Quote from: WendyA on April 09, 2016, 02:17:55 AM
The low prevalence of heart disease is not being attributed to low cholesterol. The facts are in all populations as cholesterol approaches 150mg heart attacks virtually disappear. This does not mean high cholesterol causes heart attacks.
The association between the level of cholesterol and incidence of heart attacks is just that, an ASSOCIATION. One cannot conclude from this that a cholesterol level of 150 and under will lead to no heart attacks but this is what he clearly thinks as his goal is to achieve this level in his patients and he tries to do this with the cholesterol lowering medication and diet.
QuoteThere has been no cause and effect asserted.
First he says:
"In a small group of my own patients, a 12-year follow-up shows prospective data confirming that a low-fat diet and lipid-lowering medication
causes disease to halt or regress." When clearly, we can't isolate cause and effect from this study as too many factors were manipulated. Instead, he should have said "is associated with". This suggests he is indeed biased.
Then:
"For over a decade it has been known that sufficient reduction of lipids may arrest and, in some cases, reverse coronary artery disease.7 An analysis of 35 cholesterol-lowering studies confirms that the benefits
are directly related to the degree of cholesterol reduction.8"
Bold statement, clearly implicating CAUSE, given that in these interventions, other factors are also at play like diet, or other effects of the medications/hormones involved that have nothing to do with cholesterol lowering which could have well played a role in lowering of CHD (coronary heart disease) mortality.
Circulation. 1995 Apr 15;91( 8 ):2274-82."Certain types of intervention had specific effects independent of cholesterol lowering."
In this study, if you look at findings closely, you find that the risk ratio for CHD mortality is:
- 0.889, 1.011, in all trials, from which no significant finding can be extracted as it is over and under 1.
- 0.861, 1.004, in all unifactorial trials, from which no significant finding can be extracted as it is over and under 1.
Hence, no significant findings.
Same goes for total mortality, as risk ratios are 0.957, 1.057 and 0.948, 1.085.
So when they say "The results suggest that cholesterol lowering itself is beneficial", they forget, interestingly enough to say that none of these findings are indeed significant. This, to me, reflects gross bias.
Uffe Ravnskov: High cholesterol does not cause atherosclerosis"recent studies have shown that statins (...) may exert anti-atherosclerotic effects by other mechanisms. These 'pleiotropic' effects, probably related to inhibition of the production of other isoprenoids such as geranylgeraniol or ubiquinone, are well-established in vitro, and studies are beginning to show cholesterol-independent mechanisms, including anti-inflammatory effects, in vivo as well14, 15."
Also,
http://www.ravnskov.nu/2015/12/27/myth-2/"If a high cholesterol really did promote atherosclerosis, then people with a high cholesterol should evidently be more atherosclerotic than people with a low. But it isn't so.
The pathologist Dr. Kurt Landé and the biochemist Dr. Warren Sperry at the Department of Forensic Medicine of New York University were the first to study that question. The year was 1936. To their surprise, they found absolutely no correlation between the amount of cholesterol in the blood and the degree of atherosclerosis in the arteries of a large number of individuals who had died violently. In age group after age group their diagrams looked like the starry sky. Drs. Landé and Sperry are never mentioned by the proponents of the diet-heart idea, or they misquote them and claim that they found a connection, or they ignore their results by arguing that cholesterol values in the dead are not identical with those in living people.
The latter problem was solved by Dr. J. C. Paterson from London, Canada and his team. For many years they followed about 800 war veterans. Over the years, Dr. Paterson and his coworkers regularly analyzed blood samples from these veterans. Because they restricted their study to veterans who had died between the ages of sixty and seventy, the scientists were informed about the cholesterol level over a large part of the time when atherosclerosis normally develops.Dr. Paterson and his colleagues did not find any connection either between the degree of atherosclerosis and the blood cholesterol level; those who had had a low cholesterol were just as atherosclerotic when they died as those who had had a high cholesterol. Similar studies have been performed in India, Poland, Guatemala, and in the USA, all with the same result: no correlation between the level of cholesterol in the blood stream and the amount of atherosclerosis in the vessels."
http://www.westonaprice.org/modern-diseases/the-benefits-of-high-cholesterol/"most studies of old people have shown that high cholesterol is not a risk factor for coronary heart disease. This was the result of my search in the Medline database for studies addressing that question.2 Eleven studies of old people came up with that result, and a further seven studies found that high cholesterol did not predict all-cause mortality either.
Now consider that more than 90 % of all cardiovascular disease is seen in people above age 60 also and that almost all studies have found that high cholesterol is not a risk factor for women.2 This means that high cholesterol is only a risk factor for less than 5 % of those who die from a heart attack."
QuoteCholesterol is a marker, often cholesterol is a symptom of inflammation that causes the liver to produce more cholesterol.
http://www.westonaprice.org/modern-diseases/the-benefits-of-high-cholesterol/"High cholesterol may therefore reflect mental stress, a well-known cause of high cholesterol and also a risk factor for heart disease. Again, high cholesterol is not necessarily the direct cause but may only be a marker. High cholesterol in young and middle-aged men could, for instance, reflect the body's need for more cholesterol because cholesterol is the building material of many stress hormones."
High cholesterol may be a symptom of many things and is sometimes actually associated with better outcome, although causality cannot be established.
"Consider the finding of Dr. Harlan Krumholz of the Department of Cardiovascular Medicine at Yale University, who reported in 1994 that old people with low cholesterol died twice as often from a heart attack as did old people with a high cholesterol.1"
"six of the studies found that total mortality was inversely associated with either total or LDL-cholesterol, or both. This means that it is actually much better to have high than to have low cholesterol if you want to live to be very old."
"in 19 large studies of more than 68,000 deaths, reviewed by Professor David R. Jacobs and his co-workers from the Division of Epidemiology at the University of Minnesota, low cholesterol predicted an increased risk of dying from gastrointestinal and respiratory diseases.3
Most gastrointestinal and respiratory diseases have an infectious origin. Therefore, a relevant question is whether it is the infection that lowers cholesterol or the low cholesterol that predisposes to infection? To answer this question Professor Jacobs and his group, together with Dr. Carlos Iribarren, followed more than 100,000 healthy individuals in the San Francisco area for fifteen years. At the end of the study those who had low cholesterol at the start of the study had more often been admitted to the hospital because of an infectious disease.4,5 This finding cannot be explained away with the argument that the infection had caused cholesterol to go down, because how could low cholesterol, recorded when these people were without any evidence of infection, be caused by a disease they had not yet encountered? Isn"t it more likely that low cholesterol in some way made them more vulnerable to infection, or that high cholesterol protected those who did not become infected? Much evidence exists to support that interpretation."
"those who had low cholesterol at the beginning of the study were twice as likely to test postitive for HIV compared with those with the highest cholesterol.6
Similar results come from a study of the MRFIT screenees, including more than 300,000 young and middle-aged men, which found that 16 years after the first cholesterol analysis the number of men whose cholesterol was lower than 160 and who had died from AIDS was four times higher than the number of men who had died from AIDS with a cholesterol above 240."
And this study:
Lancet. 2001 Aug 4;358(9279):351-5."Only the group with low cholesterol concentration at both examinations had a significant association with mortality (risk ratio 1.64, 95% CI 1.13-2.36)."
"We have been unable to explain our results. These data cast doubt on the scientific justification for lowering cholesterol to very low concentrations (<4.65 mmol/L) in elderly people."
4.65 mmol/L = 180 mg/dl
Cholesterol, in some cases, may also increase due to diet alone and may not be a bad thing.
Int J Clin Pract Suppl. 2009 Oct;(163):1-8, 28-36. "The degree to which serum cholesterol is increased by dietary cholesterol depends upon whether the individual's cholesterol synthesis is stimulated or down-regulated by such increased intake, and the extent to which each of these phenomena occurs varies from person to person. Several recent studies have shed additional light on the specific interplay between dietary cholesterol and cardiovascular health risk. It is evident that the dynamics of cholesterol homeostasis, and of development of CHD, are extremely complex and multifactorial. In summary, the earlier purported adverse relationship between dietary cholesterol and heart disease risk was likely largely over-exaggerated."
For instance, when I went ZERO carb and ate only protein and fat, my cholesterol went wayyyy up but so did my HDL and my Cholesterol:HDL ratio remained perfect, so did my LDL:HDL despite the fact that LDL also increased. Triglycerides having shown to be a causal agent in CHD, mine went wayyyyyyyyy down, under normal range. C-Reactive protein remained very low and there were no symptoms of inflammation whatsoever based on blood test results or how I felt and outward symptoms. Cholesterol was very high and yet everything indicated that my risk of CHD had actually gone down, my HDL being VERY high and triglycerides being very low.
QuoteYou are wrong though he does focus on one variable, heart disease. His goal was to get these patients under 150 mg of cholesterol by implementing a diet based on his best guess of what would lower cholesterol and inflammation.
Am J Cardiol. 1999 Aug 1;84(3):339-41, A8."The goal at study onset in 1985 had been to achieve a total serum cholesterol of <150 mg/dl, the level seen in cultures where coronary artery disease is virtually absent.3"
His focus seems to be heart disease, indeed. He believes that by just lowering cholesterol to under 150, heart disease will be halted, reversed and prevented when clearly, he does more than just lower cholesterol in his interventions (lowers refined carbs, for instance) which could account for results.
QuoteThe benefits of cholesterol lowering drugs are well defined. However in absolute numbers those who start taking them after they are diagnosed with heart disease after 5 years of daily statin therapy achieved a 1.2% lower chance of death, a 2.6% lower chance of heart attack, and a 0.8% lower chance of stroke. To put this in real numbers the 5-year risk is about 19% for mortality and 8% for non-fatal heart attacks.
Can you please cite source from where you get these numbers?
QuoteCompare this to the 5 year real world risk of Dr. Esselstyn's most recent group 0% deaths from coronary artery disease and 0.6% chance of non-fatal event. In relative terms this is a 98.8% reduction of risk.
True but this was mostly in men (180 out of 198) and a bunch of factors were manipulated so that we cannot pinpoint what exactly led to these findings. Was it the low fat, exclusion of refined carbs or animal protein, the lack of caffeine or fructose but doesn't fruit contain fructose?? What's the point of a study like this if we cannot find out what exactly caused what? And why would I adhere to such a diet when any of these components could prove to have no relationship to the outcomes and be something that could enhance my quality of life and overall health perhaps?
QuoteThe recently published 5 year paper has a 89.6% adherence rate after 5 years. Possibly times are changing. There are certainly many more resources available for folks these days and support groups are just a click away, both online and local via meetup.com.
"First, and quite compelling, is that 89% of patients were willing to make a substantial lifestyle transition to plant-based nutrition and sustain it for
an average of 3.7 years (for some patients up to 13 years). "
In the previous study, after 5 years, 75% adhered and by 10 yrs, 50%. After that, it fell even more, to 6 out of 22 (27%). Who's to say that eventually some of them in the new study won't also stop eating this way?
QuoteOne of the many reasons he chose such a low fat diet for his patients is because literally dietary fat quickly finds its way into the blood and takes about 6 hours to be processed. During this time the dilation of blood vessels is severely restricted. When one already has clogged arteries and is suffering from angina this is not a good thing.
In other words, you are saying dietary fat constricts blood vessels and clogs the arteries when...
Lipids. 2008 Jan;43(1):65-77"Overweight men and women with atherogenic dyslipidemia consumed ad libitum diets very low in carbohydrate (VLCKD) (1504 kcal:%CHO:fat:protein = 12:59:28) or low in fat (LFD) (1478 kcal:%CHO:fat:protein = 56:24:20) for 12 weeks."
"Total saturated fatty acids and 16:1n-7 were consistently decreased following the VLCKD."
From full study...
"Two recent studies demonstrated that consumption of a diet higher in saturated fat resulted in lower circulating palmitic acid (16:0) in cholesteryl ester compared to a diet low in saturated fat [3, 4], a paradox likely explained by the level of carbohydrate [5] whose increase is known to be associated with de novo fatty acid synthesis [6] and decreased fatty acid oxidation."
"We have previously described a comparison between a very low carbohydrate diet (VLCKD) and a low fat diet (LFD) in subjects with features of metabolic syndrome. A notable finding was an inverse relationship between dietary and plasma saturated fatty acids (SFA).
The VLCKD, with three-fold greater dietary SFA than the LFD, showed a consistently greater reduction in plasma SFA compared to the LFD [7]."
"Most striking,
we reported that despite a three-fold higher intake of dietary saturated fat during the VLCKD compared to the LFD, circulating saturated fatty acids in TAG and CE were significantly decreased, as was 16:1n-7, an endogenous marker of lipogenesis. There were profound changes, as well, in other fatty acids in circulating TG, PL, and CE fractions (Tables 2–4)."
"In the context of hypocaloric diets, we showed that reducing dietary total and saturated fat only had a small effect on circulating inflammatory markers whereas reducing carbohydrate led to considerably greater reductions in a number of proinflammatory cytokines, chemokines, and adhesion molecules.
These data implicate dietary carbohydrate rather than dietary fat as a more significant nutritional factor contributing to inflammatory processes"
"In this study, the VLCKD resulted in concurrent reductions in both 16:0 and 16:1n-7 in both TG and CE lipid fractions despite an increase in dietary saturated fat load. The significant reduction in dietary saturated fat in the LFD led to little decrease in total saturates and essentially no change in 16:1n-7, with one subject actually showing a drastic increase. The greater decrease in circulating SFA in response to carbohydrate restriction may have contributed to the larger decline in several inflammatory markers that are regulated by NF-κB [10, 11]. The decrease in circulating saturated fatty acids on the VLCKD is likely due to greater oxidation of the saturated fat from both diet and endogenous lipolysis, and a reduction in de novo lipogenesis."
BMJ. 2003 Oct 4;327(7418):777-82."These findings do not support associations between intake of total fat, cholesterol, or specific types of fat and risk of stroke in men."
Nutr Metab (Lond). 2006; 3: 24."carbohydrate restriction leads to an improvement in atherogenic lipid states in the absence of weight loss or
in the presence of higher saturated fat."
Am J Clin Nutr. 2010 Mar;91(3):535-46."A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD."
Nutrition. 2012 Feb;28(2):118-23. "Results and conclusions about saturated fat intake in relation to cardiovascular disease, from leading advisory committees, do not reflect the available scientific literature."
BMJ 2013;347:f6873"An influential Swedish health organisation has recommended a diet that is low in carbohydrates but not low in fat for people who are overweight or obese or have diabetes.
The advice from the Swedish Council on Health and Technology Assessment is the result of
a two year review of 16 000 scientific studies of diet. The recommendation contradicts the generally held belief that people should avoid foods that are rich in fat, especially those high in saturated fat."
"The council, which advises the Swedish healthcare system, concluded that
the scientific evidence did not support a low fat diet. Instead people should focus on reducing their intake of carbohydrates."
QuoteHe also encourages the small use of flax or chia seeds for omega 3 intake.
Of which less than 10% or less actually makes it into EPA and/or DHA.
Proc Nutr Soc. 2006 Feb;65(1):42-50."However, alphaLNA-feeding studies and stable-isotope studies using alphaLNA, which have addressed the question of bioconversion of alphaLNA to EPA and DHA, have concluded that in adult men conversion to EPA is limited (approximately 8%) and
conversion to DHA is extremely low (<0.1%). In women fractional conversion to DHA appears to be greater (9%)"
QuoteYou are wrong about the fact that nothing can be concluded. One conclusion is obvious, if your Dad, Uncle, Mom, Grandfather etc... died of heart disease and you have anxiety over it now there is something you can do to prevent yourself from falling victim to it.
But, just based on these studies, you can't tell what exactly you need to do without having to compromise on other things which might have nothing to do with heart disease. The studies would have been more informative had one factor just been changed, say a decrease in all refined carbs ONLY, nothing else. Perhaps, the same results would have been found. I refuse to make so many changes, not knowing what exact change will be beneficial and what other changes either make no difference at all or can actually make me healthier and increase my quality of life and the pleasure I get out of eating. This study, as far as I'm concerned, is totally useless as it reveals nothing concrete and specific. It remains too vague.
QuoteMy mistake, the on going program has been in existence for 3 decades. The first cohort started 3 decades ago the next paper is a snapshot of 198 consecutive patients but is not inclusive of the 1000s of folks that Dr. Esselstyn has counseled and trained in this way of halting and reversing heart disease.
All we have on paper (published) is those 198 patients and those other 22 or 24 patients of which 89% (176 people) and eventually 27% (6 people) adhered to the diet, respectively after an average of 3.5 yrs and after 10 yrs. Nothing else. Your original assertion of hundred(s) in 3 decades is not supported by these publications. Those 1000 folks you speak of, we first need to see actual results on paper to properly evaluate. Also, as I explained earlier, there are too many variables so one cannot establish specific cause and effect.
QuoteI simply stated what has been shown to work.
And what has been shown to work in MOSTLY men, in a small sample of individuals, is a host of things that were modified all at the same time. Far from conclusive.
QuoteBut the foods I eat now are nutritious and enjoyable and my quality of life has improved dramatically. Add to that the preponderance of evidence of the benefits of eating plants and I'll stick to it.
Despite the fact that over time (decades), the lack of fats and animal protein could possibly lead to nutrient deficiencies. You could still perhaps have a much improved quality of life and health over what you have now if you had included some things that you avoid and which might have no incidence on heart disease outcome.
QuoteFor all I know this study may be going on as we speak. Whether or not it would be sufficient for folks with advanced disease is hard to tell, but for all others it may be all that is needed. I certainly don't have the answers.
With those types of studies, we will NEVER have an answer. We need randomized controlled trials where only one variable is changed.
QuoteI agree, but did you read the article I linked to? Quite a fascinating story and the substance is already approved for use.
The evidence for it working comes from studies on MICE and in-vitro studies. Until it has actually been tested in humans, we cannot conclude anything. The treatment in the twins did not cure the illness (Niemann-Pick type C disease (NPC) but improved it and the illness is quite different from the condition of heart disease which is not necessarily caused by cholesterol accumulating in arteries but rather to initial inflammation in that area triggering cholesterol to deposit in that area to try and improve situation. This drug would not address the source of the problem but rather the factor that actually tries and helps improve the situation. Not good!
http://www.cbn.com/cbnnews/healthscience/2013/february/forget-cholesterol-inflammations-the-real-enemy/?mobile=false"Dr. Beverly Teter, a lipid biochemist at the University of Maryland, studies how the different kinds of fat in food affect our health.
Teter said scientists wrongly blamed cholesterol for heart disease when they saw high levels of it at a damaged blood vessel. Teter believes the body put the cholesterol there to fix the problem, which was actually caused by inflammation.
"It's the inflammation in the vessels that start the lesion," she explained. "
The body then sends the cholesterol like a scab to cover over it to protect the blood system and the vessel wall from further damage."
Research also shows cholesterol can protect against respiratory and gastrointestinal problems, and helps create vitamin D. People with higher cholesterol live longer.
Teter said that's a scientific fact that she can vouch for personally.
"I come from a family that has, my mother's side, had naturally high cholesterol. Her cholesterol was between 380 and 420 when I started watching her medical records, and she died at 97," she said. "So I don't think that cholesterol was too bad for her."
http://www.sott.net/article/242516-Heart-surgeon-speaks-out-on-what-really-causes-heart-disease"Simply stated, without inflammation being present in the body, there is no way that cholesterol would accumulate in the wall of the blood vessel and cause heart disease and strokes. Without inflammation, cholesterol would move freely throughout the body as nature intended. It is inflammation that causes cholesterol to become trapped."
