Rick49
02-02-2005, 11:20 PM
...As you may have observed, I tend to be a very analytical person. Until I saw an improvement in my cholesterol from a low GI diet, I really didn't think to hard about why my cholesterol was high. This board has really enlightened my knowledge and has stimulated my desire to learn more about this process.
...I have learned that cholesterol is the foundation of a lot if not all of our gland's steroids or hormones, however you wish to speak of them. I got to thinking that maybe the mechanism by which the Low GI diet lowered cholesterol was that it takes the stress off of the panceras, therefore decreasing the need for insulin, the hormone of the pancreas, thereby decreasing the need for cholesterol to make the hormone.
...With my other chronic condition, I found that the adrenal gland played a big role. I was taking corticosteroids and found out the hard way that steroids will suppress the adrenal gland. Basically the brain sees the extra steroids floating around and tells the adrenal gland to back off because there's enough. The reason that caused problem is that the adrenal gland is the back up system to prevent low glucose levels and if it's not reacting, the glucose levels can get low.
...I got to thinking that if the adrenal gland is suppressed, then the need for cholesterol would also be decreased drastically since it wouldn't need the cholesterol to make any hormones. I also figured that there has probably been some studies done in regards to prednisone (corticosteroid) and cholesterol. Prednisone while being a medicine is also used in a lot of studies to suppress the adrenal gland.
...In the three studies I found, HDL levels rose sharply in the test subjects that were given prednisone. Given that, I would think that if the opposite was true and the adrenal gland was being called on to make a lot of hormones, that the HDL would go lower than normal, which leads me to the belief that any type of chronic stress that efects the adrenal system can lower HDL. This could be Mental stress, metabolic stress, or prolonged physical exertion. Since exercise helps cholesterol levels, it could be theorised that intermitant stress couldbe a good thing. But that seems to go with life, a little is good, but when it becomes chronic things go bad.
...I would be interested in your thoughts and here's the study:
The effect of prednisone therapy on plasma lipoproteins and apolipoproteins A-I, A-II, and E levels was studied prospectively in a heterogeneous group of six male and six female subjects. All patients were in a good general condition. The patients had normal hepatocellular, renal, and thyroid functions. During the first month of therapy, the following changes were noted: Plasma triglyceride (TG) levels increased slightly in female patients only. In the entire group, plasma cholesterol level increased (17.3% of initial value, P less than 0.01). Plasma high-density lipoprotein cholesterol (HDL-C) level increased by 68% (P less than 0.001), while plasma low-density lipoprotein cholesterol (LDL-C) level increased by only 10.9% (not significant), resulting in an increased ratio of cholesterol in the two (P less than 0.01). No change in levels of plasma apolipoproteins A-I, A-II, and E was evident. The ratio of HDL-C to plasma apolipoprotein A-I increased (P less than 0.01), indicating an increased lipid to protein ratio for this lipoprotein. Most of these changes were already apparent and significant 48 hours after initiation of treatment and persisted throughout the follow-up period (up to 18 months in some patients). Our results show that in patients with no major metabolic abnormality, prednisone induces significant changes of the lipoprotein system, especially in HDL.
...I have learned that cholesterol is the foundation of a lot if not all of our gland's steroids or hormones, however you wish to speak of them. I got to thinking that maybe the mechanism by which the Low GI diet lowered cholesterol was that it takes the stress off of the panceras, therefore decreasing the need for insulin, the hormone of the pancreas, thereby decreasing the need for cholesterol to make the hormone.
...With my other chronic condition, I found that the adrenal gland played a big role. I was taking corticosteroids and found out the hard way that steroids will suppress the adrenal gland. Basically the brain sees the extra steroids floating around and tells the adrenal gland to back off because there's enough. The reason that caused problem is that the adrenal gland is the back up system to prevent low glucose levels and if it's not reacting, the glucose levels can get low.
...I got to thinking that if the adrenal gland is suppressed, then the need for cholesterol would also be decreased drastically since it wouldn't need the cholesterol to make any hormones. I also figured that there has probably been some studies done in regards to prednisone (corticosteroid) and cholesterol. Prednisone while being a medicine is also used in a lot of studies to suppress the adrenal gland.
...In the three studies I found, HDL levels rose sharply in the test subjects that were given prednisone. Given that, I would think that if the opposite was true and the adrenal gland was being called on to make a lot of hormones, that the HDL would go lower than normal, which leads me to the belief that any type of chronic stress that efects the adrenal system can lower HDL. This could be Mental stress, metabolic stress, or prolonged physical exertion. Since exercise helps cholesterol levels, it could be theorised that intermitant stress couldbe a good thing. But that seems to go with life, a little is good, but when it becomes chronic things go bad.
...I would be interested in your thoughts and here's the study:
The effect of prednisone therapy on plasma lipoproteins and apolipoproteins A-I, A-II, and E levels was studied prospectively in a heterogeneous group of six male and six female subjects. All patients were in a good general condition. The patients had normal hepatocellular, renal, and thyroid functions. During the first month of therapy, the following changes were noted: Plasma triglyceride (TG) levels increased slightly in female patients only. In the entire group, plasma cholesterol level increased (17.3% of initial value, P less than 0.01). Plasma high-density lipoprotein cholesterol (HDL-C) level increased by 68% (P less than 0.001), while plasma low-density lipoprotein cholesterol (LDL-C) level increased by only 10.9% (not significant), resulting in an increased ratio of cholesterol in the two (P less than 0.01). No change in levels of plasma apolipoproteins A-I, A-II, and E was evident. The ratio of HDL-C to plasma apolipoprotein A-I increased (P less than 0.01), indicating an increased lipid to protein ratio for this lipoprotein. Most of these changes were already apparent and significant 48 hours after initiation of treatment and persisted throughout the follow-up period (up to 18 months in some patients). Our results show that in patients with no major metabolic abnormality, prednisone induces significant changes of the lipoprotein system, especially in HDL.
Sponsor
CobaltBlue
02-03-2005, 07:55 AM
I guess this goes to show that each of us finds different parts interesting...
What struck me was that the Apo A1, A2, and E remained at the same level while HDL increased. The reason that I focused in on those findings is because for the transport form of VLDL, it needs the ApoE from HDL, so it would seem reasonable that if HDL increased, so would the level of ApoE (and ApoC2 which was not measured?) Thinking of it that way, you would expect a direct correlation. Same applies to A1, which is believed to help transport the HDL to lesions. As for the A2 protein, I am not sure that there is a definitive answer yet on it's true role--other than it seems to exert an effect opposite of A1 with respect to binding and cholesterol uptake. I suppose what I notice as "interesting" is that this part of the mechanism is unaffected by the prednisone.
Oh, another thing about stress and exercise...there are some who would argue that exercise reduces stress. Here comes my own speculation, perhaps unfounded because I have not spent any time to look this up at all: I think that one physiological effect of stress is elevated blood pressure, and if not mistaken, elevation of both systolic and diastolic pressures. However, when healthy individuals exercise (well those w/o CAD/CHD, unlike me), the normal? response is that the systolic pressure rises and the diastolic maintains or drops slightly during exertion. Perhaps there is some truth to what I heard many years ago: the diastolic pressure is the more critical of the two? Anyway, just throwing that out there since your mentioning stress had me thinking about that situation.
What struck me was that the Apo A1, A2, and E remained at the same level while HDL increased. The reason that I focused in on those findings is because for the transport form of VLDL, it needs the ApoE from HDL, so it would seem reasonable that if HDL increased, so would the level of ApoE (and ApoC2 which was not measured?) Thinking of it that way, you would expect a direct correlation. Same applies to A1, which is believed to help transport the HDL to lesions. As for the A2 protein, I am not sure that there is a definitive answer yet on it's true role--other than it seems to exert an effect opposite of A1 with respect to binding and cholesterol uptake. I suppose what I notice as "interesting" is that this part of the mechanism is unaffected by the prednisone.
Oh, another thing about stress and exercise...there are some who would argue that exercise reduces stress. Here comes my own speculation, perhaps unfounded because I have not spent any time to look this up at all: I think that one physiological effect of stress is elevated blood pressure, and if not mistaken, elevation of both systolic and diastolic pressures. However, when healthy individuals exercise (well those w/o CAD/CHD, unlike me), the normal? response is that the systolic pressure rises and the diastolic maintains or drops slightly during exertion. Perhaps there is some truth to what I heard many years ago: the diastolic pressure is the more critical of the two? Anyway, just throwing that out there since your mentioning stress had me thinking about that situation.
Lenin
02-03-2005, 01:16 PM
Though interesting there are too many imponderables here.
First off, a definition of STRESS is required. it's one of those words that two people can use to mean almost the opposite, i.e, is exercise STRESS, or does exercise RELIEVE STRESS?
What is clear is that a dose of a synthetic cortisone raises blood cholesterol components, HDL more than LDL. Also it's clear that cortisone suppresses adrenal function.
Since the adrenals pour out hormones of various types with various functions, you would need a hypothesis about which hormone is being supressed that would normally lower these cholesterol components. Perhaps it's as simple as the fact that absent the adrenal hormones we become extremely sluggish and thus aren't able to burn off blood lipids as readily and perhaps the liver isn't able to deal with them as readily.
I believe that Exercise is a "Stress" (slowly growing to hate that word) and is dependent on lots of adrenal outpouring. Since the "common wisdom" has it that exercise raises HDL there seems to be a paradox (since adrenal shutdown raises cholesterol levels, HDL and LDL.)
My solution to the paradox is from my own personal observation that hard, regular exercise DOES NOT raise HDL so all seems well in my universe:D!
An aside,
Do you have any figures on the exact number of the cholesterol raise with prednisone...my reason, if a person has an HDL of 30 and an LDL of 200 and raises both by 20 points with prednisone, you'd get HDL increasing 67% and LDL increasing 10%...just musing (trying to avoid the gym!:D)
First off, a definition of STRESS is required. it's one of those words that two people can use to mean almost the opposite, i.e, is exercise STRESS, or does exercise RELIEVE STRESS?
What is clear is that a dose of a synthetic cortisone raises blood cholesterol components, HDL more than LDL. Also it's clear that cortisone suppresses adrenal function.
Since the adrenals pour out hormones of various types with various functions, you would need a hypothesis about which hormone is being supressed that would normally lower these cholesterol components. Perhaps it's as simple as the fact that absent the adrenal hormones we become extremely sluggish and thus aren't able to burn off blood lipids as readily and perhaps the liver isn't able to deal with them as readily.
I believe that Exercise is a "Stress" (slowly growing to hate that word) and is dependent on lots of adrenal outpouring. Since the "common wisdom" has it that exercise raises HDL there seems to be a paradox (since adrenal shutdown raises cholesterol levels, HDL and LDL.)
My solution to the paradox is from my own personal observation that hard, regular exercise DOES NOT raise HDL so all seems well in my universe:D!
An aside,
Do you have any figures on the exact number of the cholesterol raise with prednisone...my reason, if a person has an HDL of 30 and an LDL of 200 and raises both by 20 points with prednisone, you'd get HDL increasing 67% and LDL increasing 10%...just musing (trying to avoid the gym!:D)
Benzi
02-03-2005, 01:37 PM
You two confuse me to death. LOL Well I have a problem that I can't get off my mind and could not in a million years put it into those kind of words (I am the artistic type) here go's: Would having severe pancreatic damage due to a car accident cause my high cholesterol and fatty liver?
Background: Car accident 1989 Pancrea's was shredded (the Dr's words not mine) Hospitalized 9 weeks just barely escaped Whipple procedure (where they remove part or all of pancrea's) only after effects have been inability to drink alcohol and eat much pork or fatty meats. Some pain. Never been checked for diabetes since I left hospital do have severe hypoglycemia that actually wakes me up at night shaking.
Thyroid cancer 1991 total thyroidectemy taking .115 synthroid, possible reocurrance waiting for a scan. Through old lab reports I discovered that my tsh was never suppressed enough to prevent cancer reoccurance.
Having lots of pain in the kidney region (both sides) this just started 4 days ago. A CT done in early Dec. showed attenuation of liver to spleen possibly because of fatty infiltration.
Having more pain than usual from area of pancrea's.
Having nausea bouts off and on mostly if I am thinking about eating or actually eating.
After the car accident my cholesterol sky rocketed to 550 which I controlled (by diet) down to where it now runs between 287 and 305. PCP just wrote prescription for Lipitor which I have not filled yet.
My blood pressure is low runs about 100 or 60 normal and if I stand up it drops to about 90 over 56
I have never been overweight, I can't drink and can't eat fatty foods so I am wondering if my pancrea's has decided to go south and mess up my liver. I am also concerned about adrenal fatigue and have started to notice my skin is getting darker no matter how much sun screen I wear. PS don't spend any time in the sun except from house to car ect.... I am exhausted all the time, crave salt like there is no tomorrow. ( it actually makes me feel better to eat a lot of salt) always thirsty (small wonder), nightsweats and low grade evening fevers, my joints and muscles hurt all the time. Have a continuous headache. bouts of anxiety if I have do do anything (like go to grocery store) I have not lost weight. My thyroid tests are coming back ok. Not Hypothyroid. Any guesses? Does it sound like adrenal fatigue? I also had a hysterectomy in Feb last year and thats when all of this started. I am not on estrogen and I am 47 yrs old. I would be grateful if anyone can help with this I am almost at then end of my rope and I think my PCP is starting to think I might be losing it. I just can not bear to ask him any more questions right now.
Background: Car accident 1989 Pancrea's was shredded (the Dr's words not mine) Hospitalized 9 weeks just barely escaped Whipple procedure (where they remove part or all of pancrea's) only after effects have been inability to drink alcohol and eat much pork or fatty meats. Some pain. Never been checked for diabetes since I left hospital do have severe hypoglycemia that actually wakes me up at night shaking.
Thyroid cancer 1991 total thyroidectemy taking .115 synthroid, possible reocurrance waiting for a scan. Through old lab reports I discovered that my tsh was never suppressed enough to prevent cancer reoccurance.
Having lots of pain in the kidney region (both sides) this just started 4 days ago. A CT done in early Dec. showed attenuation of liver to spleen possibly because of fatty infiltration.
Having more pain than usual from area of pancrea's.
Having nausea bouts off and on mostly if I am thinking about eating or actually eating.
After the car accident my cholesterol sky rocketed to 550 which I controlled (by diet) down to where it now runs between 287 and 305. PCP just wrote prescription for Lipitor which I have not filled yet.
My blood pressure is low runs about 100 or 60 normal and if I stand up it drops to about 90 over 56
I have never been overweight, I can't drink and can't eat fatty foods so I am wondering if my pancrea's has decided to go south and mess up my liver. I am also concerned about adrenal fatigue and have started to notice my skin is getting darker no matter how much sun screen I wear. PS don't spend any time in the sun except from house to car ect.... I am exhausted all the time, crave salt like there is no tomorrow. ( it actually makes me feel better to eat a lot of salt) always thirsty (small wonder), nightsweats and low grade evening fevers, my joints and muscles hurt all the time. Have a continuous headache. bouts of anxiety if I have do do anything (like go to grocery store) I have not lost weight. My thyroid tests are coming back ok. Not Hypothyroid. Any guesses? Does it sound like adrenal fatigue? I also had a hysterectomy in Feb last year and thats when all of this started. I am not on estrogen and I am 47 yrs old. I would be grateful if anyone can help with this I am almost at then end of my rope and I think my PCP is starting to think I might be losing it. I just can not bear to ask him any more questions right now.
Lenin
02-03-2005, 03:33 PM
Benzi,
Gotta take this in little bites...
First off, I'd say your intolerance to fats is from an undersupply of bile, the caustic detergent that emulsifies fats after they leave the stomach. Most likely your gallbladder or the common duct (with the pancreas might be partially blocked.)
attenuation of liver to spleen possibly because of fatty infiltration
Could you amplify that; on face value it sounds like the liver has shrunk in relationship to the spleen or the spleen has grown too large? Usually fatty infiltration refers to the liver and causes a larger rather than a smaller liver.
With the hysterectomy, the thyroidectomy and the pancreatic shredding, it sounds like you need to be under the watchful eye of a good endocrinologist. Your hormones have GOT to be messed up and replacement therapy always leaves lots to be desired.
I wouldn't dwell on the adrenals, it would just add another couple variables to an already VERY complicated picture.
I would DEFINITELY take the Lipitor to avoid throwing cardiac problems into your mix.
Gotta take this in little bites...
First off, I'd say your intolerance to fats is from an undersupply of bile, the caustic detergent that emulsifies fats after they leave the stomach. Most likely your gallbladder or the common duct (with the pancreas might be partially blocked.)
attenuation of liver to spleen possibly because of fatty infiltration
Could you amplify that; on face value it sounds like the liver has shrunk in relationship to the spleen or the spleen has grown too large? Usually fatty infiltration refers to the liver and causes a larger rather than a smaller liver.
With the hysterectomy, the thyroidectomy and the pancreatic shredding, it sounds like you need to be under the watchful eye of a good endocrinologist. Your hormones have GOT to be messed up and replacement therapy always leaves lots to be desired.
I wouldn't dwell on the adrenals, it would just add another couple variables to an already VERY complicated picture.
I would DEFINITELY take the Lipitor to avoid throwing cardiac problems into your mix.
Rick49
02-03-2005, 07:19 PM
Benzi,
...I agree that it sounds like you have a lot of issues going on here. For the pancreas to have an effect on the cholesterol and also make you have "reactive hypoglycemia" you would have to have hyperinsulinemia which in my case is caused by insulin resistance which is a metabolism type dysfunction. If that's your problem then a low gi diet could help. But there's other causes of hyperinsulinemia, so given your history, the advice to see the endo, is good.
...with your BP falling when you stand, could be an adrenal thing but the fact that you get the shakes when you get hypoglycemic, says your adrenals are working. The adrenals are the backup to the pancreas for raising blood sugar. But that also says your pancreas wasn't secreting glucagon during low sugar periods which is a sign of increased insulin levels.
Lenin,
...Adrenal stress is any stress that causes the adrenal gland to secrete it's hormones. Your right"stress" is overworked. And your right that there is a paradox and when I get a chance, I'm going to investigat the cholesterol levels of marathon runners as their exercise regime would be considered "chronic" and should push the adrenal beyond normal limits. I would expect to see marathoners to have higher than normal cholesterol levels than the general public, but I may be wrong and in that case the paradox would remain. I don't think the adrenal hormones have an effect on cholesterol but its a case of supply and demand. Cholesterol being the precurser of adrenal hormones, if no hormones are needed the the demand for cholesterol is not needed. Chicken and the egg thing. Same thing with the pancreas, if there is little demand for insulin, then the need for producing cholesterol is lessened.
Rick
...I agree that it sounds like you have a lot of issues going on here. For the pancreas to have an effect on the cholesterol and also make you have "reactive hypoglycemia" you would have to have hyperinsulinemia which in my case is caused by insulin resistance which is a metabolism type dysfunction. If that's your problem then a low gi diet could help. But there's other causes of hyperinsulinemia, so given your history, the advice to see the endo, is good.
...with your BP falling when you stand, could be an adrenal thing but the fact that you get the shakes when you get hypoglycemic, says your adrenals are working. The adrenals are the backup to the pancreas for raising blood sugar. But that also says your pancreas wasn't secreting glucagon during low sugar periods which is a sign of increased insulin levels.
Lenin,
...Adrenal stress is any stress that causes the adrenal gland to secrete it's hormones. Your right"stress" is overworked. And your right that there is a paradox and when I get a chance, I'm going to investigat the cholesterol levels of marathon runners as their exercise regime would be considered "chronic" and should push the adrenal beyond normal limits. I would expect to see marathoners to have higher than normal cholesterol levels than the general public, but I may be wrong and in that case the paradox would remain. I don't think the adrenal hormones have an effect on cholesterol but its a case of supply and demand. Cholesterol being the precurser of adrenal hormones, if no hormones are needed the the demand for cholesterol is not needed. Chicken and the egg thing. Same thing with the pancreas, if there is little demand for insulin, then the need for producing cholesterol is lessened.
Rick
Rick49
02-03-2005, 11:59 PM
Well it looks like my marathon runners have good cholesterol levels and I found one site that talked about Cushing's syndrom which is caused by excess use of corticosteroids and it talked about the danger of high cholesterol.
...Lot's of conflicting data out there. Guess I'll continue my quest. I still haven't found any info on the "cholesterol cycle" What mechanism tells our body how much cholesterol to make? It took a long time to find the info on how our metabolism worked. So it may take a while to find out the secrets of cholesterol. If your wondering what I meant by metabolism, We all know that the pancreas secretes insulin to lower blood glucose, but how many people know that the pancreas also secretes Glucagon to raise glucose levels. It's the improper operation of this system that can lead to reactive hypoglycemia. 75% of doctors will tell people to treat this condition by eating more often, yet that does nothing to address the underlying problem of hyperinsulinemia. Once that's addressed, the insulin/glucagon process will return to normal. I highly suspect a similar thing happens with the manufacture of cholesterol.
Rick
...Lot's of conflicting data out there. Guess I'll continue my quest. I still haven't found any info on the "cholesterol cycle" What mechanism tells our body how much cholesterol to make? It took a long time to find the info on how our metabolism worked. So it may take a while to find out the secrets of cholesterol. If your wondering what I meant by metabolism, We all know that the pancreas secretes insulin to lower blood glucose, but how many people know that the pancreas also secretes Glucagon to raise glucose levels. It's the improper operation of this system that can lead to reactive hypoglycemia. 75% of doctors will tell people to treat this condition by eating more often, yet that does nothing to address the underlying problem of hyperinsulinemia. Once that's addressed, the insulin/glucagon process will return to normal. I highly suspect a similar thing happens with the manufacture of cholesterol.
Rick
Lenin
02-04-2005, 09:22 AM
Rick,
Throw this fact into your research melange.
Epinephrine and nor-epinephrine are EXTREMELY tied to the ebb and flow of fats into and out of our bloodstreams and our livers. There is a very direct relationship to these catecholamines and our blood lipids.
You might look to see what happens to experimentally adrenalectomized rats (or bats, cows etc:D:D:D)
(If you get it all figured out first, I'm sure there's a Nobel Prize in it down the road.:D)
The more you dig into, the more paradoxes and contractions you'll find. Evolution did QUITE a job on these interconnected systems with unimaginable layers of feedback loops and corrective compensations. The story of the blind men describing an elephant comes to mind a lot with their desriptions depending on what PART they are holding.
Throw this fact into your research melange.
Epinephrine and nor-epinephrine are EXTREMELY tied to the ebb and flow of fats into and out of our bloodstreams and our livers. There is a very direct relationship to these catecholamines and our blood lipids.
You might look to see what happens to experimentally adrenalectomized rats (or bats, cows etc:D:D:D)
(If you get it all figured out first, I'm sure there's a Nobel Prize in it down the road.:D)
The more you dig into, the more paradoxes and contractions you'll find. Evolution did QUITE a job on these interconnected systems with unimaginable layers of feedback loops and corrective compensations. The story of the blind men describing an elephant comes to mind a lot with their desriptions depending on what PART they are holding.
CobaltBlue
02-04-2005, 11:43 AM
I still haven't found any info on the "cholesterol cycle" What mechanism tells our body how much cholesterol to make? It took a long time to find the info on how our metabolism worked.
Rick,
Try searching on "lipid metabolism" and you will find various articles on the cycles, and how much is still unknown, as you pointed out. As for marathon runners, they do in general have higher totals (slightly) than the population, but primarily due to increased HDL, even though the VLDLs are slightly decreased. The reason that there is so much debate on the minimum exercise needed to get the increased HDL benefit.
When thinking about your adrenal question, it occurred to me that one situation where the ApoC2, A1, etc. would remain the same and HDL would increase would be if it interfered with reuptake of HDL by the liver.
Finally, back to marathon runners and others who regularly do high intensity endurance exercise. The increase in lipoprotein lipase from this training results in greater HDL and lower VLDL. However, the amount of HDL can be elevated and lowered by adjusting the amount of fat intake. The question still remains if this can overcome genetics with respect to long term protection from CAD.
Rick,
Try searching on "lipid metabolism" and you will find various articles on the cycles, and how much is still unknown, as you pointed out. As for marathon runners, they do in general have higher totals (slightly) than the population, but primarily due to increased HDL, even though the VLDLs are slightly decreased. The reason that there is so much debate on the minimum exercise needed to get the increased HDL benefit.
When thinking about your adrenal question, it occurred to me that one situation where the ApoC2, A1, etc. would remain the same and HDL would increase would be if it interfered with reuptake of HDL by the liver.
Finally, back to marathon runners and others who regularly do high intensity endurance exercise. The increase in lipoprotein lipase from this training results in greater HDL and lower VLDL. However, the amount of HDL can be elevated and lowered by adjusting the amount of fat intake. The question still remains if this can overcome genetics with respect to long term protection from CAD.
Benzi
02-04-2005, 03:24 PM
Lenin and Rick,
The report reads as follows: Computed tomography of the abdomen was performed with contrast. The stomach,large and small bowel have a normal CT apperance. I see no abscess or inflamation. There is no evidence of free fluid or adenopathy. The liver is diminished in attenuation compared to spleen suggestive of some fatty infiltration of the liver.
This is what has worried me: I too thought a fatty liver was an ENLARGED liver. I went to ER with a pain in upper and lower LEFT quadrant. My spleen area HURT and felt enlarged to me.
I have a High Platelet count but not dangerously so it runs around 500.
I have had this pain now for weeks (about 6) and PCP can not run any more CTs because I can't have the Iodine in the contrast solution until after the whole body scan to be done in late Feb early March.
PCP says not to worry that this is normal and to get him to do any more tests I would have to throw a big fit.
My question is this: Should I send this CT report down to the Endo?
I know I have the hypoglycemia because of two 911 calls by friends caused my blood sugar to be checked and even after I had eaten a burger my blood sugar was 30.
I'm glad to know about the adrenals though and the shaking at least they are most likely to be ok.
I am worried now about eating and the nausea I just hate to eat anymore because I know I will hurt and feel sick.
PS What is the blood test called to check pancreatic enzymes?
Add: my Alk Phos has been raised up to higher limits it runs around 126 to 130
my BUN is always way low around 2 ref range 7-17
chloride levels are high at 111 ref range 98-107
co2 is a little low 15 ref range 20-32
sodium is usually high also as is calcium.
The report reads as follows: Computed tomography of the abdomen was performed with contrast. The stomach,large and small bowel have a normal CT apperance. I see no abscess or inflamation. There is no evidence of free fluid or adenopathy. The liver is diminished in attenuation compared to spleen suggestive of some fatty infiltration of the liver.
This is what has worried me: I too thought a fatty liver was an ENLARGED liver. I went to ER with a pain in upper and lower LEFT quadrant. My spleen area HURT and felt enlarged to me.
I have a High Platelet count but not dangerously so it runs around 500.
I have had this pain now for weeks (about 6) and PCP can not run any more CTs because I can't have the Iodine in the contrast solution until after the whole body scan to be done in late Feb early March.
PCP says not to worry that this is normal and to get him to do any more tests I would have to throw a big fit.
My question is this: Should I send this CT report down to the Endo?
I know I have the hypoglycemia because of two 911 calls by friends caused my blood sugar to be checked and even after I had eaten a burger my blood sugar was 30.
I'm glad to know about the adrenals though and the shaking at least they are most likely to be ok.
I am worried now about eating and the nausea I just hate to eat anymore because I know I will hurt and feel sick.
PS What is the blood test called to check pancreatic enzymes?
Add: my Alk Phos has been raised up to higher limits it runs around 126 to 130
my BUN is always way low around 2 ref range 7-17
chloride levels are high at 111 ref range 98-107
co2 is a little low 15 ref range 20-32
sodium is usually high also as is calcium.
Lenin
02-05-2005, 08:39 AM
Benzi,
If I had to make a stab at a flash diagnosis, the phrase that causght my eye was
I went to ER with a pain in upper and lower LEFT quadrant.
That is suggestive of a descending colon problem.
A colonoscopy is a good idea to rule out BIG problems, but the more common one, IRS (irritable bowel) won't show up.
Try taking some psyllium (like Metamucil for a couple weeks), about 2 or three doses a day. If this alleviated the pain very soon you've got a likely candidate.
I guess that the "attenuated liver" refers more to the way it appears on screen than its size. It probably appeared with less crisp outlines suggestive of fatty infiltration. BUT the term "some fatty infiltration" can probably be apt for 50% of the adult population...don't worry about it.
You might also want to Google "chronic (or even acute) pancreatitis" which seems also a possibility which would explain both fat intolerance and weird blood sugar activity.
You seemed to have eliminated the possiblility of the BIG SCARE, carcinoma of the pancreas and the common ducts...THAT'S a killer!
If I had to make a stab at a flash diagnosis, the phrase that causght my eye was
I went to ER with a pain in upper and lower LEFT quadrant.
That is suggestive of a descending colon problem.
A colonoscopy is a good idea to rule out BIG problems, but the more common one, IRS (irritable bowel) won't show up.
Try taking some psyllium (like Metamucil for a couple weeks), about 2 or three doses a day. If this alleviated the pain very soon you've got a likely candidate.
I guess that the "attenuated liver" refers more to the way it appears on screen than its size. It probably appeared with less crisp outlines suggestive of fatty infiltration. BUT the term "some fatty infiltration" can probably be apt for 50% of the adult population...don't worry about it.
You might also want to Google "chronic (or even acute) pancreatitis" which seems also a possibility which would explain both fat intolerance and weird blood sugar activity.
You seemed to have eliminated the possiblility of the BIG SCARE, carcinoma of the pancreas and the common ducts...THAT'S a killer!
Hartland
02-05-2005, 10:15 AM
Comic Sans Ms3Navy
This thread is wonderful. Thank you all for the great information
Hartland :)
This thread is wonderful. Thank you all for the great information
Hartland :)
Benzi
02-07-2005, 12:20 PM
Thanks so much for all the info I am glad to know that the CT was worth doing anyway. I had some polops removed from my colon 2 yrs ago and probably should have them checked anyway, Colon cancer runs in the family too but seems like lots of stuff runs in my family. LOL It was a little strange because the CT report did not mention it but the ER DOC said he thought I had a reoccurance of polops in my colon, and that he had seen it on the CT. But then when I got CT report there was no mention of that but just the liver. Thanks again you are all great.
CobaltBlue
02-08-2005, 12:11 PM
[QUOTE=Rick49...I would be interested in your thoughts and here's the study:
The effect of prednisone therapy on plasma lipoproteins and apolipoproteins A-I, A-II, and E levels was studied prospectively in a heterogeneous group of six male and six female subjects. Our results show that in patients with no major metabolic abnormality, prednisone induces significant changes of the lipoprotein system, especially in HDL.[/QUOTE]
Rick,
I have been meaning to get back to writing something more about this, in addition to what I was guessing at before. Prednisone (and other corticosteroids) have various effects, one of which is to interfere with the cholesteryl ester transfer protein effect (the protein that allows transport of that ester from HDL to VLDL and the movement of a TG from the VLDL to the HDL for clearance).
The net effect is as you described in this study, a rise in HDL, but there is also decreased insulin sensitivity, leading to hyperinsulemia in some, and as a result elevated TG levels. There was much excitement around the 1989 discovery that individuals who were deficient in CETP had elevated HDL. The disappointment was that this was not the magic bullet. It was found that among this group of those with CETP deficiency and elevated HDL, the incidence of heart disease was greater rather than lesser.
I suppose that one of the issues that will be discussed more in the future will how much to rely on measured "classes" of lipoprotein carriers, rather than focus on the actual types. For example, take two individuals with a total cholesterol of 140 mg/dL; one has LDL: 60, HDL: 40, TG: 200, the other LDL: 90, HDL: 40, TG: 50--I would bet that the probability of cardiovascular disease in the first would be >> than the second based upon the state of hyperinsulemia that leads to hypertriglyceridaemia, and more r**** clearance of HDL3 back out of the plasma. This situation produced more dense lipoproteins which are much less protective. This (dyslipidemia) is a situation that I once experienced.
The effect of prednisone therapy on plasma lipoproteins and apolipoproteins A-I, A-II, and E levels was studied prospectively in a heterogeneous group of six male and six female subjects. Our results show that in patients with no major metabolic abnormality, prednisone induces significant changes of the lipoprotein system, especially in HDL.[/QUOTE]
Rick,
I have been meaning to get back to writing something more about this, in addition to what I was guessing at before. Prednisone (and other corticosteroids) have various effects, one of which is to interfere with the cholesteryl ester transfer protein effect (the protein that allows transport of that ester from HDL to VLDL and the movement of a TG from the VLDL to the HDL for clearance).
The net effect is as you described in this study, a rise in HDL, but there is also decreased insulin sensitivity, leading to hyperinsulemia in some, and as a result elevated TG levels. There was much excitement around the 1989 discovery that individuals who were deficient in CETP had elevated HDL. The disappointment was that this was not the magic bullet. It was found that among this group of those with CETP deficiency and elevated HDL, the incidence of heart disease was greater rather than lesser.
I suppose that one of the issues that will be discussed more in the future will how much to rely on measured "classes" of lipoprotein carriers, rather than focus on the actual types. For example, take two individuals with a total cholesterol of 140 mg/dL; one has LDL: 60, HDL: 40, TG: 200, the other LDL: 90, HDL: 40, TG: 50--I would bet that the probability of cardiovascular disease in the first would be >> than the second based upon the state of hyperinsulemia that leads to hypertriglyceridaemia, and more r**** clearance of HDL3 back out of the plasma. This situation produced more dense lipoproteins which are much less protective. This (dyslipidemia) is a situation that I once experienced.
Lenin
02-08-2005, 12:40 PM
ubie,
I have always pictured A CERTAIN PROTEIN that attaches to cholesterol and to a number of fat molecules (triglycerides) to form VLDL, LDL, HDL, the apolipoprotein classes and perhaps even chylomicorons (maybe minus the cholesterol.)
Is that certain "carrier" protein CETP?
If not, do you have any idea of what the protein is that makes up all the LipoPROTEINS or is there a whole family of them?
Perhaps of some interest:
General Information
It has been proposed that high density lipoproteins (HDLs) function jointly with lecithin:cholesterol acyltransferase and CETP to facilitate cholesterol transport from tissues to the liver. This mechanism, referred to as reverse cholesterol transport, is physiologically important because it maintains systemic cholesterol levels.
CETP is responsible for neutral lipid transfer activity in plasma in numerous species. Since CETP is able to specifically accelerate the exchange of lipid components between pro- and anti-atherogenic lipoprotein fractions, it may be a key determinant of the global atherogenicity of the plasma lipoprotein profile and arises as a possible target in atherosclerosis prevention. In general, elevated levels of CETP have been associated with increased risk of coronary heart disease.
I have always pictured A CERTAIN PROTEIN that attaches to cholesterol and to a number of fat molecules (triglycerides) to form VLDL, LDL, HDL, the apolipoprotein classes and perhaps even chylomicorons (maybe minus the cholesterol.)
Is that certain "carrier" protein CETP?
If not, do you have any idea of what the protein is that makes up all the LipoPROTEINS or is there a whole family of them?
Perhaps of some interest:
General Information
It has been proposed that high density lipoproteins (HDLs) function jointly with lecithin:cholesterol acyltransferase and CETP to facilitate cholesterol transport from tissues to the liver. This mechanism, referred to as reverse cholesterol transport, is physiologically important because it maintains systemic cholesterol levels.
CETP is responsible for neutral lipid transfer activity in plasma in numerous species. Since CETP is able to specifically accelerate the exchange of lipid components between pro- and anti-atherogenic lipoprotein fractions, it may be a key determinant of the global atherogenicity of the plasma lipoprotein profile and arises as a possible target in atherosclerosis prevention. In general, elevated levels of CETP have been associated with increased risk of coronary heart disease.
CobaltBlue
02-08-2005, 09:27 PM
Lenin,
For a second there, I thought you and I were reading the same material :p when you quoted the LCAT info about the HDL cascade. Must mean that we have too much time on our hands.
There is a neat book (OK, well neat to people like me and this would be in a weird kind of way I supposed) called, "Lipoproteins in Health and Disease" by Betteridge, Illingworth and Shepherd. There is a whole chapter in that book dedicated to CETP; the book is about the size of a CRC Handbook of Chemistry and Physics, and I have a feeling you have seen one of those before.
There is another website that I know you are aware of, becuase you have mentioned the slides it contains in previous posts. To be honest, I think that site does a great job of making many of these things easier to understand whereas that book, in places, is pretty rough. Each chapter is written by different researchers, and just like with manuscripts, I often have to reread sections for it to sink in.
That CETP is the protein that binds them, and I think that is exactly what you are thinking of when you wrote that. Its action is specialized for the transport of the hydrophobic lipids, primarily triglycerides and cholesteryl esters between the VLDL and HDL during that cascade, but sometimes the transfer or exchange processes in LDL, VLDL, and CMs too. CETP has 3 binding sites, one for CE, one for TG and one for phospholipids. The lipoprotein lipase (LPL, that I keep mentioning in reference to exercise and HDL benefit) plays a part in the lipolytic cascade to hydrolyze the TGs from VLDLs, down to an IDL, then hepatic lipase (HL) frees up more TG to produce the ApoB-100 rich LDL. That same LPL does this to CM too, but here you get ApoAs from the CMs, whereas that VLDL yields ApoCs and ApoE (which is important to HDL).
When you mentioned the LCAT (and PCTP), you brought up an interesting part of what I wrote to Rick about the HDL cascade. Those proteins are what leads to the transition from nascent HDL to HDL3 then HDL2. (Except for the dyslipidemic, e.g. me, where almost no HDL2 exists without measures such as maintenance of proper weight and consistent exercise--absence of HDL2 is common in males, in contrast to females). This is presumably due to hormone differences between the genders....
Gee, I am rambling and off on many tangents. OK, from what I read, the composition of VLDL has surface phospholipids, cholesterol, B&C proteins, and carries almost all TG inside, in contrast to LDL, which has surface phospholipids, cholesterol, and B protein (i.e. ApoB-100) on the surface with a core of cholesteryl esters. HDLs have phospholipids and cholsterol on the surface, with A and C proteins there (ApoA, ApoC), and the core has a small amt of TG and cholesteryl esters. Oh, the CM, they have ApoA's, B-48, Cs, and E.
CMs have the most TG rich core, HDL3 and Lp(a) have the least TG inside. The free cholesterol on the surface of these (by % mass) is 2-10% for all lipoproteins, phospholipids range from 7% in CMs to 20-30% for the rest, and surface proteins are minimal in CMs (2%), to 40-55% in HDL2 and HDL3.
I have a feeling that I still haven't answered the question you asked me? Not sure if I will approach it here, but those surface apolipoproteins....there are 9 types. HDL carries ApoA1 (28 kDa relative molecular mass), ApoA2 (17 kDa)m and ApoA4 (44.5 kDa), ApoB-48 (264 kDa) in CMs [CMs contain all except B-100], ApoB-100 (550 kDa) on LDL, IDL, and VLDL, ApoC1 (6600 Da), C2 (8900 Da) and C3 (8800 Da) primarily on HDL, with some on IDL and VLDL, ApoD (22 kDa) on HDL, and ApoE (34 kDa) on HDL, IDL, and VLDL. Finally, you probably know this, but proteins are just amino acids. I have yet to see a 3-D representation of any of these, though I don't doubt they exist by now, since they know which chromosomes have the apolipoprotein genes encoded.
Now for the clincher, and funniest part of all of this, Lenin, is what you were asking buried somewhere in there between what you wanted to find out and what I wanted to ramble on about? ;)
For a second there, I thought you and I were reading the same material :p when you quoted the LCAT info about the HDL cascade. Must mean that we have too much time on our hands.
There is a neat book (OK, well neat to people like me and this would be in a weird kind of way I supposed) called, "Lipoproteins in Health and Disease" by Betteridge, Illingworth and Shepherd. There is a whole chapter in that book dedicated to CETP; the book is about the size of a CRC Handbook of Chemistry and Physics, and I have a feeling you have seen one of those before.
There is another website that I know you are aware of, becuase you have mentioned the slides it contains in previous posts. To be honest, I think that site does a great job of making many of these things easier to understand whereas that book, in places, is pretty rough. Each chapter is written by different researchers, and just like with manuscripts, I often have to reread sections for it to sink in.
That CETP is the protein that binds them, and I think that is exactly what you are thinking of when you wrote that. Its action is specialized for the transport of the hydrophobic lipids, primarily triglycerides and cholesteryl esters between the VLDL and HDL during that cascade, but sometimes the transfer or exchange processes in LDL, VLDL, and CMs too. CETP has 3 binding sites, one for CE, one for TG and one for phospholipids. The lipoprotein lipase (LPL, that I keep mentioning in reference to exercise and HDL benefit) plays a part in the lipolytic cascade to hydrolyze the TGs from VLDLs, down to an IDL, then hepatic lipase (HL) frees up more TG to produce the ApoB-100 rich LDL. That same LPL does this to CM too, but here you get ApoAs from the CMs, whereas that VLDL yields ApoCs and ApoE (which is important to HDL).
When you mentioned the LCAT (and PCTP), you brought up an interesting part of what I wrote to Rick about the HDL cascade. Those proteins are what leads to the transition from nascent HDL to HDL3 then HDL2. (Except for the dyslipidemic, e.g. me, where almost no HDL2 exists without measures such as maintenance of proper weight and consistent exercise--absence of HDL2 is common in males, in contrast to females). This is presumably due to hormone differences between the genders....
Gee, I am rambling and off on many tangents. OK, from what I read, the composition of VLDL has surface phospholipids, cholesterol, B&C proteins, and carries almost all TG inside, in contrast to LDL, which has surface phospholipids, cholesterol, and B protein (i.e. ApoB-100) on the surface with a core of cholesteryl esters. HDLs have phospholipids and cholsterol on the surface, with A and C proteins there (ApoA, ApoC), and the core has a small amt of TG and cholesteryl esters. Oh, the CM, they have ApoA's, B-48, Cs, and E.
CMs have the most TG rich core, HDL3 and Lp(a) have the least TG inside. The free cholesterol on the surface of these (by % mass) is 2-10% for all lipoproteins, phospholipids range from 7% in CMs to 20-30% for the rest, and surface proteins are minimal in CMs (2%), to 40-55% in HDL2 and HDL3.
I have a feeling that I still haven't answered the question you asked me? Not sure if I will approach it here, but those surface apolipoproteins....there are 9 types. HDL carries ApoA1 (28 kDa relative molecular mass), ApoA2 (17 kDa)m and ApoA4 (44.5 kDa), ApoB-48 (264 kDa) in CMs [CMs contain all except B-100], ApoB-100 (550 kDa) on LDL, IDL, and VLDL, ApoC1 (6600 Da), C2 (8900 Da) and C3 (8800 Da) primarily on HDL, with some on IDL and VLDL, ApoD (22 kDa) on HDL, and ApoE (34 kDa) on HDL, IDL, and VLDL. Finally, you probably know this, but proteins are just amino acids. I have yet to see a 3-D representation of any of these, though I don't doubt they exist by now, since they know which chromosomes have the apolipoprotein genes encoded.
Now for the clincher, and funniest part of all of this, Lenin, is what you were asking buried somewhere in there between what you wanted to find out and what I wanted to ramble on about? ;)
CobaltBlue
02-08-2005, 09:41 PM
Lenin, one more interesting thing that I ran across in reference to the quoted info you highlighted:
In general, elevated levels of CETP have been associated with increased risk of coronary heart disease.
A 1994 Japanese study found that the protective HDL (HDL2) from individuals that were CETP deficient had a reduced ability for inhibiting "the LDL-induced accumulation of cholesteryl ester in mouse peritoneal macrophages." Ok, yes they were studying this effect outside of the human body, but it was demonstrated that HDL2 from these patients was less protective than normal HDL2. Other studies have shown that the presence of ApoA2 plays a role in whether CETP interaction results in HDL particle sizes that are small or large...maybe that is the key as to why either elevated or deficient levels of CETP result in higher disease risk? Might be related to the concentration of ApoAs, primarily A2? (I am speculating here).
In general, elevated levels of CETP have been associated with increased risk of coronary heart disease.
A 1994 Japanese study found that the protective HDL (HDL2) from individuals that were CETP deficient had a reduced ability for inhibiting "the LDL-induced accumulation of cholesteryl ester in mouse peritoneal macrophages." Ok, yes they were studying this effect outside of the human body, but it was demonstrated that HDL2 from these patients was less protective than normal HDL2. Other studies have shown that the presence of ApoA2 plays a role in whether CETP interaction results in HDL particle sizes that are small or large...maybe that is the key as to why either elevated or deficient levels of CETP result in higher disease risk? Might be related to the concentration of ApoAs, primarily A2? (I am speculating here).
Lenin
02-09-2005, 09:30 AM
Ubernier,
I've always suspected that I had a problem with my PERITONEAL MACROPHAGES.:D:D
I guess I am going to have to bite the bullet and admit it's over my head (only a ChE.) My hat's off to you for the research you have done into the layers of this complex onion.
It does make clear how silly we are when we (and so much of medicine) try to explain this spiderweb of interwoven complexity by reducing it to "LDL BAD; HDL GOOD." Like the Frankenstein, Tarzan and Tonto routine...FIRE BAD (Frankenstein) vs FIRE GOOD, Jane (Tarzan) or FIRE NOW KEEMOSAABI (Tonto.):D
Thanks for the input...I'll work it.
If you haven't seen this paper from Taina Korholen at OULU UNIVERSITY, Finland, you might find it interesting:
http://herkules.oulu.fi/isbn9514251598/html/
I've always suspected that I had a problem with my PERITONEAL MACROPHAGES.:D:D
I guess I am going to have to bite the bullet and admit it's over my head (only a ChE.) My hat's off to you for the research you have done into the layers of this complex onion.
It does make clear how silly we are when we (and so much of medicine) try to explain this spiderweb of interwoven complexity by reducing it to "LDL BAD; HDL GOOD." Like the Frankenstein, Tarzan and Tonto routine...FIRE BAD (Frankenstein) vs FIRE GOOD, Jane (Tarzan) or FIRE NOW KEEMOSAABI (Tonto.):D
Thanks for the input...I'll work it.
If you haven't seen this paper from Taina Korholen at OULU UNIVERSITY, Finland, you might find it interesting:
http://herkules.oulu.fi/isbn9514251598/html/
CobaltBlue
02-09-2005, 10:29 AM
Lenin,
I knew you would know just how thick that CRC was (as for the ChE, even not identical, but you and I have similar backgrounds) :) Then again, you know why I study so much of this from the posts about my health history. Most people go home and read novels, I go home, exercise and read this stuff :rolleyes:
Thanks for that URL! :) The take home message that I got from that first abstract was that ApoE can, in some populations, correlate with CAD, while others not. I have seen the various types of dysfunctional lipid (genetics) broken down into at least 5 groups, of which I seem to fit best in the type IV or type V grouping (metabolic syndrome, low HDL and small dense HDLs, hypertension, hypertriglyceridaemia, insulin resistance-type II diabetes, etc.).
Oh the other take home msg was the GI effects for those statins. I guess I should be thankful that I do not need a statin :eek:
You are right though, the deeper we dig, the more we see it's particles (like ApoE) that reside on particles (like HDL, or VLDL) and different phenotypes of those very particles (like the various E alleles) that come into play in the overall picture of how each of us need to handle our lifestyles to prevent or reduce the development/progression of CAD.
I knew you would know just how thick that CRC was (as for the ChE, even not identical, but you and I have similar backgrounds) :) Then again, you know why I study so much of this from the posts about my health history. Most people go home and read novels, I go home, exercise and read this stuff :rolleyes:
Thanks for that URL! :) The take home message that I got from that first abstract was that ApoE can, in some populations, correlate with CAD, while others not. I have seen the various types of dysfunctional lipid (genetics) broken down into at least 5 groups, of which I seem to fit best in the type IV or type V grouping (metabolic syndrome, low HDL and small dense HDLs, hypertension, hypertriglyceridaemia, insulin resistance-type II diabetes, etc.).
Oh the other take home msg was the GI effects for those statins. I guess I should be thankful that I do not need a statin :eek:
You are right though, the deeper we dig, the more we see it's particles (like ApoE) that reside on particles (like HDL, or VLDL) and different phenotypes of those very particles (like the various E alleles) that come into play in the overall picture of how each of us need to handle our lifestyles to prevent or reduce the development/progression of CAD.
Lenin
02-09-2005, 11:07 AM
Ubie,
Make sure you open some of the links in the TABLE OF CONTENTS if you haven't. It's quite a text all in itself!
Make sure you open some of the links in the TABLE OF CONTENTS if you haven't. It's quite a text all in itself!
CobaltBlue
02-10-2005, 09:48 AM
Lenin,
I did, I did ;) It is a great reference--lots of good stuff in there.
I did, I did ;) It is a great reference--lots of good stuff in there.