NHone
03-13-2006, 08:10 PM
Just heard on the CBS evening news that a recent Crestor trial decreased plaque in the arteries. They gave the participants 40 mg of Crestor a day...a high dose. Something that wasn't quiet right about the study was that NONE of the participants reported any side effects. Thats not quiet right. Even with the best medication, someone will have a side effect. Of course, none of the information on the participants was told on the news. The really important information was missing. It is also contrary to what we read on the message boards. Looks like it is close to time to report 1st quarter earnings and sales...?????
Sponsor
JJ
03-13-2006, 08:38 PM
Just heard on the CBS evening news that a recent Crestor trial decreased plaque in the arteries. They gave the participants 40 mg of Crestor a day...a high dose. Something that wasn't quiet right about the study was that NONE of the participants reported any side effects. Thats not quiet right. Even with the best medication, someone will have a side effect. Of course, none of the information on the participants was told on the news. The really important information was missing. It is also contrary to what we read on the message boards. Looks like it is close to time to report 1st quarter earnings and sales...?????
I saw that on ABC WNT. Seems kind of strange to me as well, as even folks who take statins say Crestor is the strongest and worst. Oh well, maybe sales were down.......... :D
As I have said before, believe half of what U hear and see..... ;)
I saw that on ABC WNT. Seems kind of strange to me as well, as even folks who take statins say Crestor is the strongest and worst. Oh well, maybe sales were down.......... :D
As I have said before, believe half of what U hear and see..... ;)
ARIZONA73
03-13-2006, 09:38 PM
Of course, none of the information on the participants was told on the news. The really important information was missing.
You noticed that too, huh? It seems like whenever they come out with one of these studies, there are always far more questions than answers. Besides, this isn't the first time a regression of plaque was observed. A Canadian physician, G.C. Willis, observed a similar effect on human subjects by administering 1500mg vitamin C. And this was back in 1954!
You noticed that too, huh? It seems like whenever they come out with one of these studies, there are always far more questions than answers. Besides, this isn't the first time a regression of plaque was observed. A Canadian physician, G.C. Willis, observed a similar effect on human subjects by administering 1500mg vitamin C. And this was back in 1954!
Stumper
03-13-2006, 10:02 PM
Of course Statins clean plaque.. That's just common knowledge anymore.
Johns Hopkins University already has done the research..BUT the numbers gotta get LOW...LOW...
And the ONLY way to do that is with Statins.
Plaque cleaning drugs.
I doubt very much that G. C. Willis observed much of anything. They didn't have magnetic imaging like they do today back then.
Johns Hopkins University already has done the research..BUT the numbers gotta get LOW...LOW...
And the ONLY way to do that is with Statins.
Plaque cleaning drugs.
I doubt very much that G. C. Willis observed much of anything. They didn't have magnetic imaging like they do today back then.
NHone
03-13-2006, 10:57 PM
Of course Statins clean plaque.. That's just common knowledge anymore.
Johns Hopkins University already has done the research..BUT the numbers gotta get LOW...LOW...
And the ONLY way to do that is with Statins.
Plaque cleaning drugs.
I doubt very much that G. C. Willis observed much of anything. They didn't have magnetic imaging like they do today back then.
That is not common knowledge.. Especially since plaque has very little cholesterol in it. In fact Researchers at St. Louis University say that it is impractical to think this. In 1954 there were other ways to observe conditions. Some of the ways were called autopsy.
Johns Hopkins University already has done the research..BUT the numbers gotta get LOW...LOW...
And the ONLY way to do that is with Statins.
Plaque cleaning drugs.
I doubt very much that G. C. Willis observed much of anything. They didn't have magnetic imaging like they do today back then.
That is not common knowledge.. Especially since plaque has very little cholesterol in it. In fact Researchers at St. Louis University say that it is impractical to think this. In 1954 there were other ways to observe conditions. Some of the ways were called autopsy.
ARIZONA73
03-13-2006, 11:13 PM
I doubt very much that G. C. Willis observed much of anything. They didn't have magnetic imaging like they do today back then.
I disagree. In fact, Dr. Willis did see a reduction or stabilization in most patients, but that a smaller number of patients experienced no reduction in plaque size, or that it got worse. But overall, the results were quite positive. And he only used 1500mg vitamin C, which is a very modest dose. Higher dosages would probably have resulted in even greater benefits. As I understand it, he tried to persuade the medical profession to further examine his findings, and conduct further studies, but his efforts were ignored.
I disagree. In fact, Dr. Willis did see a reduction or stabilization in most patients, but that a smaller number of patients experienced no reduction in plaque size, or that it got worse. But overall, the results were quite positive. And he only used 1500mg vitamin C, which is a very modest dose. Higher dosages would probably have resulted in even greater benefits. As I understand it, he tried to persuade the medical profession to further examine his findings, and conduct further studies, but his efforts were ignored.
Stumper
03-14-2006, 08:23 AM
That is not common knowledge.. Especially since plaque has very little cholesterol in it. In fact Researchers at St. Louis University say that it is impractical to think this. In 1954 there were other ways to observe conditions. Some of the ways were called autopsy.
Yeah, riiight.... :D
How many times you gonna kill a person to discover how much plaque is reduced ? Twice? :D :D
Yeah, riiight.... :D
How many times you gonna kill a person to discover how much plaque is reduced ? Twice? :D :D
Stumper
03-14-2006, 08:26 AM
I disagree. In fact, Dr. Willis did see a reduction or stabilization in most patients, but that a smaller number of patients experienced no reduction in plaque size, or that it got worse. But overall, the results were quite positive. And he only used 1500mg vitamin C, which is a very modest dose. Higher dosages would probably have resulted in even greater benefits. As I understand it, he tried to persuade the medical profession to further examine his findings, and conduct further studies, but his efforts were ignored.
Yes, and just HOW was Mr. Willis determining plaque reductions?
This sounds like just another rumor from the supplement industry with no actual facts or data !
From 1954 yet !
Back then Cholesterol was hardly or never brought up !
Yes, and just HOW was Mr. Willis determining plaque reductions?
This sounds like just another rumor from the supplement industry with no actual facts or data !
From 1954 yet !
Back then Cholesterol was hardly or never brought up !
Lenin
03-14-2006, 09:42 AM
I was pleased to hear about the superb reductions from Crestor that were apparent after only 2 months od dosing (high dosing alas.)
My only worry is that as a plaque is reduced does it retain its integrity. I'd hate to think that while reducing them we are making them less stable and thus mor prone to ruture.
Oh, the Vitamin C cures everything again argument. No, 1500 mg. Ascorbic acid doesn't reduce plaque...not in 2 years nor in 30.
My only worry is that as a plaque is reduced does it retain its integrity. I'd hate to think that while reducing them we are making them less stable and thus mor prone to ruture.
Oh, the Vitamin C cures everything again argument. No, 1500 mg. Ascorbic acid doesn't reduce plaque...not in 2 years nor in 30.
janeslk
03-14-2006, 11:29 AM
I know only one person who has taken Crestor. She is a borderline diabetic and after taking Crestor she developed permanent neuropathy in her feet. I don't think I will be buying stock anytime soon. I have noticed that not too many people on this board are taking Crestor. Are doctors reluctant to prescribe it or it is only for people known to have plaque buildup? I would imagine after this study it will become the statin of choice for doctors.
Jane
Jane
liverock
03-14-2006, 12:01 PM
The Journal of the American Medical Asssociation, JAMA, has given a more cautious welcome to the Crestor(ASTEROID) Trial.
www.jama.ama-assn.org/cgi/content/full/295.13.jed60019v1
Among its reservations and comments are;
Only subjects with a coronary stenosis of under 50% were included in the trial.
The mean values of the subjects on the start of the trial were HDL43 LDL 130 which indicated that the effect on more acute coronary cases could not be evaluated from this trial.
There was no adverse clinical symptoms reported.
Another recent trial (REVERSAL) examined the effects of plaque regression using IVUS (intervascular ultrasound), the method used in this trial, on coronary lumen size.
In the REVERSAL trial a decrease in the cross sectional area of the external lumen area was associated with no change in coronary lumen area.
No data regarding change in lumen volume or size was reported in the ASTEROID trial leaving open the possibility that changes in atheroma volume may have been deduced from the reduced cross sectional area of the external elastic membrane, with potentially unchanged or no reduction in coronary lumen size.
It was also reported in Reuters that the main author of the report stated that reducing the cholesterol to that level would leave behind a 'mainly fibrous plaque tissue."
This I would have thought would increase the chances of destabalising the plaque.
The mean reduction in atheroma volume was from 39.6% to 38.6% which doesnt seem a lot, considering in my view, the possible increased plaque instability.
Perhaps it would be more prudent in non chronic cases, to reduce LDL to a level were there was no reduction in plaque and no increase either, a happy median.... :)
.
www.jama.ama-assn.org/cgi/content/full/295.13.jed60019v1
Among its reservations and comments are;
Only subjects with a coronary stenosis of under 50% were included in the trial.
The mean values of the subjects on the start of the trial were HDL43 LDL 130 which indicated that the effect on more acute coronary cases could not be evaluated from this trial.
There was no adverse clinical symptoms reported.
Another recent trial (REVERSAL) examined the effects of plaque regression using IVUS (intervascular ultrasound), the method used in this trial, on coronary lumen size.
In the REVERSAL trial a decrease in the cross sectional area of the external lumen area was associated with no change in coronary lumen area.
No data regarding change in lumen volume or size was reported in the ASTEROID trial leaving open the possibility that changes in atheroma volume may have been deduced from the reduced cross sectional area of the external elastic membrane, with potentially unchanged or no reduction in coronary lumen size.
It was also reported in Reuters that the main author of the report stated that reducing the cholesterol to that level would leave behind a 'mainly fibrous plaque tissue."
This I would have thought would increase the chances of destabalising the plaque.
The mean reduction in atheroma volume was from 39.6% to 38.6% which doesnt seem a lot, considering in my view, the possible increased plaque instability.
Perhaps it would be more prudent in non chronic cases, to reduce LDL to a level were there was no reduction in plaque and no increase either, a happy median.... :)
.
NHone
03-14-2006, 01:57 PM
I was pleased to hear about the superb reductions from Crestor that were apparent after only 2 months od dosing (high dosing alas.)
My only worry is that as a plaque is reduced does it retain its integrity. I'd hate to think that while reducing them we are making them less stable and thus mor prone to ruture.
Oh, the Vitamin C cures everything again argument. No, 1500 mg. Ascorbic acid doesn't reduce plaque...not in 2 years nor in 30.
That is an excellent , excellent point. It has been looked at before, and some data shows that while there is a reduction, the plaque did become unstable. I guess its kind of like taking dirt off of one side of the dam and saying, guess we didn't need such a big dam anyway. Some day you'll cause a dam break.
My only worry is that as a plaque is reduced does it retain its integrity. I'd hate to think that while reducing them we are making them less stable and thus mor prone to ruture.
Oh, the Vitamin C cures everything again argument. No, 1500 mg. Ascorbic acid doesn't reduce plaque...not in 2 years nor in 30.
That is an excellent , excellent point. It has been looked at before, and some data shows that while there is a reduction, the plaque did become unstable. I guess its kind of like taking dirt off of one side of the dam and saying, guess we didn't need such a big dam anyway. Some day you'll cause a dam break.
ARIZONA73
03-14-2006, 06:58 PM
Oh, the Vitamin C cures everything again argument. No, 1500 mg. Ascorbic acid doesn't reduce plaque...not in 2 years nor in 30.
Evidently vitamin C has been shown to reduce plaque, and the results of the Willis study appeared in the Canadian Medical Association Journal.
Evidently vitamin C has been shown to reduce plaque, and the results of the Willis study appeared in the Canadian Medical Association Journal.
JJ
03-14-2006, 07:24 PM
I know only one person who has taken Crestor. She is a borderline diabetic and after taking Crestor she developed permanent neuropathy in her feet. I don't think I will be buying stock anytime soon. I have noticed that not too many people on this board are taking Crestor. Are doctors reluctant to prescribe it or it is only for people known to have plaque buildup? I would imagine after this study it will become the statin of choice for doctors.
Jane
A friend of mine has taken Lipitor, even at 80 mgs., but when her dr. switched her to Crestor she got quite ill from it, and it was not a high dose. Dr. switched her back to the Lipitor but it still didn't bring her numbers down much, so they are trying her on Vytorin. Like U, I know noone on Crestor, so maybe drs. just aren't comfortable with it???
She has a horrible time trying to get her numbers down, yet she had a cath 2 years ago and it showed her with NO plaque. Only thing she did get was the PN and she isn't a diabetic, but got that while on Lipitor, not Crestor. Even with the high doses of statins, she hits maybe 255 and can't seem to get lower. I know she tries to eat well, is only maybe 15 lbs. over weight, but her biggest downfall is being from the south, she loves her stuff fried. Like I told her, bout time she started giving that up, it just might help.
Jane
A friend of mine has taken Lipitor, even at 80 mgs., but when her dr. switched her to Crestor she got quite ill from it, and it was not a high dose. Dr. switched her back to the Lipitor but it still didn't bring her numbers down much, so they are trying her on Vytorin. Like U, I know noone on Crestor, so maybe drs. just aren't comfortable with it???
She has a horrible time trying to get her numbers down, yet she had a cath 2 years ago and it showed her with NO plaque. Only thing she did get was the PN and she isn't a diabetic, but got that while on Lipitor, not Crestor. Even with the high doses of statins, she hits maybe 255 and can't seem to get lower. I know she tries to eat well, is only maybe 15 lbs. over weight, but her biggest downfall is being from the south, she loves her stuff fried. Like I told her, bout time she started giving that up, it just might help.
balleteach
03-14-2006, 11:24 PM
Hi all, I follow this board regularly, but this is my first post here. I've had high LDL that I've always been able to lower with diet. My HDL is high, with numbers in the 70's and 80's. Also very low trig levels. I feel pretty fortunate so far, but intend to keep getting checked every year or two. The study about Crestor was in our morning paper and caught my eye. Whenever anything comes out like this, I make sure to check who paid for the study. In this case, the sponsor was AstraZenecaPLC, Crestors maker. I have no idea whether this makes any difference or would skew the results, but I found it interesting. Any way, good luck to everyone....balleteach
ARIZONA73
03-14-2006, 11:47 PM
The study about Crestor was in our morning paper and caught my eye. Whenever anything comes out like this, I make sure to check who paid for the study. In this case, the sponsor was AstraZenecaPLC, Crestors maker. I have no idea whether this makes any difference or would skew the results, but I found it interesting.
Yes, whenever you read about some study, always follow the money, and then draw your own conclusions. Well, in this case, it was about Crestor, a drug which has received some bad publicity as of late. So, a little boost in sales just might serve their purpose. So again, just follow the money, remember who sponsored the study, and then draw your own conclusions. Just remember one thing. Drug companies exert a very powerful influence. They've got a tremendous amount of money to spread around, and they can slant their studies to their favor. But, in my opinion, statins are dangerous drugs which should be avoided except in cases in which there is a dire need for them.
Yes, whenever you read about some study, always follow the money, and then draw your own conclusions. Well, in this case, it was about Crestor, a drug which has received some bad publicity as of late. So, a little boost in sales just might serve their purpose. So again, just follow the money, remember who sponsored the study, and then draw your own conclusions. Just remember one thing. Drug companies exert a very powerful influence. They've got a tremendous amount of money to spread around, and they can slant their studies to their favor. But, in my opinion, statins are dangerous drugs which should be avoided except in cases in which there is a dire need for them.
NHone
03-15-2006, 12:37 AM
Arizona....Was just going over the Crestor study in JAMA... It is in JAMA with charts..i looked up Asteroid Study Crestor. IT MAKES ME ANGRY. THis was a definite stock prop up. Look at the results. (I'll tell more about them later)..But for now...507 people started, of that 158 didn't finish. WHY? As in their table 5, under drug discontinuations: muscle pain or weakness 19, gastronintestinal complaints 2, cardiovascular disorders 22, and a few more things. Total adverse effects 62. But also .."of the 3 remaining deaths, 2 were due to sudden cardiac death and 1 to gastric carcinoma. I thought Astrazeneca was touting this as so special because they had no adverse effects????? Also look at the financial interest section!!! There don't seem to be individual results either.
vipergg22
03-15-2006, 12:17 PM
Hi all, I follow this board regularly, but this is my first post here. I've had high LDL that I've always been able to lower with diet. My HDL is high, with numbers in the 70's and 80's. Also very low trig levels. I feel pretty fortunate so far, but intend to keep getting checked every year or two. The study about Crestor was in our morning paper and caught my eye. Whenever anything comes out like this, I make sure to check who paid for the study. In this case, the sponsor was AstraZenecaPLC, Crestors maker. I have no idea whether this makes any difference or would skew the results, but I found it interesting. Any way, good luck to everyone....balleteach
Follow your instincts , have you ever seen a study funded by the drug company ever put out to media with unfavorable results ? Of course not . I'd trust that study about as far as I could throw it .
Follow your instincts , have you ever seen a study funded by the drug company ever put out to media with unfavorable results ? Of course not . I'd trust that study about as far as I could throw it .
liverock
03-31-2006, 10:44 AM
The thing I have trouble understanding in the JAMA report by the authors of the ASTEROID (Crestor)study are the two "before and after "photographs showing the cross section of the arteries.
www. jama.ama-assn.org/cgi/content/full/295.13.jpc60002v1/JPC60002F2
From what I can see, while the plaque has indeed been reduced by 40%, the cross sectional area of the external elastic membrane has also been reduced . This shrinkage appears to have taken up all the area vacated by the plaque reduction and and this has meant that there is virtually the same lumen area of the artery(actually there is a 3% reduction).
This point was also taken up by the 2 cardiologists who reviewed the study and they commented;
" A recent substudy of the REVERSAL trial (another plaque reduction trial done recently), examined the effects of plaque progression and regression on coronary lumen size. In patients manifesting plaque regression, a decrease in the cross sectional area of the external elastic membrane was associated with no change in coronary lumen area.
No data regarding changes in lumen volume or size are reported in the ASTEROID study leaving open the possibility that changes in atheroma volume may be due to reduced cross sectional area of the external elastic membrane with potentially unchanged or reduced coronary lumen size suggested by figure 2"
www.jama.ama-assn.org/cgi/content/full/295.13.jed60019v1
So after a 40% plaque reduction there is no change in coronary artery blood flow according to these ultrasound pictures? Am I reading this right?
www. jama.ama-assn.org/cgi/content/full/295.13.jpc60002v1/JPC60002F2
From what I can see, while the plaque has indeed been reduced by 40%, the cross sectional area of the external elastic membrane has also been reduced . This shrinkage appears to have taken up all the area vacated by the plaque reduction and and this has meant that there is virtually the same lumen area of the artery(actually there is a 3% reduction).
This point was also taken up by the 2 cardiologists who reviewed the study and they commented;
" A recent substudy of the REVERSAL trial (another plaque reduction trial done recently), examined the effects of plaque progression and regression on coronary lumen size. In patients manifesting plaque regression, a decrease in the cross sectional area of the external elastic membrane was associated with no change in coronary lumen area.
No data regarding changes in lumen volume or size are reported in the ASTEROID study leaving open the possibility that changes in atheroma volume may be due to reduced cross sectional area of the external elastic membrane with potentially unchanged or reduced coronary lumen size suggested by figure 2"
www.jama.ama-assn.org/cgi/content/full/295.13.jed60019v1
So after a 40% plaque reduction there is no change in coronary artery blood flow according to these ultrasound pictures? Am I reading this right?
Lenin
03-31-2006, 12:03 PM
It was also reported in Reuters that the main author of the report stated that reducing the cholesterol to that level would leave behind a 'mainly fibrous plaque tissue."
This I would have thought would increase the chances of destabalising the plaque.
Liverock,
Your assumption is not correct. A typical plaque (non-calcified) has a fibrous cap covering a necrotic lipid core. The thicker the fibrous cap, the less chance of rupture. Studies have shown a 50 micron thick cap rutures easily and a 150 micron thick cap doesn't.
If one could eliminate most of the lipid leaving behind "fibrous plaque tissue" one will produce a plaque that is ultimately completely stable with almost NO chance of rupture...it's just an empty shell with nothing to "rupture out;" probably scar tissue is a good way to think about it.
Alas, it still takes up space in an artery but less than if it were filled with "pus-laden grease!"
This I would have thought would increase the chances of destabalising the plaque.
Liverock,
Your assumption is not correct. A typical plaque (non-calcified) has a fibrous cap covering a necrotic lipid core. The thicker the fibrous cap, the less chance of rupture. Studies have shown a 50 micron thick cap rutures easily and a 150 micron thick cap doesn't.
If one could eliminate most of the lipid leaving behind "fibrous plaque tissue" one will produce a plaque that is ultimately completely stable with almost NO chance of rupture...it's just an empty shell with nothing to "rupture out;" probably scar tissue is a good way to think about it.
Alas, it still takes up space in an artery but less than if it were filled with "pus-laden grease!"
liverock
04-01-2006, 01:04 PM
Fine Lenin, but what about the ultrasound pictures at www.jama.ama-assn.org/cgi/content/full/295.13.jpc60002v1/JPC60002F2 showing a reduced lumen area from 6.1sq.mm to 5.96sq.mm after 2 years of statin therapy which to my understanding (and I am willing to be corrected) means a 3% reduction in blood flow volume?
Lenin
04-01-2006, 02:37 PM
I'm thinking about that, liverock.
THis is cutting edge stuff and measurements and the methodologies are not precise.
I looked and looked at those 4 arteriographs...I'm not sure I get it.
What is the "external elastic membrane...it looks very INTERNAL to the artery...lots of gray stuff OUTSIDE it.
Is there a statistical difference between 5.98 and 6.19, they both round off to 6. It's bad science when someone overdefines their decimal points...and from these photos, calling them both 6 seems right to me.
Obviously if the volume of the the plaque fell nearly in half but the lumen decreased in size, there is either something else going on with that artery than atherosclerosis or it's partial abatement.
My problem on looking at the 4 pictures comes from what seems to me the rather arbitrary choice of boundaries.
Look at the bottom 2...check the 10 o'clock position. Why did that gray area that is NOT atheroma, nor lumen become so much thicker? Why should reducing an atheroma make an artery wall thicker?
These are very first approximation pix and should be useful in a huge body of evidence. But alone they don't tell much pro or con...IMHO (Humble, MOI? :D:D)
I must admit I came in on the tail end of this conversation ...I'll work harder on it.
THis is cutting edge stuff and measurements and the methodologies are not precise.
I looked and looked at those 4 arteriographs...I'm not sure I get it.
What is the "external elastic membrane...it looks very INTERNAL to the artery...lots of gray stuff OUTSIDE it.
Is there a statistical difference between 5.98 and 6.19, they both round off to 6. It's bad science when someone overdefines their decimal points...and from these photos, calling them both 6 seems right to me.
Obviously if the volume of the the plaque fell nearly in half but the lumen decreased in size, there is either something else going on with that artery than atherosclerosis or it's partial abatement.
My problem on looking at the 4 pictures comes from what seems to me the rather arbitrary choice of boundaries.
Look at the bottom 2...check the 10 o'clock position. Why did that gray area that is NOT atheroma, nor lumen become so much thicker? Why should reducing an atheroma make an artery wall thicker?
These are very first approximation pix and should be useful in a huge body of evidence. But alone they don't tell much pro or con...IMHO (Humble, MOI? :D:D)
I must admit I came in on the tail end of this conversation ...I'll work harder on it.
liverock
04-03-2006, 01:04 PM
I emailed Dr Nissen and now I've got the explanation.
According to him the conventional theory that the artery acts like a copper pipe on your heating system gradually being uniformally silted up is erroneous.
What really happens is that as plaque builds up THE ARTERY MEMBRANE EXPANDS TO MAINTAIN THE EXISTING LUMEN AREA AND BLOODFLOW.
Only when the artery has expanded as much as possible does the continued build up of plaque cause the lumen area to decrease and eventually stenosis occurs.
Likewise when arterial plaque regression occurs the artery shrinks to maintain the existing lumen area. It seems that the bodies intelligence is always trying to maintain a certain lumen area, and the artery membrane responds accordingly.
This doesnt to me explain the thickening of the membrane, but as long as the lumen area is not reduced (which it more or less it isn't), this may be a structural strength advantage for coronary arteries that are going like cocktail shakers for 24/7 year after year.
There is a comprehensive lecture by Dr Nissen on all this and a lot more at:
www.medscape.com/viewprogram/2590_pnt
You will have to scroll down the page about a quarter way before you get to his lecture but its very informative and complete with slides.
I must warn you after viewing you will never trust an angiogram again ! :
.
According to him the conventional theory that the artery acts like a copper pipe on your heating system gradually being uniformally silted up is erroneous.
What really happens is that as plaque builds up THE ARTERY MEMBRANE EXPANDS TO MAINTAIN THE EXISTING LUMEN AREA AND BLOODFLOW.
Only when the artery has expanded as much as possible does the continued build up of plaque cause the lumen area to decrease and eventually stenosis occurs.
Likewise when arterial plaque regression occurs the artery shrinks to maintain the existing lumen area. It seems that the bodies intelligence is always trying to maintain a certain lumen area, and the artery membrane responds accordingly.
This doesnt to me explain the thickening of the membrane, but as long as the lumen area is not reduced (which it more or less it isn't), this may be a structural strength advantage for coronary arteries that are going like cocktail shakers for 24/7 year after year.
There is a comprehensive lecture by Dr Nissen on all this and a lot more at:
www.medscape.com/viewprogram/2590_pnt
You will have to scroll down the page about a quarter way before you get to his lecture but its very informative and complete with slides.
I must warn you after viewing you will never trust an angiogram again ! :
.
Lenin
04-04-2006, 09:11 AM
liverock,
I'll visit the site this morning. I DO know that the coronary arteries are very elastic with muscular control of lumen size to throttle blood flow and thus can expand readily to compensate for some plaquing.
So far my only personal choice was to use angioplasty to open one widely, to over 3 mm., that had been completerly closed. For that, the angiogram was quite trustworthy and the increase in lumen size rather startling.
Presumably the pictured artery was not one that caused pain on exertion in either the BEFORE or AFTER state...or else evolution has made a very bad turn. It seems logical that an artery that is closed enough to cause a deficit of bloood wouldn't continue to shrink its "elastic membrane" <more later> to continue at the diameter that is insufficient to provide good blood flow.
The most logical process is that with large plaque formation the artery is stretched to it's limit in order to keep the lumen open as much as possible and to do the opposite when the plaque is regressed, to shrink back to normal. I would imagine the same thing would happen if a plaque were suddenly carved out and removed in a atherectomy.
And since you said pretty much the same thing:
What really happens is that as plaque builds up THE ARTERY MEMBRANE EXPANDS TO MAINTAIN THE EXISTING LUMEN AREA AND BLOODFLOW.
Only when the artery has expanded as much as possible does the continued build up of plaque cause the lumen area to decrease and eventually stenosis occurs. I agree completely. :D
If the artery shown is representative, I would expect that FURTHER regression of plaque would get to the point of increasing lumen size as the stretched artery returns to its to it's preobstruction size.
It is also quite possible that the artery shown is NOT representative of most of the coronary arteries.
Aside,
In your first post you mentioned "external elastic membrane." Can you define it for me. The discussion seems to focus on something that might more logically be called the "internal elastic membrane", if such a thing exists. To me "external elastic membrane seems to define the outer covereing of the artery...like paint on the outside of pipe. Are they talking about some membrane that might be thought of as paint on the INSIDE surface of a pipe?
The net effect of the Crestor study is that plaque regressed measurably in 2 years from the probable huge LDL decrease and modes HDL increase. For many people merely holding the status quo means the difference between life and death, and an angina-free existence. If modest plaque regression alone isn't enough to restore complete arterial flow, so be it. Perhaps 10 years of Crestor might.
Another aside: Back to that artery with the 6 square mm. lumen before and after the large plaque regression: is it possible to know the lumen size BEFORE the plaque formed...perhaps it was also 6 square millimeters then? ;)
I'll visit the site this morning. I DO know that the coronary arteries are very elastic with muscular control of lumen size to throttle blood flow and thus can expand readily to compensate for some plaquing.
So far my only personal choice was to use angioplasty to open one widely, to over 3 mm., that had been completerly closed. For that, the angiogram was quite trustworthy and the increase in lumen size rather startling.
Presumably the pictured artery was not one that caused pain on exertion in either the BEFORE or AFTER state...or else evolution has made a very bad turn. It seems logical that an artery that is closed enough to cause a deficit of bloood wouldn't continue to shrink its "elastic membrane" <more later> to continue at the diameter that is insufficient to provide good blood flow.
The most logical process is that with large plaque formation the artery is stretched to it's limit in order to keep the lumen open as much as possible and to do the opposite when the plaque is regressed, to shrink back to normal. I would imagine the same thing would happen if a plaque were suddenly carved out and removed in a atherectomy.
And since you said pretty much the same thing:
What really happens is that as plaque builds up THE ARTERY MEMBRANE EXPANDS TO MAINTAIN THE EXISTING LUMEN AREA AND BLOODFLOW.
Only when the artery has expanded as much as possible does the continued build up of plaque cause the lumen area to decrease and eventually stenosis occurs. I agree completely. :D
If the artery shown is representative, I would expect that FURTHER regression of plaque would get to the point of increasing lumen size as the stretched artery returns to its to it's preobstruction size.
It is also quite possible that the artery shown is NOT representative of most of the coronary arteries.
Aside,
In your first post you mentioned "external elastic membrane." Can you define it for me. The discussion seems to focus on something that might more logically be called the "internal elastic membrane", if such a thing exists. To me "external elastic membrane seems to define the outer covereing of the artery...like paint on the outside of pipe. Are they talking about some membrane that might be thought of as paint on the INSIDE surface of a pipe?
The net effect of the Crestor study is that plaque regressed measurably in 2 years from the probable huge LDL decrease and modes HDL increase. For many people merely holding the status quo means the difference between life and death, and an angina-free existence. If modest plaque regression alone isn't enough to restore complete arterial flow, so be it. Perhaps 10 years of Crestor might.
Another aside: Back to that artery with the 6 square mm. lumen before and after the large plaque regression: is it possible to know the lumen size BEFORE the plaque formed...perhaps it was also 6 square millimeters then? ;)
liverock
04-04-2006, 01:21 PM
Lenin
To me "external elastic membrane" seems to define the outer covering of the artery..like paint on the outside of a pipe. Are they talking about some membrane that might be thought of as paint on the INSIDE surface of a pipe?
External Elastic Membrane is just the name used for the whole artery membrane, not some sort of coat on the outside of the artery. There is no internal artery membrane term used in the study.
Another aside: Back to that artery with the 6 square mm. lumen before and after the large plaque regression: is it possible to know the lumen size BEFORE the plaque formed...perhaps it was also 6 square millimeters then? ;)
Indeed, as I understand it, once the artery starts moving back from its expanded state the lumen area will be as it was before there was any plaque formed. If the original lumen area could not be maintained then the artery would not be shrinking.
Further plaque recession will not increase the lumen area-which is the the thing that baffled me originally :confused: :confused:
Without this artery expansion as plaque is formed our arteries would silt up much quicker with the resulting much earlier deaths from CHD.
After you have visited the site you will be much clearer-I think! :D
To me "external elastic membrane" seems to define the outer covering of the artery..like paint on the outside of a pipe. Are they talking about some membrane that might be thought of as paint on the INSIDE surface of a pipe?
External Elastic Membrane is just the name used for the whole artery membrane, not some sort of coat on the outside of the artery. There is no internal artery membrane term used in the study.
Another aside: Back to that artery with the 6 square mm. lumen before and after the large plaque regression: is it possible to know the lumen size BEFORE the plaque formed...perhaps it was also 6 square millimeters then? ;)
Indeed, as I understand it, once the artery starts moving back from its expanded state the lumen area will be as it was before there was any plaque formed. If the original lumen area could not be maintained then the artery would not be shrinking.
Further plaque recession will not increase the lumen area-which is the the thing that baffled me originally :confused: :confused:
Without this artery expansion as plaque is formed our arteries would silt up much quicker with the resulting much earlier deaths from CHD.
After you have visited the site you will be much clearer-I think! :D
Lenin
04-05-2006, 10:40 AM
liverock,
I'm having a problem alas. Damn slides require RealPlayer and I use WindowsMediaPlayer...thus for me, it's all reading and NO video...so I'm missing the boat.
Some thoughts:
Glagov was right on target. We now know that between 95% and 99% of this disease, which kills one-third to one-half the population, occurs at sites without luminal narrowing. That is to say, only 1 in 20 to 1 in 100 plaques actually cause luminal narrowing. Thus, the angiograms we perform so commonly have really misled us.
Okay, what does this say:
1. that plaque problems are FAR worse than one sees on an angiogram and that a clean one may not be so clean.
2. IF the plaques that show up represent only 1 in 20 or 1 in 100, then we'd expect heart attacks in people with failed angiograms at the same rate as those who passed with flying colors (give or take a couple percent.) I don't think this is what we actually see in fact. I think he is vastly overstating the case.
IF 1/2 to 2/3 of the peope are killed by sites WITH shrunken lumina, then that alone is a very good argument FOR angiography...if ony 1-5% of plaques shrink the lumen but kill 60%, it is STILL this kind of plaque that we must find.
Should we not intervene at all? No, of course not. We should intervene to relieve angina, but we should not expect that intervention to treat the underlying arterial plaque. The intervention is going to treat the 1% of the plaque that the angiographer can see; it's not going to treat the 99% of the plaque that the angiographer can't see.
That seem quite obvious to me. Of course somebody who has been laying down plaque for decades and decades of fat coursing through his blood vessels is goint to show a distribution from tiny to humongous. THe humongous plaque will close down the lumen, and HURT. Such a plaque should be opened for pain relief. THat's not to say that the hundreds of others that don't hurt won't kill.
If anything, the presence of disease that cannot be surgically treated seems the very best reason for plaque reducing statin drugs since removing the fat is the only resasonable way to shrink a couple hundred plaques in the heart...certainly can't stent them.
If I had to summarize the results of the lecture, vis a vie, statins, it would be with this statement:
Now what about the lumen, did it get any bigger? It did not. There was no change in the hole. There was only change in the disease. At follow-up, the plaque was about half the size it was at baseline.
For me and most people with proven heart disease who are agressively lowering LDL with agents like Crestor the appproach is angiography to find closing or nonexistent lumens and force them open...and then assume there are MANY MANY partial blockages, the disease, that must be treated to maintain status quo or regression.
The lecture is quite good (I did 2/3 of the 32 pages.) It is probably the best summary of why one should stating drugs that I've seen. I didn't get the same negative view of angiography that you did. It painted angiography for what it is, a way to ascertain areas that are causing ischemia by closing off the lumen of a major artery. What it DOES indicate is that one shouldn't take an angiographic clean bill of health to the bank...there may be LOTS going on.
(oops I seem to have gone seamlessly from Dr. Nissen's article to Dr. Jones'...but they are related.)
I look forwward to revisiting the lecture when I can more fully appreciate it (if I ever load RealPlayer) alas my one attemp to run both media players was a disaster of overcompetition between them! :D) I would have liked to view th video presentations...maybe I'll sneak over to friend.
I'm having a problem alas. Damn slides require RealPlayer and I use WindowsMediaPlayer...thus for me, it's all reading and NO video...so I'm missing the boat.
Some thoughts:
Glagov was right on target. We now know that between 95% and 99% of this disease, which kills one-third to one-half the population, occurs at sites without luminal narrowing. That is to say, only 1 in 20 to 1 in 100 plaques actually cause luminal narrowing. Thus, the angiograms we perform so commonly have really misled us.
Okay, what does this say:
1. that plaque problems are FAR worse than one sees on an angiogram and that a clean one may not be so clean.
2. IF the plaques that show up represent only 1 in 20 or 1 in 100, then we'd expect heart attacks in people with failed angiograms at the same rate as those who passed with flying colors (give or take a couple percent.) I don't think this is what we actually see in fact. I think he is vastly overstating the case.
IF 1/2 to 2/3 of the peope are killed by sites WITH shrunken lumina, then that alone is a very good argument FOR angiography...if ony 1-5% of plaques shrink the lumen but kill 60%, it is STILL this kind of plaque that we must find.
Should we not intervene at all? No, of course not. We should intervene to relieve angina, but we should not expect that intervention to treat the underlying arterial plaque. The intervention is going to treat the 1% of the plaque that the angiographer can see; it's not going to treat the 99% of the plaque that the angiographer can't see.
That seem quite obvious to me. Of course somebody who has been laying down plaque for decades and decades of fat coursing through his blood vessels is goint to show a distribution from tiny to humongous. THe humongous plaque will close down the lumen, and HURT. Such a plaque should be opened for pain relief. THat's not to say that the hundreds of others that don't hurt won't kill.
If anything, the presence of disease that cannot be surgically treated seems the very best reason for plaque reducing statin drugs since removing the fat is the only resasonable way to shrink a couple hundred plaques in the heart...certainly can't stent them.
If I had to summarize the results of the lecture, vis a vie, statins, it would be with this statement:
Now what about the lumen, did it get any bigger? It did not. There was no change in the hole. There was only change in the disease. At follow-up, the plaque was about half the size it was at baseline.
For me and most people with proven heart disease who are agressively lowering LDL with agents like Crestor the appproach is angiography to find closing or nonexistent lumens and force them open...and then assume there are MANY MANY partial blockages, the disease, that must be treated to maintain status quo or regression.
The lecture is quite good (I did 2/3 of the 32 pages.) It is probably the best summary of why one should stating drugs that I've seen. I didn't get the same negative view of angiography that you did. It painted angiography for what it is, a way to ascertain areas that are causing ischemia by closing off the lumen of a major artery. What it DOES indicate is that one shouldn't take an angiographic clean bill of health to the bank...there may be LOTS going on.
(oops I seem to have gone seamlessly from Dr. Nissen's article to Dr. Jones'...but they are related.)
I look forwward to revisiting the lecture when I can more fully appreciate it (if I ever load RealPlayer) alas my one attemp to run both media players was a disaster of overcompetition between them! :D) I would have liked to view th video presentations...maybe I'll sneak over to friend.
heartcreature
04-05-2006, 01:22 PM
I've seen the damage Crestor can do to a person. My brother was on it and I believe if he had continued he would have ended up with a permanent disability or dead. The scary part is that the doctor didn't think it was the Crestor so I'm sure it was not reported. Thankfully after coming off the Crestor he had no permanent injuries and the terrible side effects were gone.
Lenin
04-05-2006, 01:31 PM
heartcreature,
Perhaps if his doctor didn't think the Crestor had any part in his semi-disability, it didn't. People got disabled before statins were invented 15 years ago.
Maybe the doctors are right sometimes.
If we don't believe them, perhaps the right approach would be to stop going to doctors; it's certainly the LOGICAL approach! It will save is a GREAT deal of money.
From previous posts, I think YOU take statins: which do you like best?
Perhaps if his doctor didn't think the Crestor had any part in his semi-disability, it didn't. People got disabled before statins were invented 15 years ago.
Maybe the doctors are right sometimes.
If we don't believe them, perhaps the right approach would be to stop going to doctors; it's certainly the LOGICAL approach! It will save is a GREAT deal of money.
From previous posts, I think YOU take statins: which do you like best?
HubbleRules
04-05-2006, 07:35 PM
heartcreature,
Perhaps if his doctor didn't think the Crestor had any part in his semi-disability, it didn't. People got disabled before statins were invented 15 years ago.
Maybe the doctors are right sometimes.
If we don't believe them, perhaps the right approach would be to stop going to doctors; it's certainly the LOGICAL approach! It will save is a GREAT deal of money.
From previous posts, I think YOU take statins: which do you like best?
Lenin,
Surely you don't really believe this...
If someone starts experiencing pains they never had before shortly after going on a drug, it's probably the drug that is causing it...
Doctors don't like to admit anything they prescribed or did caused a patient problem for a very, very good reason - FEAR OF MALPRACTICE SUITS... They are deathly afraid of saying or doing anything that could imply in any way, shape or form liability...
HubbleRules
:cool:
Perhaps if his doctor didn't think the Crestor had any part in his semi-disability, it didn't. People got disabled before statins were invented 15 years ago.
Maybe the doctors are right sometimes.
If we don't believe them, perhaps the right approach would be to stop going to doctors; it's certainly the LOGICAL approach! It will save is a GREAT deal of money.
From previous posts, I think YOU take statins: which do you like best?
Lenin,
Surely you don't really believe this...
If someone starts experiencing pains they never had before shortly after going on a drug, it's probably the drug that is causing it...
Doctors don't like to admit anything they prescribed or did caused a patient problem for a very, very good reason - FEAR OF MALPRACTICE SUITS... They are deathly afraid of saying or doing anything that could imply in any way, shape or form liability...
HubbleRules
:cool:
liverock
04-06-2006, 09:40 AM
Lenin,
It will be interesting to see whether reducing plaque to the extent that this study recommends does in fact cut down the number of cardiac events or all causes mortality, particularly cancer which has associations with low cholesterol levels.
The main problem I forsee will be how many people can stand taking 40mg of a gorilla statin like Crestor. William Davies, the cardiologist who wrote the bestseller,"Track Your Plaque" has treated hundreds of CAD patients with high statin doses(he also believes in reducing LDL to <60), and he reckons 30% of his patients have side effects. He was one himself and had to take a large dose of CoQ10 to reduce his muscle problems.
Another interesting point that has emerged from this trial is the fact that lower plaque can be associated with no increase in lumen area and at the same time the artery membrane can thicken.
5 years ago the press tore into a Vitamin C trial on reducing plaque in carotid arteries by announcing that "Vitamin C does not increase lumen size and causes an increase in artery thickness", exactly the same as the Crestor Trial did.
Could it be that Vitamin C was reducing plaque in this trial after all? :D :D
It will be interesting to see whether reducing plaque to the extent that this study recommends does in fact cut down the number of cardiac events or all causes mortality, particularly cancer which has associations with low cholesterol levels.
The main problem I forsee will be how many people can stand taking 40mg of a gorilla statin like Crestor. William Davies, the cardiologist who wrote the bestseller,"Track Your Plaque" has treated hundreds of CAD patients with high statin doses(he also believes in reducing LDL to <60), and he reckons 30% of his patients have side effects. He was one himself and had to take a large dose of CoQ10 to reduce his muscle problems.
Another interesting point that has emerged from this trial is the fact that lower plaque can be associated with no increase in lumen area and at the same time the artery membrane can thicken.
5 years ago the press tore into a Vitamin C trial on reducing plaque in carotid arteries by announcing that "Vitamin C does not increase lumen size and causes an increase in artery thickness", exactly the same as the Crestor Trial did.
Could it be that Vitamin C was reducing plaque in this trial after all? :D :D
Lenin
04-06-2006, 10:13 AM
liverock,
Another interesting point that has emerged from this trial is the fact that lower plaque can be associated with no increase in lumen area and at the same time the artery membrane can thicken.
I didn't really catch that. My impression was that the big ballooned arteries (viewed from outside) that had their plaque removed seemed to return to more normal size. Again, I don't really know what the "artery membrane" is...remember, I didn't have any of the slide projections. There doesn't seem to be a logical mechanism for the muscular walls of the artery to grow in response to lowered pressure from plaque regression.
Another weakness that might slant results away from an increasing lumen with plaque regression is the fact that the mecanics (and ethics) of the testing meant that they angioplasied those plaques that they thought might be causing ischemia. Thus they removed from consideration what might have happened to those lumina from 2 years of strong statin therapy. A good presumption is that with plaque diminution, the lumina would have likely increased in size. They thus studied only small plaques and "fixed" the rest...that skews results.
Here's another interesting take: My completely blocked (or nearly so) RCA was VERY distended on either side of the closure, such that it was more than twice the size of any other coronary for a centimeter or more. This indicated very clearly to me that the plug had caused increased pressure and swelling/ballooning of the artery probably for years during the plaque formation in an attempt to keep me alive (and heart attack free :bouncing: ) Since this was viewed angiographically, of course it was the lumen I was looking at. I would imagine that the lumen on either side of the blockage would have shrunk back to normal as the artery came back to approximate normal size once the large block of gluey fat fiber and pus was opened. Of course, right AT the plaque, the arterial distension was probably greatest because the angioplasty opened it as wide as the surrounding artery and the plaque was still there, just squooshed.
I guess, tying some good 64 slice CAT scans to show the outside of arteries in with both angiography and the intra-artery ultra sound to give the whole picture will be the grand finale. "We'll need to do some thorough testing on you sir; the cost should be around $2 million." :D:
On the concern for long term ability to take 40 mg. Crestor, I'm with you. Bumping up my Lipitor from 10 to 20 mg. in order to get my LDL into the 60's gave me great pause. After all, for me I'll be taking this med (or a generic variant like simvastain) til the day I die.
What impressed me was the ability to get such results from a mere 2 years of Crestor. I'm thinking very positively about the changes I might have gotten over the last 8 years of Lipitor.
I think the ultimate study of studies is to take a large population 20 year olds whose grandparents had heart disease and give half of them free Lipitor in 10 mg. doses for the rest of their lives. Let both groups eat the "typical American diet", i.e., too much wretched food, their whole lives and document what illnesses they get and what they die from and at what age. The government would have to pay the cost (like Framingham) because no drug company would pick up the costs to determine their drug was superb but the patent had run out 30 years ago!:D:D
You don't want to get me started about Vitamin C...then I'd have to go to the HIGH BLOOD PRESSURE page and start a thread: TALKING ABOUT VITAMIN C CURES CAUSES HYPERTENSION :D:D It didn't work for plaque regression because it doesn't work for ANYTHING except preventing scurvy in tiny doses. "Vitamin C CURES EVERYTHING" is the biggest supplement scam of the 20th century...and now the 21st. A remarkable feat of publicity over common sense and facts...like selling cigarettes for 60 years after people started calling them "coffin nails." ;)
Take care; nice chatting with you.
Another interesting point that has emerged from this trial is the fact that lower plaque can be associated with no increase in lumen area and at the same time the artery membrane can thicken.
I didn't really catch that. My impression was that the big ballooned arteries (viewed from outside) that had their plaque removed seemed to return to more normal size. Again, I don't really know what the "artery membrane" is...remember, I didn't have any of the slide projections. There doesn't seem to be a logical mechanism for the muscular walls of the artery to grow in response to lowered pressure from plaque regression.
Another weakness that might slant results away from an increasing lumen with plaque regression is the fact that the mecanics (and ethics) of the testing meant that they angioplasied those plaques that they thought might be causing ischemia. Thus they removed from consideration what might have happened to those lumina from 2 years of strong statin therapy. A good presumption is that with plaque diminution, the lumina would have likely increased in size. They thus studied only small plaques and "fixed" the rest...that skews results.
Here's another interesting take: My completely blocked (or nearly so) RCA was VERY distended on either side of the closure, such that it was more than twice the size of any other coronary for a centimeter or more. This indicated very clearly to me that the plug had caused increased pressure and swelling/ballooning of the artery probably for years during the plaque formation in an attempt to keep me alive (and heart attack free :bouncing: ) Since this was viewed angiographically, of course it was the lumen I was looking at. I would imagine that the lumen on either side of the blockage would have shrunk back to normal as the artery came back to approximate normal size once the large block of gluey fat fiber and pus was opened. Of course, right AT the plaque, the arterial distension was probably greatest because the angioplasty opened it as wide as the surrounding artery and the plaque was still there, just squooshed.
I guess, tying some good 64 slice CAT scans to show the outside of arteries in with both angiography and the intra-artery ultra sound to give the whole picture will be the grand finale. "We'll need to do some thorough testing on you sir; the cost should be around $2 million." :D:
On the concern for long term ability to take 40 mg. Crestor, I'm with you. Bumping up my Lipitor from 10 to 20 mg. in order to get my LDL into the 60's gave me great pause. After all, for me I'll be taking this med (or a generic variant like simvastain) til the day I die.
What impressed me was the ability to get such results from a mere 2 years of Crestor. I'm thinking very positively about the changes I might have gotten over the last 8 years of Lipitor.
I think the ultimate study of studies is to take a large population 20 year olds whose grandparents had heart disease and give half of them free Lipitor in 10 mg. doses for the rest of their lives. Let both groups eat the "typical American diet", i.e., too much wretched food, their whole lives and document what illnesses they get and what they die from and at what age. The government would have to pay the cost (like Framingham) because no drug company would pick up the costs to determine their drug was superb but the patent had run out 30 years ago!:D:D
You don't want to get me started about Vitamin C...then I'd have to go to the HIGH BLOOD PRESSURE page and start a thread: TALKING ABOUT VITAMIN C CURES CAUSES HYPERTENSION :D:D It didn't work for plaque regression because it doesn't work for ANYTHING except preventing scurvy in tiny doses. "Vitamin C CURES EVERYTHING" is the biggest supplement scam of the 20th century...and now the 21st. A remarkable feat of publicity over common sense and facts...like selling cigarettes for 60 years after people started calling them "coffin nails." ;)
Take care; nice chatting with you.
ARIZONA73
04-06-2006, 11:34 PM
You don't want to get me started about Vitamin C...then I'd have to go to the HIGH BLOOD PRESSURE page and start a thread: TALKING ABOUT VITAMIN C CURES CAUSES HYPERTENSION :D:D It didn't work for plaque regression because it doesn't work for ANYTHING except preventing scurvy in tiny doses.
As far as vitamin C is concerned, it has been shown to reduce plaque. What? It doesn't do anything except prevent scurvy in tiny doses? That's a very primitive way of thinking. After all, we're living in the 21st century, not the 18th century. Dr. Willis has clearly demonstrated that vitamin C can reduce plaque way back in 1954!!
As far as vitamin C is concerned, it has been shown to reduce plaque. What? It doesn't do anything except prevent scurvy in tiny doses? That's a very primitive way of thinking. After all, we're living in the 21st century, not the 18th century. Dr. Willis has clearly demonstrated that vitamin C can reduce plaque way back in 1954!!
Lenin
04-07-2006, 10:01 AM
The Willis/Pauling version of "clearly demonstrated" is a perfect example of faith based medicine. Willis' results/ hypotheses/theories/guesses are not clear or demonstrated by ANY stretch of medical imagination.
A lot of murky nonsense geared towards selling megavitamins and books.
If 1500 mg. of Vitamin C reversed plaque...my plaques would have been impossible to form, since I'd taken more than that for 20 years. Vitamin C does NOT reverse or prevent heart disease...nor is heart disease scurvy.
VITMIN C is the lead horse in the quackery race...in a truly civilized society, people who made irresponsible medical claims like that would be jailed for fraud.
A lot of murky nonsense geared towards selling megavitamins and books.
If 1500 mg. of Vitamin C reversed plaque...my plaques would have been impossible to form, since I'd taken more than that for 20 years. Vitamin C does NOT reverse or prevent heart disease...nor is heart disease scurvy.
VITMIN C is the lead horse in the quackery race...in a truly civilized society, people who made irresponsible medical claims like that would be jailed for fraud.
ARIZONA73
04-07-2006, 07:32 PM
It's not faith-based medicine. It was a legitimate study that Willis performed, and it is documented in the Canadian Medical Journal. He reported that 60% of those taking vitamin C improved, that is, their plaques were reduced. In 30% the plaques remained about the same, and in 10% he saw their plaques increase slightly. NONE of the control's plaques were reduced.
Incidentaly, when Linus Pauling published his book "Vitamin C and the Common Cold" in 1970, sales of vitamin C immediately skyrocketed, with some amazing results, such as the number of deaths attributed to heart disease plummeting by a staggering 40% in the next decade. This was observed only in the United States, where sales of vitamin C increased dramatically, not elsewhere in the world.
Incidentaly, when Linus Pauling published his book "Vitamin C and the Common Cold" in 1970, sales of vitamin C immediately skyrocketed, with some amazing results, such as the number of deaths attributed to heart disease plummeting by a staggering 40% in the next decade. This was observed only in the United States, where sales of vitamin C increased dramatically, not elsewhere in the world.
Lenin
04-07-2006, 07:53 PM
As Stumnper said, how many autipsies can you do on one heart.
An X-ray of the 50's saw broken bones and NOTHING in the heart.
Willis provided no evidence of cardio-protective qualities of Vitamin C.
God...what total nonsense about plummetting rates of heart disease with mega vitamin C dosage. Please tell me you don't REALLY believe there are demogaphics to show there was a 40% fall in heart disease in the 80's because of Vitamin C megadosing.
You CANNOT really believe nonsense like that; Can you?
I mean, honestly, my hope for the survival of common sense for mankind is on the line here?
A 40% decrease in heart disease in the 80's....OY!
An X-ray of the 50's saw broken bones and NOTHING in the heart.
Willis provided no evidence of cardio-protective qualities of Vitamin C.
God...what total nonsense about plummetting rates of heart disease with mega vitamin C dosage. Please tell me you don't REALLY believe there are demogaphics to show there was a 40% fall in heart disease in the 80's because of Vitamin C megadosing.
You CANNOT really believe nonsense like that; Can you?
I mean, honestly, my hope for the survival of common sense for mankind is on the line here?
A 40% decrease in heart disease in the 80's....OY!
ARIZONA73
04-07-2006, 11:38 PM
Well, for your information, Willis WAS able to take pictures of the human artery, even back in 1954. And, as far as the 40% drop in heart disease is concerned, you can believe whatever you want. But one thing is for certain: statins, for the majority of people, haven't done crap, except to cause a lot of pain and suffering!