-2002, 11:06 PM
Hi arkie,
I guess you totally ignored the scientific references they use to support their stance since the direction of the article didn't agree with your narrow view, that is, assuming you even read the article.
Mary Enig (weston price), Gary Tauber (reporter), and Uffe Ravnskov (trying to sell a book), are hardly what I consider scientific references. Weston Price has been dead for 54 years. He was a dentist who maintained that sugar causes not only tooth decay but physical, mental, moral, and social decay as well. Price made a whirlwind tour of primitive areas, examined the natives superficially, and jumped to simplistic conclusions. While extolling their health, he ignored their short life expectancy and high rates of infant mortality, endemic diseases, and malnutrition. While praising their diets for not producing cavities, he ignored the fact that malnourished people don't usually get many cavities. The Weston Price Memorial Foundation and it's newsletter, book catalog, and information service promote food faddism, megavitamin therapy, homeopathy, chelation therapy, and many other dubious practices.
Carreen, you always defend the medical/pharmaceutical establishment and the status quo in medicine in your posts (in this forum and others). I sense that your financial well being is somehow tied to this profession. Is that correct? If you don't mind, how about telling the folks here what you do for a living.
You say this as if it's a bad thing. :) I'm a research scientist in genzyme molecular oncology (the study of how enzymes and genes relate to cancer and treatment for cancer). Before I became a researcher, I practiced medicine. I don't defend "the medical/pharmaceutical establishment and the status quo in medicine", I defend the relevance of using rigorously controlled, objectively interpreted independent clinical trials as the basis for medical evidence and treatment. Bottom line is anyone can write a book or make a webpage saying whatever they want. <<This isn't science. The critical factor is objective, scientific, evidence-based data collected from carefully drawn experiments and clinical trials, which are then used to show that clinical care and medicines used are sound, scientific, effective, not harmful, and beneficial. <<This is science.
Ok, you've made the claim, now show me some sound scientific references to support that claim. I honestly can't find them, especially if you look deeper into the studies than just the conclusions reached. Maybe you have better resources at locating them than me.
References used for the NCEP(National Cholesterol Education Program):
Scandinavian Simvastatin Survival Study (Scandinavian
Simvastatin Survival Study Group 1994)
Asymptomatic Carotid Atherosclerosis Study (Executive
Committee for the Asymptomatic Carotid Atherosclerosis Study
1995)
Air Force/Texas Coronary Atherosclerosis Prevention Study
(Downs et al., 1998)
Antihypertensive and Lipid Lowering Treatment to Prevent Heart
Attack Trial (Davis et al., 1996)
Atherosclerosis Risk in Communities (Bensen et al., 1999)
Atorvastatin Versus Revascularization Trial (Pitt et al., 1999)
Bezafibrate Coronary Atherosclerosis Intervention Trial (Ericsson
et al., 1996)
Boeing Employees Fat Intervention Trial (Walden et al., 2000)
Bezafibrate Infarction Prevention (Bezafibrate Infarction
Prevention [BIP] Study 2000)
Cholesterol and Recurrent Events Trial (Sacks et al., 1996)
Beta-Carotene and Retinol Efficacy Trial (Omenn et al., 1996)
Coronary Artery Regression Study Group (Tamura et al., 1997)
Carotid Artery Stenosis with Asymptomatic Narrowing: Operation
Versus Aspirin (The CASANOVA Study Group 1991)
Canadian Coronary Atherosclerosis Intervention Trial (Waters
et al., 1994)
Coronary Drug Project (Coronary Drug Project Research Group
1975)
Cambridge Heart Antioxidant Study (Stephens et al., 1996)
Multicenter Coronary Intervention Study (Bestehorn et al., 1997)
Cholesterol Lowering Atherosclerosis Study (Blankenhorn et al.,
Comparative dose efficacy study of atorvastatin versus simvastatin,
pravastatin, lovastatin and fluvastatin in patients with
hypercholesterolemia (Jones et al., 1998)
Diet and Reinfarction Trial (Burr et al., 1989)
Diabetes Control and Complications Trial (Diabetes Control and
Complications Trial 1993)
Dietary Intervention Study in Children (Obarzanek et al., 1997)
European Carotid Surgery Trial (Barnett et al., 1998; Randomised
trial . . . carotid stenosis 1998)
Expanded Clinical Evaluation of Lovastatin (Bradford et al., 1991)
Familial Atherosclerosis Treatment Study (Brown et al., 1990)
Harvard Atherosclerosis Reversibility Project (Sacks et al., 1994)
HDL Atherosclerosis Treatment Study (Brown et al., 2000a)
Heidelberg (Schuler et al., 1992)
Helsinki Heart Study (Frick et al., 1987; Huttunen et al., 1991;
1994)
Heart and Estrogen/Progestin Replacement Study (Hulley et al.,
1998)
Heart Outcomes Prevention Evaluation Study (Heart Outcomes
Prevention Evaluation Study Investigators 2000a,b)
International Nifedipine Trial on Antiatherosclerotic Therapy
(Lichtlen et al., 1990)
LDL-Apheresis Atherosclerosis Regression Study (Kroon et al.,
1996)
Lipoprotein and Coronary Atherosclerosis Study (West et al.,
1996)
Lifestyle Heart Trial (Ornish et al., 1990)
Long-term Intervention with Pravastatin in Ischaemic Disease
(Long-term Intervention with Pravastatin in Ischaemic Disease
[LIPID] Study Group 1998)
Lopid Coronary Angiography Trial (Frick et al., 1997)
Lipid Research Clinics Coronary Primary Prevention Trial (Glueck
et al., 1986)
Multicentre Anti-Atheroma Study (MAAS Investigators 1994)
Monitored Atherosclerosis Regression Study (Blankenhorn et al.,
1993)
Mayo Asymptomatic Carotid Endarterectomy Study (Mayo Asymptomatic Carotid Endarterectomy Study Group 1992)
Myocardial Ischemia Reduction with Aggressive Cholesterol
Lowering (Schwartz et al., 2001)
Montreal Heart Institute Study (Waters et al., 1990)
Multiple Risk Factor Intervention Trial (Multiple Risk Factor
Intervention Trial Research Group 1982)
North American Symptomatic Carotid Endarterectomy Trial
(Ferguson et al., 1999)
NHLBI Type II Coronary Intervention Study (Brensike et al.,
1984)
Pathobiological Determinants of Atherosclerosis in Youth Study
(Strong et al., 1997; 1999)
Postmenopausal Estrogen/Progestin Interventions (Cushman et al.,
1999)
Pravastatin Limitation of Atherosclerosis in the Coronary Arteries
(Pitt et al., 1995)
Program on the Surgical Control of the Hyperlipidemias
(Buchwald et al., 1990)
Post Coronary Artery Bypass Graft (Post Coronary Artery Bypass
Graft Trial Investigators 1997)
Regression Growth Evaluation Statin Study (Jukema et al., 1995;
Aengevaeren et al., 1997)
San Francisco Arteriosclerosis Specialized Center of Research
(Kane et al., 1990)
Stanford Coronary Risk Intervention Project (Haskell et al., 1994)
Systolic Hypertension in Elderly Program (SHEP Cooperative
Research Group 1991)
St.Thomas’ Atherosclerosis Regression Study (Watts et al., 1992)
United Kingdom Prospective Diabetes Study (UK Prospective
Diabetes Study [UKPDS] Group 1998a,b,c,d)
Veterans Affairs HDL Intervention Trial (Rubins et al., 1999)
Veterans Affairs Cooperative Study Group (Hobson et al., 1993)
World Health Organization Clofibrate Study (Committee of
Principal Investigators 1978)
West of Scotland Coronary Prevention Study (Shepherd et al.,
1995a)
Here are another 99 pages of references used in the ATP3 (Adult Treatment Panel III)
http://www.nhlbi.nih.gov/guidelines/cholesterol/referenc.pdf
I guess you totally ignored the scientific references they use to support their stance since the direction of the article didn't agree with your narrow view, that is, assuming you even read the article.
Mary Enig (weston price), Gary Tauber (reporter), and Uffe Ravnskov (trying to sell a book), are hardly what I consider scientific references. Weston Price has been dead for 54 years. He was a dentist who maintained that sugar causes not only tooth decay but physical, mental, moral, and social decay as well. Price made a whirlwind tour of primitive areas, examined the natives superficially, and jumped to simplistic conclusions. While extolling their health, he ignored their short life expectancy and high rates of infant mortality, endemic diseases, and malnutrition. While praising their diets for not producing cavities, he ignored the fact that malnourished people don't usually get many cavities. The Weston Price Memorial Foundation and it's newsletter, book catalog, and information service promote food faddism, megavitamin therapy, homeopathy, chelation therapy, and many other dubious practices.
Carreen, you always defend the medical/pharmaceutical establishment and the status quo in medicine in your posts (in this forum and others). I sense that your financial well being is somehow tied to this profession. Is that correct? If you don't mind, how about telling the folks here what you do for a living.
You say this as if it's a bad thing. :) I'm a research scientist in genzyme molecular oncology (the study of how enzymes and genes relate to cancer and treatment for cancer). Before I became a researcher, I practiced medicine. I don't defend "the medical/pharmaceutical establishment and the status quo in medicine", I defend the relevance of using rigorously controlled, objectively interpreted independent clinical trials as the basis for medical evidence and treatment. Bottom line is anyone can write a book or make a webpage saying whatever they want. <<This isn't science. The critical factor is objective, scientific, evidence-based data collected from carefully drawn experiments and clinical trials, which are then used to show that clinical care and medicines used are sound, scientific, effective, not harmful, and beneficial. <<This is science.
Ok, you've made the claim, now show me some sound scientific references to support that claim. I honestly can't find them, especially if you look deeper into the studies than just the conclusions reached. Maybe you have better resources at locating them than me.
References used for the NCEP(National Cholesterol Education Program):
Scandinavian Simvastatin Survival Study (Scandinavian
Simvastatin Survival Study Group 1994)
Asymptomatic Carotid Atherosclerosis Study (Executive
Committee for the Asymptomatic Carotid Atherosclerosis Study
1995)
Air Force/Texas Coronary Atherosclerosis Prevention Study
(Downs et al., 1998)
Antihypertensive and Lipid Lowering Treatment to Prevent Heart
Attack Trial (Davis et al., 1996)
Atherosclerosis Risk in Communities (Bensen et al., 1999)
Atorvastatin Versus Revascularization Trial (Pitt et al., 1999)
Bezafibrate Coronary Atherosclerosis Intervention Trial (Ericsson
et al., 1996)
Boeing Employees Fat Intervention Trial (Walden et al., 2000)
Bezafibrate Infarction Prevention (Bezafibrate Infarction
Prevention [BIP] Study 2000)
Cholesterol and Recurrent Events Trial (Sacks et al., 1996)
Beta-Carotene and Retinol Efficacy Trial (Omenn et al., 1996)
Coronary Artery Regression Study Group (Tamura et al., 1997)
Carotid Artery Stenosis with Asymptomatic Narrowing: Operation
Versus Aspirin (The CASANOVA Study Group 1991)
Canadian Coronary Atherosclerosis Intervention Trial (Waters
et al., 1994)
Coronary Drug Project (Coronary Drug Project Research Group
1975)
Cambridge Heart Antioxidant Study (Stephens et al., 1996)
Multicenter Coronary Intervention Study (Bestehorn et al., 1997)
Cholesterol Lowering Atherosclerosis Study (Blankenhorn et al.,
Comparative dose efficacy study of atorvastatin versus simvastatin,
pravastatin, lovastatin and fluvastatin in patients with
hypercholesterolemia (Jones et al., 1998)
Diet and Reinfarction Trial (Burr et al., 1989)
Diabetes Control and Complications Trial (Diabetes Control and
Complications Trial 1993)
Dietary Intervention Study in Children (Obarzanek et al., 1997)
European Carotid Surgery Trial (Barnett et al., 1998; Randomised
trial . . . carotid stenosis 1998)
Expanded Clinical Evaluation of Lovastatin (Bradford et al., 1991)
Familial Atherosclerosis Treatment Study (Brown et al., 1990)
Harvard Atherosclerosis Reversibility Project (Sacks et al., 1994)
HDL Atherosclerosis Treatment Study (Brown et al., 2000a)
Heidelberg (Schuler et al., 1992)
Helsinki Heart Study (Frick et al., 1987; Huttunen et al., 1991;
1994)
Heart and Estrogen/Progestin Replacement Study (Hulley et al.,
1998)
Heart Outcomes Prevention Evaluation Study (Heart Outcomes
Prevention Evaluation Study Investigators 2000a,b)
International Nifedipine Trial on Antiatherosclerotic Therapy
(Lichtlen et al., 1990)
LDL-Apheresis Atherosclerosis Regression Study (Kroon et al.,
1996)
Lipoprotein and Coronary Atherosclerosis Study (West et al.,
1996)
Lifestyle Heart Trial (Ornish et al., 1990)
Long-term Intervention with Pravastatin in Ischaemic Disease
(Long-term Intervention with Pravastatin in Ischaemic Disease
[LIPID] Study Group 1998)
Lopid Coronary Angiography Trial (Frick et al., 1997)
Lipid Research Clinics Coronary Primary Prevention Trial (Glueck
et al., 1986)
Multicentre Anti-Atheroma Study (MAAS Investigators 1994)
Monitored Atherosclerosis Regression Study (Blankenhorn et al.,
1993)
Mayo Asymptomatic Carotid Endarterectomy Study (Mayo Asymptomatic Carotid Endarterectomy Study Group 1992)
Myocardial Ischemia Reduction with Aggressive Cholesterol
Lowering (Schwartz et al., 2001)
Montreal Heart Institute Study (Waters et al., 1990)
Multiple Risk Factor Intervention Trial (Multiple Risk Factor
Intervention Trial Research Group 1982)
North American Symptomatic Carotid Endarterectomy Trial
(Ferguson et al., 1999)
NHLBI Type II Coronary Intervention Study (Brensike et al.,
1984)
Pathobiological Determinants of Atherosclerosis in Youth Study
(Strong et al., 1997; 1999)
Postmenopausal Estrogen/Progestin Interventions (Cushman et al.,
1999)
Pravastatin Limitation of Atherosclerosis in the Coronary Arteries
(Pitt et al., 1995)
Program on the Surgical Control of the Hyperlipidemias
(Buchwald et al., 1990)
Post Coronary Artery Bypass Graft (Post Coronary Artery Bypass
Graft Trial Investigators 1997)
Regression Growth Evaluation Statin Study (Jukema et al., 1995;
Aengevaeren et al., 1997)
San Francisco Arteriosclerosis Specialized Center of Research
(Kane et al., 1990)
Stanford Coronary Risk Intervention Project (Haskell et al., 1994)
Systolic Hypertension in Elderly Program (SHEP Cooperative
Research Group 1991)
St.Thomas’ Atherosclerosis Regression Study (Watts et al., 1992)
United Kingdom Prospective Diabetes Study (UK Prospective
Diabetes Study [UKPDS] Group 1998a,b,c,d)
Veterans Affairs HDL Intervention Trial (Rubins et al., 1999)
Veterans Affairs Cooperative Study Group (Hobson et al., 1993)
World Health Organization Clofibrate Study (Committee of
Principal Investigators 1978)
West of Scotland Coronary Prevention Study (Shepherd et al.,
1995a)
Here are another 99 pages of references used in the ATP3 (Adult Treatment Panel III)
http://www.nhlbi.nih.gov/guidelines/cholesterol/referenc.pdf
Carreen
03-12-2002, 11:22 PM
I've written all I'm going write on this subject as time doesn't permit me to continue with these lenghthy replies.
People will believe whatever they want and I suspect that I could post here till I'm "blue in the face" and it wouldn't change anything. :) Here's to hoping that we all learned something.
Eat well, live long.
People will believe whatever they want and I suspect that I could post here till I'm "blue in the face" and it wouldn't change anything. :) Here's to hoping that we all learned something.
Eat well, live long.
LooneyJM
03-13-2002, 10:17 AM
1. From my earlier post -
Even LIPITOR claims it hasn't been proved on thier website. It's been proved that it causes cancer and many side effects.
Anyone wish to comment?
2. Am I to believe my primary physician and cardio? They have NEVER commented/asked about my diet, loss of 50 lbs or ANY bloodwork other than LDL. My tri's went from 600 to 108 (on a diet advice found on the internet) and they say NOTHING.
3. So going with the LDL theory - If my number is 153, I'm at risk - if I take drugs and get it below 100, I can live happily everafter. I don't buy it.
4. I am hearing more and more that it's HDL and Trig's that predict heart disease.
Even LIPITOR claims it hasn't been proved on thier website. It's been proved that it causes cancer and many side effects.
Anyone wish to comment?
2. Am I to believe my primary physician and cardio? They have NEVER commented/asked about my diet, loss of 50 lbs or ANY bloodwork other than LDL. My tri's went from 600 to 108 (on a diet advice found on the internet) and they say NOTHING.
3. So going with the LDL theory - If my number is 153, I'm at risk - if I take drugs and get it below 100, I can live happily everafter. I don't buy it.
4. I am hearing more and more that it's HDL and Trig's that predict heart disease.
arkie6
03-14-2002, 01:30 AM
Originally posted by Carreen:
I think that sticking with the guidelines researched, used and approved by the agencies below is more indicative of how cholesterol and heart disease occurs as compared to some extremists on the fringe.
The question is are we getting positive benefits from following the standard advice? I think not considering the epidemic levels of diabetes and the continuing rise in heart disease even while the consumption of saturated fat has declined over the past 50 or so years. We, the consumers and taxpayers, are getting screwed by following this advice. The only ones that benefit are the health professionals, hospitals, and the pharmaceutical industry.
The National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH) launched the National Cholesterol Education Program (NCEP) in November 1985. The goal of the NCEP is to contribute to reducing illness and death from coronary heart disease (CHD) in the United States by reducing the percentage of Americans with high blood cholesterol. Through educational efforts directed at health professionals and the public, the NCEP aims to raise awareness and understanding about high blood cholesterol as a risk factor for CHD and the benefits of lowering cholesterol levels as a means of preventing CHD.
Member Organizations of the NCEP Coordinating Committee:
American Academy of Family Physicians
American Academy of Pediatrics
American Association of Occupational Health Nurses
American College of Cardiology
American College of Chest Physicians
American College of Nutrition
American College of Obstetricians and Gynecologists
American College of Occupational Medicine
American College of Preventive Medicine
American Diabetes Association, Inc.
American Dietetic Association
American Heart Association
American Hospital Association
American Medical Association
American Nurses Association
American Osteopathic Association
American Pharmaceutical Association
American Public Health Association
American Red Cross
Association of Black Cardiologists
Association of Life Insurance Medical Directors of America
Association of State and Territorial Health Officials
Citizens for Pubic Action on Blood Pressure and Cholesterol, Inc.
National Black Nurses Association, Inc.
National Heart, Lung, and Blood Institute
National Medical Association
Society for Nutrition Education
Society for Public Health Education
Associate Member Organizations of the NCEP Coordinating Committee
American Association of Office Nurses
Federal Agencies
NHLBI Ad Hoc Committee on Minority Populations
Agency for Healthcare Research and Quality
Centers for Disease Control and Prevention
Coordinating Committee for the Community Demonstration Studies
Department of Agriculture
Department of Defense
Food and Drug Administration
Health Resources and Services Administration
National Cancer Institute
National Center for Health Statistics
Office of Disease Prevention and Health Promotion
Department of Veterans Affairs
Many liberal, cause-oriented, organizations aren't really interested in eliminating the problem they are "addressing". If they ever actually solved the problem, that would eliminate their fund raising as well as their source of employment. They would rather talk about it, fear-monger it, raise more money to "fight for the cause". But heaven help us, don't actually fix the problem!
Alan
I think that sticking with the guidelines researched, used and approved by the agencies below is more indicative of how cholesterol and heart disease occurs as compared to some extremists on the fringe.
The question is are we getting positive benefits from following the standard advice? I think not considering the epidemic levels of diabetes and the continuing rise in heart disease even while the consumption of saturated fat has declined over the past 50 or so years. We, the consumers and taxpayers, are getting screwed by following this advice. The only ones that benefit are the health professionals, hospitals, and the pharmaceutical industry.
The National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH) launched the National Cholesterol Education Program (NCEP) in November 1985. The goal of the NCEP is to contribute to reducing illness and death from coronary heart disease (CHD) in the United States by reducing the percentage of Americans with high blood cholesterol. Through educational efforts directed at health professionals and the public, the NCEP aims to raise awareness and understanding about high blood cholesterol as a risk factor for CHD and the benefits of lowering cholesterol levels as a means of preventing CHD.
Member Organizations of the NCEP Coordinating Committee:
American Academy of Family Physicians
American Academy of Pediatrics
American Association of Occupational Health Nurses
American College of Cardiology
American College of Chest Physicians
American College of Nutrition
American College of Obstetricians and Gynecologists
American College of Occupational Medicine
American College of Preventive Medicine
American Diabetes Association, Inc.
American Dietetic Association
American Heart Association
American Hospital Association
American Medical Association
American Nurses Association
American Osteopathic Association
American Pharmaceutical Association
American Public Health Association
American Red Cross
Association of Black Cardiologists
Association of Life Insurance Medical Directors of America
Association of State and Territorial Health Officials
Citizens for Pubic Action on Blood Pressure and Cholesterol, Inc.
National Black Nurses Association, Inc.
National Heart, Lung, and Blood Institute
National Medical Association
Society for Nutrition Education
Society for Public Health Education
Associate Member Organizations of the NCEP Coordinating Committee
American Association of Office Nurses
Federal Agencies
NHLBI Ad Hoc Committee on Minority Populations
Agency for Healthcare Research and Quality
Centers for Disease Control and Prevention
Coordinating Committee for the Community Demonstration Studies
Department of Agriculture
Department of Defense
Food and Drug Administration
Health Resources and Services Administration
National Cancer Institute
National Center for Health Statistics
Office of Disease Prevention and Health Promotion
Department of Veterans Affairs
Many liberal, cause-oriented, organizations aren't really interested in eliminating the problem they are "addressing". If they ever actually solved the problem, that would eliminate their fund raising as well as their source of employment. They would rather talk about it, fear-monger it, raise more money to "fight for the cause". But heaven help us, don't actually fix the problem!
Alan
arkie6
03-14-2002, 01:43 AM
Originally posted by Carreen:
References used for the NCEP(National Cholesterol Education Program): ...................
Well, I see you posted lots of study titles.
Without seeing at least the abstracts and conclusions, no conclusion can be drawn from these. Did the studies show any significant connection between diet, cholesterol levels, and heart disease? Who knows based on the info provided. And like you, I don't have the time to dig up every one of these studies and review the study design and conclusions. I did note that many of the studies involved statin drugs, no doubt funded by pharmaceutical companies. I sometimes wonder what is the real goal of NCEP. Is it to improve peoples health or to assist the pharmaceutical industry in peddling its products?
Alan
References used for the NCEP(National Cholesterol Education Program): ...................
Well, I see you posted lots of study titles.
Without seeing at least the abstracts and conclusions, no conclusion can be drawn from these. Did the studies show any significant connection between diet, cholesterol levels, and heart disease? Who knows based on the info provided. And like you, I don't have the time to dig up every one of these studies and review the study design and conclusions. I did note that many of the studies involved statin drugs, no doubt funded by pharmaceutical companies. I sometimes wonder what is the real goal of NCEP. Is it to improve peoples health or to assist the pharmaceutical industry in peddling its products?
Alan
Carreen
03-15-2002, 08:10 AM
Loonyjm,
1. From my earlier post -
Even LIPITOR claims it hasn't been proved on thier website. It's been proved that it causes cancer and many side effects.
Anyone wish to comment?
I did comment. :) Lipitor(or other statin) don't claim to prevent heart disease or heart attacks. It's a synthetic lipid lowering agent not a heart attack preventer. Show us some medical studies or proof of your claim that Lipitor causes cancer.
2. Am I to believe my primary physician and cardio? They have NEVER commented/asked about my diet, loss of 50 lbs or ANY bloodwork other than LDL. My tri's went from 600 to 108 (on a diet advice found on the internet) and they say NOTHING.
The ineptness of your physicians doesn't indicate that all the research ever done is invalid.
3. So going with the LDL theory - If my number is 153, I'm at risk - if I take drugs and get it below 100, I can live happily everafter. I don't buy it.
Not exactly, there are other risk factors to consider and even if you do everything "by the book" you could still have a coronary event. There is no guarantee. It's all about risk. You can choose "not to buy it" but that doesn't make it not so.
4. I am hearing more and more that it's HDL and Trig's that predict heart disease.
HDL and Trigs are part of the picture but not the finished product.
1. From my earlier post -
Even LIPITOR claims it hasn't been proved on thier website. It's been proved that it causes cancer and many side effects.
Anyone wish to comment?
I did comment. :) Lipitor(or other statin) don't claim to prevent heart disease or heart attacks. It's a synthetic lipid lowering agent not a heart attack preventer. Show us some medical studies or proof of your claim that Lipitor causes cancer.
2. Am I to believe my primary physician and cardio? They have NEVER commented/asked about my diet, loss of 50 lbs or ANY bloodwork other than LDL. My tri's went from 600 to 108 (on a diet advice found on the internet) and they say NOTHING.
The ineptness of your physicians doesn't indicate that all the research ever done is invalid.
3. So going with the LDL theory - If my number is 153, I'm at risk - if I take drugs and get it below 100, I can live happily everafter. I don't buy it.
Not exactly, there are other risk factors to consider and even if you do everything "by the book" you could still have a coronary event. There is no guarantee. It's all about risk. You can choose "not to buy it" but that doesn't make it not so.
4. I am hearing more and more that it's HDL and Trig's that predict heart disease.
HDL and Trigs are part of the picture but not the finished product.
Carreen
03-15-2002, 10:05 AM
HI arkie,
The question is are we getting positive benefits from following the standard advice? I think not considering the epidemic levels of diabetes and the continuing rise in heart disease even while the consumption of saturated fat has declined over the past 50 or so years. We, the consumers and taxpayers, are getting screwed by following this advice. The only ones that benefit are the health professionals, hospitals, and the pharmaceutical industry.
There has been no continuing rise in heart diease. In fact Age-adjusted death rates per 100,000 persons (standardized to the 1940 U.S. population) for diseases of the heart (i.e., coronary heart disease, hypertensive heart disease, and rheumatic heart disease) have decreased from a peak of 307.4 in 1950 to 134.6 in 1996, an overall decline of 56%.
Age-adjusted death rates for stroke have declined steadily since the beginning of the century. Since 1950, stroke rates have declined 70%, from 88.8 in 1950 to 26.5 in 1996.
Reasons for the declines in heart disease and stroke may vary by period and across region or socioeconomic groups (e.g., age, sex, and racial/ethnic groups). Prevention efforts and improvements in early detection, treatment, and care have resulted in a number of beneficial trends which may have contributed to declines in heart disease and stroke. These trends include:
**a decline in cigarette smoking among adults aged greater than or equal to 18 years from approximately 42% in 1965 to 25% in 1995
**a decrease in mean blood pressure levels in the U.S. population
**an increase in the percentage of persons with hypertension who have the condition treated and controlled
**a decrease in mean blood cholesterol levels
**changes in the U.S. diet. Data based on surveys of food supply suggest that consumption of saturated fat and cholesterol has decreased since 1909. Data from the National Health and Nutrition Examination surveys suggest that decreases in the percentage of calories from dietary fat and the levels of dietary cholesterol coincide with decreases in blood cholesterol levels.
**improvements in medical care, including advances in diagnosing and treating heart disease and stroke, development of effective medications for treatment of hypertension and hypercholesterolemia, greater numbers of specialists and health-care providers focusing on CVD, an increase in emergency medical services for heart attack and stroke, and an increase in coronary-care units.
These developments have contributed to lower case-fatality rates, lengthened survival times, and shorter hospital stays for persons with CVD.
Diabetes is on the increase. Effective intervention strategies are urgently needed for the primary prevention of diabetes. Currently, clinical trials are ongoing to determine whether type 2 diabetes (the most prevalent form of diabetes, accounting for 90%-95% of diabetes) and type 1 diabetes can be prevented.
Many liberal, cause-oriented, organizations aren't really interested in eliminating the problem they are "addressing". If they ever actually solved the problem, that would eliminate their fund raising as well as their source of employment. They would rather talk about it, fear-monger it, raise more money to "fight for the cause". But heaven help us, don't actually fix the problem!
Arkie, you're using flawed logic, engaging in clever usage and misapplications of terms, and accuse others of "conspiracy theories", and other bogeymen, to suggest that some pharmaceutical company-medical establishment cartel is trying to keep "them" from "saving money" for the public by withholding treatments and methods which allegedly "work", but can be done for very little money by medically unqualified individuals. Nothing is further from factual reality. This is simply paranoid.
The "medical establishment" is not a single entity. The health-care industry includes physicians, nurses, other health professionals, insurance companies, private consumer organizations, universities, government agencies, hospitals, insurance programs, professional organizations, pharmaceutical companies, and other private corporations. These groups may have competing interests. Within each group, individual members may also have competing interests, and many have no financial stake in patient care. It would take one heck of a cover up to keep these thousands of people quiet.
Remember, too, that physicians, basic scientists, and even pharmaceutical company executives, are people with family and loved ones of their own. Conspiracy theorists seem to ignore the fact that the very people who are supposed to be suppressing cures, might need them for their family and friends, or for themselves. It is difficult to imagine that anyone could be greedy and shortsighted enough to condemn their loved ones -- and even themselves -- to a premature death, no matter what the possible gain. In other words, most of us wouldn't sell our kids down the river to "supress" a cure for a disease because we'd fear some unknown pharmaceutical hitman would be waiting for us.
There are thousands of diseases to work on and cure. I don't think anyone is going to run out of work to do soon.
Well, I see you posted lots of study titles.
Without seeing at least the abstracts and conclusions, no conclusion can be drawn from these. Did the studies show any significant connection between diet, cholesterol levels, and heart disease? Who knows based on the info provided. And like you, I don't have the time to dig up every one of these studies and review the study design and conclusions. I did note that many of the studies involved statin drugs, no doubt funded by pharmaceutical companies.
I didn't know you wanted me to do your work too. ;) Listen, you don't have to take one look at any of those or try and learn anything. You asked me to post proof and I posted proof. You, being the one who requested it may have had the time to look up a few to see if indeed you could be mistaken. You've never proven anything you've said here. It's all just what you think. Show us some research to prove your ascertations I'd really like to see it.
Live long, Eat well
The question is are we getting positive benefits from following the standard advice? I think not considering the epidemic levels of diabetes and the continuing rise in heart disease even while the consumption of saturated fat has declined over the past 50 or so years. We, the consumers and taxpayers, are getting screwed by following this advice. The only ones that benefit are the health professionals, hospitals, and the pharmaceutical industry.
There has been no continuing rise in heart diease. In fact Age-adjusted death rates per 100,000 persons (standardized to the 1940 U.S. population) for diseases of the heart (i.e., coronary heart disease, hypertensive heart disease, and rheumatic heart disease) have decreased from a peak of 307.4 in 1950 to 134.6 in 1996, an overall decline of 56%.
Age-adjusted death rates for stroke have declined steadily since the beginning of the century. Since 1950, stroke rates have declined 70%, from 88.8 in 1950 to 26.5 in 1996.
Reasons for the declines in heart disease and stroke may vary by period and across region or socioeconomic groups (e.g., age, sex, and racial/ethnic groups). Prevention efforts and improvements in early detection, treatment, and care have resulted in a number of beneficial trends which may have contributed to declines in heart disease and stroke. These trends include:
**a decline in cigarette smoking among adults aged greater than or equal to 18 years from approximately 42% in 1965 to 25% in 1995
**a decrease in mean blood pressure levels in the U.S. population
**an increase in the percentage of persons with hypertension who have the condition treated and controlled
**a decrease in mean blood cholesterol levels
**changes in the U.S. diet. Data based on surveys of food supply suggest that consumption of saturated fat and cholesterol has decreased since 1909. Data from the National Health and Nutrition Examination surveys suggest that decreases in the percentage of calories from dietary fat and the levels of dietary cholesterol coincide with decreases in blood cholesterol levels.
**improvements in medical care, including advances in diagnosing and treating heart disease and stroke, development of effective medications for treatment of hypertension and hypercholesterolemia, greater numbers of specialists and health-care providers focusing on CVD, an increase in emergency medical services for heart attack and stroke, and an increase in coronary-care units.
These developments have contributed to lower case-fatality rates, lengthened survival times, and shorter hospital stays for persons with CVD.
Diabetes is on the increase. Effective intervention strategies are urgently needed for the primary prevention of diabetes. Currently, clinical trials are ongoing to determine whether type 2 diabetes (the most prevalent form of diabetes, accounting for 90%-95% of diabetes) and type 1 diabetes can be prevented.
Many liberal, cause-oriented, organizations aren't really interested in eliminating the problem they are "addressing". If they ever actually solved the problem, that would eliminate their fund raising as well as their source of employment. They would rather talk about it, fear-monger it, raise more money to "fight for the cause". But heaven help us, don't actually fix the problem!
Arkie, you're using flawed logic, engaging in clever usage and misapplications of terms, and accuse others of "conspiracy theories", and other bogeymen, to suggest that some pharmaceutical company-medical establishment cartel is trying to keep "them" from "saving money" for the public by withholding treatments and methods which allegedly "work", but can be done for very little money by medically unqualified individuals. Nothing is further from factual reality. This is simply paranoid.
The "medical establishment" is not a single entity. The health-care industry includes physicians, nurses, other health professionals, insurance companies, private consumer organizations, universities, government agencies, hospitals, insurance programs, professional organizations, pharmaceutical companies, and other private corporations. These groups may have competing interests. Within each group, individual members may also have competing interests, and many have no financial stake in patient care. It would take one heck of a cover up to keep these thousands of people quiet.
Remember, too, that physicians, basic scientists, and even pharmaceutical company executives, are people with family and loved ones of their own. Conspiracy theorists seem to ignore the fact that the very people who are supposed to be suppressing cures, might need them for their family and friends, or for themselves. It is difficult to imagine that anyone could be greedy and shortsighted enough to condemn their loved ones -- and even themselves -- to a premature death, no matter what the possible gain. In other words, most of us wouldn't sell our kids down the river to "supress" a cure for a disease because we'd fear some unknown pharmaceutical hitman would be waiting for us.
There are thousands of diseases to work on and cure. I don't think anyone is going to run out of work to do soon.
Well, I see you posted lots of study titles.
Without seeing at least the abstracts and conclusions, no conclusion can be drawn from these. Did the studies show any significant connection between diet, cholesterol levels, and heart disease? Who knows based on the info provided. And like you, I don't have the time to dig up every one of these studies and review the study design and conclusions. I did note that many of the studies involved statin drugs, no doubt funded by pharmaceutical companies.
I didn't know you wanted me to do your work too. ;) Listen, you don't have to take one look at any of those or try and learn anything. You asked me to post proof and I posted proof. You, being the one who requested it may have had the time to look up a few to see if indeed you could be mistaken. You've never proven anything you've said here. It's all just what you think. Show us some research to prove your ascertations I'd really like to see it.
Live long, Eat well
LooneyJM
03-15-2002, 01:19 PM
Carreen,
I was referring to the data sheet about the Lipitor. After my eye doctor tols me about the dangers of statins, I read the entire thing and was scared to death! Tumors, brain seizures, etc. etc.
What scares me more are the posts here and on other message boards from users who have sleep problems, aches and pains, etc. There are no long-term statin users since they are all new - Cancer takes years to develop. Then we had the Baycol thing which may be a good thing since the lawyers are digging into the reasearch behind this.
I'm totally frustrated because everyone claims to have the answers, books, and studies to back it up.
Ornish, Gould, Pauling-Rath, Atkins and the many others. I've read many posts on newsgroups from people with perfectly normal lipid levels, yet they have heart attacks. I realize as you said, the other risk factors can't be ignored. This internet is a blessing and a curse!!!
Now I read interviews and bios from Debakey of Baylor - someone I would consider a pioneer, and he says we still don't know what causes it.
The part that irritates me is how the marketing campaign of the drug companies are trying to make it a black and white issue. Almost all my friends hear the same story - go to the doctor, cholesterol a bit high, take drugs. They rarely give them the total picture or all the options. As you say, they may be poor doctors. Perhaps they just blindly bought into the statin campaign too. I've heard many stories from a guy I know whose wife worked for a cardiology group about the way the companies wine and dine the MD salesman.
OK - I'll get off my soapbox cause I feel better now! Thanks :-)
PS - You said you're a "research scientist in genzyme molecular oncology (the study of how enzymes and genes relate to cancer and treatment for cancer)." I have no idea what is (I'm a nerdy computer scientist) but what do you think of Linus Pauling's theory? If you work with animals in research, is it true they never get heart disease?
I was referring to the data sheet about the Lipitor. After my eye doctor tols me about the dangers of statins, I read the entire thing and was scared to death! Tumors, brain seizures, etc. etc.
What scares me more are the posts here and on other message boards from users who have sleep problems, aches and pains, etc. There are no long-term statin users since they are all new - Cancer takes years to develop. Then we had the Baycol thing which may be a good thing since the lawyers are digging into the reasearch behind this.
I'm totally frustrated because everyone claims to have the answers, books, and studies to back it up.
Ornish, Gould, Pauling-Rath, Atkins and the many others. I've read many posts on newsgroups from people with perfectly normal lipid levels, yet they have heart attacks. I realize as you said, the other risk factors can't be ignored. This internet is a blessing and a curse!!!
Now I read interviews and bios from Debakey of Baylor - someone I would consider a pioneer, and he says we still don't know what causes it.
The part that irritates me is how the marketing campaign of the drug companies are trying to make it a black and white issue. Almost all my friends hear the same story - go to the doctor, cholesterol a bit high, take drugs. They rarely give them the total picture or all the options. As you say, they may be poor doctors. Perhaps they just blindly bought into the statin campaign too. I've heard many stories from a guy I know whose wife worked for a cardiology group about the way the companies wine and dine the MD salesman.
OK - I'll get off my soapbox cause I feel better now! Thanks :-)
PS - You said you're a "research scientist in genzyme molecular oncology (the study of how enzymes and genes relate to cancer and treatment for cancer)." I have no idea what is (I'm a nerdy computer scientist) but what do you think of Linus Pauling's theory? If you work with animals in research, is it true they never get heart disease?
Carreen
03-15-2002, 04:23 PM
I think one thing that tends to happen on message boards is that they are predominately people who are having some type of trouble, side effect or undiagnosed illness. What I mean is, people who are perfectly healthy don't bother signing up to a forum to say "hey, nothing is wrong with me, I'm just fine." That tends to give us a view slanted to the negative of how severe side effects or other trouble can be. Every drug will have a side effect.
I think what happens with doctors is, that we, as the patients go in and are told we have high cholesterol. They tell us loose weight, eat right, excercise, bla bla bla :) Really we get told that for everything. Most of us don't wanna do those things so we're more than willing to take a pill that will lower our cholesterol. Doctors know no one wants to hear this either. In other cases, people have fathers or mothers who dropped dead at 50 from a heart attack and they're scared. So they WANT help, they WANT to lower their risk of heart disease badly. Then there are others who think 'well I feel ok so I'll just ignore it and maybe it will go away" and still others who don't give a flying rip what their cholesterol is. :)
If you can lower your cholesterol to a safer level without any drugs that is the optimum. Or if you feel that the risk of side effects outweighs the risk of having a coronary event then don't take the drugs. But also remember MOST people don't have bad side effects. You could be one who doesn't have side effects or you could be one who doesn't give a flying rip. Bottom line is, you're in charge.
Now about Paulings:
I think Paulings did us all a disservice by continuing to rant about the greatness of vitamin c as a cure for everything including cancer when test after test and trial after trial of his theory showed he was wrong. He didn't like to be wrong :D Arthur Robinson, Ph.D was Paulings assistant. While working at the Linus Pauling Institute for Science and Medicine, Robinson conducted four studies in which cancerous mice were given different diets and vitamin supplement regimens. Nearly all of the mice developed skin cancers (squamous cell carcinomas) following exposure to ultraviolet radiation.
In 1999, Robinson commented:
The results of these experiments caused an argument between Linus and me, which ended our 16-year period of work together. He was not willing to accept the experimentally proved fact that vitamin C in ordinary doses accelerated the growth rate of squamous cell carcinoma in these mice.
At the time, Linus was promoting his claim that "75% of all cancer can be prevented and cured by vitamin C alone." This claim proved to be without experimental foundation and not true. . . . Vitamin C increased the rate of growth of cancer at human equivalents of 1 to 5 grams per day, but suppressed the cancer growth rate at doses on the order of 100 grams per day (near the lethal dose), as do other measures of malnutrition. [Robinson AB. Nutrition and Cancer. Nutrition and Cancer Web site, Dec 1999.]
Paulings died of prostate cancer. No, it isn't true that animals never get heart disease.
PS. I fall into the category of "I don't give a flying rip what my cholesterol is" :D I've never even had it tested.
[This message has been edited by Carreen (edited 03-15-2002).]
I think what happens with doctors is, that we, as the patients go in and are told we have high cholesterol. They tell us loose weight, eat right, excercise, bla bla bla :) Really we get told that for everything. Most of us don't wanna do those things so we're more than willing to take a pill that will lower our cholesterol. Doctors know no one wants to hear this either. In other cases, people have fathers or mothers who dropped dead at 50 from a heart attack and they're scared. So they WANT help, they WANT to lower their risk of heart disease badly. Then there are others who think 'well I feel ok so I'll just ignore it and maybe it will go away" and still others who don't give a flying rip what their cholesterol is. :)
If you can lower your cholesterol to a safer level without any drugs that is the optimum. Or if you feel that the risk of side effects outweighs the risk of having a coronary event then don't take the drugs. But also remember MOST people don't have bad side effects. You could be one who doesn't have side effects or you could be one who doesn't give a flying rip. Bottom line is, you're in charge.
Now about Paulings:
I think Paulings did us all a disservice by continuing to rant about the greatness of vitamin c as a cure for everything including cancer when test after test and trial after trial of his theory showed he was wrong. He didn't like to be wrong :D Arthur Robinson, Ph.D was Paulings assistant. While working at the Linus Pauling Institute for Science and Medicine, Robinson conducted four studies in which cancerous mice were given different diets and vitamin supplement regimens. Nearly all of the mice developed skin cancers (squamous cell carcinomas) following exposure to ultraviolet radiation.
In 1999, Robinson commented:
The results of these experiments caused an argument between Linus and me, which ended our 16-year period of work together. He was not willing to accept the experimentally proved fact that vitamin C in ordinary doses accelerated the growth rate of squamous cell carcinoma in these mice.
At the time, Linus was promoting his claim that "75% of all cancer can be prevented and cured by vitamin C alone." This claim proved to be without experimental foundation and not true. . . . Vitamin C increased the rate of growth of cancer at human equivalents of 1 to 5 grams per day, but suppressed the cancer growth rate at doses on the order of 100 grams per day (near the lethal dose), as do other measures of malnutrition. [Robinson AB. Nutrition and Cancer. Nutrition and Cancer Web site, Dec 1999.]
Paulings died of prostate cancer. No, it isn't true that animals never get heart disease.
PS. I fall into the category of "I don't give a flying rip what my cholesterol is" :D I've never even had it tested.
[This message has been edited by Carreen (edited 03-15-2002).]
arkie6
03-15-2002, 04:49 PM
Originally posted by Carreen:
I've written all I'm going write on this subject as time doesn't permit me to continue with these lenghthy replies.
Really?
I've written all I'm going write on this subject as time doesn't permit me to continue with these lenghthy replies.
Really?
Carreen
03-15-2002, 05:18 PM
Arkie, too bad you don't have anything more than that to contribute to the conversation.
Magpiezoe
03-15-2002, 05:34 PM
Hello Maximize22, It look like we all got into a little debate session, instead of trying to help. Sorry. I'm finding it's so easy people to debate on this board for some strange reason. A low carb. diet might work for some, but not other. The same goes for the low total fat/low cal. diet works for some and not others. Then there's the Meditarainian diet, which I haven't heard anyone mention. I had high cholesterol too. It was 239. (One point away from medicine.) Now the doctors are starting to look at the LDL/HDL ratio, because it is supposed to give a better idea of how you're doing. My doctor had me go on the low fat diet with 1400 cal. and 16-39 gram of fat, but I'm 115 lbs. My cholesterol did drop to 203, then 195. I just got my blood work back and will be picking up a copy of it for my files. I'm so HAPPY! I'm down to 179, but he said I have to stay on the diet since high cholesterol is in my history and my family's history. I still eat whatever I want, but I really keep my fat intake and cal. in check.
I really believe you have to change your diet as well as exercise. I'm a cheese lover too. I eat a lot of low-fat string cheese. (Almost 1/day.) It has 2.5 grams of total fat and 60 cal. I occationally treat myself to light cream cheese or low fat chedder. (Cracker Barrel) I hear Burger King is going to have a vegie burger, which might be ok once in a while. I have finally reached my night-time goal of exercising 60 min. I walk for 1/2 hour every morning in addition. I try to alternate days of weight barring exercise and aerobics. I hope this helps.
------------------
Magpie
I really believe you have to change your diet as well as exercise. I'm a cheese lover too. I eat a lot of low-fat string cheese. (Almost 1/day.) It has 2.5 grams of total fat and 60 cal. I occationally treat myself to light cream cheese or low fat chedder. (Cracker Barrel) I hear Burger King is going to have a vegie burger, which might be ok once in a while. I have finally reached my night-time goal of exercising 60 min. I walk for 1/2 hour every morning in addition. I try to alternate days of weight barring exercise and aerobics. I hope this helps.
------------------
Magpie
vipergg22
03-15-2002, 08:41 PM
After trying all these nice statins , I'm with you I have had it with them , willing to take this "risk" . That's all it is too a risk , doesn't mean anything will even happen to you . I've come to the conclusion it's less of a risk than driving a car.
PS. I fall into the category of "I don't give a flying rip what my cholesterol is" :D I've never even had it tested.
[This message has been edited by Carreen (edited 03-15-2002).][/B][/QUOTE]
PS. I fall into the category of "I don't give a flying rip what my cholesterol is" :D I've never even had it tested.
[This message has been edited by Carreen (edited 03-15-2002).][/B][/QUOTE]
arkie6
03-16-2002, 01:08 AM
Originally posted by Carreen:
Arkie, too bad you don't have anything more than that to contribute to the conversation.
Well, I didn't have much time for a reply when I made that previous post. I just thought it was rather odd to find three lengthy replies on this topic from you after you said you were through posting on this subject. I'll get back to the discussion at hand, even if we have strayed from the original question posed in this topic.
Alan
Arkie, too bad you don't have anything more than that to contribute to the conversation.
Well, I didn't have much time for a reply when I made that previous post. I just thought it was rather odd to find three lengthy replies on this topic from you after you said you were through posting on this subject. I'll get back to the discussion at hand, even if we have strayed from the original question posed in this topic.
Alan
arkie6
03-16-2002, 03:06 AM
Originally posted by Carreen:
There has been no continuing rise in heart diease. In fact Age-adjusted death rates per 100,000 persons (standardized to the 1940 U.S. population) for diseases of the heart (i.e., coronary heart disease, hypertensive heart disease, and rheumatic heart disease) have decreased from a peak of 307.4 in 1950 to 134.6 in 1996, an overall decline of 56%.
Whoa now. We're mixing words and terminology up here. I said heart disease has increased, not deaths from heart disease. There is a difference which I will explain.
I stated that there has been an increase in the incidence of heart disease and I stand by that statement.
The following is from the American Heart Association:
Nearly 62 million Americans have some form of cardiovascular disease, and nearly a million die from such conditions each year. Heart disease is by far the number one killer in the United States. Heart disease accounted for 40 percent of all deaths in the United States in 1999. Cardiovascular disease kills more Americans than the next seven causes combined -- including cancer -- the AHA report states. "The most surprising finding is that heart disease and stroke numbers are not going down," Dr. David Faxon, president of the AHA, told Reuters Health. "For many years, they did, but now we are seeing a leveling off, and in fact, we are seeing an increase in some groups such as African-American women." According to Faxon, reasons for the leveling off in numbers include the aging of the population and the "growing problem" of diabetes and obesity, both of which greatly increase heart disease risk.
Now deaths from heart disease have gone down, no doubt. But this isn't because of prevention measures such as lowering cholesterol. This lowering of deaths is due to better surgical techniques (coronary bypass surgury, angioplasty, etc.) and more frequent use of these measures. I have seen the numbers posted before, but couldn't locate them at the moment, but if my memory serves me correctly, there were on the order of 50,000 coronary bypass surgeries performed in the US in 1970 vs. 500,000 in 1990. This is why deaths from heart disease have gone down while the incidence of the disease has not.
Alan
There has been no continuing rise in heart diease. In fact Age-adjusted death rates per 100,000 persons (standardized to the 1940 U.S. population) for diseases of the heart (i.e., coronary heart disease, hypertensive heart disease, and rheumatic heart disease) have decreased from a peak of 307.4 in 1950 to 134.6 in 1996, an overall decline of 56%.
Whoa now. We're mixing words and terminology up here. I said heart disease has increased, not deaths from heart disease. There is a difference which I will explain.
I stated that there has been an increase in the incidence of heart disease and I stand by that statement.
The following is from the American Heart Association:
Nearly 62 million Americans have some form of cardiovascular disease, and nearly a million die from such conditions each year. Heart disease is by far the number one killer in the United States. Heart disease accounted for 40 percent of all deaths in the United States in 1999. Cardiovascular disease kills more Americans than the next seven causes combined -- including cancer -- the AHA report states. "The most surprising finding is that heart disease and stroke numbers are not going down," Dr. David Faxon, president of the AHA, told Reuters Health. "For many years, they did, but now we are seeing a leveling off, and in fact, we are seeing an increase in some groups such as African-American women." According to Faxon, reasons for the leveling off in numbers include the aging of the population and the "growing problem" of diabetes and obesity, both of which greatly increase heart disease risk.
Now deaths from heart disease have gone down, no doubt. But this isn't because of prevention measures such as lowering cholesterol. This lowering of deaths is due to better surgical techniques (coronary bypass surgury, angioplasty, etc.) and more frequent use of these measures. I have seen the numbers posted before, but couldn't locate them at the moment, but if my memory serves me correctly, there were on the order of 50,000 coronary bypass surgeries performed in the US in 1970 vs. 500,000 in 1990. This is why deaths from heart disease have gone down while the incidence of the disease has not.
Alan
arkie6
03-16-2002, 05:23 AM
Originally posted by Carreen:
Arkie, you're using flawed logic, engaging in clever usage and misapplications of terms, and accuse others of "conspiracy theories", and other bogeymen, to suggest that some pharmaceutical company-medical establishment cartel is trying to keep "them" from "saving money" for the public...
Whoa again. You are attributing words to me that I never stated. I never claimed there was a "conspiracy theory". In fact, I don't believe that to be the case. Definition of conspire as implied herein: To join in a secret agreement to do an unlawful or wrongful act or to use such means to accomplish a lawful end. I really don't believe that the food manufacturers, pharmaceutical companies, hospitals, and various health organizations have conspired and planned the current state of affairs. It is just a matter of making money - Capitalism 101. The way things currently operate, these entities make a healthy profit and they are resistant to any changes that might impact the status quo.
Take the American Heart Associaton. It recieves most of its funding from donations. Who are the biggest donors to the AHA? Pharmaceutical companies and major food manufacturers are at the top of the list in their annual report. Now do you think they they would continue to get these donations if they advocated a position that hurt these companies financially? I think not.
Take research funding for example. Who pays for it? More and more is payed for by corporations. Now do you think they will continue providing funding to research organizations that get results that hurt the sales of their products, whether it be food or pharmaceuticals? Not likely. That is why most studies are designed with the desired results in mind ahead of time. We all know that just about any data can be manipulated enough to get the desired results.
Alan
Arkie, you're using flawed logic, engaging in clever usage and misapplications of terms, and accuse others of "conspiracy theories", and other bogeymen, to suggest that some pharmaceutical company-medical establishment cartel is trying to keep "them" from "saving money" for the public...
Whoa again. You are attributing words to me that I never stated. I never claimed there was a "conspiracy theory". In fact, I don't believe that to be the case. Definition of conspire as implied herein: To join in a secret agreement to do an unlawful or wrongful act or to use such means to accomplish a lawful end. I really don't believe that the food manufacturers, pharmaceutical companies, hospitals, and various health organizations have conspired and planned the current state of affairs. It is just a matter of making money - Capitalism 101. The way things currently operate, these entities make a healthy profit and they are resistant to any changes that might impact the status quo.
Take the American Heart Associaton. It recieves most of its funding from donations. Who are the biggest donors to the AHA? Pharmaceutical companies and major food manufacturers are at the top of the list in their annual report. Now do you think they they would continue to get these donations if they advocated a position that hurt these companies financially? I think not.
Take research funding for example. Who pays for it? More and more is payed for by corporations. Now do you think they will continue providing funding to research organizations that get results that hurt the sales of their products, whether it be food or pharmaceuticals? Not likely. That is why most studies are designed with the desired results in mind ahead of time. We all know that just about any data can be manipulated enough to get the desired results.
Alan
arkie6
03-16-2002, 05:35 AM
Originally posted by Carreen:
I didn't know you wanted me to do your work too. Listen, you don't have to take one look at any of those or try and learn anything. You asked me to post proof and I posted proof. You, being the one who requested it may have had the time to look up a few to see if indeed you could be mistaken. You've never proven anything you've said here. It's all just what you think. Show us some research to prove your ascertations I'd really like to see it.
Based on your logic above, I offer the following proof that the current diet-heart hypothesis is nothing more than wishful thinking. These studies by and large show no positive connection between the consumption of saturated animal fat and heart disease, cancer, diabetes, or obesity. In fact, they show an inverse relationship – the more animal protein and fat consumed, the less prevalent was the disease studied. What is implicated as causal factors in these all too common health concerns today is the increased consumption of sugar, refined flour, and polyunsaturated vegetable oils. Here are the studies:
Allred, JB, Too much of a good thing? An overemphasis on eating low-fat foods may be contributing to the alarming increase in overweight among US adults, J Amer Dietetic Assoc, April 1995;95(4):417-18.
Block, G, et al, Nutrient sources in the American diet: Quantitative data from the NHANES II survey, Amer J Epidemiol, 1985;122:27-40.
Hampl, JS and Betts, NM, Comparisons of dietary intake and sources of fat in low- and high-fat diets of 18- to 24-year-olds, J Amer Dietetic Assoc, August 1995;95(8):893-418.
Johnson, MA, The Georgia centenarian study: Nutritional patterns of centenarians, Intl J Aging and Human Development, 1992;34(1):57-76.
Kant, AK, and Schatzkin, A, Consumption of energy-dense, nutrient-poor foods by the US population: Effect on nutrient profiles, J Amer College Nutr, 1994;13(3):285-91.
Lieb, CW, The effects of an exclusive, long-continued meat diet, JAMA, 1926;87(1):25-26
Lieb, CW, The effects on human beings of a twelve-months exclusive meat diet, JAMA, 1929;93(1):20-22.
Williamson, DF, et al, The 10-year incidence of overweight and major weight gain in US adults, Arch Int Med, Mar 1990;150:665-72.
Eschwege, E, et al, The epidemiology of coronary heart disease in glucose-intolerant and diabetic subjects, J Int Med, 1994; 236(suppl 736):5-11.
Ferrannini, E, et al, Insulin resistance in essential hypertension, NEJM, 1987;317:350-7.
Ferrannini, E, et al, Hyperinsulinaemia: The key feature of a cardiovascular and metabolic syndrome, Diabetologia, 1991;34:416-22.
Hamsten, A, et al, Interactions amongst insulin, lipoproteins and haemostatic function relevant to coronary heart disease, J Int Med, 1994;236(suppl 736):75-88.
Lesourd, B, Protein undernutrition as the major cause of decreased immune function in the elderly: clinical and functional implications, Nutrition Reviews, 1995;53:86s-94s.
Reaven, GM and Hoffman, BB, Hypertension as a disease of carbohydrate and lipoprotein metabolism, Amer J Medicine, Dec 1989;87(supp 6A):6A-2S.
Reaven, GM and Hoffman, BB, A role for insulin in the aetiology and course of hypertension? The Lancet, August 22, 1987:435-7.
Smith, RL, Dietary lipids and heart disease: The contriving of a relationship, in American Clinical Laboratory, November 1989, pp 26-33.
Belfiore, F, et al, Metabolic effects of short-term fasting in obese hyperglycaemic humans and mice, Intl J Obesity, 1987;11:631-40.
Bevilacqua, S, et al, Operation of Randle's Cycle in patients with NIDDM, Diabetes, March 1990;39:383-9.
Cahill, GF, Physiology of insulin in man, Diabetes, 1971;20(12):785-99.
Caro, JF, Clinical Review 26: Insulin resistance in obese and nonobese man, J Clin Endocrinol and Metab, 1991;73(4):691-5.
Cerami, et al, Glucose and aging, Scientific American, May 1987:90-6.
Crapo, PA, et al, Plasma glucose and insulin responses to orally administered simple and complex carbohydrates, Diabetes, 1976;25:741-7.
Crapo, PA, et al, Postprandial plasma-glucose and -insulin responses to different complex carbohydrates, Diabetes, 1977;26:1178-83.
Crapo, PA, et al, Comparison of serum glucose, insulin, and glucagon responses to different types of complex carbohydrate in non-insulin-dependent diabetic patients, Amer J Clin Nutr, 1981;34:184-90.
DeFronzo, RA, Lilly Lecture 1987, The Triumvirate: B-cell, muscle, liver: A collusion responsible for NIDDM, Diabetes, June 1988;37:667-87.
DeFronzo, RA and Ferrannini, E, Insulin Resistance: A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease, Diabetes Care, March 1991;14(3):173-94.
Dudl, JR and Ensinck, JW, Insulin and glucagon relationships during aging in man, Metabolism, Jan 1977;26(1):33-41.
Farquhar, JW, et al, Glucose, insulin, and triglyceride responses to high and low carbohydrate diets in man, J Clin Invest, 1966;45(10):1648-56.
Ferrara, A, et al, Sex differences in insulin levels in older adults and the effect of body size, estrogen replacement therapy, and glucose tolerance status: The Rancho Bernardo Study, 1984-87, Diabetes Care, February 1995;18(2):220-5.
Flakoll, PJ, et al, The role of glucagon in the control of protein and amino acid metabolism in vivo, Metabolism, December 1994;43(12):1509-16.
Foster, DW, The Banting Lecture 1984. From glycogen to ketones--and back, Diabetes, 1984;33:1188-99.
Friedman, JE, et al, Glucose metabolism in incubated human muscle: Effect of obesity and non-insulin-dependent diabetes mellitus, Metabolism, August 1994;43(8):1047-54.
Griffiths, AJ, et al, Immediate metabolic availability of dietary fat in combination with carbohdyrate, Am J Clin Nutr, 1994;59:53-9.
Hainer, V, et al, Body fat distribution, metabolic and hormonal indices in obese patients treated initially by very low calorie diet, in Obesity: Dietary Factors and Control, Romsos, Himms-Hagen, and Suzuki, eds., Japan Scientific Societies Press:Tokyo, 1991, pp 215-26.
Inoue, S, et al, Effects of high sucrose diet and its components on glucose tolerance and serum lipids, Obesity: Dietary Factors and Control, Romsos, Himms-Hagen, and Suzuki, eds., Japan Scientific Societies Press:Tokyo, 1991, pp 159-67.
Islam, AHM W, et al, Fasting plasma insulin level is an important risk factor for the development of complications in Japanese obese children -- results from a cross-sectional and a longitudinal study, Metabolism, April 1995;44(4):478-85.
Landau, RL, et al, The protein-sparing action of protein feeding: absence of relationship to insulin secretion, Am J Clin Nutr, 1981;34:1300-04.
LeBlanc, J, Hormonal and metabolic responses to meals of various composition, in Obesity: Dietary Factors and Control, Romsos, DR et al, eds, Japan Sci. Soc. Press:Tokyo, 1991, pp 59-66.
Liu, GC, et al, Effect of high-carbohydrate-low-fat diets on plasma glucose, insulin and lipid responses in hypertriglyceridemic humans, Metabolism, 1983;:32(8):750-3.
McGarry, JD, New perspective in the regulation of ketogenesis, Diabetes, 1979;28:517-23.
McGarry, JD and Foster, DW, Regulation of hepatic fatty acid oxidation and ketone body production, Ann Rev Biochem, 1980;49:395-420.
McGarry, JD, et al, From dietary glucose to liver glycogen: The full circle round, Ann Rev Nutr, 1987;7:51-73.
Moan, A, et all, Mental stress increases glucose uptake during hyperinsulinemia: associations with sympathetic and cardiovascular responsiveness, Metabolism, Oct 1995;44(10):1303-7.
Modan, M, et al, Hyperinsulinemia: A link between hypertension obesity and glucose intolerance, J Clin Invest, 1985;75:809-17.
Muller, WA, et al, The influence of the antecedent diet upon glucagon and insulin secretion, NEJM, 1971;285:1450-4.
Nutall, FQ and Gannon, MC, Plasma glucose and insulin response to macronutrients in nondiabetic and NIDDM subjects, Diabetes Care, Sep 1991;14(9):824-38.
Okayama, A, et al, Changes in total serum cholesterol and other risk factors for cardiovascular disease in Japan, 1980-1989, Intl J Epidemiol, 1993;22(6):1038-47.
Oppert, J-M, et al, Plasma glucose, insulin, and glucagon before and after long-term overfeeding in identical twins, Metabolism, January 1995;44(1):96-105.
Parillo, M, et al, A high-monounsaturated-fat/low-carbohydrate diet improves peripheral insulin sensitivity in non-insulin dependent diabetic patients, Metabolism, December 1992;41(12):1373-8.
Pasquali, R, et al, Interrelationships between dietary carbohydrates, B-cell function, and rate of ketogenesis during underfeeding in obese patients, Ann. Nutr. Metab., 31:219-30, 1987.
Piatti, PM, et al, Hypocaloric high-protein diet improves glucose oxidation and spares lean body mass: Comparison to hypocaloric high-carbohydrate diet, Metabolism, December 1994;43(12):1481-7.
Raitakari, OT, et al, The role of insulin in clustering of serum lipids and blood pressure in children and adolescents: the cardiovascular risk in young Finns study, Diabetologia, 1995;38:1042-50.
Reaven, GM, Banting Lecture 1988: Role of insulin resistance in human disease, Diabetes, Dec 1988;37:1595-1607.
Sevak, L, et al, Relationship of hyperinsulinemia to dietary intake in South Asian and European men, Amer J Clin Nutr, 1994;59:1069-74.
Slabber, M, et al, Effect of a low-insulin-response, energy-restricted diet on weight loss and plasma insulin concentration in hyperinsulinemic obese females, Amer J Clin Nutr, 1994;60:48-53.
Sosenko JMm, et al, High-density lipoprotein and glycosylated hemoglobin in nondiabetic individuals, Arch Int Med, Aug 1986;146:1521-4.
Swislocki, ALM, et al, Insulin resistance, glucose intolerance and hyperinsulinemia in patients with hypertension, Amer J Hypertension, May 1989;2(5 part 1):419-23.
Urberg, M, and Rajdev, K, A correlation between serum cholesterol and glycosylated hemoglobin in nondiabetic humans, J Fam Pract, 1989;28(3):269-74.
Urberg, M, et al, Glycosylated hemoglobin in acute myocardial infarction, J Fam Pract, 1990;30(2):215-16.
Unger, RH, Glucagon and the insulin:glucagon ratio in diabetes and other catabolic illnesses, Diabetes, 1971;20:834-8.
Westphal, SA, et al, Metabolic response to glucose ingested with various amounts of protein, Amer J Clin Nutr, 1990;52:267-72.
Yudkin, J, Sucrose, Coronary Heart Disease, Diabetes, and Obesity: Do Hormones Provide a Link? American Heart Journal, February 1988;115(2):493-8.
Yudkin, J, Diet and coronary thrombosis: Hypothesis and fact, The Lancet, July 20, 1957:155-62.
Yudkin, J, Dietary factors in atherosclerosis, Lipids, 1978; 13:370-2.
Yudkin, J, Dietary fat and dietary sugar in relation to ischaemic heart-disease and diabetes, The Lancet, July 4, 1964:4-5.
Yudkin, J, et al, Effects of high dietary sugar, BMJ, 1980;281:1396.
Yudkin, J, Whither sugar consumption? , South African Medical Journal, Jan 13, 1973;47(2):44.
Yudkin, J, Nutrition and palatability with special reference to obesity, myocardial infarction, and other diseases of civilisation, The Lancet, June 22, 1963:1335-8.
Yudkin, JS, Coronary heart disease and diabetes mellitus: Three new risk factors and a unifying hypothesis," J Int Med, 1995;238:21-30.
Ashwell J, et al, Obesity: new insight into the anthropometric classification of fat distribution shown by computed tomography, BMJ, June 8, 1985;290:1692-4.
Barakat, HS, et al, Body fat distribution, plasma lipoproteins and the risk of coronary heart disease of male subjects, Intl J Obesity, 1988;12:473-80.
Bjorntorp, P, Regional patterns of fat distribution, Ann Int Med, 1985;103(6 pt 2):994-5.
Borkam, GA, et al, Assessment of abdominal fat content by computed tomography, Amer J Clin Nutr, July 1982;36:172-7.
Brodie, DA, Techniques of measurement of body composition part I, Sports Medicine 1988;5:11-40.
Despres, JP, et al, Abdominal adipose tissue and serum HDL-cholesterol association: Independent from obesity and serum triglyceride concentration, Intl J Obesity, 1988;12:1-3.
Dixon, AK, Abdominal fat assessed by computed tomography: Sex difference in distribution, Clin Radiol, 1983; 34:189-91.
Houmard, JA, et al, Effects of fitness level and the regional distribution of fat on carbohydrate metabolism and plasma lipids in middle- to older-aged men, Metabolism, July 1991:40(7):714-19.
Jensen, MD, et al, Measurement of abdominal and visceral fat with computed tomography and dual-energy x-ray absorptiometry, Amer J Clin Nutr, 1995;61:274-8.
Mueller, WH, et al, Body circumference as alternatives to skinfold measurement of body fat distribution in Mexican-Americans, Intl J Obesity, 1987;11:309-18.
Parker, DR, et al, Relationship of dietary saturated fatty acids and body habitus to serum insulin concentrations: the Normative Aging Study, Amer J Clin Nutr, 1993;58:129-36.
Peiris, AN, et al, Relationship of body fat distribution to the metabolic clearance of insulin in premenopausal women, Intl J Obesity, 1987;11:581-9.
Rissanen, J, et al, Visceral adiposity, androgens, and plasma lipids in obese men, Metabolism, October 1994,;43(10):1318-23.
Seidell, JC, et al, The sagittal waist diameter and mortality in men: the Baltimore Longitudinal Study on Aging, Intl J Obesity, 1994;18:61-7.
Tokunaga, K, et al, A novel technique for the determination of body fat by computed tomography, Intl J Obesity, 1983;7:437-45.
Vansant, G, et al, Body fat distribution and the prognosis for weight reduction: Preliminary observations, Intl J Obesity, 1988;12:133-40.
Blum, M, et al, Protein Intake and kidney function in humans: Its effect on 'Normal Aging', Arch Int Med, Jan 1989;149:211-12.
Emmett, PM and Heaton, KW, Is extrinsic sugar a vehicle for dietary fat? The Lancet, June 17, 1995;345:1537-40.
Facchini, F, et al, Light-to-moderate alcohol intake is associated with enhanced insulin sensitivity, Diabetes Care, February 1994;17(2):115-9.
Ferro-Luzzi, A and Branca, F, Mediterranean diet, Italian-style: prototype of a healthy diet , Amer J Clin Nutr, 1995;61(suppl):1338s-45S.
Finer, N, Sugar substitutes in the treatment of obesity and diabetes mellitus, Clinical Nutrition, November-December 1985;4(6):207-14.
Frankel, EN, et al, Inhibition of oxidation of human low-density lipoprotein by phenolic substances in red wine, The Lancet, February 20, 1993;341:454-7.
Hunt, JR, et al, High- versus low-meat diets: effects on zinc absorption iron status, and calcium, copper, iron, magnesium, manganese, nitrogen, phosphorous, and zinc balance in postmenopausal women, Amer J Clin Nutr, 1995;62:621-32.
Jenkins, DJA, et al, Glycemic index of foods: A physiological basis for carbohydrate exchange, Amer J Clin Nutr, 1981;34:362-66.
Jenkins, DJA, et al, Metabolic effects of a low-glycemic index diet, Amer J Clin Nutr, 1987;46:968-75.
Kern, W, et al, Evidence for effects of insulin on sensory processing in humans, Diabetes, March 1994;43:351-6.
Nutrition Reviews, How ketones spare protein in starvation, 1989;47(3):80-1.
Remer, T and Manz, F, Dietary protein as a modulator of the renal net acid excretion capacity: Evidence that an increased protein intake improves the capability of the kidney to excrete ammonium, Nutritional Biochemistry, 1995;6:431-37.
Spencer, H, et al, Further studies of the effect of a high protein diet as meat on calcium metabolism, Am J Clin Nutr, 1983;37:924-29.
Spencer, H, et al, Do protein and phosphorous cause calcium loss?, J Nutr, 1988;118:657-60.
Stryer, L, Biochemistry, New York: W H Freeman and Company, 1988.
Tappy, L, et al, Thermic effect of infused amino acids in healthy humans and in subjects with insulin resistance, Amer J Clin Nutr, 1993;57:912-6.
von Borstel, RW, Metabolic and physiologic effects of sweeteners, Clinical Nutrition, 1985;4(6):215-20.
Young, VR and Pellett, P, Protein intake and requirements with reference to diet and health, Amer J Clin Nutr, 1987;45:1323-43.
Yudkin, J and Smith, EE, The low-carbohydrate diet in the treatment of chronic dyspepsia, Proceedings of the Nutrition Society, May 1972;31(1):12A.
Yudkin, J and Carey, M, The treatment of obesity by the "high-fat" diet. The inevitability of calories, The Lancet, 1960, ii:939-41.
Bulpitt, CJ, Vitamin C and vascular disease, (letter) BMJ, June 17, 1995;310:1548-9.
dePee, S, et al, Lack of improvement in vitamin A status with increased consumption of dark-green leafy vegetables, The Lancet, July 8, 1995;346:75-81.
Gale, CR, et al, Vitamin C and risk of death from stroke and coronary heart disease in cohort of elderly people, BMJ, 1995;310:1563-6.
Khaw, K-T and Woodhouse, P, Interrelation of vitamin C, infection, haemostatic factors, and cardiovascular disease, BMJ, 1995;310:1559-63.
Kozlovsky, AS, et al, Effects of diets high in simple sugars on urinary chromium losses, Metabolism, 1986;35(6):515-18.
Nicholson, Al and Yudkin, J, The nutritional value of low-carbohydrate diet used in the treatment of obesity, Proceedings of the Nutrition Society, Mar 1969;28(1):13A.
Nutrition Reviews, Vitamin D and insulin secretion, November 1986;44(11):375-6.
Paolisso, G, et al, Pharmacologic doses of vitamin E improve insulin action in healthy subjects and non-insulin-dependent diabetic patients, Amer J Clin Nutr, 1993;57:650-6.
Umegaki, K, et al, Beta-carotene prevents x-ray induction of micronuclei in human lymphocytes, Amer J Clin Nutr, 1994;59:409-12.
Urb, M and Zemel, MB, Evidence for synergism between chromium and nicotinic acid in the control of glucose tolerance in elderly humans, Metabolism, 1987;36(9):896-98.
Zimmermann, MB and Shane, B, Supplemental folic acid, Amer J Clin Nutr, 1993;58:127-8.
Andreotti, AC, et al, Acute pharmacologic blockade of lipolysis normalizes nocturnal growth hormone levels and pulsatility in obese subjects, Metabolism, October 1994;43(10):1207-13.
Cappon, JP, et al, Acute effects of high fat and high glucose meals on the growth hormone response to exercise, J Clin Endocrinol, 1992;76(6):1418-22.
Corpas, E, et al, Human growth hormone and human aging, Endocrin Rev, 1993;14(1):20-39.
Cutler, DL, Gray, C, et al, Low-carbohydrate diet alters intracellular glucose metabolism but not overall glucose disposal in exercise-trained subjects, Metabolism, Oct 1995;44(10):1264-70.
Despres, JP, Obesity, regional adipose tissue distribution, and metabolism: Effect of exercise, in Obesity: Dietary Factors and Control, Romsos, Himms-Hagen, and Suzuki, eds., Japan Scientific Societies Press:Tokyo, 1991, pp 251-9.
Eiffert, KC, et al, High sucrose diet and exercise: Effects on insulin-receptor function of 12- and 24-mo-old Sprague-Dawley rats, J Nutr, 1991;121:1081-9.
Hardman, AE, et al, Brisk walking and plasma high density lipoprotein cholesterol concentration in previously sedentary women, BMJ, November 1989;299:1204-5.
Horowitz, JF and Coyle, EF, Metabolic responses to preexercise meals containing various carbohydrates and fat, Amer J Clin Nutr 1993;58:235-41.
Kraemer, WJ, Influence of the endocrine system on resistance training adaptations, Natl Strength and Conditioning Assoc. J, 1992;14(2):47-53.
Medeiros-Neto, G, et al, The effect of hypocaloric diet with and without d-fenfluramine treatment on growth hormone release after growth hormone-releasing factor stimulation in patients with android obesity, Metabolism, August 1994;43(8):969-73.
Neufeld, ND, et al, Effects of caloric restriction and exercise on insulin receptors in obesity: Associated with changes in membrane lipids, Metabolism, 1986;35:580-7.
Rasmussen, MH et al, Massive weight loss restores 24-hour growth hormone release profiles and serum insulin-like growth factor-I levels in obese subjects, J Clin Endocrinol and Metab, 1995;80(4):1407-15.
Rudman, D, et al, Effect of growth hormone in men over 60 years old, NEJM, 1990;323:1-6.
Rudman, D, et al, Impaired growth hormone secretion in the adult population: relation to age and adiposity, J Clin Invest, 1981;67:1361-69.
Thissen, JP, et al, Nutritional regulation of the insulin-like growth factors, Endocrine Reviews, 1994;15(1):80-101.
Acheson, KJ, et al, Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man, Amer J Clin Nutr, 1988;48:240-7.
Ahrens, RA, Sucrose, hypertension, and heart disease, Amer J Clin Nutr, March 1975;28:195-202.
Ahrens, RA, Sucrose, hypertension, and heart disease: an historical perspective, Amer J Clin Nutr, April 1974;27:403-22.
Bernstein, RK, Effects of low insulin and low carbohydrate on frequency and severity of hypoglycemia, (letter), Amer J Med, March 1992;92:39.
Blankenhorn, DH, et al, The influence of diet on the appearance of new lesions in human coronary arteries, JAMA, March 23/30, 1990;263(12):1646-52.
Bonadonna, RC, et al, Obesity and insulin resistance in humans: A dose-response study, Metabolism, 1990;39:452-9.
Bonora, E, et al, Effect of glipizide on insulin secretion and insulin metabolism in obese type II diabetic patients, Diabetes Care, November-December 1987;10(6).
Boyko, EJ, et al, Visceral adiposity, fasting plasma insulin, and blood pressure in Japanese-Americans, Diabetes Care, February 1995;18(2):174-81.
Brownell, KD and Wadden, TA, Etiology and treatment of obesity: Understanding a serious prevalent, and refractory disorder, J Consult and Clin Psych, 1992;60(4):505-17.
Campbell, LV, et al, The high-monounsaturated fat diet as a practical alternative for NIDDM, Diabetes Care, March 1994;17(3):177-82.
Cigolini, M. et al, Fasting serum insulin in relation to components of the metabolic syndrome in European healthy men: The European Fat Distribution Study, Metabolism, January 1995;44(1):35-40.
Cohen, MP, et al, High prevalence of diabetes in young adult Ethiopian immigrants to Israel, Diabetes, June 1988;37:824-8.
Cruz, AB et al, Effect of intra-arterial insulin on tissue cholesterol and fatty acids in alloxan-diabetic dogs, Circulation Research, January 1961;IX:39-43.
Daly, PA and Landsberg, L, Hypertension in obesity and NIDDM: The role of insulin and sympathetic nervous system, Diabetes Care, March 1991;14(3):240-8.
DeFronzo, RA, Insulin secretion, insulin resistance, and obesity, Intl J Obesity, 1982;6(suppl 1):73-82.
Dinneen, S, et al, Carbohydrate metabolism in non-insulin-dependent diabetes mellitus, Sem Med Beth Israel Hosp, 1992;327(10):707-13.
Donahue, RP and Orchard, TJ, Diabetes mellitus and macrovascular complications, Diabetes Care, September 1992;15(9):1141-55.
Donnan, PT, et al, Diet as a risk factor for peripheral arterial disease in the general population: The Edinburgh Artery Study, Amer J Clin Nutr, 1993;57:917-21.
Dulloo, AG et al, Differential effects of high fat diets varying in fatty acid composition on the efficiency of lean and fat tissue deposition during weight recovery after low food intake, Metabolism, February 1995;44(2):273-9.
Durrington, PN, Is insulin atherogenic? Diabetic Medicine, 1992;9:597-600.
Eckel, RH, Lipoprotein lipase: A multifunctional enzyme relevant to common metabolic diseases, NEJM, 1989;320:1060-8.
Eliasson, M, et al, Hyperinsulinemia predicts low tissue plasminogen activator activity in a healthy population: The northern Sweden MONICA study, Metabolism, December 1994;43(12):1579-86.
Flatt, J-P, Use and storage of carbohydrate and fat, Amer J Clin Nutr, 1995;61(suppl):952S-9S.
Garg, A, High monounsaturated fat diet for diabetic patients, Diabetes Care, March 1994;17(3):242-7.
Garg, A, et al, Effects of varying carbohydrate content of diet in patients with non-insulin dependent diabetes mellitus, JAMA, May 11, 1994;271(18):1421-8.
Garg, A, et al, Comparison of a high-carbohydrate diet with a high-monounsaturated-fat diet in patients with non-insulin-dependent diabetes mellitus, NEJM, 1988;319:829-34.
Kaplan, N, The Deadly Quartet, Arch Int Med, July 1989;149:1514-20.
Kekwick, A and Pawan, GLS, Metabolic study in human obesity with isocaloric diets high in fat, protein or carbohydrate, Metabolism, 1957;6:447-60.
Kekwick, A and Pawan, GLS, Calorie intake in relation to body-weight changes in the obese, The Lancet, July 28, 1956:155-61.
Kekwick, A, et al, Resistance to ketosis in obese subjects, The Lancet, December 26, 1959: 1157-9.
Kiens, B, et al, Lipoprotein lipase activity and intramuscular triglyceride stores after long-term high-fat and high-carbohydrate diets in physically trained men, Clinical Physiology (1987)7:1-9.
Laakso, M, et al, Asymptomatic atherosclerosis and insulin resistance, Arteriosclerosis and Thrombosis, Jul-Aug 1991;11(4):1069-77.
Laville, M, et al, Decreased glucose-induced thermogenesis at the onset of obesity, Amer J Clin Nutr, 1993;57:851-6.
Quinn, D, et al, Lipoprotein lipase: Mechanism of action and role in lipoprotein metabolism, Prog Lipid Res, 1982;22:35-78.
Raison, J, et al, Regional differences in adipose tissue lipoprotein lipase activity in relation to body fat distribution and menopausal status in obese women, Intl J Obesity, (1988)12:465-72.
Reaven, GM, The role of insulin resistance and hyperinsulinemia in coronary heart disease, Metabolism, May 1992;41(5 suppl 1):16-19.
Rossetti, L, et al, Glucose toxicity, Diabetes Care, 1990;13:610-30.
Ross, R, The pathogenesis of atherosclerosis - an update, NEJM, Feb 20, 1986;314(8):488-500.
Rothwell, NJ and Stock, MJ, Insulin and thermogenesis, Intl J Obesity, 1988;12:93-102.
Saudek, CD, and Brach, EL, Cholesterol metabolism in diabetes: The effect of diabetic control on sterol balance, Diabetes, Nov 1978;27:1059-64.
Schwartz, CJ, et al, Pathophysiology of the atherogenic process, Amer J Cardiology, October 3, 1989;64:23G-31G.
Schwartz, CJ, et al, The pathogenesis of atherosclerosis: An overview, Clin Cardiol, 1991;14(I):1-16.
Schwartz, CJ, et al, Pathogenesis of the Atherosclerotic Lesion: Implications for diabetes mellitus, Diabetes Care, Sep 1992;15(9):1156-67.
Stehouwer, CDA and Donker AJM, Endothelial function in metabolic disease, Diabetes Complications, 1995; 9:7-22.
Steinberg, D, et al, Beyond Cholesterol: Modification of low-density lipoprotein that increases its atherogenicity, NEJM, April 6, 1989;320(14):915-24.
Stout, RW, Insulin and Atheroma: 20 year perspective, Diabetes Care, June 1990;13(6):631-54.
Stout, RW, Insulin as a mitogenic factor: Role in the pathogenesis of cardiovascular disease, Amer J Med, Feb 21, 1991;90(suppl 2A):62S-65S.
Stubbs, RJ, et al, Carbohydrate balance and the regulation of day-to-day food intake in humans, Amer J Clin Nutr, 1993;57:897-903.
Swai, ABM, et al, Diabetes in tropical Africa: a prospective study, 1981-7, BMJ, Apr 1990;300:1103-10.
Vinik, AI and Wing, R, The good, the bad, and the ugly in diabetic diets, Endocrinology and Metabolism Clinics of North America, June 1992;21(2):237-71.
Watts, NB, et al, Prediction of glucose response to weight loss in patients with non-insulin-dependent diabetes mellitus, Arch Int Med, April 1990;150:803-6.
Witztum, JL, The oxidation hypothesis of atherosclerosis, The Lancet, September 17, 1994;344:793-5.
Worthington, BS and Taylor, LE, Balanced low-calorie vs. High-protein-low-carbohydrate reducing diets, Research, January 1974;64:47-55.
Yudkin, J, The low-carbohydrate diet in the treatment of obesity, Postgraduate Med, 1972;51(5).
Yudkin, J and Szanto, S, Hyperinsulinism and atherogenesis, BMJ, Feb 6, 1971;1(744):349.
Zavaroni, I, et al, Hyperinsulinaemia, obesity, and syndrome X, J Int Med, 1994;235:51-6.
Zimmet, PZ, Hyperinsulinemia - How innocent a bystander? Diabetes Care, 1993;16(suppl 3):56-70.
Zimmet, P, Type 2 (non insulin dependent) diabetes - An epidemiological overview, Diabetologia, 1982;22:399-411.
I didn't know you wanted me to do your work too. Listen, you don't have to take one look at any of those or try and learn anything. You asked me to post proof and I posted proof. You, being the one who requested it may have had the time to look up a few to see if indeed you could be mistaken. You've never proven anything you've said here. It's all just what you think. Show us some research to prove your ascertations I'd really like to see it.
Based on your logic above, I offer the following proof that the current diet-heart hypothesis is nothing more than wishful thinking. These studies by and large show no positive connection between the consumption of saturated animal fat and heart disease, cancer, diabetes, or obesity. In fact, they show an inverse relationship – the more animal protein and fat consumed, the less prevalent was the disease studied. What is implicated as causal factors in these all too common health concerns today is the increased consumption of sugar, refined flour, and polyunsaturated vegetable oils. Here are the studies:
Allred, JB, Too much of a good thing? An overemphasis on eating low-fat foods may be contributing to the alarming increase in overweight among US adults, J Amer Dietetic Assoc, April 1995;95(4):417-18.
Block, G, et al, Nutrient sources in the American diet: Quantitative data from the NHANES II survey, Amer J Epidemiol, 1985;122:27-40.
Hampl, JS and Betts, NM, Comparisons of dietary intake and sources of fat in low- and high-fat diets of 18- to 24-year-olds, J Amer Dietetic Assoc, August 1995;95(8):893-418.
Johnson, MA, The Georgia centenarian study: Nutritional patterns of centenarians, Intl J Aging and Human Development, 1992;34(1):57-76.
Kant, AK, and Schatzkin, A, Consumption of energy-dense, nutrient-poor foods by the US population: Effect on nutrient profiles, J Amer College Nutr, 1994;13(3):285-91.
Lieb, CW, The effects of an exclusive, long-continued meat diet, JAMA, 1926;87(1):25-26
Lieb, CW, The effects on human beings of a twelve-months exclusive meat diet, JAMA, 1929;93(1):20-22.
Williamson, DF, et al, The 10-year incidence of overweight and major weight gain in US adults, Arch Int Med, Mar 1990;150:665-72.
Eschwege, E, et al, The epidemiology of coronary heart disease in glucose-intolerant and diabetic subjects, J Int Med, 1994; 236(suppl 736):5-11.
Ferrannini, E, et al, Insulin resistance in essential hypertension, NEJM, 1987;317:350-7.
Ferrannini, E, et al, Hyperinsulinaemia: The key feature of a cardiovascular and metabolic syndrome, Diabetologia, 1991;34:416-22.
Hamsten, A, et al, Interactions amongst insulin, lipoproteins and haemostatic function relevant to coronary heart disease, J Int Med, 1994;236(suppl 736):75-88.
Lesourd, B, Protein undernutrition as the major cause of decreased immune function in the elderly: clinical and functional implications, Nutrition Reviews, 1995;53:86s-94s.
Reaven, GM and Hoffman, BB, Hypertension as a disease of carbohydrate and lipoprotein metabolism, Amer J Medicine, Dec 1989;87(supp 6A):6A-2S.
Reaven, GM and Hoffman, BB, A role for insulin in the aetiology and course of hypertension? The Lancet, August 22, 1987:435-7.
Smith, RL, Dietary lipids and heart disease: The contriving of a relationship, in American Clinical Laboratory, November 1989, pp 26-33.
Belfiore, F, et al, Metabolic effects of short-term fasting in obese hyperglycaemic humans and mice, Intl J Obesity, 1987;11:631-40.
Bevilacqua, S, et al, Operation of Randle's Cycle in patients with NIDDM, Diabetes, March 1990;39:383-9.
Cahill, GF, Physiology of insulin in man, Diabetes, 1971;20(12):785-99.
Caro, JF, Clinical Review 26: Insulin resistance in obese and nonobese man, J Clin Endocrinol and Metab, 1991;73(4):691-5.
Cerami, et al, Glucose and aging, Scientific American, May 1987:90-6.
Crapo, PA, et al, Plasma glucose and insulin responses to orally administered simple and complex carbohydrates, Diabetes, 1976;25:741-7.
Crapo, PA, et al, Postprandial plasma-glucose and -insulin responses to different complex carbohydrates, Diabetes, 1977;26:1178-83.
Crapo, PA, et al, Comparison of serum glucose, insulin, and glucagon responses to different types of complex carbohydrate in non-insulin-dependent diabetic patients, Amer J Clin Nutr, 1981;34:184-90.
DeFronzo, RA, Lilly Lecture 1987, The Triumvirate: B-cell, muscle, liver: A collusion responsible for NIDDM, Diabetes, June 1988;37:667-87.
DeFronzo, RA and Ferrannini, E, Insulin Resistance: A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease, Diabetes Care, March 1991;14(3):173-94.
Dudl, JR and Ensinck, JW, Insulin and glucagon relationships during aging in man, Metabolism, Jan 1977;26(1):33-41.
Farquhar, JW, et al, Glucose, insulin, and triglyceride responses to high and low carbohydrate diets in man, J Clin Invest, 1966;45(10):1648-56.
Ferrara, A, et al, Sex differences in insulin levels in older adults and the effect of body size, estrogen replacement therapy, and glucose tolerance status: The Rancho Bernardo Study, 1984-87, Diabetes Care, February 1995;18(2):220-5.
Flakoll, PJ, et al, The role of glucagon in the control of protein and amino acid metabolism in vivo, Metabolism, December 1994;43(12):1509-16.
Foster, DW, The Banting Lecture 1984. From glycogen to ketones--and back, Diabetes, 1984;33:1188-99.
Friedman, JE, et al, Glucose metabolism in incubated human muscle: Effect of obesity and non-insulin-dependent diabetes mellitus, Metabolism, August 1994;43(8):1047-54.
Griffiths, AJ, et al, Immediate metabolic availability of dietary fat in combination with carbohdyrate, Am J Clin Nutr, 1994;59:53-9.
Hainer, V, et al, Body fat distribution, metabolic and hormonal indices in obese patients treated initially by very low calorie diet, in Obesity: Dietary Factors and Control, Romsos, Himms-Hagen, and Suzuki, eds., Japan Scientific Societies Press:Tokyo, 1991, pp 215-26.
Inoue, S, et al, Effects of high sucrose diet and its components on glucose tolerance and serum lipids, Obesity: Dietary Factors and Control, Romsos, Himms-Hagen, and Suzuki, eds., Japan Scientific Societies Press:Tokyo, 1991, pp 159-67.
Islam, AHM W, et al, Fasting plasma insulin level is an important risk factor for the development of complications in Japanese obese children -- results from a cross-sectional and a longitudinal study, Metabolism, April 1995;44(4):478-85.
Landau, RL, et al, The protein-sparing action of protein feeding: absence of relationship to insulin secretion, Am J Clin Nutr, 1981;34:1300-04.
LeBlanc, J, Hormonal and metabolic responses to meals of various composition, in Obesity: Dietary Factors and Control, Romsos, DR et al, eds, Japan Sci. Soc. Press:Tokyo, 1991, pp 59-66.
Liu, GC, et al, Effect of high-carbohydrate-low-fat diets on plasma glucose, insulin and lipid responses in hypertriglyceridemic humans, Metabolism, 1983;:32(8):750-3.
McGarry, JD, New perspective in the regulation of ketogenesis, Diabetes, 1979;28:517-23.
McGarry, JD and Foster, DW, Regulation of hepatic fatty acid oxidation and ketone body production, Ann Rev Biochem, 1980;49:395-420.
McGarry, JD, et al, From dietary glucose to liver glycogen: The full circle round, Ann Rev Nutr, 1987;7:51-73.
Moan, A, et all, Mental stress increases glucose uptake during hyperinsulinemia: associations with sympathetic and cardiovascular responsiveness, Metabolism, Oct 1995;44(10):1303-7.
Modan, M, et al, Hyperinsulinemia: A link between hypertension obesity and glucose intolerance, J Clin Invest, 1985;75:809-17.
Muller, WA, et al, The influence of the antecedent diet upon glucagon and insulin secretion, NEJM, 1971;285:1450-4.
Nutall, FQ and Gannon, MC, Plasma glucose and insulin response to macronutrients in nondiabetic and NIDDM subjects, Diabetes Care, Sep 1991;14(9):824-38.
Okayama, A, et al, Changes in total serum cholesterol and other risk factors for cardiovascular disease in Japan, 1980-1989, Intl J Epidemiol, 1993;22(6):1038-47.
Oppert, J-M, et al, Plasma glucose, insulin, and glucagon before and after long-term overfeeding in identical twins, Metabolism, January 1995;44(1):96-105.
Parillo, M, et al, A high-monounsaturated-fat/low-carbohydrate diet improves peripheral insulin sensitivity in non-insulin dependent diabetic patients, Metabolism, December 1992;41(12):1373-8.
Pasquali, R, et al, Interrelationships between dietary carbohydrates, B-cell function, and rate of ketogenesis during underfeeding in obese patients, Ann. Nutr. Metab., 31:219-30, 1987.
Piatti, PM, et al, Hypocaloric high-protein diet improves glucose oxidation and spares lean body mass: Comparison to hypocaloric high-carbohydrate diet, Metabolism, December 1994;43(12):1481-7.
Raitakari, OT, et al, The role of insulin in clustering of serum lipids and blood pressure in children and adolescents: the cardiovascular risk in young Finns study, Diabetologia, 1995;38:1042-50.
Reaven, GM, Banting Lecture 1988: Role of insulin resistance in human disease, Diabetes, Dec 1988;37:1595-1607.
Sevak, L, et al, Relationship of hyperinsulinemia to dietary intake in South Asian and European men, Amer J Clin Nutr, 1994;59:1069-74.
Slabber, M, et al, Effect of a low-insulin-response, energy-restricted diet on weight loss and plasma insulin concentration in hyperinsulinemic obese females, Amer J Clin Nutr, 1994;60:48-53.
Sosenko JMm, et al, High-density lipoprotein and glycosylated hemoglobin in nondiabetic individuals, Arch Int Med, Aug 1986;146:1521-4.
Swislocki, ALM, et al, Insulin resistance, glucose intolerance and hyperinsulinemia in patients with hypertension, Amer J Hypertension, May 1989;2(5 part 1):419-23.
Urberg, M, and Rajdev, K, A correlation between serum cholesterol and glycosylated hemoglobin in nondiabetic humans, J Fam Pract, 1989;28(3):269-74.
Urberg, M, et al, Glycosylated hemoglobin in acute myocardial infarction, J Fam Pract, 1990;30(2):215-16.
Unger, RH, Glucagon and the insulin:glucagon ratio in diabetes and other catabolic illnesses, Diabetes, 1971;20:834-8.
Westphal, SA, et al, Metabolic response to glucose ingested with various amounts of protein, Amer J Clin Nutr, 1990;52:267-72.
Yudkin, J, Sucrose, Coronary Heart Disease, Diabetes, and Obesity: Do Hormones Provide a Link? American Heart Journal, February 1988;115(2):493-8.
Yudkin, J, Diet and coronary thrombosis: Hypothesis and fact, The Lancet, July 20, 1957:155-62.
Yudkin, J, Dietary factors in atherosclerosis, Lipids, 1978; 13:370-2.
Yudkin, J, Dietary fat and dietary sugar in relation to ischaemic heart-disease and diabetes, The Lancet, July 4, 1964:4-5.
Yudkin, J, et al, Effects of high dietary sugar, BMJ, 1980;281:1396.
Yudkin, J, Whither sugar consumption? , South African Medical Journal, Jan 13, 1973;47(2):44.
Yudkin, J, Nutrition and palatability with special reference to obesity, myocardial infarction, and other diseases of civilisation, The Lancet, June 22, 1963:1335-8.
Yudkin, JS, Coronary heart disease and diabetes mellitus: Three new risk factors and a unifying hypothesis," J Int Med, 1995;238:21-30.
Ashwell J, et al, Obesity: new insight into the anthropometric classification of fat distribution shown by computed tomography, BMJ, June 8, 1985;290:1692-4.
Barakat, HS, et al, Body fat distribution, plasma lipoproteins and the risk of coronary heart disease of male subjects, Intl J Obesity, 1988;12:473-80.
Bjorntorp, P, Regional patterns of fat distribution, Ann Int Med, 1985;103(6 pt 2):994-5.
Borkam, GA, et al, Assessment of abdominal fat content by computed tomography, Amer J Clin Nutr, July 1982;36:172-7.
Brodie, DA, Techniques of measurement of body composition part I, Sports Medicine 1988;5:11-40.
Despres, JP, et al, Abdominal adipose tissue and serum HDL-cholesterol association: Independent from obesity and serum triglyceride concentration, Intl J Obesity, 1988;12:1-3.
Dixon, AK, Abdominal fat assessed by computed tomography: Sex difference in distribution, Clin Radiol, 1983; 34:189-91.
Houmard, JA, et al, Effects of fitness level and the regional distribution of fat on carbohydrate metabolism and plasma lipids in middle- to older-aged men, Metabolism, July 1991:40(7):714-19.
Jensen, MD, et al, Measurement of abdominal and visceral fat with computed tomography and dual-energy x-ray absorptiometry, Amer J Clin Nutr, 1995;61:274-8.
Mueller, WH, et al, Body circumference as alternatives to skinfold measurement of body fat distribution in Mexican-Americans, Intl J Obesity, 1987;11:309-18.
Parker, DR, et al, Relationship of dietary saturated fatty acids and body habitus to serum insulin concentrations: the Normative Aging Study, Amer J Clin Nutr, 1993;58:129-36.
Peiris, AN, et al, Relationship of body fat distribution to the metabolic clearance of insulin in premenopausal women, Intl J Obesity, 1987;11:581-9.
Rissanen, J, et al, Visceral adiposity, androgens, and plasma lipids in obese men, Metabolism, October 1994,;43(10):1318-23.
Seidell, JC, et al, The sagittal waist diameter and mortality in men: the Baltimore Longitudinal Study on Aging, Intl J Obesity, 1994;18:61-7.
Tokunaga, K, et al, A novel technique for the determination of body fat by computed tomography, Intl J Obesity, 1983;7:437-45.
Vansant, G, et al, Body fat distribution and the prognosis for weight reduction: Preliminary observations, Intl J Obesity, 1988;12:133-40.
Blum, M, et al, Protein Intake and kidney function in humans: Its effect on 'Normal Aging', Arch Int Med, Jan 1989;149:211-12.
Emmett, PM and Heaton, KW, Is extrinsic sugar a vehicle for dietary fat? The Lancet, June 17, 1995;345:1537-40.
Facchini, F, et al, Light-to-moderate alcohol intake is associated with enhanced insulin sensitivity, Diabetes Care, February 1994;17(2):115-9.
Ferro-Luzzi, A and Branca, F, Mediterranean diet, Italian-style: prototype of a healthy diet , Amer J Clin Nutr, 1995;61(suppl):1338s-45S.
Finer, N, Sugar substitutes in the treatment of obesity and diabetes mellitus, Clinical Nutrition, November-December 1985;4(6):207-14.
Frankel, EN, et al, Inhibition of oxidation of human low-density lipoprotein by phenolic substances in red wine, The Lancet, February 20, 1993;341:454-7.
Hunt, JR, et al, High- versus low-meat diets: effects on zinc absorption iron status, and calcium, copper, iron, magnesium, manganese, nitrogen, phosphorous, and zinc balance in postmenopausal women, Amer J Clin Nutr, 1995;62:621-32.
Jenkins, DJA, et al, Glycemic index of foods: A physiological basis for carbohydrate exchange, Amer J Clin Nutr, 1981;34:362-66.
Jenkins, DJA, et al, Metabolic effects of a low-glycemic index diet, Amer J Clin Nutr, 1987;46:968-75.
Kern, W, et al, Evidence for effects of insulin on sensory processing in humans, Diabetes, March 1994;43:351-6.
Nutrition Reviews, How ketones spare protein in starvation, 1989;47(3):80-1.
Remer, T and Manz, F, Dietary protein as a modulator of the renal net acid excretion capacity: Evidence that an increased protein intake improves the capability of the kidney to excrete ammonium, Nutritional Biochemistry, 1995;6:431-37.
Spencer, H, et al, Further studies of the effect of a high protein diet as meat on calcium metabolism, Am J Clin Nutr, 1983;37:924-29.
Spencer, H, et al, Do protein and phosphorous cause calcium loss?, J Nutr, 1988;118:657-60.
Stryer, L, Biochemistry, New York: W H Freeman and Company, 1988.
Tappy, L, et al, Thermic effect of infused amino acids in healthy humans and in subjects with insulin resistance, Amer J Clin Nutr, 1993;57:912-6.
von Borstel, RW, Metabolic and physiologic effects of sweeteners, Clinical Nutrition, 1985;4(6):215-20.
Young, VR and Pellett, P, Protein intake and requirements with reference to diet and health, Amer J Clin Nutr, 1987;45:1323-43.
Yudkin, J and Smith, EE, The low-carbohydrate diet in the treatment of chronic dyspepsia, Proceedings of the Nutrition Society, May 1972;31(1):12A.
Yudkin, J and Carey, M, The treatment of obesity by the "high-fat" diet. The inevitability of calories, The Lancet, 1960, ii:939-41.
Bulpitt, CJ, Vitamin C and vascular disease, (letter) BMJ, June 17, 1995;310:1548-9.
dePee, S, et al, Lack of improvement in vitamin A status with increased consumption of dark-green leafy vegetables, The Lancet, July 8, 1995;346:75-81.
Gale, CR, et al, Vitamin C and risk of death from stroke and coronary heart disease in cohort of elderly people, BMJ, 1995;310:1563-6.
Khaw, K-T and Woodhouse, P, Interrelation of vitamin C, infection, haemostatic factors, and cardiovascular disease, BMJ, 1995;310:1559-63.
Kozlovsky, AS, et al, Effects of diets high in simple sugars on urinary chromium losses, Metabolism, 1986;35(6):515-18.
Nicholson, Al and Yudkin, J, The nutritional value of low-carbohydrate diet used in the treatment of obesity, Proceedings of the Nutrition Society, Mar 1969;28(1):13A.
Nutrition Reviews, Vitamin D and insulin secretion, November 1986;44(11):375-6.
Paolisso, G, et al, Pharmacologic doses of vitamin E improve insulin action in healthy subjects and non-insulin-dependent diabetic patients, Amer J Clin Nutr, 1993;57:650-6.
Umegaki, K, et al, Beta-carotene prevents x-ray induction of micronuclei in human lymphocytes, Amer J Clin Nutr, 1994;59:409-12.
Urb, M and Zemel, MB, Evidence for synergism between chromium and nicotinic acid in the control of glucose tolerance in elderly humans, Metabolism, 1987;36(9):896-98.
Zimmermann, MB and Shane, B, Supplemental folic acid, Amer J Clin Nutr, 1993;58:127-8.
Andreotti, AC, et al, Acute pharmacologic blockade of lipolysis normalizes nocturnal growth hormone levels and pulsatility in obese subjects, Metabolism, October 1994;43(10):1207-13.
Cappon, JP, et al, Acute effects of high fat and high glucose meals on the growth hormone response to exercise, J Clin Endocrinol, 1992;76(6):1418-22.
Corpas, E, et al, Human growth hormone and human aging, Endocrin Rev, 1993;14(1):20-39.
Cutler, DL, Gray, C, et al, Low-carbohydrate diet alters intracellular glucose metabolism but not overall glucose disposal in exercise-trained subjects, Metabolism, Oct 1995;44(10):1264-70.
Despres, JP, Obesity, regional adipose tissue distribution, and metabolism: Effect of exercise, in Obesity: Dietary Factors and Control, Romsos, Himms-Hagen, and Suzuki, eds., Japan Scientific Societies Press:Tokyo, 1991, pp 251-9.
Eiffert, KC, et al, High sucrose diet and exercise: Effects on insulin-receptor function of 12- and 24-mo-old Sprague-Dawley rats, J Nutr, 1991;121:1081-9.
Hardman, AE, et al, Brisk walking and plasma high density lipoprotein cholesterol concentration in previously sedentary women, BMJ, November 1989;299:1204-5.
Horowitz, JF and Coyle, EF, Metabolic responses to preexercise meals containing various carbohydrates and fat, Amer J Clin Nutr 1993;58:235-41.
Kraemer, WJ, Influence of the endocrine system on resistance training adaptations, Natl Strength and Conditioning Assoc. J, 1992;14(2):47-53.
Medeiros-Neto, G, et al, The effect of hypocaloric diet with and without d-fenfluramine treatment on growth hormone release after growth hormone-releasing factor stimulation in patients with android obesity, Metabolism, August 1994;43(8):969-73.
Neufeld, ND, et al, Effects of caloric restriction and exercise on insulin receptors in obesity: Associated with changes in membrane lipids, Metabolism, 1986;35:580-7.
Rasmussen, MH et al, Massive weight loss restores 24-hour growth hormone release profiles and serum insulin-like growth factor-I levels in obese subjects, J Clin Endocrinol and Metab, 1995;80(4):1407-15.
Rudman, D, et al, Effect of growth hormone in men over 60 years old, NEJM, 1990;323:1-6.
Rudman, D, et al, Impaired growth hormone secretion in the adult population: relation to age and adiposity, J Clin Invest, 1981;67:1361-69.
Thissen, JP, et al, Nutritional regulation of the insulin-like growth factors, Endocrine Reviews, 1994;15(1):80-101.
Acheson, KJ, et al, Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man, Amer J Clin Nutr, 1988;48:240-7.
Ahrens, RA, Sucrose, hypertension, and heart disease, Amer J Clin Nutr, March 1975;28:195-202.
Ahrens, RA, Sucrose, hypertension, and heart disease: an historical perspective, Amer J Clin Nutr, April 1974;27:403-22.
Bernstein, RK, Effects of low insulin and low carbohydrate on frequency and severity of hypoglycemia, (letter), Amer J Med, March 1992;92:39.
Blankenhorn, DH, et al, The influence of diet on the appearance of new lesions in human coronary arteries, JAMA, March 23/30, 1990;263(12):1646-52.
Bonadonna, RC, et al, Obesity and insulin resistance in humans: A dose-response study, Metabolism, 1990;39:452-9.
Bonora, E, et al, Effect of glipizide on insulin secretion and insulin metabolism in obese type II diabetic patients, Diabetes Care, November-December 1987;10(6).
Boyko, EJ, et al, Visceral adiposity, fasting plasma insulin, and blood pressure in Japanese-Americans, Diabetes Care, February 1995;18(2):174-81.
Brownell, KD and Wadden, TA, Etiology and treatment of obesity: Understanding a serious prevalent, and refractory disorder, J Consult and Clin Psych, 1992;60(4):505-17.
Campbell, LV, et al, The high-monounsaturated fat diet as a practical alternative for NIDDM, Diabetes Care, March 1994;17(3):177-82.
Cigolini, M. et al, Fasting serum insulin in relation to components of the metabolic syndrome in European healthy men: The European Fat Distribution Study, Metabolism, January 1995;44(1):35-40.
Cohen, MP, et al, High prevalence of diabetes in young adult Ethiopian immigrants to Israel, Diabetes, June 1988;37:824-8.
Cruz, AB et al, Effect of intra-arterial insulin on tissue cholesterol and fatty acids in alloxan-diabetic dogs, Circulation Research, January 1961;IX:39-43.
Daly, PA and Landsberg, L, Hypertension in obesity and NIDDM: The role of insulin and sympathetic nervous system, Diabetes Care, March 1991;14(3):240-8.
DeFronzo, RA, Insulin secretion, insulin resistance, and obesity, Intl J Obesity, 1982;6(suppl 1):73-82.
Dinneen, S, et al, Carbohydrate metabolism in non-insulin-dependent diabetes mellitus, Sem Med Beth Israel Hosp, 1992;327(10):707-13.
Donahue, RP and Orchard, TJ, Diabetes mellitus and macrovascular complications, Diabetes Care, September 1992;15(9):1141-55.
Donnan, PT, et al, Diet as a risk factor for peripheral arterial disease in the general population: The Edinburgh Artery Study, Amer J Clin Nutr, 1993;57:917-21.
Dulloo, AG et al, Differential effects of high fat diets varying in fatty acid composition on the efficiency of lean and fat tissue deposition during weight recovery after low food intake, Metabolism, February 1995;44(2):273-9.
Durrington, PN, Is insulin atherogenic? Diabetic Medicine, 1992;9:597-600.
Eckel, RH, Lipoprotein lipase: A multifunctional enzyme relevant to common metabolic diseases, NEJM, 1989;320:1060-8.
Eliasson, M, et al, Hyperinsulinemia predicts low tissue plasminogen activator activity in a healthy population: The northern Sweden MONICA study, Metabolism, December 1994;43(12):1579-86.
Flatt, J-P, Use and storage of carbohydrate and fat, Amer J Clin Nutr, 1995;61(suppl):952S-9S.
Garg, A, High monounsaturated fat diet for diabetic patients, Diabetes Care, March 1994;17(3):242-7.
Garg, A, et al, Effects of varying carbohydrate content of diet in patients with non-insulin dependent diabetes mellitus, JAMA, May 11, 1994;271(18):1421-8.
Garg, A, et al, Comparison of a high-carbohydrate diet with a high-monounsaturated-fat diet in patients with non-insulin-dependent diabetes mellitus, NEJM, 1988;319:829-34.
Kaplan, N, The Deadly Quartet, Arch Int Med, July 1989;149:1514-20.
Kekwick, A and Pawan, GLS, Metabolic study in human obesity with isocaloric diets high in fat, protein or carbohydrate, Metabolism, 1957;6:447-60.
Kekwick, A and Pawan, GLS, Calorie intake in relation to body-weight changes in the obese, The Lancet, July 28, 1956:155-61.
Kekwick, A, et al, Resistance to ketosis in obese subjects, The Lancet, December 26, 1959: 1157-9.
Kiens, B, et al, Lipoprotein lipase activity and intramuscular triglyceride stores after long-term high-fat and high-carbohydrate diets in physically trained men, Clinical Physiology (1987)7:1-9.
Laakso, M, et al, Asymptomatic atherosclerosis and insulin resistance, Arteriosclerosis and Thrombosis, Jul-Aug 1991;11(4):1069-77.
Laville, M, et al, Decreased glucose-induced thermogenesis at the onset of obesity, Amer J Clin Nutr, 1993;57:851-6.
Quinn, D, et al, Lipoprotein lipase: Mechanism of action and role in lipoprotein metabolism, Prog Lipid Res, 1982;22:35-78.
Raison, J, et al, Regional differences in adipose tissue lipoprotein lipase activity in relation to body fat distribution and menopausal status in obese women, Intl J Obesity, (1988)12:465-72.
Reaven, GM, The role of insulin resistance and hyperinsulinemia in coronary heart disease, Metabolism, May 1992;41(5 suppl 1):16-19.
Rossetti, L, et al, Glucose toxicity, Diabetes Care, 1990;13:610-30.
Ross, R, The pathogenesis of atherosclerosis - an update, NEJM, Feb 20, 1986;314(8):488-500.
Rothwell, NJ and Stock, MJ, Insulin and thermogenesis, Intl J Obesity, 1988;12:93-102.
Saudek, CD, and Brach, EL, Cholesterol metabolism in diabetes: The effect of diabetic control on sterol balance, Diabetes, Nov 1978;27:1059-64.
Schwartz, CJ, et al, Pathophysiology of the atherogenic process, Amer J Cardiology, October 3, 1989;64:23G-31G.
Schwartz, CJ, et al, The pathogenesis of atherosclerosis: An overview, Clin Cardiol, 1991;14(I):1-16.
Schwartz, CJ, et al, Pathogenesis of the Atherosclerotic Lesion: Implications for diabetes mellitus, Diabetes Care, Sep 1992;15(9):1156-67.
Stehouwer, CDA and Donker AJM, Endothelial function in metabolic disease, Diabetes Complications, 1995; 9:7-22.
Steinberg, D, et al, Beyond Cholesterol: Modification of low-density lipoprotein that increases its atherogenicity, NEJM, April 6, 1989;320(14):915-24.
Stout, RW, Insulin and Atheroma: 20 year perspective, Diabetes Care, June 1990;13(6):631-54.
Stout, RW, Insulin as a mitogenic factor: Role in the pathogenesis of cardiovascular disease, Amer J Med, Feb 21, 1991;90(suppl 2A):62S-65S.
Stubbs, RJ, et al, Carbohydrate balance and the regulation of day-to-day food intake in humans, Amer J Clin Nutr, 1993;57:897-903.
Swai, ABM, et al, Diabetes in tropical Africa: a prospective study, 1981-7, BMJ, Apr 1990;300:1103-10.
Vinik, AI and Wing, R, The good, the bad, and the ugly in diabetic diets, Endocrinology and Metabolism Clinics of North America, June 1992;21(2):237-71.
Watts, NB, et al, Prediction of glucose response to weight loss in patients with non-insulin-dependent diabetes mellitus, Arch Int Med, April 1990;150:803-6.
Witztum, JL, The oxidation hypothesis of atherosclerosis, The Lancet, September 17, 1994;344:793-5.
Worthington, BS and Taylor, LE, Balanced low-calorie vs. High-protein-low-carbohydrate reducing diets, Research, January 1974;64:47-55.
Yudkin, J, The low-carbohydrate diet in the treatment of obesity, Postgraduate Med, 1972;51(5).
Yudkin, J and Szanto, S, Hyperinsulinism and atherogenesis, BMJ, Feb 6, 1971;1(744):349.
Zavaroni, I, et al, Hyperinsulinaemia, obesity, and syndrome X, J Int Med, 1994;235:51-6.
Zimmet, PZ, Hyperinsulinemia - How innocent a bystander? Diabetes Care, 1993;16(suppl 3):56-70.
Zimmet, P, Type 2 (non insulin dependent) diabetes - An epidemiological overview, Diabetologia, 1982;22:399-411.
Carreen
03-16-2002, 10:35 AM
This discussion is about coronary heart disease and how cholesterol effects it. Taking these referances out of micheal eades book may be ok if we were discussing a low carb diet or insulin resistance. It has nothing to do with this discussion. Which of these "studies" have to do with how cholesterol effects heart disease or lipid lowering drugs?
hunter44
03-16-2002, 11:25 PM
Careen - I have a simple question, and I think I am correct in saying this. If 50% of the people that have heart attacks have low or slightly evalated cholesterol levels and 50% have high cholesterol levels, how can taking a statin to lower cholesterol change your risk, if both groups are 50%?
Carreen
03-17-2002, 12:26 AM
Well Hunter, there are other reasons that people have heart attacks besides high cholesterol. You can have a heart attack and have low or normal cholesterol for the following reasons (risk factors):
Increasing age. About four out of five people who die of coronary heart disease are 65 or older.
Male sex (gender) Men have a greater risk of heart attack than women do, and they have attacks earlier in life.
Heredity (including Race)
Smoking
High Cholesterol
High Blood Pressure
Physical inactivity
Obesity and overweight
Diabetes mellitus
All of the above are risk factors for heart attacks. Having high cholesterol is just one risk. The more you have the higher your chances. Lowing your cholesterol is just one thing you can do. Others include lose weight, quit smoking, excercise, control your blood pressure.
You asked how can taking a statin to lower cholesterol change your risk (no matter what the percentages are)the answer is.
Lowering cholesterol can prevent heart attacks and reduce death in men and women who already have heart disease and high cholesterol. Lowering LDL-C can reduce the severity of heart disease, reduce the risk of a non-fatal heart attack and reduce the need for bypass surgery or angioplasty.
Increasing age. About four out of five people who die of coronary heart disease are 65 or older.
Male sex (gender) Men have a greater risk of heart attack than women do, and they have attacks earlier in life.
Heredity (including Race)
Smoking
High Cholesterol
High Blood Pressure
Physical inactivity
Obesity and overweight
Diabetes mellitus
All of the above are risk factors for heart attacks. Having high cholesterol is just one risk. The more you have the higher your chances. Lowing your cholesterol is just one thing you can do. Others include lose weight, quit smoking, excercise, control your blood pressure.
You asked how can taking a statin to lower cholesterol change your risk (no matter what the percentages are)the answer is.
Lowering cholesterol can prevent heart attacks and reduce death in men and women who already have heart disease and high cholesterol. Lowering LDL-C can reduce the severity of heart disease, reduce the risk of a non-fatal heart attack and reduce the need for bypass surgery or angioplasty.
arkie6
03-17-2002, 03:28 AM
Originally posted by Carreen:
This discussion is about coronary heart disease and how cholesterol effects it. Taking these referances out of micheal eades book may be ok if we were discussing a low carb diet or insulin resistance. It has nothing to do with this discussion. Which of these "studies" have to do with how cholesterol effects heart disease or lipid lowering drugs?
Carreen, I thought we were discussing the relationship between abnormal blood lipids (cholesterol, triglycerides, etc.) and heart disease. Are you not familiar with the term “Syndrome X” and insulin resistance? The majority of the references I posted are related to this subject.
Syndrome X is a cluster of risk factors for heart disease associated with insulin resistance. These risk factors include: hypertriglyceridemia, low HDL-cholesterol, hyperinsulinemia (high blood insulin), often hyperglycemia (high blood glucose), and hypertension (high blood pressure).
Doctors have known for years that each of these health problems can increase the risk of other diseases, such as heart disease and diabetes. However, until relatively recently, they failed to connect the dots and see these health problems as part of a syndrome. We now know that eating large amounts of dietary carbohydrates (such as sweets, pastas, and breads) can raise cholesterol, triglyceride, and insulin levels. We know also that elevated insulin can promote obesity and high blood pressure. Because these problems are related and tend to occur in clusters, they form a syndrome.
Almost all individuals with type 2 diabetes mellitus (diabetes) and many with hypertension, cardiovascular disease, and obesity are insulin resistant. About 20-25% of the healthy population is estimated to be insulin resistant.
For more reading on the subject go to this link: http://syndromex.stanford.edu/InsulinResistance.htm or just do a search for “syndrome x insulin resistance” using www.google.com (http://www.google.com)
Also reference Reaven, GM. Syndrome X:6 years later. Journal of Internal Medicine. 1994; 236 (Supplement 736): 13-22
Until 1988, researchers studying insulin resistance focused on its role in diabetes. Then, Gerald M. Reaven, M.D., of the Stanford University Medical Center, built a strong case for insulin resistance as a cause of obesity, hypertension, and coronary heart disease.
"The fact that an insulin-resistant subject may not become diabetic does not mean that they suffer no untoward consequences," Reaven wrote in the journal Diabetes. "Indeed, an argument can be made that the more insulin sensitive [in contrast to insulin resistant] an individual, the better off he or she is, and that the attempt to compensate for insulin resistance sets in motion of series of events that play an important role in the development of both hypertension and coronary heart disease.
Reaven coined the term "Syndrome X," to describe how insulin resistance sets the stage for more serious disease. The syndrome is characterized by six traits: insulin resistance, glucose intolerance, abnormally high insulin levels, high triglycerides, low high-density lipoprotein (the "good" cholesterol), and hypertension. "The common feature of the proposed syndrome is insulin resistance," he explained, "and all other changes are likely to be secondary to this basic abnormality.".
Here is more info on carbs, insulin, and heart disease:
A ten-year followup study (Liu, Willet, Stampfer, et al. A prospective study of dietary glycemic load, carbohydrate intake, and risk of coronary heart disease in US women.,American Journal of Clinical Nutrition, 2000 71: 6; 1455-1461) of 75,521 women suggests that a high dietary glycemic load from refined carbohydrates increases the risk of coronary heart disease, independent of known coronary disease risk factors. Women who consumed the largest amounts of refined starchy carbohydrates: potatoes, white rice, white bread, and sugar had an 85% greater risk of heart attack. Glycemic index was a stronger predictor of coronary heart disease than the usual classification of complex vs. simple carbohydrates.
The whole idea of “treating” high cholesterol with a drug is fundamentally wrong. Period. High cholesterol is not a disease, but merely a symptom of a problem. And has been shown in these discussions, high cholesterol does not “cause” heart disease. So, lowering cholesterol levels through the use of drugs is not the answer to the problem of heart disease. This symptom oriented treatment of problems is what is wrong with modern medicine. Got high cholesterol? Here, take this pill. Got high bloodpressure? Here, take this pill. Got Type II diabetes? Here, take this pill. Treating each of these symptoms does not fix the problem. Treating the symptoms may delay or reduce the end result, but it doesn’t get at the root of the problem, which in the vast majority of cases is insulin resistance brought about by poor diet that places too much emphasis on refined carbohydrates.
Alan
This discussion is about coronary heart disease and how cholesterol effects it. Taking these referances out of micheal eades book may be ok if we were discussing a low carb diet or insulin resistance. It has nothing to do with this discussion. Which of these "studies" have to do with how cholesterol effects heart disease or lipid lowering drugs?
Carreen, I thought we were discussing the relationship between abnormal blood lipids (cholesterol, triglycerides, etc.) and heart disease. Are you not familiar with the term “Syndrome X” and insulin resistance? The majority of the references I posted are related to this subject.
Syndrome X is a cluster of risk factors for heart disease associated with insulin resistance. These risk factors include: hypertriglyceridemia, low HDL-cholesterol, hyperinsulinemia (high blood insulin), often hyperglycemia (high blood glucose), and hypertension (high blood pressure).
Doctors have known for years that each of these health problems can increase the risk of other diseases, such as heart disease and diabetes. However, until relatively recently, they failed to connect the dots and see these health problems as part of a syndrome. We now know that eating large amounts of dietary carbohydrates (such as sweets, pastas, and breads) can raise cholesterol, triglyceride, and insulin levels. We know also that elevated insulin can promote obesity and high blood pressure. Because these problems are related and tend to occur in clusters, they form a syndrome.
Almost all individuals with type 2 diabetes mellitus (diabetes) and many with hypertension, cardiovascular disease, and obesity are insulin resistant. About 20-25% of the healthy population is estimated to be insulin resistant.
For more reading on the subject go to this link: http://syndromex.stanford.edu/InsulinResistance.htm or just do a search for “syndrome x insulin resistance” using www.google.com (http://www.google.com)
Also reference Reaven, GM. Syndrome X:6 years later. Journal of Internal Medicine. 1994; 236 (Supplement 736): 13-22
Until 1988, researchers studying insulin resistance focused on its role in diabetes. Then, Gerald M. Reaven, M.D., of the Stanford University Medical Center, built a strong case for insulin resistance as a cause of obesity, hypertension, and coronary heart disease.
"The fact that an insulin-resistant subject may not become diabetic does not mean that they suffer no untoward consequences," Reaven wrote in the journal Diabetes. "Indeed, an argument can be made that the more insulin sensitive [in contrast to insulin resistant] an individual, the better off he or she is, and that the attempt to compensate for insulin resistance sets in motion of series of events that play an important role in the development of both hypertension and coronary heart disease.
Reaven coined the term "Syndrome X," to describe how insulin resistance sets the stage for more serious disease. The syndrome is characterized by six traits: insulin resistance, glucose intolerance, abnormally high insulin levels, high triglycerides, low high-density lipoprotein (the "good" cholesterol), and hypertension. "The common feature of the proposed syndrome is insulin resistance," he explained, "and all other changes are likely to be secondary to this basic abnormality.".
Here is more info on carbs, insulin, and heart disease:
A ten-year followup study (Liu, Willet, Stampfer, et al. A prospective study of dietary glycemic load, carbohydrate intake, and risk of coronary heart disease in US women.,American Journal of Clinical Nutrition, 2000 71: 6; 1455-1461) of 75,521 women suggests that a high dietary glycemic load from refined carbohydrates increases the risk of coronary heart disease, independent of known coronary disease risk factors. Women who consumed the largest amounts of refined starchy carbohydrates: potatoes, white rice, white bread, and sugar had an 85% greater risk of heart attack. Glycemic index was a stronger predictor of coronary heart disease than the usual classification of complex vs. simple carbohydrates.
The whole idea of “treating” high cholesterol with a drug is fundamentally wrong. Period. High cholesterol is not a disease, but merely a symptom of a problem. And has been shown in these discussions, high cholesterol does not “cause” heart disease. So, lowering cholesterol levels through the use of drugs is not the answer to the problem of heart disease. This symptom oriented treatment of problems is what is wrong with modern medicine. Got high cholesterol? Here, take this pill. Got high bloodpressure? Here, take this pill. Got Type II diabetes? Here, take this pill. Treating each of these symptoms does not fix the problem. Treating the symptoms may delay or reduce the end result, but it doesn’t get at the root of the problem, which in the vast majority of cases is insulin resistance brought about by poor diet that places too much emphasis on refined carbohydrates.
Alan
Maximize22
03-18-2002, 02:41 PM
Thanks for the input, but the majority of the thread is waaay off of the original question (simply - exercise and the impact on cholesterol).
Anyway, I've taken a look at a couple of sites - the secondopinions was very interesting, but as always taken with a grain of salt.
For right now, I'm keeping an eye on what I eat (watching the cholesterol and saturated fat) and trying to increase fruit and veg intake. And getting to the gym as often as possible - I was doing 2 twenty minute sessions a couple of times a week (20 mins running, 20 mins on exercise bike) - and looking to increase my exercise time. And I'll see in 3 months how/if that has an affect.
Thanks for the input!
Max
Anyway, I've taken a look at a couple of sites - the secondopinions was very interesting, but as always taken with a grain of salt.
For right now, I'm keeping an eye on what I eat (watching the cholesterol and saturated fat) and trying to increase fruit and veg intake. And getting to the gym as often as possible - I was doing 2 twenty minute sessions a couple of times a week (20 mins running, 20 mins on exercise bike) - and looking to increase my exercise time. And I'll see in 3 months how/if that has an affect.
Thanks for the input!
Max
TB
03-19-2002, 08:36 AM
arkie6, I would like to know have you had a heart attack or been diagnosed with high cholesterol?
TB
03-19-2002, 09:18 AM
hunter44,I am not as articulate as some of the others that post on this board,but I will try and answer your lower your risk question.
Let us take a revolver that has 11 chambers.I know they do not make one,but bear with me.Each of the risk factors is a bullet.We take one bullet and load it,this represents the unknown.People who have heart attacks that have no commonality with anyone else.The stuff happens bullet.Load another bullet to represent the age factor if it applies.Gender,load another if it applies.Heredity,use of tobacco,etc.I am sure you get the idea.
If you now look at the loaded gun ,you will have multiple bullets in the chamber depending on your risk factors.Spin the chamber.That represents your everyday life.Put it to your heart and pull the trigger.If you are REAL lucky you hit an empty chamber day after day.One day it WILL go off.Now,if you survive,you are laying in the hospital bed and you have the Dr. telling you about all of your risk factors.You begin to wonder how you could be so stupid with your life and vow to change.So the Dr. has you change and you start taking the bullets out of the gun.You quit using tobacco,remove a bullet,you control your BP,remove a bullet,lower your cholesterol,remove a bullet,etc.
Now,you go through life with fewer bullets in the gun and when you spin the chamber and pull the trigger there are more empty holes then there are bullets.
As you go along in life,human nature takes over.People get lazy as well as cynical,and before you know it,they have added a few more bullets to the gun.
You are correct that you have no guarantee that you will not have a heart attack,but you can sure increase your chances of not getting one.
Until you have had one ,you do not know.I asked before on another post,how many have HAD heart attacks.I do not recall anyone coming forward and saying that yes they had one.The people who have had one do not live by statistics,or all of the studies posted.We live day to day and want more out of life,We got a second chance.We ask ourselves why did this happen to me and will it happen to me again.
The survivors ARE THE GUINEA PIGS.We are the ones who are being looked at.What happens with us has a profound effect on how some of you who have not had a heart attack are treated for prevention of this.
I feel that is the goal that all of you who are here are striving for.You do not want to have the heart attack.If that is not your goal,then why are your here?
Let us take a revolver that has 11 chambers.I know they do not make one,but bear with me.Each of the risk factors is a bullet.We take one bullet and load it,this represents the unknown.People who have heart attacks that have no commonality with anyone else.The stuff happens bullet.Load another bullet to represent the age factor if it applies.Gender,load another if it applies.Heredity,use of tobacco,etc.I am sure you get the idea.
If you now look at the loaded gun ,you will have multiple bullets in the chamber depending on your risk factors.Spin the chamber.That represents your everyday life.Put it to your heart and pull the trigger.If you are REAL lucky you hit an empty chamber day after day.One day it WILL go off.Now,if you survive,you are laying in the hospital bed and you have the Dr. telling you about all of your risk factors.You begin to wonder how you could be so stupid with your life and vow to change.So the Dr. has you change and you start taking the bullets out of the gun.You quit using tobacco,remove a bullet,you control your BP,remove a bullet,lower your cholesterol,remove a bullet,etc.
Now,you go through life with fewer bullets in the gun and when you spin the chamber and pull the trigger there are more empty holes then there are bullets.
As you go along in life,human nature takes over.People get lazy as well as cynical,and before you know it,they have added a few more bullets to the gun.
You are correct that you have no guarantee that you will not have a heart attack,but you can sure increase your chances of not getting one.
Until you have had one ,you do not know.I asked before on another post,how many have HAD heart attacks.I do not recall anyone coming forward and saying that yes they had one.The people who have had one do not live by statistics,or all of the studies posted.We live day to day and want more out of life,We got a second chance.We ask ourselves why did this happen to me and will it happen to me again.
The survivors ARE THE GUINEA PIGS.We are the ones who are being looked at.What happens with us has a profound effect on how some of you who have not had a heart attack are treated for prevention of this.
I feel that is the goal that all of you who are here are striving for.You do not want to have the heart attack.If that is not your goal,then why are your here?
Carreen
03-19-2002, 11:28 AM
Very good analogy TB.
hunter44
03-19-2002, 11:42 AM
Thank You - But how is it a risk factor if, by lowering your lipid levels through statins, you still fall within the same percentile = 50%. So, is it really a risk factor? I believe you can't put a bullet in your gun unless it shows to be a risk factor. Let me put the question another way. How specifically is high cholesterol a risk factor if 50% of all people who have heart attacts have normal or low cholesterol. The Framingham Study has since showed this not to be true. Can you show me another study of it's granduer?
TB
03-19-2002, 12:59 PM
hunter44,Good question.
The studies are nice.You need to put that aside.The studies,the statistics.They do not really matter,nor do they show the true facts.
Here is the difference.A heart attack occure when there is an interruption in the blood flow going to the heart.Other then the collapsing of an artery,the majority of heart attacks are due to a blockage.A blood clot that travels to the heart,or the build up in the artery that ruptures and blocks the artery. The numbers can say what they want.The fact is that you have a blockage in your artery and it is killing of your heart muscle.SOMETHING caused this to happen.Statistics or studies aside.They do not apply to you because you are trying to survive,hoping to get through this.I must correct the statistics part slightly.The only statistic that runs through your mind that matters is that 2/3 of the people that have a heart attack DIE.
Anyway,your Dr. tells you that although your numbers were not that bad,you still have build up in your coronary arteries,and that they want to help prevent another heart attack. What options do you have? There are a few,but you cannot play around with this anymore.You know that you have build up,and you now have to work closely with the Dr. in anything you try because of the medication you are on.Time is not on your side.You want to do ALL that you can so you do not experience that again.
After going through the experience,I told my wife that although there are no guarantees that I will not have another heart attack,that I can accept having another heart attack if I did everything I could no matter how small to help myself.Chalk it up to fate,the one bullet in the gun that is always there.
It is human nature to want answers.Especially if you go through something traumatic.With the study and statistics the only thing the Dr. would be able to tell a heart attack patient is we do not know why you have clogged arteries,and there is nothing we can do to help you to prevent you from having another one.Let me tell you,that is an unacceptable answer when you are laying there.
The fact that there are people participating in this board or any of the other boards on heart disease,cholesterol,high BP,etc,means that if you have not had a heart attack,you are trying not to have one.That,to me,throws out the study and statistic for the people here.It may apply on paper,but it does no apply to people.hunter44,you would not be here discussing this stuff if you REALLY held those studies and statistics as gospel.There would be no use in trying to prevent something that was going to happen no matter what you did,because the commonality of the stats is that ALL of those people had heart attacks.
The studies are nice.You need to put that aside.The studies,the statistics.They do not really matter,nor do they show the true facts.
Here is the difference.A heart attack occure when there is an interruption in the blood flow going to the heart.Other then the collapsing of an artery,the majority of heart attacks are due to a blockage.A blood clot that travels to the heart,or the build up in the artery that ruptures and blocks the artery. The numbers can say what they want.The fact is that you have a blockage in your artery and it is killing of your heart muscle.SOMETHING caused this to happen.Statistics or studies aside.They do not apply to you because you are trying to survive,hoping to get through this.I must correct the statistics part slightly.The only statistic that runs through your mind that matters is that 2/3 of the people that have a heart attack DIE.
Anyway,your Dr. tells you that although your numbers were not that bad,you still have build up in your coronary arteries,and that they want to help prevent another heart attack. What options do you have? There are a few,but you cannot play around with this anymore.You know that you have build up,and you now have to work closely with the Dr. in anything you try because of the medication you are on.Time is not on your side.You want to do ALL that you can so you do not experience that again.
After going through the experience,I told my wife that although there are no guarantees that I will not have another heart attack,that I can accept having another heart attack if I did everything I could no matter how small to help myself.Chalk it up to fate,the one bullet in the gun that is always there.
It is human nature to want answers.Especially if you go through something traumatic.With the study and statistics the only thing the Dr. would be able to tell a heart attack patient is we do not know why you have clogged arteries,and there is nothing we can do to help you to prevent you from having another one.Let me tell you,that is an unacceptable answer when you are laying there.
The fact that there are people participating in this board or any of the other boards on heart disease,cholesterol,high BP,etc,means that if you have not had a heart attack,you are trying not to have one.That,to me,throws out the study and statistic for the people here.It may apply on paper,but it does no apply to people.hunter44,you would not be here discussing this stuff if you REALLY held those studies and statistics as gospel.There would be no use in trying to prevent something that was going to happen no matter what you did,because the commonality of the stats is that ALL of those people had heart attacks.
hunter44
03-19-2002, 04:48 PM
Having heart disease and not having heart disease are two different issues in taking the statins. But, did elevated cholesterol levels cause your heart disease? And, will it prevent you from having another heart attack?(studies show it might slightly improve your odds) I have read that the blood thinning properties in the statins could be the real answer because the lowering of total cholesterol has not been proven to eleminate the cause of heart disease. Aspirin does the same. I'm referring more to healthy people with no evidence of heart disease but with elevated cholesterol and all the doctors are putting them on these powerful statin drugs when in actuality they have no diffinitive proof that elevated cholesterol has any effect in preventing heart disease and heart attacks. I've done a ton of reading on this subject and the body needs cholesterol. Either through diet or manufactured by the liver. It is strtegic in the structure and maintenance of every living cell. And, the body takes in or manufactures more when the cells need repair because they are damaged in some way = elevated cholesterol. That damage could be from the bodies overproduction of insulin. So, if you prevent the overproduction of insulin, you reduce the increased cholesterol which in turn could posibly prevent the plaque buildup = healthy plumbing system. Increase HDL to remove LDL, and reduce Trigs. These are the approaches that more and more researchers are finding. The way to do that is reduce carbohydrates, increase saturated fats and protein. Eliminate vegetable oils, especially hydrogenated oils and reduce grains. I wish you well. My approach right now is I am what I eat and I want to learn exactly how my body utilizes what I put into it. Ten years ago, when I was younger, this approach was effective for me and my doctor was shocked when I told him that I did not take the statin he prescribed. Now I've adapted that way of eating again, I feel great and I report my bloodwork in a couple of weeks. This time I don't think I'll return to the AMA food pyramid.
arkie6
03-19-2002, 05:44 PM
Originally posted by TB:
arkie6, I would like to know have you had a heart attack or been diagnosed with high cholesterol?
Nope. No heart attack and as far as I know I never had high cholesterol, but I never had it checked before starting a low carbohydrate diet about 4 years ago at 32 years of age. About a year or so after starting that diet and losing about 40 pounds, my total cholesterol was 198 or so. My most recent test (about a year ago) shows TC=187, HDL=60, triglycerides=115, and I forget the LDL, but it was "normal".
My father on the other hand has significant cardiovascular disease. He didn't have a heart attack, but due to severe angina they found significant blockage in 4 of his coronary arteries. He had bypass surgery about 8 years ago for that. About 5 years prior to that they found significant blockage in his carotid arteries. Both of those were opened up via surgery. Most recently, he had an arterial bypass on his right leg due to blockage. He still has the staples in his leg from that, but is doing ok considering he is 77 years old, still drinks and smokes, and won't eat like I tell him he ought to - these parents, they just won't listen ;) By the way, my dad's cholesterol level was 240 when he was around 70 years old. 240 is not really that high considering his age.
I'm not sure how much of his problems are caused by smoking and how much by a less than ideal diet over the years, but I'm trying to take measures to avoid what he has gone through. I never smoked, so that's not something I have to worry about. I've learned over the past few years through quite a bit of reading (books and net) that this low carb diet is the best thing I can do to avoid the complications he has went through. I want to stress that this low carb diet that I follow (similar to "Protein Power LifePlan") revolves around whole natural foods, not convenience or highly processed foods. I eat things like grass fed beef, venison, eggs, poultry, pork, fish, some dairy, and lots of green vegetables with a few low-sugar fruits thrown in. This diet (it is really a way of life now) works for me, and that is based on objective evidence - close to ideal bodyweight (6'0" tall, 185#, 15% bodyfat - if I would get away from this computer and exercise a little more I could drop that last few pounds), "normal" cholesterol levels, good lipid ratios (triglyceride/HDL < 2.0), normal/low bloodpressure (typically 105-115/55-65), and a normal CBC.
Alan
arkie6, I would like to know have you had a heart attack or been diagnosed with high cholesterol?
Nope. No heart attack and as far as I know I never had high cholesterol, but I never had it checked before starting a low carbohydrate diet about 4 years ago at 32 years of age. About a year or so after starting that diet and losing about 40 pounds, my total cholesterol was 198 or so. My most recent test (about a year ago) shows TC=187, HDL=60, triglycerides=115, and I forget the LDL, but it was "normal".
My father on the other hand has significant cardiovascular disease. He didn't have a heart attack, but due to severe angina they found significant blockage in 4 of his coronary arteries. He had bypass surgery about 8 years ago for that. About 5 years prior to that they found significant blockage in his carotid arteries. Both of those were opened up via surgery. Most recently, he had an arterial bypass on his right leg due to blockage. He still has the staples in his leg from that, but is doing ok considering he is 77 years old, still drinks and smokes, and won't eat like I tell him he ought to - these parents, they just won't listen ;) By the way, my dad's cholesterol level was 240 when he was around 70 years old. 240 is not really that high considering his age.
I'm not sure how much of his problems are caused by smoking and how much by a less than ideal diet over the years, but I'm trying to take measures to avoid what he has gone through. I never smoked, so that's not something I have to worry about. I've learned over the past few years through quite a bit of reading (books and net) that this low carb diet is the best thing I can do to avoid the complications he has went through. I want to stress that this low carb diet that I follow (similar to "Protein Power LifePlan") revolves around whole natural foods, not convenience or highly processed foods. I eat things like grass fed beef, venison, eggs, poultry, pork, fish, some dairy, and lots of green vegetables with a few low-sugar fruits thrown in. This diet (it is really a way of life now) works for me, and that is based on objective evidence - close to ideal bodyweight (6'0" tall, 185#, 15% bodyfat - if I would get away from this computer and exercise a little more I could drop that last few pounds), "normal" cholesterol levels, good lipid ratios (triglyceride/HDL < 2.0), normal/low bloodpressure (typically 105-115/55-65), and a normal CBC.
Alan
TB
03-19-2002, 06:46 PM
hunter44,thanks for your answer.At least you do see the difference.One thing to remember.There are people like myself that come here to get information to help ourselves.The perspective changes if you have had a heart attack or have CAD.I hope that it works for you and I am hoping to hear good news from you on your results.It may be something I can look into,and apply the parts that I can to my situation.
Cholesterol readings were not that bad for me.My TC was always in the 170-180 range.My HDL was low at 29.I had the other risk factors which I am sure contributed to my heart attacks.
As for the blood thinning properties of the statin,that may be true.I only know that for the first year I was on Lescol,a baby apsirin,and Coumadin.I would think that there would be a minimal thinning if any on the statin.
I am currently taking Zocor and Niaspan.They are trying to see if my blockages can be reversed with this therapy.You can say that I am a guinea pig.
Arkie6,thanks for your answer.You have a higher risk because of your father.You seem to be doing things the right way.It is hard to overcome heredity.My father had his first at 45.Best of luck to both you and your father.
Both of you have validated my earlier point.You are trying to do things to improve your chances,your cholesterol levels,even though there are statistics and studies that show otherwise.You do not want to be where I am at.That is commendable.
Cholesterol readings were not that bad for me.My TC was always in the 170-180 range.My HDL was low at 29.I had the other risk factors which I am sure contributed to my heart attacks.
As for the blood thinning properties of the statin,that may be true.I only know that for the first year I was on Lescol,a baby apsirin,and Coumadin.I would think that there would be a minimal thinning if any on the statin.
I am currently taking Zocor and Niaspan.They are trying to see if my blockages can be reversed with this therapy.You can say that I am a guinea pig.
Arkie6,thanks for your answer.You have a higher risk because of your father.You seem to be doing things the right way.It is hard to overcome heredity.My father had his first at 45.Best of luck to both you and your father.
Both of you have validated my earlier point.You are trying to do things to improve your chances,your cholesterol levels,even though there are statistics and studies that show otherwise.You do not want to be where I am at.That is commendable.
LooneyJM
03-20-2002, 12:21 PM
What a great thread!
I'm here too, to learn about prevention since having angioplasty 18 months ago.
I have come to the conclusion that Triglycerides and HDL play a bigger factor than LDL. My Tri's were 573 and HDL 33 when they found the blockage in a stress test (at 41). I had been on a low-fat diet for almost 10 years at the time (with sugar/carb ignorance).
My dad had a fatal MI back in the 60's at 33! The first didn't kill him but the doctors gave him diet pills to loose weight. Guess it was standard back then. He lost the weight but his brother claimed the 'speed' gave him the 2nd fatal 1 year later.
Diet alone solved my bad numbers. My trigs are 108 and HDL are 45 (and rising). I found out about Syndrome-X on the web - sure enough, it was the cure (along with daily cardio workout).
As for the statins, I was getting aches and pains. My boss recently said he noticed a change in my attitude and I seemed 'pissed off' alot. There were times I felt 'not suicidal - more homicidal'. I quit taking them last week and will let you know!
I'm here too, to learn about prevention since having angioplasty 18 months ago.
I have come to the conclusion that Triglycerides and HDL play a bigger factor than LDL. My Tri's were 573 and HDL 33 when they found the blockage in a stress test (at 41). I had been on a low-fat diet for almost 10 years at the time (with sugar/carb ignorance).
My dad had a fatal MI back in the 60's at 33! The first didn't kill him but the doctors gave him diet pills to loose weight. Guess it was standard back then. He lost the weight but his brother claimed the 'speed' gave him the 2nd fatal 1 year later.
Diet alone solved my bad numbers. My trigs are 108 and HDL are 45 (and rising). I found out about Syndrome-X on the web - sure enough, it was the cure (along with daily cardio workout).
As for the statins, I was getting aches and pains. My boss recently said he noticed a change in my attitude and I seemed 'pissed off' alot. There were times I felt 'not suicidal - more homicidal'. I quit taking them last week and will let you know!
hunter44
03-20-2002, 12:35 PM
Arkie6 - Can you send me some venison since I didn't get my deer this year? Bottom line is that most doctors treat the symptom rather than the cause. Here - take this pill, and, some people think they are cured!
TB
03-20-2002, 04:00 PM
LooneyJM,good to see you on the board.
What prompted the stress test?
If diet lowered your numbers then why did the Dr. put you on a statin? What were your other numbers? Are these new numbers with or without the statin? Which statin and what dosage?
You have to remember that you are now in a different risk factor.You do not have the luxury of "playing" with these numbers as alot of people here can. If diet alone keeps your numbers down,which you already know are lower then the current standards,then great.If not then you need to pursue this aggressively.You are on a short time scale.The plasty usually lasts 3-5 years before it has to be repeated.You should be on some of the newer pharmacology treatments to help keep your arteries from blocking again.
Your sysmptoms are somewhat common.You need to remember that you already have the disease,and that you are fighting heredity with the cholesterol.I experience aches and pains from time to time.If yours were constant and severe then you needed to go back to the Dr. and see what could be done.As far as the mood goes,you need to work at it.It takes conscious effort to keep it under control.
Best of luck.
What prompted the stress test?
If diet lowered your numbers then why did the Dr. put you on a statin? What were your other numbers? Are these new numbers with or without the statin? Which statin and what dosage?
You have to remember that you are now in a different risk factor.You do not have the luxury of "playing" with these numbers as alot of people here can. If diet alone keeps your numbers down,which you already know are lower then the current standards,then great.If not then you need to pursue this aggressively.You are on a short time scale.The plasty usually lasts 3-5 years before it has to be repeated.You should be on some of the newer pharmacology treatments to help keep your arteries from blocking again.
Your sysmptoms are somewhat common.You need to remember that you already have the disease,and that you are fighting heredity with the cholesterol.I experience aches and pains from time to time.If yours were constant and severe then you needed to go back to the Dr. and see what could be done.As far as the mood goes,you need to work at it.It takes conscious effort to keep it under control.
Best of luck.
Carreen
03-21-2002, 12:17 AM
Loonyjm, Syndrome X or Metabolic Syndrome is a cluster of risk factors. The cause isn't fully understood but people who have this are at higher risk of coronary artery disease. Syndrome X has been observed in people who are insulin-resistant. One such group is people with diabetes, who have a defect in insulin action and can't maintain a proper level of glucose in their blood. Are you diabetic? Another is people, mainly those with high blood pressure, who are nondiabetic and insulin-resistant but who compensate by secreting large amounts of insulin. This condition is known as hyperinsulinemia. A third group is heart attack survivors who, unlike people with hypertension, have hyperinsulinemia without having abnormal glucose levels.
I'm assuming you think you have syndrome x and I just wondered if you had been tested and diagnosed with this.
The cluster of risks include:
central obesity (excessive fat tissue in the abdominal region) Are you fat around the middle?
glucose intolerance-Have you ever had your glucose monitored? One of the main concerns with impaired fasting glucose is that it is often seen in people who also have high blood pressure and elevated cholesterol or triglyceride (blood fat) levels. A major reason why impaired fasting glucose should be treated before it even progresses to diabetes is to reduce the blood glucose levels, which may also reduce triglycerides and other measures.
hyperlipidemia - primarily high triglycerides and low HDL cholesterol I see you have this.
high blood pressure -Do you have high blood pressure?
If you don't have these conditions, it's unlikely that you have metabolic syndrome and that cholesterol may indeed play a bigger role than you realise.
This condition can be diagnosed fairly easily.
You need to get your blood sugar checked (over 100 may be a sign of insulin resistance) and your insulin level as well. If you do a glucose tolerance test (2hr GTT) also have your doctor order a fasting and 2 hr insulin level.
I'm just saying it's in your best health interest to know FOR SURE you have this instead of guessing so that a proper diagnosis and treament can be reached.
I'm assuming you think you have syndrome x and I just wondered if you had been tested and diagnosed with this.
The cluster of risks include:
central obesity (excessive fat tissue in the abdominal region) Are you fat around the middle?
glucose intolerance-Have you ever had your glucose monitored? One of the main concerns with impaired fasting glucose is that it is often seen in people who also have high blood pressure and elevated cholesterol or triglyceride (blood fat) levels. A major reason why impaired fasting glucose should be treated before it even progresses to diabetes is to reduce the blood glucose levels, which may also reduce triglycerides and other measures.
hyperlipidemia - primarily high triglycerides and low HDL cholesterol I see you have this.
high blood pressure -Do you have high blood pressure?
If you don't have these conditions, it's unlikely that you have metabolic syndrome and that cholesterol may indeed play a bigger role than you realise.
This condition can be diagnosed fairly easily.
You need to get your blood sugar checked (over 100 may be a sign of insulin resistance) and your insulin level as well. If you do a glucose tolerance test (2hr GTT) also have your doctor order a fasting and 2 hr insulin level.
I'm just saying it's in your best health interest to know FOR SURE you have this instead of guessing so that a proper diagnosis and treament can be reached.
LooneyJM
03-22-2002, 01:27 PM
I never had a test for diabetes and didn't have any symptoms of heart disease. I had risk factors, high LDL, low HDL, very high triglycerides, and overweight/no excercise.
My brother has a very wise doctor who suggested he have a stress test done (bro has same symptoms). He had the test done, it was positive and he had angiplasty.
I told my doc and he sent me for one - same results - DOH. It makes me wonder if folks in high risk should get one done as a standard 'over 40' test?
Anyway, I made radical changes in diet, excercise daily and lost 50lbs. Take lots of supplements and was taking Lipitor until last week - too many problems. I'm not sure what he'll suggest to replace it yet.
C ya
My brother has a very wise doctor who suggested he have a stress test done (bro has same symptoms). He had the test done, it was positive and he had angiplasty.
I told my doc and he sent me for one - same results - DOH. It makes me wonder if folks in high risk should get one done as a standard 'over 40' test?
Anyway, I made radical changes in diet, excercise daily and lost 50lbs. Take lots of supplements and was taking Lipitor until last week - too many problems. I'm not sure what he'll suggest to replace it yet.
C ya
arkie6
03-23-2002, 02:00 PM
While not strictly related to the topic of exercise and cholesterol, the following link does relate to the direction of where this topic has headed, that being the relationship between cholesterol and coronary heart disease (CHD). This link: http://www.hsph.harvard.edu/reviews/transfats.html from the Harvard School of Public Health is titled “TRANS FATTY ACIDS AND CORONARY HEART DISEASE”
This article paints a picture that the past focus on saturated fats as being the culprit behind coronary heart disease has been misguided for the most part. The primary focus on the causes behind coronary heart disease should have been on trans fatty acids, which are formed during the creation of partially hydrogenated vegetable oils - one of the major frankenfoods created during the 20th century.
Here are some excerpts from the article:
“Concerns have been raised for several decades that consumption of trans fatty acids might have contributed to the 20th century epidemic of coronary heart disease...
...Metabolic studies have shown that trans fats have adverse effects on blood lipid levels--increasing LDL ("bad") cholesterol while decreasing HDL ("good") cholesterol. This combined effect on the ratio of LDL to HDL cholesterol is double that of saturated fatty acids...
...Trans fats have also been associated with an increased risk of coronary heart disease in epidemiologic studies...
...Trans fats are produced commercially in large quantities to harden vegetable oils into shortening and margarine. Food manufacturers also use partial hydrogenation of vegetable oil to destroy some fatty acids, such as linolenic and linoleic acid, which tend to oxidize, causing fat to become rancid with time. The oils used to cook french fries and other fast food are usually this kind of partially hydrogenated oil, containing trans fats. Commercial baked goods frequently include trans fats to protect against spoilage...
...The combined results of metabolic and epidemiologic studies strongly support an adverse effect of trans fat on risk of CHD. Furthermore, two independent methods of estimation indicate that the adverse effect of trans fat is stronger than that of saturated fat. By our most conservative estimate, replacement of partially hydrogenated fat in the U.S. diet with natural unhydrogenated vegetable oils would prevent approximately 30,000 premature coronary deaths per year, and epidemiologic evidence suggests this number is closer to 100,0000 premature deaths annually. These reductions are higher than what could be achieved with realistic reductions in saturated fat intake...
...Thus there appear to be no likely alternative to the hypothesis that high trans intake increases the risk of CHD...
...In summary, prospective studies provide strong evidence that trans fatty acids consumption increases substantially the risk of CHD...
...Five years ago evidence was strong that trans fat had deleterious impacts on blood lipids; ensuing studies have confirmed these metabolic findings and strengthened epidemiologic support for an important adverse effect on risk of coronary heart disease.”
End of article.
Natural saturated fats like those found in animal products, which humans have consumed for thousands of years, get blamed for all of societies relatively recent health ills and attention gets diverted from the real culprits - highly processed foods, partially hydrogenated vetegable oils in particular. Here is an interesting article that discusses how we ended up in this predicament: http://www.westonaprice.org/know_your_fats/oiling.html
It takes a lot of money to perform rigorous scientific studies. Over the last 20-30 years, the share of scientific research funded by governments has declined dramatically. Corporations now control the research agenda, even at prestigious universities. Enormously wealthy and powerful agribusiness cartels like Archer-Daniels Midland and Cargill have absolutely no interest in funding research which might prove their multi-billion-dollar product lines are slowly killing millions worldwide. If agribusiness does fund research, you can bet it will be either "inconclusive" (researcher wants another fat contract) or will claim the harm is negligible or imaginary (corporation feels it has paid enough). Medical research funded by manufacturers of the product being researched is biased, highly suspect, and likely corrupt in my opinion.
Alan
This article paints a picture that the past focus on saturated fats as being the culprit behind coronary heart disease has been misguided for the most part. The primary focus on the causes behind coronary heart disease should have been on trans fatty acids, which are formed during the creation of partially hydrogenated vegetable oils - one of the major frankenfoods created during the 20th century.
Here are some excerpts from the article:
“Concerns have been raised for several decades that consumption of trans fatty acids might have contributed to the 20th century epidemic of coronary heart disease...
...Metabolic studies have shown that trans fats have adverse effects on blood lipid levels--increasing LDL ("bad") cholesterol while decreasing HDL ("good") cholesterol. This combined effect on the ratio of LDL to HDL cholesterol is double that of saturated fatty acids...
...Trans fats have also been associated with an increased risk of coronary heart disease in epidemiologic studies...
...Trans fats are produced commercially in large quantities to harden vegetable oils into shortening and margarine. Food manufacturers also use partial hydrogenation of vegetable oil to destroy some fatty acids, such as linolenic and linoleic acid, which tend to oxidize, causing fat to become rancid with time. The oils used to cook french fries and other fast food are usually this kind of partially hydrogenated oil, containing trans fats. Commercial baked goods frequently include trans fats to protect against spoilage...
...The combined results of metabolic and epidemiologic studies strongly support an adverse effect of trans fat on risk of CHD. Furthermore, two independent methods of estimation indicate that the adverse effect of trans fat is stronger than that of saturated fat. By our most conservative estimate, replacement of partially hydrogenated fat in the U.S. diet with natural unhydrogenated vegetable oils would prevent approximately 30,000 premature coronary deaths per year, and epidemiologic evidence suggests this number is closer to 100,0000 premature deaths annually. These reductions are higher than what could be achieved with realistic reductions in saturated fat intake...
...Thus there appear to be no likely alternative to the hypothesis that high trans intake increases the risk of CHD...
...In summary, prospective studies provide strong evidence that trans fatty acids consumption increases substantially the risk of CHD...
...Five years ago evidence was strong that trans fat had deleterious impacts on blood lipids; ensuing studies have confirmed these metabolic findings and strengthened epidemiologic support for an important adverse effect on risk of coronary heart disease.”
End of article.
Natural saturated fats like those found in animal products, which humans have consumed for thousands of years, get blamed for all of societies relatively recent health ills and attention gets diverted from the real culprits - highly processed foods, partially hydrogenated vetegable oils in particular. Here is an interesting article that discusses how we ended up in this predicament: http://www.westonaprice.org/know_your_fats/oiling.html
It takes a lot of money to perform rigorous scientific studies. Over the last 20-30 years, the share of scientific research funded by governments has declined dramatically. Corporations now control the research agenda, even at prestigious universities. Enormously wealthy and powerful agribusiness cartels like Archer-Daniels Midland and Cargill have absolutely no interest in funding research which might prove their multi-billion-dollar product lines are slowly killing millions worldwide. If agribusiness does fund research, you can bet it will be either "inconclusive" (researcher wants another fat contract) or will claim the harm is negligible or imaginary (corporation feels it has paid enough). Medical research funded by manufacturers of the product being researched is biased, highly suspect, and likely corrupt in my opinion.
Alan
arkie6
04-11-2003, 04:51 PM
I just wanted to bump this thread back up near the top so that those new to the boards could find it and read it if so inclined.
CobaltBlue
04-13-2003, 11:16 AM
Originally posted by arkie6:
These studies by and large show no positive connection between the consumption of saturated animal fat and heart disease, cancer, diabetes, or obesity. In fact, they show an inverse relationship – the more animal protein and fat consumed, the less prevalent was the disease studied. What is implicated as causal factors in these all too common health concerns today is the increased consumption of sugar, refined flour, and polyunsaturated vegetable oils.
Alan,
I still think what Magpie said is just about right on when she said "different diets work for different people." The foods you eat were part of my "diet" when I had near 300 total cholesterol levels (was 290 in 1997 before being placed on Tricor). I posted my typical fast food meal in here, but my usual weeknight dinner favorite was deli meats sandwiched between pieces of swiss and cheddar cheese. My weekend breakfasts had eggs plus either sausage or bacon. I loved sausage, including hot dogs. My Saturday dinner consisted of the a rare prime rib heated for a short time in the oven. I would eat the leftovers of this for the next few days. Not sure how much weight of prime rib I was eating per night, but it was certainly 3-4 half inch thick slices off the roast. Forget the breads, desserts and the vegetables, I was a meat and cheese person--didn't even care for potatoes. That diet plus sedentary lifestyle earned me a blocked RCA and a blocked LAD at age 35, plus some irregularites were already seen in my circumflex.
By cutting out the red meat, large amounts of saturated fat in meats and cheeses, my cholesterol now hovers around 100 (between 94 and 102). My HDL is higher than ever noted in past lipid profiles, even when my total was 300.
I dropped low fat dairy products a few months back and went to soy milk and soy based cheeses only. This diet is the right one for me based not only the numbers but how I feel. My tolerance for exercise has increased greatly, such than I can run 3.1 miles every morning, doing about 8 min miles (when I started it was well over 10 min miles and I still felt angina). I have not felt angina now for over 6 months.
Some of us are best on an Atkins or other protein based diet, others are better on a low fat diet. I am not sure where I fit in now--possibly closer to some kind of vegetarian low-sat fat/avoid trans fat diet :)
These studies by and large show no positive connection between the consumption of saturated animal fat and heart disease, cancer, diabetes, or obesity. In fact, they show an inverse relationship – the more animal protein and fat consumed, the less prevalent was the disease studied. What is implicated as causal factors in these all too common health concerns today is the increased consumption of sugar, refined flour, and polyunsaturated vegetable oils.
Alan,
I still think what Magpie said is just about right on when she said "different diets work for different people." The foods you eat were part of my "diet" when I had near 300 total cholesterol levels (was 290 in 1997 before being placed on Tricor). I posted my typical fast food meal in here, but my usual weeknight dinner favorite was deli meats sandwiched between pieces of swiss and cheddar cheese. My weekend breakfasts had eggs plus either sausage or bacon. I loved sausage, including hot dogs. My Saturday dinner consisted of the a rare prime rib heated for a short time in the oven. I would eat the leftovers of this for the next few days. Not sure how much weight of prime rib I was eating per night, but it was certainly 3-4 half inch thick slices off the roast. Forget the breads, desserts and the vegetables, I was a meat and cheese person--didn't even care for potatoes. That diet plus sedentary lifestyle earned me a blocked RCA and a blocked LAD at age 35, plus some irregularites were already seen in my circumflex.
By cutting out the red meat, large amounts of saturated fat in meats and cheeses, my cholesterol now hovers around 100 (between 94 and 102). My HDL is higher than ever noted in past lipid profiles, even when my total was 300.
I dropped low fat dairy products a few months back and went to soy milk and soy based cheeses only. This diet is the right one for me based not only the numbers but how I feel. My tolerance for exercise has increased greatly, such than I can run 3.1 miles every morning, doing about 8 min miles (when I started it was well over 10 min miles and I still felt angina). I have not felt angina now for over 6 months.
Some of us are best on an Atkins or other protein based diet, others are better on a low fat diet. I am not sure where I fit in now--possibly closer to some kind of vegetarian low-sat fat/avoid trans fat diet :)
mvbech
04-14-2003, 10:51 AM
Some great posts - very helpful. I found that dietary changes alone didn't have the impact I'd hoped on my numbers. Excercise helped alot. I think the best approach is to address total lifestyle. Eat better - the partially hydrogenized fats in my opinion are the real concern, along with refined sugars in things like donuts and other pastries. Stay away from these and I think you'll see a change. Excercise is important for complete health. No doubt you will feel better physically and mentally, the benefits are tremendous. Good luck
Coureur
04-14-2003, 08:47 PM
Originally posted by hunter44:
Careen - I have a simple question, and I think I am correct in saying this. If 50% of the people that have heart attacks have low or slightly evalated cholesterol levels and 50% have high cholesterol levels, how can taking a statin to lower cholesterol change your risk, if both groups are 50%?
What you are saying would be true if 50% of the population had elevated cholesterol. But the number of people with elevated cholesterol is lower than 50%.
I don't know the exact numbers, but lets say that 10% of the population has elevated cholesterol and 90% is normal, then we'd have 10% of the population (the high cholesterol group)having 50% of the heart attacks and 90%(the normal/low cholesterol group) having the other 50% of the heart attacks.
As you can see with this example, the risk of heart attack would be much greater for the high cholesterol group even though 50% of the heart attacks occur in the low cholesterol group.
The point of the statin drugs is that they move you out of the high risk group and put you in the lower risk group. Doesn't mean that you can't still have a heart attack - just that the risk is lower.
Careen - I have a simple question, and I think I am correct in saying this. If 50% of the people that have heart attacks have low or slightly evalated cholesterol levels and 50% have high cholesterol levels, how can taking a statin to lower cholesterol change your risk, if both groups are 50%?
What you are saying would be true if 50% of the population had elevated cholesterol. But the number of people with elevated cholesterol is lower than 50%.
I don't know the exact numbers, but lets say that 10% of the population has elevated cholesterol and 90% is normal, then we'd have 10% of the population (the high cholesterol group)having 50% of the heart attacks and 90%(the normal/low cholesterol group) having the other 50% of the heart attacks.
As you can see with this example, the risk of heart attack would be much greater for the high cholesterol group even though 50% of the heart attacks occur in the low cholesterol group.
The point of the statin drugs is that they move you out of the high risk group and put you in the lower risk group. Doesn't mean that you can't still have a heart attack - just that the risk is lower.
Gatormom
04-15-2003, 04:38 PM
Just an interested reader here.... wishing to say THANKS to all the folks who have posted so much valuable info! It's very educational just reading through the whole dialogue. Thank you all.
brad61tn
05-02-2003, 10:27 PM
Originally posted by LooneyJM:
1. From my earlier post -
Even LIPITOR claims it hasn't been proved on thier website. It's been proved that it causes cancer and many side effects.
Anyone wish to comment?
2. Am I to believe my primary physician and cardio? They have NEVER commented/asked about my diet, loss of 50 lbs or ANY bloodwork other than LDL. My tri's went from 600 to 108 (on a diet advice found on the internet) and they say NOTHING.
3. So going with the LDL theory - If my number is 153, I'm at risk - if I take drugs and get it below 100, I can live happily everafter. I don't buy it.
4. I am hearing more and more that it's HDL and Trig's that predict heart disease.
What diet did you use?
1. From my earlier post -
Even LIPITOR claims it hasn't been proved on thier website. It's been proved that it causes cancer and many side effects.
Anyone wish to comment?
2. Am I to believe my primary physician and cardio? They have NEVER commented/asked about my diet, loss of 50 lbs or ANY bloodwork other than LDL. My tri's went from 600 to 108 (on a diet advice found on the internet) and they say NOTHING.
3. So going with the LDL theory - If my number is 153, I'm at risk - if I take drugs and get it below 100, I can live happily everafter. I don't buy it.
4. I am hearing more and more that it's HDL and Trig's that predict heart disease.
What diet did you use?
arkie6
10-20-2004, 07:28 PM
Time to bump this thread back to the top.
Writergrl
10-26-2004, 06:07 PM
Exercise in and of itself does not reduce total cholesterol...your parents (what's in your genes) as well as what you eat determine that...what exercise does do, though, is RAISE HDL, or the good cholesterol. And more importantly are the numbers associated with cholesterol, mainly your heart disease "risk factor" ratio. What that is, is your total cholesterol divided by your HDL. (TC/HDL) A ratio of 4.5 or less is desirable. Your triglycerides should be below 150; your HDL should be above 40, the higher the better, and your LDL should be less than 130.
I might note here, also, that studies have proven that the percentage of those with total cholesterol levels lower than 200, have still been found to have heart attacks. So more care needs to be taken in not only the total cholesterol, but also what I have included above as well.
in good health,
Writergrl.
I might note here, also, that studies have proven that the percentage of those with total cholesterol levels lower than 200, have still been found to have heart attacks. So more care needs to be taken in not only the total cholesterol, but also what I have included above as well.
in good health,
Writergrl.
Dave440
10-27-2004, 07:22 PM
maybe I'm a bit late here but what I do know about exersise and cholesterol is it can really benefit in lowering LDL but studies have shown that you would need to keep up a really decent exercise program for at least 6 months before you start to see an elevation in HDL. This info comes from a couple college friends of mine, one being a doctor and another is a fitness trainer and chiropractor. But even that they said won't gaurentee an increase in HDL and will really make a difference in LDL and VLDL levels.
I was concerned about it since I had an HDL of 36 a little while ago (LDL of 115 and Trig of 50) and wanted to know if exercise would raise my HDL. I was told on focusing on just naturally lowering my LDL and I at the current state since I'm young (29) and only slightly overweight, I don't have to stress out and they told me that my numbers were totally fine.
I was concerned about it since I had an HDL of 36 a little while ago (LDL of 115 and Trig of 50) and wanted to know if exercise would raise my HDL. I was told on focusing on just naturally lowering my LDL and I at the current state since I'm young (29) and only slightly overweight, I don't have to stress out and they told me that my numbers were totally fine.
jtu91952
10-27-2004, 07:31 PM
Dave, i was told ldl was lowered with exercise also.
CobaltBlue
10-28-2004, 08:24 AM
I was concerned about it since I had an HDL of 36 a little while ago (LDL of 115 and Trig of 50) and wanted to know if exercise would raise my HDL. I was told on focusing on just naturally lowering my LDL and I at the current state since I'm young (29) and only slightly overweight, I don't have to stress out and they told me that my numbers were totally fine.
In many cases it will raise it Dave, but what is left out from the thinking (and may become increasingly important as more is understood) is the distribution of the particle sizes of the lipoprotein groups. The data indicate that there is an association between the size of the HDL (and LDL) particles and increased heart disease risk. It's the smaller dense particles that are worse (for LDL, IDL, VLDL) and smaller, dense HDL are not associated with being the most beneficial types of HDL. Two ways to shift the particle sizes to the larger form are exercise and high doses of niacin.
I found diet to play a larger role in reduction of LDL levels (and actually it lowered my HDL too). Exercise and weight loss did lower my VLDL by a huge amount, however. Exercise did raise my HDL level--more than doubled it.
In many cases it will raise it Dave, but what is left out from the thinking (and may become increasingly important as more is understood) is the distribution of the particle sizes of the lipoprotein groups. The data indicate that there is an association between the size of the HDL (and LDL) particles and increased heart disease risk. It's the smaller dense particles that are worse (for LDL, IDL, VLDL) and smaller, dense HDL are not associated with being the most beneficial types of HDL. Two ways to shift the particle sizes to the larger form are exercise and high doses of niacin.
I found diet to play a larger role in reduction of LDL levels (and actually it lowered my HDL too). Exercise and weight loss did lower my VLDL by a huge amount, however. Exercise did raise my HDL level--more than doubled it.
zip2play
10-28-2004, 09:42 AM
Dave,
A potent excercise program since January has given me markedly LOWERED HDL. It's a big disappointment but I will just need more devious means to get it back up. For me, it seems moderate drinking is the way to go (rather than teetotalling.)
Unfortunately for me, the two words MODERATE and DRINKING never seem to belong in the same sentence, nor even the same PARAGRAPH! But I will persevere with hypnosis and will try my damndest to make my next stab at drinking TWO DRINKS A DAY, no more, no less!
A potent excercise program since January has given me markedly LOWERED HDL. It's a big disappointment but I will just need more devious means to get it back up. For me, it seems moderate drinking is the way to go (rather than teetotalling.)
Unfortunately for me, the two words MODERATE and DRINKING never seem to belong in the same sentence, nor even the same PARAGRAPH! But I will persevere with hypnosis and will try my damndest to make my next stab at drinking TWO DRINKS A DAY, no more, no less!
ARIZONA73
10-28-2004, 11:01 AM
Zip2play,
Well, if you want to keep the number of drinks to a minimum, just use a larger glass. :D
Well, if you want to keep the number of drinks to a minimum, just use a larger glass. :D
Dave440
10-28-2004, 01:29 PM
Dave,
A potent excercise program since January has given me markedly LOWERED HDL. It's a big disappointment but I will just need more devious means to get it back up. For me, it seems moderate drinking is the way to go (rather than teetotalling.)
Unfortunately for me, the two words MODERATE and DRINKING never seem to belong in the same sentence, nor even the same PARAGRAPH! But I will persevere with hypnosis and will try my damndest to make my next stab at drinking TWO DRINKS A DAY, no more, no less!
too funny. Yeah you know when I went in for my physical, I had been on a really rough and regimental exercise program for about 2 or 3 months prior. It was the first time EVER that doctor ever brought up cholesterol since prior to that there was no issue with my numbers and the only thing he was concerned about was my HDL.
I don't drink and tried to start a regimine of drinking a glass of red wine a night but it just doesn't stick since I've never been one to drink much alcohol (other than a few stupid parties in college!). So these days I'm eating more red grapes instead since I read it's the same thing. That along with flax seed oil and olive oil with salads and cut out over half my carbs.
A potent excercise program since January has given me markedly LOWERED HDL. It's a big disappointment but I will just need more devious means to get it back up. For me, it seems moderate drinking is the way to go (rather than teetotalling.)
Unfortunately for me, the two words MODERATE and DRINKING never seem to belong in the same sentence, nor even the same PARAGRAPH! But I will persevere with hypnosis and will try my damndest to make my next stab at drinking TWO DRINKS A DAY, no more, no less!
too funny. Yeah you know when I went in for my physical, I had been on a really rough and regimental exercise program for about 2 or 3 months prior. It was the first time EVER that doctor ever brought up cholesterol since prior to that there was no issue with my numbers and the only thing he was concerned about was my HDL.
I don't drink and tried to start a regimine of drinking a glass of red wine a night but it just doesn't stick since I've never been one to drink much alcohol (other than a few stupid parties in college!). So these days I'm eating more red grapes instead since I read it's the same thing. That along with flax seed oil and olive oil with salads and cut out over half my carbs.
ARIZONA73
10-28-2004, 01:45 PM
Zip2play,
Let's see now. We need to get your HDL back on track. May I offer a suggestion? Well, for dinner tonight, how does a nice thick Porterhouse steak topped with mushrooms and onions sound? Medium-rare of course. But hold the potatoes. Instead, make a nice big salad smothered in olive oil dressing, topped with chopped raw onions, garlic, and tomatoes. A nice glass of Burgundy wine offers a perfect compliment to such a meal.
Let's see now. We need to get your HDL back on track. May I offer a suggestion? Well, for dinner tonight, how does a nice thick Porterhouse steak topped with mushrooms and onions sound? Medium-rare of course. But hold the potatoes. Instead, make a nice big salad smothered in olive oil dressing, topped with chopped raw onions, garlic, and tomatoes. A nice glass of Burgundy wine offers a perfect compliment to such a meal.
zip2play
10-28-2004, 03:49 PM
"Get thee behind me, Atkins!"<holding two crucifixes in front of Arizona>
Gonna be roast chicken and Brussels sprouts with cheese sauce. I know, pretty Low carb...but Chocolate Chips Deluxe were half price at Shoprite today:D:D so I may have to TASTE one or sixteen! ...but I'll hold the wine til I make a sensible plan (and a hypnosis tape) for this drinking thing. If I just plunge in without prepping, I'll be drinking my typical 4 martinis by Monday (12 ounces of gin) which I do not want or need.
Gonna be roast chicken and Brussels sprouts with cheese sauce. I know, pretty Low carb...but Chocolate Chips Deluxe were half price at Shoprite today:D:D so I may have to TASTE one or sixteen! ...but I'll hold the wine til I make a sensible plan (and a hypnosis tape) for this drinking thing. If I just plunge in without prepping, I'll be drinking my typical 4 martinis by Monday (12 ounces of gin) which I do not want or need.
ARIZONA73
10-28-2004, 04:51 PM
Roast chicken and brussel sprouts are fine, but take those cookies back to Shop-Rite. From now on your snacks are to consist of walnuts, almonds, cashews, pecans, brazil, and hazelnuts. When it comes to seafood, salmon, sardines, and bluefish (my favorite :D ) are excellent.
zip2play
10-29-2004, 09:06 AM
No ARIZONA, I went the Atkins route 3 times since the 70's when it first reared its head.
The LAST time I became the king of the Low Carb boards amassing some 30,000 posts. I even found some of my recommendations echoed in several of the 65 "new editions" of the same Atkins' preaching. I could tell because often the wording was EXACTLY mine!
No force on the planet can convince me to even BEGIN to think in those terms again. I found the diet DANGEROUS and a sure way to destroy my heart, as it did the "good" doctor's.
Even the newly added gospel additions like the "limit the cheese; and only a couple Tbsp of heavy cream; and the monosaturated fats instead of saturated" do not impress me that high fat eating...including the force fed macadamias:D...is in any way less dangerous than we were led to believe in the decades B.A. (before Atkins.)
"I have been to the mountain...and I ESCAPED!"...zip2play memoirs.
Bluefish...yeccch. I'll have a nice grilled trout, thank you! :bouncing:
The LAST time I became the king of the Low Carb boards amassing some 30,000 posts. I even found some of my recommendations echoed in several of the 65 "new editions" of the same Atkins' preaching. I could tell because often the wording was EXACTLY mine!
No force on the planet can convince me to even BEGIN to think in those terms again. I found the diet DANGEROUS and a sure way to destroy my heart, as it did the "good" doctor's.
Even the newly added gospel additions like the "limit the cheese; and only a couple Tbsp of heavy cream; and the monosaturated fats instead of saturated" do not impress me that high fat eating...including the force fed macadamias:D...is in any way less dangerous than we were led to believe in the decades B.A. (before Atkins.)
"I have been to the mountain...and I ESCAPED!"...zip2play memoirs.
Bluefish...yeccch. I'll have a nice grilled trout, thank you! :bouncing:
heart44
10-31-2004, 01:25 AM
Not sure if anyone has mentioned this, but statins can make a person "exercise intolerant". Interesting that our doctors tell us to exercise, but this drug can prevent us from doing one of the most important things to help us.
QUOTE: The reduction of CoQ10 levels might be associated with myopathy, a rare adverse effect associated with statin drugs. This metabolic myopathy is related to ubiquinone (CoQ10) deficiency in muscle cell mitochondria, disturbing normal cellular respiration and causing adverse effects such as rhabdomyolysis, exercise intolerance, and recurrent myoglobinuria. (DiMuro S., Exercise intolerance and the mitochondrial respiratory chain. Ital J Neurol Sci. Dec. 1999.... END QUOTE
QUOTE: The reduction of CoQ10 levels might be associated with myopathy, a rare adverse effect associated with statin drugs. This metabolic myopathy is related to ubiquinone (CoQ10) deficiency in muscle cell mitochondria, disturbing normal cellular respiration and causing adverse effects such as rhabdomyolysis, exercise intolerance, and recurrent myoglobinuria. (DiMuro S., Exercise intolerance and the mitochondrial respiratory chain. Ital J Neurol Sci. Dec. 1999.... END QUOTE
zip2play
10-31-2004, 06:53 AM
Well, certainly any myopatic procces would leave most of us "exercise intolerant" in the same way that a pulled muscle would. But I doubt there is anything more direct.
Myopathy hurts (it means muscle pain), and those people who get it bad from statins would probably discontinue them.
Really your quote actually says that low levels of CoQ10 cause pain and make people exercise intorlerant
Myopathy hurts (it means muscle pain), and those people who get it bad from statins would probably discontinue them.
Really your quote actually says that low levels of CoQ10 cause pain and make people exercise intorlerant
heart44
11-01-2004, 01:02 AM
Myopathy hurts (it means muscle pain), and those people who get it bad from statins would probably discontinue them.
Myopathy is more than just "muscle pain". Myopathy can range from a cramp to Rhabdomyolysis [Rhabdomyolysis is the breakdown of muscle fibers resulting in the release of muscle fiber contents into the circulation. Some of these are toxic to the kidney and frequenty result in kidney damage.]
Definition from the National Institute of Neurological Disorders and Stroke:
What is Myopathy?
The myopathies are neuromuscular disorders in which the primary symptom is muscle weakness due to dysfunction of muscle fiber. Other symptoms of myopathy can include muscle cramps, stiffness, and spasm. Myopathies can be inherited (such as the muscular dystrophies) or acquired (such as common muscle cramps).
Myopathies are grouped as follows:
- a simple classification of myopathy:-
Hereditary
muscular dystrophies
congenital myopathies
myotonias
channelopathies (periodic paralysis syndromes)
metabolic myopathies
mitochondrial myopathies
Acquired
inflammatory myopathy
endocrine myopathies
drug-induced/toxic myopathies
myopathy associated with systemic illness
**************************************** ****************
Drug-induced myopathy
lipid-lowering agents (statins, clofibrate and gemfibrizol)
agents that cause hypokalemia (diuretics, theophylline, amphotericin B)
lithium
succinylcholine
antibiotics (trimethoprim, isoniazid)
anticonvulsants (valproic acid, lamotrigine, prolonged propofol infusion)
vasopressin
colchicine, episilon aminocaproic acid, high dose alfa-interferon
illicit drugs (cocaine, heroin, phencyclidine, amphetamines)
**************************************** ****************
My point was that statins deplete the body of CoQ10. Low levels of CoQ10
can cause myopathy. Myopathy can make it difficult or impossible to
exercise. A rather vicious circle.
Myopathy is more than just "muscle pain". Myopathy can range from a cramp to Rhabdomyolysis [Rhabdomyolysis is the breakdown of muscle fibers resulting in the release of muscle fiber contents into the circulation. Some of these are toxic to the kidney and frequenty result in kidney damage.]
Definition from the National Institute of Neurological Disorders and Stroke:
What is Myopathy?
The myopathies are neuromuscular disorders in which the primary symptom is muscle weakness due to dysfunction of muscle fiber. Other symptoms of myopathy can include muscle cramps, stiffness, and spasm. Myopathies can be inherited (such as the muscular dystrophies) or acquired (such as common muscle cramps).
Myopathies are grouped as follows:
- a simple classification of myopathy:-
Hereditary
muscular dystrophies
congenital myopathies
myotonias
channelopathies (periodic paralysis syndromes)
metabolic myopathies
mitochondrial myopathies
Acquired
inflammatory myopathy
endocrine myopathies
drug-induced/toxic myopathies
myopathy associated with systemic illness
**************************************** ****************
Drug-induced myopathy
lipid-lowering agents (statins, clofibrate and gemfibrizol)
agents that cause hypokalemia (diuretics, theophylline, amphotericin B)
lithium
succinylcholine
antibiotics (trimethoprim, isoniazid)
anticonvulsants (valproic acid, lamotrigine, prolonged propofol infusion)
vasopressin
colchicine, episilon aminocaproic acid, high dose alfa-interferon
illicit drugs (cocaine, heroin, phencyclidine, amphetamines)
**************************************** ****************
My point was that statins deplete the body of CoQ10. Low levels of CoQ10
can cause myopathy. Myopathy can make it difficult or impossible to
exercise. A rather vicious circle.
zip2play
11-01-2004, 09:05 AM
So, take CoQ-10...it's not rocket science!