Tuesday, October 30, 2012

Healthy Longevity: Diet, Blood Cholesterol, Blood Pressure and Risk of Stroke

Healthy Longevity: Diet, Blood Cholesterol, Blood Pressure and Risk of Stroke:  Part I

The controversy surrounding the lipid hypothesis, in particular the relationship between elevated total and LDL cholesterol and coronary heart disease was considered largely resolved and regarded as scientific fact within the scientific community by 1984 when the expert panel from the National Institutes of Health (NIH) reviewed the relevant literature and agreed that the relationship was causal.1 2 The panel concluded:
Elevated blood cholesterol level is a major cause of coronary artery disease. It has been established beyond a reasonable doubt that lowering definitely elevated blood cholesterol levels (specifically blood levels of low-density lipoprotein cholesterol) will reduce the risk of heart attacks due to coronary heart disease… Further, we are persuaded that the blood cholesterol level of most Americans is undesirably high, in large part because of our high dietary intake of calories, saturated fat, and cholesterol… There is no doubt that appropriate changes in our diet will reduce blood cholesterol levels.
Since 1984 evidence accumulated from over 100 randomized controlled trials of various medical and dietary based lipid modifying interventions has further established that lowering LDL cholesterol significantly decreases the risk of coronary heart disease and all-cause mortality, independent of changes to HDL cholesterol and triglycerides, and non-lipid effects of specific drugs.3 4



Jozef Varhaník said...

Don please, what is your opinion about this study?

Jozef Varhaník said...

damn captcha spoiled my link


Brian J. MacLean said...

Re the study cited by Jozef: a cursory read of the paper suggests reverse causality may be a plausible explanation for low LDL levels being associated with higher CHF. The authors state: "It is possible, however, that decreased levels of cholesterol may simply be an effect of advanced HF. It has been thought that decreased levels of LDL are associated with cardiac cachexia, which is a state independently associated with increased mortality in HF.30 Alternatively, in vitro studies have suggested that circulating cytokines may act to decrease lipoprotein levels by decreasing hepatic lipoprotein production and increasing LDL receptor activity.31 These circulating cytokines may instead be the causative agent of the increased mortality in HF rather than a decrease in lipoprotein levels...
and, as such, cause and effect of the influence of LDL levels on outcomes cannot be conclusively proven from our study."

Jane said...

So Healthy Longevity is Nancy Rodriguez, a professor of nutritional science? Why does she not mention iron overload or copper deficiency? This is the real problem with animal products, because meat is so high in iron and dairy is so low in copper. Saturated fat inhibits copper absorption, and Leslie Klevay found years ago that a high-fat diet causing heart disease in mice did not do so if they were given extra copper.

Healthy Longevity said...

I am not Nancy Rodriguez. Please let me know if I wrote something in a way that would give someone the false impression that I am Nancy.

Jane said...

@Healthy Longevity
I'm so sorry. You posted this link
and I thought that meant you were her.

I looked her up and I can see why you might not want to be mistaken for her.
'.. Individuals who stop eating meat and dairy products are at risk of not getting enough calcium, vitamin D, protein, vitamin B12, zinc and iron in their diets—all nutrients that come mostly from food products derived from animals. ..'

This is almost complete nonsense.

Peter said...

Excellent paper input from Healthy Longevity. This really destroys the nonsense over the alleged dangers of physiological cholesterol concentrations.

BTW! I am concerned over the health status of misled fools who read Stephen Guyenets blog and think that diet has no role in serum lipids. These same people have often borrowed the creationist mind set and tend to overlook all animal data from closely related mammalians.

Arterial endothelial dysfunction in baboons fed a high-cholesterol, high-fat diet

"In summary, our results clearly show that the HCHF (high cholesterol and high fat) diet resulted not only in increased serum cholesterol concentrations but also in inflammation and endothelial dysfunction"


Peter said...

Campbell & Junshi (1994) reported that elevated serum cholesterol concentrations within a population with low-cholesterol as a baseline was a chief correlate to all disease of affluence (p = 0.01) including cancers.

"These findings suggest that even small intakes of foods of animal origin are associated with significant increases in plasma cholesterol concentrations, which are associated, in turn, with significant increases in chronic degenerative disease mortality rates".


Jane said...

'.. I am concerned over the health status of misled fools who read Stephan Guyenet's blog...'

My health is pretty good, thanks.

Anonymous said...

Stephan Guyenet is more scientific than any of you people. I respect him a TON. He REALIZES that science knows far too little about nutrition.

ALL is see HERE is a BELIEF SYSTEM. PLant based diets are NOT a health panacea. THAT IS HUCKSTER NONSENSE.

PLENTY of vegans get heart disease TOO.

Anonymous said...

The cholesterol hypothesis has MAJOR problems. This is glaringly obvious:

Atherosclerosis does NOT devlop "willy nilly" NOR does it devlop uniformly.

Atherosclerosis only devlops in KINKS and areas of DAMAGE to the artery.

Did you know VEVEN THE TINIEST VEINS NEVER become atherosclerotic? They have just as much cholesterol flowng through them.

This is all evidence that contradicts the cholesterol hypothesis.

The cholesterol hypothesis is an OBVIOUS HUGE FAILURE that continues to be promoted because of:





Healthy Longevity said...


Steinberg explains about developing atherosclerosis in veins.

Steinberg: Monocytes penetrate into vessels throughout the circulatory system at some rate, but they never accumulate in veins. Atherosclerosis simply does not develop in veins. But, if you surgically move a vein into the arterial system (as in a coronary bypass operation, for example), so that it is exposed to the high pressure of the arterial system, the vein will develop atherosclerosis. This process then is in fact quite similar to the process in arteries, including the migration of monocytes into the vessel wall and the accumulation of cholesterol, etc., etc..

Are you suggesting that if we find plenty of non-smokers with lung cancer that this somehow proves that smoking is not a cause of lung cancer, and that diseases can simply not have more than one risk factor involved? Or is this just another desperate attempt to push an unhealthy diet?

Healthy Longevity said...

It seems even the cholesterol denialists believe the RAZZ is a troll. Here are some pieces that Colpo posted:

For several years now, this individual has trolled and terrorized the Internet using monikers such as “Razzi”, “Razwell”, “Chris Razwell”, “Chris Downey”, and “Dr Susan Harmony”. At one point, this truly demented individual professed to be a huge fan of yours truly and Dr. Uffe Ravnskov (author of The Cholesterol Myths), posting in ALL-CAPS all over the Internet about our findings on the untenable cholesterol hypothesis of heart disease.


My website has picked up a lot of new readers since that article was written, so here’s a quick recap: “Razwell” is an anonymous troll who pollutes every diet, health and even MMA blog and forum he can access. In addition, he sends vulgar and highly abusive emails to those who have incurred his wrath, often several times a day. I know, because I’ve been on the receiving end of his harassment.

Aaron said...

I think I come to this blog to see what kind of nonsense is possible in the health community.

As Bill Maher would say -- paleo bloggers are living in some type of bubble that seems to ignore facts. No doubt there are positives about the paleo diet -- but high meat and fat intake is just not optimal for longevity.

Razz, I'll grant you that inflammation is what we need to be targeting. Problem is, high fat intake is more inflammatory than a lower fat intake based on fats like extra virgin olive oil and such.

On high fat diets -- bodies produce more cholesterol to deal with the arachadonic acid and other factors that might be damaging your body (from your high fat intake). So while cholesterol itself isn't bad. You need to worry why the body needs so much cholesterol to repair things.

malena said...

What Razz is suggesting here, I believe, is that the body is simply not a machine, or a chemical soup, that is a total victim to our life style. The cause and effect explanation in today's theory doesn't take into account that the body has itself an infinite wisdom and at very second makes intelligent choices.

If there was a straight relationship between fat/cholesterol and atherosclerosis, we would indeed first see the problem in the tiny veins, where there's the highest probability of congestion. Ask a plumber - where do you find congestion, in the tiny pipes or in the large ones with the best flow?

So, why then do we find atherosclerosis close to the heart, in the large arteries with the best flow?

A reasonable explanation is, as Razz alluded, that there is injury to the arteries and that the intelligent body uses whatever smart material it has available to make a temporary fix - that is - mending the arteries with a cholesterol lining. This explains why we find atherosclerosis close to the heart. If there would be a rupture in an artery close to the heart, where we find the highest pressure, the largest blood flow, the body would risk a major damage, and the body, with its infinite wisdom, therefore choses to mend the arteries here.

It is not the cholesterol causing the problem, the problem is already there. Cholesterol is the symptom of something else going on - the real cause.

So why do we have injured veins? Apparently there's a weakness in the body's structural tissues, perhaps caused by nutritional deficiency. It can of course be any kind of nutritional deficiency, my guess is that many people today lack vitamin c, and that the daily recommendations are far to low.

Then we have the emotional factor. Unfortunately allopathic medicine today is not even near touching that subject, except perhaps for epigenetics.

The discussion here, that is only focused on a symptom and not the cause, is a very good illustration of the healthcare industry today. So many people here thinking that they don't agree with the industry, but the reasoning is just the same. Symptom and not the cause is still on the agenda.

Anonymous said...

Saturated fat inversely associated with stroke in Japan http://www.ncbi.nlm.nih.gov/pubmed/20685950

Loook at all of the reviews and meta analyses of dairy that don't show higher stroke risk http://www.ncbi.nlm.nih.gov/pubmed/21068345



Full fat dairy associated with lower risk for cardiovascular disease http://www.nature.com/ejcn/journal/v64/n6/abs/ejcn201045a.html

Full fat dairy not associated with stroke, cardiovascular disease or diabetes http://www.ncbi.nlm.nih.gov/pubmed/22810464

Uh ohs, are vegans far more likely to die than lacto-ovo vegetarians, even from heart attacks? http://www.ncbi.nlm.nih.gov/pubmed/10479225 Better get some of that sweet sweet moo juice into your belly before you die.

And women before they get breast cancer http://www.ncbi.nlm.nih.gov/pubmed/21442197 (actually not milk, just cheese and other dairy)

Or it could be that simply because there are statistical associations between things doesn't mean that there is a causal relationship and there are usually confounding factors that nobody has looked at.

Healthy Longevity said...

I briefly covered macronutrient intake and risk of stroke in Part II.

These meta-analyses show that increased intake of dairy primarily at the expense of foods such as refined sugars, red and processed meat, typical in the Western diets failed to lower the risk of all-cause mortality. I do not see how this justifies increase intake of dairy, especially considering the evidence linking increased intake to prostate and ovarian cancers and Parkinson’s disease. Not surprisingly, meta-analyses and systematic reviews found that compared to all other sources of energy combined, refined grains do not increase the risk of cardiovascular disease or all-cause mortality.

Stamler demonstrated in a meta-analysis that an increased intake of saturated fat primarily at the expense of refined carbohydrates increased the risk of coronary heart disease mortality, and a recent study found that intake of saturated fat increased the risk of all-cause mortality in Japanese women.

Don said...


Arteries throughout the body develop atherosclerosis, not only those you mentioned. Also, when we absorb long-chain fats (most saturated and unsaturated fats have long chains) they enter the lymph, and are transported to the superior vena cava, so the heart's arteries are the first exposed to ingested fats. They therefore capture more of the ingested fats, like a sieve, leaving less to be distributed throughout the body. Naturally, these tissues are therefore more susceptible to the damage from dietary fat, as they are, so to speak, on the frontline of exposure.

Don said...

All but one of the studies cited by Stabby are limited because they involve populations wherein almost no one has a zero intake of dairy products, which means that all could be above the threshold for harm.

As for the vegans having a higher rate of CHD in the one study, this could have a number of reasons, including:

Vegans include people who have adopted a zero intake of animal products because of established CHD.

A significant number of free-living vegans neglect to ensure adequate B12 intake.

A significant number of vegans don't care about their own health, and eat plenty of refined foods including trans fats, refined oils, etc.

A significant number of vegans eat high fat diets. Surveys show that in the UK, the average vegan consumes a diet providing 35-45% of energy as fat, no better than the average non-vegan, too high for excellent cardiovascular health.

Don said...

For example of the limits I spoke of and acknowledged by the study authors, if you check this one cited by Stabby,


the authors state:

"Conclusions from this meta-analysis only apply to the small proportion of analyzable study populations included in this work, within milk intakes of
~200–600 mL/d (see supplemental Table 2 under “Supplemental data” in the online issue)."

Anonymous said...

Healthy Longevity: interesting theory but that is a big assumption, it's not like all people eat is red meat, refined carbohydrates or dairy. Dietary factors cluster together, and since dairy fat has been demonized for so long the people who are consuming less of it will be more likely to eat the foods that are recommended: whole grains and vegetables and fruits and lean proteins.

Butter-avoiders aren't really living on processed carbs and meat. People who eat all of the high fat dairy they want are most definitely apathetic towards health save for the Weston Pricers. There are so many factors at play that we could never control for all of them, but I would wager that eating pizza and butter and full-fat ice cream correlates with worse habits than better ones across the board.

Looking at pastoral cultures is interesting too, but it could be a low carbohydrate intake or certain nutritional deficiencies at play too.

A more recent paper by Walter Willet et al suggests that actually refined carbohydrates are associated with worse outcomes than saturated fats http://www.ncbi.nlm.nih.gov/pubmed/21270379

Bottom line: the evidence from epidemiology that dairy fat causes stroke is not supportive of your recommendations to eat a vegan diet. Dairy fat can raise LDL which can be correlated with a disease is not better evidence than correlations between dairy fat and diseases.

Anonymous said...

Don: Indeed it could be that barely any is just as bad as tons of dairy. It is highly dubious considering the argument in this article relies heavily on blood cholesterol which is increased in a dose-dependent manner by cholesterol and saturated fat until a rather high intake. One would expect people barely consuming any dairy fat to be less affected by dairy fat than people eating more.

Re: vegans. It was actually 4 studies. Those are valid criticisms of trying to prove something with epidemiology, but I think that you're missing the point. You like to use epidemiology that suffers from the exact same criticisms. Some vegans neglect their health, but they are far more health-conscious than omnivores on average, and considering that for the longest time cholesterol and saturated fat have been demonized I don't think that lacto-ovos are less health-conscious than vegans.

Some neglect B12, this is true, but if that is the big reason why they are more likely to die then you have to maintain that that B12 is more important than dietary saturated fat and cholesterol when determining heart risk. You just recently argued that the differences aren't that profound.

Some people may become vegans because they have heart disease, and these people are eliminated from such studies of mortality. No heart patients are included in studies of prognosis. As you know tons of people stop being vegan because they develop health problems. Not necessarily because the vegan diet caused health problems, but it certainly removes their bad health from the statistic. Many of them start again with dairy.

As I said, I don't put much faith in statistical associations (and I don't think that other people should either). There are so many confounding factors and contextual factors at play that it provides a low level of evidence. There could be causality, but there could be no causality under other circumstances.

Saturated fat can injure the endothelium... http://atvb.ahajournals.org/content/25/6/1274.long

But that damage to the endothelium can be prevented by improving lipid metabolism to prevent lipotoxicity http://www.ncbi.nlm.nih.gov/pubmed/21831993 http://www.ncbi.nlm.nih.gov/pubmed/16896723
or improving nitric oxide synthesis http://www.ncbi.nlm.nih.gov/pubmed/17659795 Something that the successful statins do http://www.cholesterol-and-health.com/Rho-Activation.html

Feeding rabbits cholesterol tends to produce atherosclerotic lesions but there is a pronounced protective effect of nitric oxide and antioxidants that is independent of cholesterol levels http://circ.ahajournals.org/content/96/4/1282 http://www.ncbi.nlm.nih.gov/pubmed/15725692 Levels remain astronomically high, atherosclerosis is sliced.

So we again have to modify associations between certain factors like LDL or saturated fat by controlling for factors that directly protect against their effects; not something that epidemiology tends to do.

We could talk about B12 in vegans or we could just leave it as is. Or we could try to talk about nitric oxide and lipid metabolism and antioxidant status in LDL and saturated fat epidemiology instead of leaving it as-is, which is what I propose, and also propose leaving the vegans-have-more-heart-attacks-than-egg-and-dairy-eaters studies be and focus on controlled trials and experimentation with epidemiology as a hypothesis-generator only.

And you do talk about that, so this is good. One tip I would have is to try to falsify hypotheses you have that X thing kills people more. There are alternative hypotheses to the LDL-kills-you theory that can use the exact same evidence like the one Chris Masterjohn espouses. Why not the time spent in the blood rather the amount that passes through the blood?

Anonymous said...

@ Healthy Longevity: Actually I'm not sure if you're advocating a vegan diet or not, you seem to espouse the beliefs that would lead to it, or at least plant-based dieting. You said that all sorts of plant foods lower blood pressure and this explains the blood-pressure-lowering effects of vegetarian and vegan diets, which isn't necessarily an endorsement. I agree that plants can help bigtime, but in case you're suggesting that one should eliminate meat to get those benefits because meat is bad, or simply useless, I really doubt that this is true, and including meat may be beneficial...

Most of those studies are observational; yeah I know that the standard vegetarian diet is probably better than the standard omnivore diet, and the former includes more beneficial plant foods on average, but it is actually rather easy to get all of the nutrients one needs and eat meat. Vegetables fruits, teas, spices, cocoa and the like can be incorporated into a diet without having to eliminate meat, and meat may have beneficial properties.

Two studies have replaced carbohydrates with red meat and demonstrated significant reductions in blood pressure http://redalyc.uaemex.mx/redalyc/pdf/1702/170216824004.pdf http://ajcn.nutrition.org/content/83/4/780.full It was mostly starch foods that they replaced, breads, cereals, potatoes, etc. And while there may have been some refined carbohydrates in there last time I checked potatoes and cereals reduced blood pressure in their own right. It really depends on the kind of cereal, though. If not evidence that meat can benefit blood pressure, perhaps an illustration of how easy it is to bias a diet trial.

Plant protein may work too, and indeed it is probably not lack of meat but inclusion of more of other foods that accounts for lower vegetarian blood pressure, as a very tightly controlled trial showed no difference between meat and non-meat proteins http://www.ncbi.nlm.nih.gov/pubmed/3293891 But maybe we could combine them? Soy has tons of magnesium and other nutrients, and in the 2006 study I cited they suggest that meat's taurine content could be beneficial. It's an excellent source of alpha-lipoic acid and carnitine and those lower blood pressure http://www.ncbi.nlm.nih.gov/pubmed/17396066


Anonymous said...

I mean meat can get along with plants, they are certainly delicious together. And you might think that there are other reasons to avoid meat, but that is mostly based on epidemiology and often overlooks the overcooking of meat. High heat cooking produces carcinogens and low heat cooking methods minimize the formation. It is interesting that there is little evidence that low heat techniques cause cancer



Sometimes even being inversely associated.



And numerous others. And I can see one possible retort, that it's just trading bad and worse, but this is total intake of low and high heat cooked meat, and it may simply reflect preference rather than health-consciousness.

There are also protective factors like our detoxification systems that can be increased by nutrition and protect us http://www.ncbi.nlm.nih.gov/pubmed/10202396 Would small amounts of HCA's matter then? And there are of course marinades that eliminate the problem.

But back to the main topic, it's not just cancer that is affected by these damaging compounds but everything. And cooking intensity hasn't been controlled for properly in most studies. I see that as the next step in scientists trying to falsify the meat-is-deadly hypotheses.

You mentioned iron in your article, and I can see it as a concern, particularly for colon health, but some scientists thing that the nitrosation is causes can be prevented by eating calcium and chlorophyll at meals to bind the heme iron http://cancerpreventionresearch.aacrjournals.org/content/4/2/177.full?cited-by=yes&legid=canprevres;4/2/177 There's a neat chart at the bottom.

There are trials where it caused DNA adducts http://www.ncbi.nlm.nih.gov/pubmed/16452248 But there are also trials where high calcium foods were preventative of nitrosation http://www.ncbi.nlm.nih.gov/pubmed/12235653 And there is the role of highly fermentable fiber http://www.ncbi.nlm.nih.gov/pubmed/21963168 The butyrate the highly fermentable kinds produce is very protective of the GI tract and I would say that the GI tract becomes very sensitive to a lot of things without it.

On top oxidative stress in the body. That's a decent assumption but is it really true that meat causes iron overload? Increasing red meat greatly at the expense of starch can lower iron levels, reduce oxidative stress and inflammation http://jn.nutrition.org/content/137/2/363.full And they mention in the discussion section that many other studies have shown either a reduction of iron or no difference. It seems that the body regulates its iron absorption save for cases of hemochromatosis.

There is the hypothesis that fatty red meat could increase iron levels pathologically by facilitating the absorption of iron (and other minerals). It is being tested and so far unproven. I don't think that meat causing higher iron is a great explanation for associations. Meat contains carnosine which chelates iron and has numerous other benefits http://thatpaleoguy.com/2011/02/21/carnosine-colons-and-cancer/

And it may be hyperinsulinemia that is responsible for dysregulation of iron levels and iron levels rise too high when on the path to diabetes. Red meat could be the nail in the coffin and there could be benefit of a vegetarian diet then if iron absorption is dysregulated, but perhaps not for healthy people. http://www.ncbi.nlm.nih.gov/pubmed/14592787

Anonymous said...

You mentioned dairy being associated with certain cancers. This is a legitimate concern because of IGF-1 signaling, which is elevated by dairy. IGF-1 has many benefits but it's mitogenic. However the mitogenic effect of a hormone is never just determined by its status in the blood but by its receptor activity too. It turns out that vitamin d's metabolites are regulators of this and it may only be people with vitamin d utilization issues or deficiencies that need to worry about IGF-1

http://www.ncbi.nlm.nih.gov/pubmed/22216097 http://www.ncbi.nlm.nih.gov/pubmed/9379127 It also works for estrogen http://www.ncbi.nlm.nih.gov/pubmed/20156557

So I am left with a seemingly arbitrary decision. Meat and dairy are wonderfully nutritious foods that have things that plants don't. But on the other hand there are some concerns. I haven't yet found a concern that would sway my views, I think that a nutritious diet ameliorates all problems and leaves these foods as a net positive. I don't expect you to change what you're doing or saying, I'm just sharing my view on things. That epidemiology, while valuable in some cases, has a long way to go before it can really prove that something is unhealthy. And most of the controlled trials for vegetarian diets are poorly controlled. Loren Cordain's paleo diet, while flawed, is an excellent example of a combination of the best of both worlds. Although I could never eat that much meat and doubt that real grains are bad.

My bias seems to be that meat is such a good food and makes me feel good with high levels of nutrients like carnosine, its precusor beta alanine, taurine, carnitine, creatine, cholesterol, and others that whatever minor problems it may have should be battled intensely. Not that evidence should be ignored, but we should try hard to falsify the notion that a food is harmful before radically changing diets. Has epidemiology really satisfied the conditions for causation? Certainly not -necessary- causation.

Peter said...
This comment has been removed by the author.
Peter said...

A fresh paper on vegeterian mortality and metabolic risk is on the print. It's part of the seventh day adventist study with participant size almost 100 000. Loads of vegans included. It's the first paper ever that addresses the topic with adequate follow-up, volume and statistical power.

Vegans have lower serum cholesterol levels and lower blood pressure than the general population have and the vegans will be living longer lives than the general population. This is a bullet-proof fact and will be obvious immeadiately when the follow-up is long enough and the particpant size big enough. This is already nicely illustrated among the Okinawa folk whose traditional diet that was reported in the 1940's was almost as near as a vegan diet as it gets.

The only issue is to what extent high-fat Western vegans have lower cholesterol and blood pressure next to general population.

"It's the cholesterol idiot"

Anonymous said...
This comment has been removed by a blog administrator.
Anonymous said...

Well it's clearly not the cholesterol if in most of the other studies done on vegetarians and vegans the vegans were more likely to die of heart attacks than lacto-ovos. Don's new view that B12 is at the "heart" of it all is more tenable. Not that it's all that tenable.

It's interesting that the only studies that actually tend to show that vegetarians live longer than omnivores are from the Seventh Day Adventists where vegetarianism is actually a religion and is absolutely synonymous with health-consciousness, they drink and smoke less and have a myriad of other factors going for them. The Health-shoppers study was a nail in the coffin of the idea that it's somehow the meat. ajcn.nutrition.org/content/70/3/516s.full.pdf Sure the vegetarian/vegans tended to have lower CVD mortality in most of them (not lower mortality, the vegans were dragging the veggies down as I posted earlier) but when trying to control for health-consciousness, not even controlling for cooking techniques and processed meat, there was no difference. Surprise surprise.

The Japanese monks and the EPIC study that came later don't really help. Japanese monks, that couldn't possibly have been confounded! No not at all. And the EPIC study found no difference in all-cause mortality again http://www.veganhealth.org/articles/dxrates#fn12

You are sounding awfully religious, Peter, perhaps you would do well living with the Adventists. Whether or not you believe in their god you could worship veganism quite comfortably there.

As for cholesterol, the idea that the serum concentration is what matters and that anything that increases serum concentration at all is going to increase atherosclerosis has no basis in fact and has nothing going for it except for cherry-picked correlations and just-so explanations. How about you debate Chris Masterjohn http://www.cholesterol-and-health.com/Does-Cholesterol-Cause-Heart-Disease-Myth.html He's less big and scary than Anthony Colpo but better on the science. Colpo did quite a number on your little cherry-picking fests though. Not perfect but certainly very embarrassing for you and your doctrine.

Endothelial function, blood flow, oxidized LDL and the vascular injury leading to adhesion to the artery, inflammation causing progression, and I doubt we know it all yet. What part of epidemiology-has-not-accounted-for-that-yet don't you get? Every bit of evidence that could be used to argue for LDL concentration mattering can also be used to argue that it's oxidized LDL and the time it spends in the blood becoming damaged that matters. Poor T3 and insulin signaling produce the truly high cholesterol, not eating cholesterol, that is why there is such variance between increases in response to it. So many things affect LDL cholesterol, how many papers are there demonstrating that nutrients lower cholesterol? How many of those nutrients also impact inflammatory, oxidative, and endothelial status? So why the lower cholesterol and not the other things they do? Why is it the amount of LDL and not the time that the LDL spends in circulation, increased by poor clearance, which also increases levels? Vitamin e's inefficacy maybe? No those supplements are harmful in many ways.

Statin drugs? Inflammation and endothelial nitric oxide. Dean Ornish? Entire lifestyle interventions.

Supposing that for the first time ever vegans are healthier than vegetarians in this new study, how would that constitute evidence that it is any particular feature of their lifestyle of physiology that accounted for it? More cholesterol-CVD correlations and blustering? Vegans don't overcook meat because they don't eat it, don't eat processed meat, and stop being vegans once they run into health problems. But one can just eat fresh meat that has been properly cooked. Is that being accounted for or is this yet another study from the religious vegetarians trying to prove that their way of life is the best to the world via observational evidence?

Anonymous said...

By the way Peter and Don, I have saved you from an error. It seems that arachidonic acid in the diet has no impact on inflammatory arachidonic acid metabolites in the body http://www.ncbi.nlm.nih.gov/pubmed/22188761

You see there are these things called controlled trials, and people give one group something and don't give another group another thing, and hopefully that is the -only- difference between the groups or else the study can't demonstrate much of anything. They are better than observational studies, in vitro studies, and other lesser forms of evidence.

I wouldn't retort that the miniscule AA intake of the control group was comparable to the enormous amounts the other got. The intervention groups' membrane phospholipids are packed with AA and it's making a few beneficial cytokines, but they have extremely low inflammatory markers, barely any CRP. Gotta love Japan. Their fish and soy intake may also provide the omega-3s to modulate the enzymes that produce eicosanoids.

It is so cute how you guys get so excited about mining new evidence to push your ideologically-based beliefs. Okinawans may have gone through times of poverty, which is an excellent hypothesis for longevity by the way (starvation of mothers and epigenetic programming), but there is no reason to think that their pork consumption is bad for them. Animal foods, saturated fat and animal protein can predict improved longevity in older Japanese people. http://www.ncbi.nlm.nih.gov/pubmed/1407826

The Japanese have an amazing diet, but the great epidemiology gods say that they could have used more meat all along. If things start to change and we start seeing tiny increases in stroke risk or heart disease with saturated fat intake, this could be because of industrialization and the rise of fast food. So much meat is consumed at fast food restaurants with trans fats and soda and fries cooked in oils and that is apparently "meat" in most epidemiological studies. Not that it's associated yet http://www.ncbi.nlm.nih.gov/pubmed/22333876 1.10 HR from highest to lowest is not being associated. Confounding factors, mmkay?

Healthy Longevity and Don are going to jump in and say that 10g per day is just as bad as 77g per day! Well of course, if they just get rid of that fork-full of steak their mortality will plummet. And 100g sure isn't the North American intake. Well maybe some people would prefer eating that than none, hmm? Not you guys, you will never eat meat again and have vowed to prove that it is bad for everybody else.

For your benefit of course, I'm an epidemiology agnostic. Maybe it helps maybe it doesn't, it's good for infectious diseases and hypotheses. But when trying to prove that some biomarker or food is relevant there are mountains of detail and context that get washed away.

Anonymous said...

Oh some more for you guys, remember how meat raises inflammation postprandially? It's the fat, intestinal permeability and the endotoxemia, but it is really easy to prevent. They have done it with orange juice http://www.ncbi.nlm.nih.gov/pubmed/20200256 and grape http://www.ncbi.nlm.nih.gov/pubmed/21289251 I wish they had just used meat and not egg-sausage mcmuffins which have plenty wrong with them aside from the eggs and the sausage, but it counts to prove a point.

And it is unproven in humans but mice on a high fat diet are totally protected from intestinal permeability if all they do is increase their fermentable fiber to generate butyrate which protects the barrier. http://www.ncbi.nlm.nih.gov/pubmed/17823788

I wouldn't look at it as "meat bad, fat bad, fiber good", just that without a lot of butyrate production and high bifidobacteria population the GI tract is rather dysfunctional and sensitive.

So again, we have to adjust statistical models, not only for fiber and fruit, but consistent intake of fiber and fruit at the right times. And overall gut flora status, which hasn't happened. Bye bye most meat epidemiology, come back when you have grown up.

Peter said...

1) The reported dietary fat intake among Okinawans stood at 6% which corresponded with very low serum cholesterol levels (traditional dietary setting).

2) Elevated LDL cholesterol induces atherosclerosis and coronary artery disease mortality in every mammalian specimen (birds and insects included). Humans in Western socities typically show LDL cholesterol levels that are +200% to what is physiologically normal, that is levels that has been observed in a) free-ranging mammalians that do not develope atherosclerosis, b) healthy neonates and c) members living in societies where chronic disease including atherosclerosis is near-asbsent.

Perhaps the considerations expressed above influenced this article published in a peer-reviewed scientific journal

Cholesterol myth club on par with flat earth society

3) The very same foods that causes elevation in serum cholesterol promotes endothelium dysfunction, LDL oxidation, lipid peroxidation and inflamation. These are the conditions that are raised by cholesterol denialists in an attempt to confuse and sabotage the truth around cholesterol and heart disease

a) Consumption of eggs with meals increases the susceptibility of human plasma and low-density lipoprotein to lipid peroxidation

b) Dietary cholesterol oxidizes LDL, whereas oxidized omega6's do not

c) Fish high in mercury promotes lipid peroxidation

d) Arterial endothelial dysfunction in baboons fed a high-cholesterol, high-fat diet

“In summary, our results clearly show that the HCHF (high cholesterol and high fat) diet resulted not only in increased serum cholesterol concentrations but also in inflammation and endothelial dysfunction”


4) How do I fight against Chris Masterjohn? Well, incase you want us to believe that the biomedical community has managed to pull a massive, worldwide conspiracy, then have it!

Diagnostic Criteria for Dyslipidemia

“Low-density lipoprotein cholesterol (LDL-C) is identified in the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) report as the most abundant and clearly causal atherogenic lipoprotein on the basis of many observational and experimental studies over several decades.1 Guidelines from the American Association of Clinical Endocrinologists (AACE) are in agreement with NCEP ATP III that LDL-C is central in the diagnosis of dyslipidemia. Any LDL-C level above 100 mg/dL appears to promote atherogenesis”


Peter said...

You are right about b-12 though. Very low levels of b-12 clearly offset the benefits of low-cholesterol levels, given that the studies you recited had controlled for the "sick quitter effect".

I reformulate myself: b-12 supplemented dietary patterns that revolve around minimally processed whole plant-foods are likely to lead to multiple health promoting benefits and manifest clearly in lower serum cholesterol concentration and low blood pressure. This is why it's fully expected that vegans show significantly lower all-cause mortality when the follow-up is long enough and participant size big enough.

Studies showing the causal relationship between lowering LDL and decreased mortality from coronary artery disease.

Recently published in the JACC

1) Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease A Mendelian Randomization Analysis

Number of participants in meta-analysis = 1,003,207

Prolonged exposure to lower LDL-C beginning early in life associated with 3-fold greater clinical benefit for each unit lower LDL (1mmol/l) than treatment with a statin started later in life (Mean age at randomization in statin trials: 63 years; p = 0.00000000000000000843)

Absence of Heterogeneity: Suggests the effect of each of included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL-C, rather than through some other pleiotropic effect.

The increased clinical benefit associated with lowering LDL-C beginning early in life appears to be independent of the mechanism by which LDL-C is lowered. Diet and exercise are probably as effective as other therapies at reducing the risk of CHD (per unit reduction in LDL-C


2) Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysis

The meta-regression analysis included 108 randomised trials involving 299 310 participants at risk of cardiovascular events.

Results: lowering LDL cholesterol significantly decreased the risk of coronary heart disease and all-cause mortality, whereas modifying HDL, triglycerides or the non-lipid lowering effects of the drugs provided no benefit after controlling for LDL cholesterol.


Peter said...

3) Prevention of heart disease: LDL reduction is the outcome of choice? Absolutely yes.

"There is only one well-established relationship between blood cholesterol lipid fraction and coronary artery disease (CAD) That meets all the Heiss and Tyroler criteria of causality. While there are a number of blood lipid fraction, only LDL cholesterol satisfies These criteria"


4) Evidence Mandating Earlier and More Aggressive Treatment of Hypercholesterolemia (Steinberg, 2008)

“Armstrong et al and Armstrong and Megan showed that in cholesterol-fed nonhuman primates, virtually total regression could ultimately be achieved, but it took 40 months after return to a cholesterol-free diet to undo the damage done during 17 months of prior cholesterol feeding. The remarkable thing about these studies is that not only was almost all of the lipid gone from the arteries but also virtually all signs of the inflammatory process were gone. The remains of the lesions were basically scar tissue with no signs of cellular infiltrates. In other words, it appeared that in the absence of continuing hypercholesterolemia, the inflammatory process was not self-sustaining. Simply arresting the hypercholesterolemia by reverting to a normal monkey chow diet caused virtually complete lesion regression without the need for intervention directed specifically at the inflammatory process, results recently confirmed in an elegant series of studies in rabbits.59–61″

“Taken together, all of these findings suggest that the inflammation associated with atherogenesis is not sufficient in itself to cause further lesion progression or even to maintain lesions at a steady state once the hypercholesterolemia has been fully corrected. In other words, many (or even most) of the inflammatory processes in the advancing lesion are downstream responses ultimately traceable to hyperlipidemia and its consequences.Consequently, early and aggressive correction of hypercholesterolemia may be sufficient. On the other hand, if hypolipidemic therapy is initiated at, say, 40 or 50 years of age, optimal intervention will no doubt also require attention to inflammation, thrombosis, and hemodynamic factors”.


5) Conclusion:

Evidence from over 100 randomized controlled trials, mendelian randomized control trials consisting of over one million individuals, and prospective studies consisting of several million individuals have firmly established a causal relationship between lowering LDL and non-HDL cholesterol and a decreased risk of coronary heart disease, cardiovascular disease and all-causes mortality (references below).


Jane said...

Here's something Ron Krauss said earlier this year about the combination of red meat and saturated fat, and how it raises LDL cholesterol.

'...we analyzed total cholesterol and the number of LDL particles and blood sugar measurements and inflammation measurements, and we didn’t see anything particularly dangerous occurring when people ate lots of red meat but kept the saturated fat very low.

...we expected that because these diets have low carbohydrate, when we fed the high saturated fat level along with the red meat, we would see a pretty benign metabolic risk profile. Just as we did with low saturated fat and red meat.

...the surprise was that the combination of the high beef diet and the high saturated fat diet caused very serious increases in all of the cholesterol related risk factors we had been measuring, including total particle numbers, small LDL, total LDL cholesterol, inflammation, whatever we looked at, we saw an adverse effect.

...This was in contrast with our earlier studies where the same amount of saturated fat and very similar carbohydrate intake but a diet not loaded up with red meat, had no adverse effect even if it had lots of saturated fat in it.

...it’s known from genetic, metabolic and population studies that [if] the iron content of the liver...is excessive, it can lead to impaired sugar metabolism and predispose even to diabetes in the extreme case. High levels of iron in the liver also can be associated with abnormal lipid profiles, with higher amounts of small particle LDL.

...In checking to see why saturated fat could potentially increase the amount of iron coming in from beef, what I discovered buried in the literature is that certain kinds of saturated fat, beef tallow being one of them, and the saturated fat called stearic acid being another, both promote the absorption of heme iron...'


Don said...

I do not know of any randomized controlled clinical trials done on humans lasting more than 12 weeks or so. We don't do such trials on humans because they have a very high cost and require keeping humans under constant surveillance 24/7 and completely controlling every morsel of food they consume.

Also, RCTs require blinding. How will you create a trial in which you can have some people eating real red meat, and others a substitute that NO ONE will recognize as faux meat for 10+ years?

Most chronic diseases develop over periods of 10+ years. We won't see any such trials on humans to track development of CHD or cancer.

Therefore, controlled clinical trials do not serve as the gold standard for evidence in nutrition research. The best possible evidence comes from Cohort studies and meta-analyses.


The French eat their meat with wine (grape juice), vegetables, garlic, etc. i.e. the protective factors.

Time lag can explain their currently low CHD rate (compared to US), as they have only recently had an increase in meat, dairy, and fat consumption (like Japanese).


Moreover, the French rate of CHD death is 40 per 100,000, with the benefit of modern emergency medicine. Between 1973-1975 in Sichuan and Guizhou counties of China, zero deaths from CHD occurred in individuals less than 64y of age in a population of 246K men and 181K women, without the benefit of modern emergency medicine.

Meat eaters have an ideology, called carnism, which maintains that eating animals is natural, normal, and necessary. I don't accept the idea that meat-eaters have superior objectivity to people who abstain from eating flesh.

Don said...

Denialists love the idea that only RCTs provide reliable evidence because the RCTs they demand will NEVER occur due to expense, blinding difficulties, ethical concerns, etc. This allows them to rate the bulk of evidence as useless, while the scientists in the field continue to rely on epidemiology, particularly cohort studies, because they know that we won't or can't do the RCTs in humans.

Anonymous said...

I'm not counting it out completely forever, I alluded to the possibility that it could be useful, but it's just that it is of such poor quality that very little of it should be taken seriously for anything other than a hypothesis to test. Controlling for confounding factors is seriously important and especially in instances of contextual differences. You need to control for a lot more things before you can call something reliable, but most epidemiology controls for a handful of factors only. sometimes you get a really half-hearted analysis of whole foods in the diet. Never do you, or could you look at the full gamut of processed foods and additives in the American diet.

Anonymous said...


1. Yes indeed at some point in time their fat intake was low. So what? So was their intake of pretty much every processed food. And it hasn't been low the whole time. There has been a significant amount of time where Okinawans have eaten lard and maintained their longevity http://nourishedkitchen.com/hara-hachi-but.

On a side note I agree that vegans having more heart-attacks than vegetarians doesn’t implicate vegan diets per se. It does however argue for endothelial function being the big important factor amongst other non-LDL-concentration-related things, which we will get to.

2. Wolves and other meat-eating animals do not develop atherosclerosis except for when given hypothyroidism (low T3 is the relevant marker in humans And it is dubious that rabbits will develop atherosclerosis under certain conditions, as I posted before, some antioxidants and nitric oxide precursors amongst other things protect rabbits. Seeing as how humans have far better clearance than any of the animals tested in labs including all other primates this should cast doubt on the idea that humans eating healthy diets should be concerned with LDL raising foods. And there is no logical path to your view that it is the concentration that matters rather than the time spent in the blood. You give cholesterol to animals with little evolutionary adaptation to it and the cholesterol stagnates and oxidizes in the blood for long periods of time, they can‘t clear it. That is different than having more of it to pass through the blood because you ate cholesterol and saturated fat. The cholesterol concentration hypothesis needs to answer to the alternative hypothesis. It has not, every bit of evidence for the former helps argue for the latter.

I should make myself more clear though, I’m not saying that if you have an LDL of 300 you should do nothing about it, just that it isn’t reasonable to assume that because there is a correlation between LDL and CVD in many populations that anything that increases LDL at all raises your risk by virtue of raising LDL, because there are many things that affect cholesterol levels in different ways. Low thyroid hormone signalling and insulin resistance as well as nutritional deficiencies explain most of LDL concentration variance, it is perfectly possible that these things produce the conditions that actually set atherosclerosis in motion and not simply that you ate cholesterol and that caused more LDL to flow through your blood.

But if certain foods really do worsen inflammation , LDL oxidation and endothelial function, that would provide a reason not to consume them regardless of their effects on LDL. However if they only do sometimes and don’t other times, this makes epidemiology a lot more complicated . Let’s look at your references.


Anonymous said...

A and B: It does in the in vitro copper oxidation assay, and in regular eggs. But as we will see, the copper oxidation test is a little iffy for proving that something is bad for you. It also depends on the type of egg consumed, the commercial eggs really have little going for them, but when hens are fed a diet where they naturally produce more antioxidants seem to eliminate significant differences http://pubs.acs.org/doi/abs/10.1021/jf073549r These kinds of eggs are widely available, mostly they are fed with flax. . I buy the idea that dietary cholesterol by itself could produce oxidized LDL by forcing the body to produce more LDL even if it doesn’t have the antioxidants to package it and transport it safely, but the pastured and flax-fed eggs have opposite effects and I think that they are the answer because of their effects in the body. Regular eggs raise blood glucose, maybe because they produce oxLDL and that damages beta cells. But the eggs with more antioxidants (called omega-3 eggs, fed with flax, but the nutritional content is the real game changer in my view) do the opposite http://www.ncbi.nlm.nih.gov/pubmed/18991244 If the eggs are high in vitamin e it may be that this is not a problem in vivo. Oxidants are protected by antioxidants, it is important to look at their interactions. The susceptibility to LDL may also depend on general metabolic health, as in some studies only diabetes are at an increased risk form high egg consumption http://www.ncbi.nlm.nih.gov/pubmed/17179903 Makes sense to me, high glucose oxidized lipoproteins, although that’s just epidemiology and there is eggs-are-bad epidemiology out there.

There is also the matter of cooking intensity to consider; the high heat methods may be different from the low heat ones in oxidatively modifying components of eggs.

But like I mentioned I don’t think that the copper test tells us much about what causes oxidized LDL in vivo. It could very well tell us what protects LDL from oxidants, particularly copper in a petri dish, but the idea that n-6 doesn’t produce more oxidized LDL than SFAs is just false and Anthony Colpo pointed that out in your exchange with him. http://atvb.ahajournals.org/content/17/10/2088.full http://anthonycolpo.com/why-primitivenutrition-aka-plant-positive-is-a-shameless-and-cowardly-liar/ So I would call the whole copper oxidation test into question except for when looking at the efficacy of antioxidants under certain conditions. The controlled trials on vegetable oils vs. saturated fats don’t look so hot for the LDL-lowering n-6 as opposed to the LDL-raising saturated fats. http://www.ncbi.nlm.nih.gov/pubmed/21118617 There are many misconceptions about all of the old trials, maybe because the people who have pushed their theory for so long don’t want to say that seed oils are worse than saturated fats.

Although there are limitations; seed oils used could have been oxidized or not enough vitamin e was provided. But in that case this argues powerfully for LDL oxidation and not levels being the most important.

Anonymous said...

C. Yes maybe mercury causes lipid per oxidation, maybe it’s not good to eat high mercury fish. I just want to eat what’s healthy not defend or vilify all food from animal origins. Mercury has little to do with the subject matter. What about low mercury fish?

D. I am aware of these kinds of studies but for most researchers they aren’t used as evidence that a high fat diet or cholesterol are bad for you but just to study the conditions of poorly regulated LDL clearance. It is really easy to look through the literature on rabbits and rats and whatnot and find evidence that falsifies the notion that fat and cholesterol damages the arteries.

L-arginine (alone, Not even in synergy with other nutrients) has a profound effect on endothelial health and atherosclerosis in the rabbit atherosclerosis models


circ.ahajournals.org/content/96/4/1282 Cholesterol still wickedly elevated, but profound protection. Not complete protection, but what about humans?

All manner of nutrients help to protect rabbit arteries

http://www.ncbi.nlm.nih.gov/pubmed/12754174 Exercise.

“In conclusion, parallel exercise training almost completely reverses the early-stage endothelial dysfunction caused by high-cholesterol diet feeding”

I am doubtful that rabbits would see any atherosclerosis from the amount of cholesterol humans get if they were just well-nourished and healthy. What if you combine all of the relevant protective factors? I would enjoy seeing the medical community and various health gurus attempt to falsify the hypothesis that it is cholesterol that unconditionally results in atherosclerosis. We have pretty good diets with all of the nutrients we need (although vegans will always have lower levels of creatine, carnitine carnosine, and many others), I really doubt that lab animals or the Inuit are a great extrapolation to us. Low carb diets even lower T3, that could explain the Inuit atherosclerosis too.

High fat intake may produce lipotoxicity, except for when it doesn’t. The idea that fats just damage the endothelium and there is nothing to be done about it has been falsified in humans and is obvious if one simply does what a good skeptic ought to do and try to falsify it.


It’s no wonder that Anthony Colpo and Art Devany are in such great shape after all of these years of eating fat and cholesterol! It seems that simply having a nutritious diet and healthy lifestyle prevent all of the potential problems, thus explaining why hunter-gatherers don’t get atherosclerosis and some pastoralists do.

Lipotoxicity is an interesting phenomenon and its prevention is even more interesting. I urge you to look into all of the mechanisms and how food impacts it. AMPK, PPARs, uncoupling proteins, it’s fascinating.. Fat’s not the bad guy any more than glucose is the bad guy in hyperglycemia.

4. Appeal to authority isn’t refuting Masterjohn, adequately addressing the points that he makes would be.

Anonymous said...

Many doctors have been convinced that LDL concentration was what truly mattered ever since they could measure LDL and had something to tell their patients to work on. The statin industry has been influential in the rise of LDL as a risk factor in its own right. How many studies control for everything including glucose, blood pressure T3, antioxidant status, nitric oxide and everything else under the sun? None? Why not? I don’t think that everyone is conspiring, but certainly some people are. The evidence is the evidence at the end of the day, but let‘s just take a step back and look at where the money is and who funds much of this research and proportion or skepticism accordingly. Statin drugs improve nitric oxide levels and are anti-inflammatory, that is quite the big deal according to all of the evidence we have seen. Sweeping lifestyle interventions do not isolate the effect on cholesterol-raising foods and could be explained by increase clearance due to healthier physiology. It is all rather simple and easy to just say “LDL bad, lower LDL” and perhaps that’s its charm. That statins can help people in other ways is a relief for patients. It takes a certain degree of wisdom to understand the whole picture, and a certain degree of character to admit that you were wrong for years and that may have affected peoples’ health.

So I can see how you guys can believe some of the things that you do, but I hope you can see why I’m not at all convinced of what you’re convinced of.. Maybe high mercury fish is undesirable. Maybe some eggs are bad for LDL’s in vitro. Maybe high heat cooking of meat really is carcinogenic and there’s nothing our bodies can do to prevent it (doubtful though, but I‘m still siding with low heat techniques), I will make all sorts of changes to how I eat but not unnecessary ones. Meat is an extremely nutritious food and if there really are no legitimate concerns if I just eat a nutritious diet, it would seem to be desirable to eat for health.

Anonymous said...

Indeed Jane, he's testing that. But even lean meat has saturated fat so I'm not confident that it's the iron. It is probably that people think that lean meat is healthy and fatty meat is not. There are also many interactions between insulin and antioxidants to consider when looking at iron.

Don said...


The ARA supplementation RCT you cited lasted 4 weeks, and used purified ARA, not foods rich in ARA like meat. This doesn't tell us anything about how eating meat or eggs rich in ARA affects people over 10, 20, 30, or 60 years. Nutrients interact to produce effects. Giving a lot of isolated ARA to Japanese who have high tissue levels of omega-3 and a previous history of low intake of meat rich in ARA doesn't tell us much if anything about the long term effect of eating meat, which provides ARA, excess cholesterol, heme iron, excess methionine, etc., which interact.

Example; Significant evidence indicates that dietary saturated contributes to hyperinsulinemia, which may promote negative effects of heme iron, as you noted.

Thus, even if isolated ARA was proven harmless in a 4 week trial, it doesn't tell us the effect of years of eating meat providing an excess of ARA, cholesterol, protein, methionine, heme iron, and neu5G Sialic acid, to name a few.

Denialists simply do not understand the fallacy of appeal to authority. The fallacy is appeal to FALSE authority. Peter has not appealed to any false authority, he has referred to peer-reviewed scientific consensus.

Peter said...


A leap of faith and high-dose of conviction is needed if believing that the harms of elevated LDL could be offset by choosing a diet that is "nutrious" by the stardards of you and A. Colpo.

1) The "sine qua" for the induction of experimental atherosclerosis is dietary cholesterol, which can induce atherosclerosis in virtually any animal model that it elevates serum cholesterol in, even when the elevation is considered to be small.

2) The National Institutes of Health came to the conclusion that total and LDL cholesterol is causally linked to coronary heart disease in 1984, at a time when the statin industry was virtually non-existent. These conclusions cannot be explained by conflicts of interest.

3) It is important to take into account that pre-contact Inuit and nomadic Kirghiz plainsmen who subsisted primarily on organic animal foods and had little or no access to refined foods developed severe premature atherosclerosis. Furthermore, it has been observed that among free-ranging non-human primates consuming only foods found in their natural habitat, higher cholesterol concentrations have been associated with atherosclerosis. In other words, the negative effects CAUSED by elevated LDL cholesterol are likely to accrue independent of the scheme used (athrogenic diet, LDL receptor inactivity, etc).Your prediction is merely wishful thinking and endangers other uninformed people.

Elevated cholesterol (LDL > 1.8mmol) puts free-ranging wild primates at the risk of atherosclerosis. The baseline LDL levels for free-ranging primates that do not develope atherosclerosis is 1-1.8mmol/l in the LDL fraction.

There are over 100 hundred experiments demonstrating that dietary cholesterol induces experimental atherosclerosis in a variety of species, including non-human primates. This persisted even when researchers made sure that micronutrient intake requirements were being met.

4) As for Masterjohn, it is highly unlikely that only oxidised LDL-C can induce atherosclerosis. Meta-analyses of randomized controlled trials of various different lipid modification intervention’s controlling for non-lipid effects of specific drug specific and mendalian randomization studies of various different genetic polymorphisms have generally shown consistent reductions in the risk of CHD per unit lower LDL-C despite lowering LDL-C through a number of different mechanisms.

Here is an interview with Steinberg

Passwater : Is it accurate to say that only oxidized-LDL starts the plaque process?

Steinberg: No,it seems to me very likely that other modified forms of LDL are involved in plaque formation. What we know so far is that the use of antioxidants can decrease the rate of progression of lesions by 50-80%. That would speak to a major involvement of oxidation, but other things can also lead to foam cell formation. Studies by Dr. John C. Khoo in my laboratory have shown that aggregation of LDL with itself markedly increases the rate of uptake by macrophages. [15] The uptake in that case occurs by way of the native LDL receptor, not the acetyl LDL receptor or oxidized LDL receptor.

Studies by Drs. J. S. Frank and A. M. Fogelman at UCLA have demonstrated the generation LDL aggregates in the subendothelial space. [16] Aggregation does not depend upon prior oxidative modification. So here is a quite distinct mechanism by which LDL uptake into the macrophages can be accelerated and can perhaps initiate the fatty streak lesion.


Peter said...

I think it's clear that Stabby is a denialist. Let see some of the steps identified by Diethelm (2009) in regards to the various gimmicks denialist utilize in order to push their faith-based arguments

1) In regards to statin the industry:

"The first is the identification of conspiracies. When the overwhelming body of scientific opinion believes that something is true, it is argued that this is not because those scientists have independently studied the evidence and reached the same conclusion. It is because they have engaged in a complex and secretive conspiracy"

2) In regards to the use of names such as Colpo and Masterjohn in away that may lead the reader to assume the arguments raised by these debators are part of a legitimate scientific discourse:

"The second is the use of fake experts. These are individuals who purport to be experts in a particular area but whose views are entirely inconsistent with established knowledge. They have been used extensively by the tobacco industry since 1974, when a senior executive with R J Reynolds devised a system to score scientists working on tobacco in relation to the extent to which they were supportive of the industry's position"

3) Whether Stabby has learned the anti-epidemiology maneuvers directly from the tobabbo-industry remains an interesting question:

"The fourth is the creation of impossible expectations of what research can deliver.... In the early 1990s, Philip Morris tried to promote a new standard, entitled Good Epidemiological Practice (GEP) for the conduct of epidemiological studies. Under the GEP guidelines, odds ratios of 2 or less would not be considered strong enough evidence of causation, invalidating in one sweep a large body of research on the health effects of many exposures.24 Although Philip Morris eventually scaled back its GEP programme, as no epidemiological body would agree to such a standard, British American Tobacco still uses this criterion to refute the risk associated with passive smoking".25

"Stanton Glantz, professor of medicine at the University of California, San Francisco and who has made a great contribution to exposing tobacco industry tactics, is a frequent target for tobacco denialists. He is described on the Forces website as ‘infamous for being the boldest of liars in “tobacco control” that most ethically challenged gang of con artists’, adding that ‘he cynically implies his research into smoking is science, banking on the sad fact that politicians, let alone the media, have no idea that epidemiology is not real science and that his studies define the term junk science"


Swede said...

"Meat eaters have an ideology, called carnism, which maintains that eating animals is natural, normal, and necessary. I don't accept the idea that meat-eaters have superior objectivity to people who abstain from eating flesh."

Plant eaters have an ideology, called veganism, which maintains that only eating plants is natural, normal, and necessary. I don't accept the idea that plant-eaters have superior objectivity to people who do not abstain from eating flesh.

Anonymous said...

That there are some scientists who believe something that has been dogma for a very long time, way before we had so much evidence, and that there are multi-billion dollar industries built around, that the government endorses, and who haven't even addressed the criticisms of rival theories, and who pump enormous amounts of money into research is not a valid authority. A bio teacher on mitosis is a valid authority. There are plenty of people who do not espouse this theory because it is based around the false cause fallacy and every bit of evidence that could support it supports other hypotheses. You don't get to declare yourself the arbiter of what constitutes the illustrious consensus that with whom anyone who disagrees is automatically wrong. Appeal to authority isn't to prove things to other people, it is for deciding what to believe when you can't evaluate the evidence by yourself and need the most accurate belief, and that’s reasonable but then you can’t expect other people to follow suit.

The AHA has declared themselves to be an authority, wow I’m so impressed. Politicians decided something scientific decades ago and the pressure to maintain it is unrelenting. If you disagree with a single “consensus” amongst self-important clusters of scientists, you are hypocrite. If you don’t then you clearly aren’t thinking for yourself on very much.

I’m no expert, but it is plainly obvious that the conditions for -necessary causation- have not been fulfilled, that would involve controlling for all of the things I mentioned before, and the poor LDL clearance can easily explain LDL levels being associated with heart disease without implicating increases in synthesis and supply. Can we agree that a knife in the chest will probably kill you? Yes, but what if you are wearing steel armour? Context is key, and nutritional epidemiologists are pretty lazy in general; getting better, maybe they will impress me some day.

The arachidonic acid was arachidonic acid, it raised markers that are derived from arachidonic acid (not the pro-inflammatory ones), and that is the best evidence for arachidonic acid there is. Better than epidemiological or "low arachidonic acid diet" which radically alters dietary composition, or in vitro tests. You would expect there to be some difference in metabolites after 4 weeks if their phospholipids are jam-packed with biologically active arachidonic acid and phospholipid AA contributes to excess synthesis of these metabolites

Anonymous said...

And I never said that it falsified the idea that anything from meat was bad at all, just that arachidonic acid could not be demonstrated to increase pathological inflammation, because that is one point that you make. Although I did post a study before where they dramatically increased red meat intake at the expense of starch foods and their CRP dropped. It's not a perfect experiment, but trials of "vegetarian diets" that make numerous changes certainly aren't either. Are there tightly controlled trials where there is only one variable and that’s meat? Nope. I’m enjoying my extremely CRP though so it’s a bit moot for me.

Saturated fat causes hyperinsulinemia? Maybe in models of sedentary nutrient-deficient rats with poor lipid metabolism, but then like fats with endothelial function, (which has been totally falsified because we know under which conditions fatty acids are metabolized safely and it is remarkably easy to do) many researchers have used this phenomenon to study how fatty acids are metabolized and which nutrients and lifestyle factors help us do it safely and avoid cellular nutrient overload and insulin resistance.


AMPK, PPAR’s, inflammation, all of the factors that go into determining lipid metabolism are very important, just like insulin sensitivity with glucose. This is the contextual issue again, context which needs to be taken into account in full. We need to try to falsify necessary causation at any chance to maintain integrity. As for why fish oil doesn’t help diabetics more, prevention isn’t the same as treatment. And they may be more likely to have it turned into ALEs which are functionless and harmful. Vitamin e levels have a profound effect on the efficacy of n-3s in controlling lipid metabolism and diabetics are depleted http://www.ncbi.nlm.nih.gov/pubmed/1995786 (you need 4.5iu per gram to prevent the rise of glucose from what I assume to be beta cell death http://www.deepdyve.com/lp/elsevier/vitamin-e-supplementation-counteracts-the-fish-oil-induced-increase-of-9cMrd2wAm0 but then you’re in the money)

Anonymous said...


I don’t think that “elevated LDL” is the right view, I don’t think that LDL concentration is harmful in and of itself, but that in these animal models and in humans the super high LDL comes along with poor clearance and greater oxidation, which is the real determinant of the propensity to form plaques, along with endothelial function and inflammation. I differ from Anthony Colpo in many regards, but point out what I agree with him on. I don’t have experts who I appeal to, merely people who I think have good arguments that it would behove anybody to address in full.

1. I could use that to argue for LDL oxidation being the dominant factor. Any model that causes LDL to be cleared less efficiently and stagnate in the blood producing LDL oxidation will increase the risk for atherosclerosis via the interaction of oxidized LDL with the endothelium which doesn‘t happen in any parts of the body except for where there is high pressure on the arteries. It’s the same evidence, those studies don’t show that the same things happen in humans, humans have a far greater capacity to clear LDL from the blood.

2. Indeed I’m not saying that they were biased then, they were just jumping the gun, but the statin industry thrives on the LDL concentration hypothesis and it won’t let it go away now. And the AHA can’t reverse its position because it would have to retract its profitable endorsements of processed food with no cholesterol in it. Doctors can’t live with the guilt of having been wrong for so long, it is just too embarrassing. This happens with all drugs. They are just like you and Don, completely unable to admit that they are wrong. I’m not saying that there’s no possibility that you’re right, but you will never admit it if you‘re not. I will if I truly think that I’m going to suffer a heart attack. I already stopped grilling and started drinking green tea because I think that HCAs are bad, that was tragic. Tragic!

Anonymous said...

3. There are plenty of explanations for Inuit atherosclerosis which don’t have to do with consuming dietary cholesterol and SFAs. They were known to cook with seal oil, basically consuming fried food which produces oxLDL. They were low carb which lowers T3, which reduces the LDL receptor expression and causes greater LDL oxidation. They were lacking many nutrients, and lived in a house of smoke. http://huntgatherlove.com/content/stop-mummy-abuse I repeat, house of smoke.

Why not metabolic syndrome and low carb causing low T3 causing stagnation of LDL in the blood and greater oxidation? http://blog.cholesterol-and-health.com/2011/08/central-role-of-thyroid-hormone-in.html

LDL goes up and atherosclerosis goes up doesn’t mean that it is the concentration in the blood, it could be the amount of time each individual LDL particle spends in the blood. Under the latter condition we can’t say that having slightly more synthesis or supply is this big deal. More cars on the road driving smoothly or a traffic jam?

4. That’s an interesting interview and I’ll look into it more. LDL oxidation isn’t the only factor of course, Masterjohn clearly thinks that endothelial function and inflammation are important, although that oxLDL is most important (clearly it is then). If antioxidants have prevented 50-80% of plaque, that doesn’t suggest that more and better antioxidants and lower oxidation from higher clearance and less oxidants wouldn’t prevent that further even further.

Nothing that guy is saying really implicates LDL concentration, though. He talks about LDL modification; perhaps modification can be targeted for prevention? When they talk about monocyte recruitment, it may not be that LDL is the root factor of this phenomenon but that poorly regulated inflammatory cascades are. Omega-3s help prevent this http://www.ncbi.nlm.nih.gov/pubmed/22814747 Macrophages creating foam cells is probably dependent on…macrophages. It’s tempting to say that LDL concentration would matter, but if it does at all, it is obviously a lot less than 100%

Anonymous said...

“ Furthermore, omega-3 fatty acids favorably alter monocyte subsets independently from effects on plasma cholesterol and reduce monocyte recruitment into atherosclerotic lesions.”

If we are to use primates as an example, we must add nitric-oxide-dependent vasodilation and endothelial function to the mix. Clearly the animals in the paper you posted earlier weren’t getting all of the nutrients required for proper nitric oxide synthesis because monkeys see a profound reduction in atherosclerosis from l-arginine alone without altering LDL at all http://www.ncbi.nlm.nih.gov/pubmed/15786711 Hypercholesterolemia doesn’t harm their endothelium if their nitric oxide synthesis is high and over the course of 6 months the progression of atherosclerosis is greatly slashed, and even a little better than the non-cholesterol-non-arginine control group; although a little worse than the group with arginine and no cholesterol. A job for more nitric oxide synthesis? It’s probably not maxed out with just l-arginine. A job for more anti-inflammatory nutrients or antioxidants? Probably, arginine can‘t be expected to be the be-all-end-all of inflammation and oxidative stress. So what if they had antioxidants and anti-inflammatory nutrients, and what if they were healthy meat and egg-eating humans who maybe had an LDL of 120? This is assuming that LDL concentration matters, this is for your benefit. Nitric oxide’s role could either be explained by greater blood flow and less LDL contact with the endothelium, or it could be explained by something else. It would probably behove scientists to look for nutritional treatments that totally prevent atherosclerosis and get off the statins, why don’t they try to do this? Why have I never seen all of the nutritional interventions that have been shown to be effective in animal models put together?

Anonymous said...

It appears to be that atherosclerosis is accounted for without appealing to LDL levels. In fact they didn’t change and they were astronomical, but there were massive reductions with just arginine. Of course I would be worried about astronomically high LDL because it is indicative of poor LDL receptor activity, but that doesn’t mean that I should fear anything that increases LDL concentrations ever so slightly.

Like I said before, if there is this massive correlation between something and a disease, usually a pathogen, I will take that as good evidence until it’s properly tested. But correlations are not very robust in nutrition, all of the meta-analyses for red meat are inconclusive, very very modest and confounder-prone (they can’t tell how much of it was Mcdonalds) and not controlling for cooking intensity. If we took every single contextual factor and confounding factor that we know of that and controlled for them, that would be good epidemiology. This doesn’t happen. Asking for the “experts” to address all of the scientific literature is not unreasonable.

Masterjohn and Colpo are not my experts, I simply said that they should take what they have to say into consideration because they make some good points. Masterjohn more than Colpo, I mentioned Masterjohn as a guy, now a scientist, with many criticisms of the lipid hypothesis that have gone unaddressed.

When there is clear financial interest, billions of dollars worth in statins, I act sceptically. I don‘t think that there is a massive conspiracy encompassing everyone, there are conspirators with billions of dollars and in bed with doctors and they make their money not when LDL receptor activity and antioxidant status are bad, but when LDL is high, that is a bit of a red flag and you should be less willing to side with a “consensus“ amongst these people.

I have to maintain that guys like Willet are just confused, have too much faith in their statistical associations, and don’t want to have to take back what they wrote about and caused people to alter their diets over. People prescribed statins which caused many side-effects which may have been avoided by using LDL receptor agonists or nitric oxide boosters rather than HMG coA reductase inhibitors. Sorry if I’m not surprised that they’re sticking to their guns after this stuff became public policy and official dogma decades ago. If it was proven back then why the continued research and the consensus now? It was proven back then right?

Peter said...

Stabby wrote:

"It’s no wonder that Anthony Colpo and Art Devany are in such great shape after all of these years of eating fat and cholesterol! It seems that simply having a nutritious diet and healthy lifestyle prevent all of the potential problems, thus explaining why hunter-gatherers don’t get atherosclerosis and some pastoralists do"

Just to be on the safe-side it helps to have a low serum cholesterol levels just like all the HG-groups have. I wonder whether HG-groups that show TC cholesterol above 3.88mmol/l (150mg/dl)or LDL cholesterol above 1.9 (mmol/l (73mg/dl) even exist. Perhaps the inuits make an exception.

A leap of faith is needed while aiming for physiologically normal cholesterol levels in a sterile eno-niche where the cholesterol lowering parasites in the blood stream are absent.

Optimal low-density lipoprotein is 50 to 70 mg/dl: Lower is better and physiologically normal

"The average total cholesterol level in American adults today is 208 mg/dl (corresponding to an LDL of approximately 130 mg/dl) (13). In this case, average is not normal because atherosclerosis is present in up to 40% to 50% of women and men by age 50 (14). Atherosclerosis is endemic in our population in part because the average person's LDL level is approximately twice the normal physiologic level"


Anonymous said...

I’ll believe that I should stop eating meat and eggs when an LDL of 120 is still worse than an LDL of 90 with extremely low inflammation, glucose, high T3 signalling, optimal nitric oxide, high antioxidant status, low blood pressure, exercise, and any other factors that have been established to modify relationships. It’s not me who is being unreasonable, it is completely possible to control for all of the relevant confounding factors. That some people are so apathetic to accuracy is not my fault. I have declared conditions when epidemiology could be valid: when it actually addresses all of the literature in its multivariate analyses. How hard is that? My criticism of nutritional epidemiology goes way beyond confounding factors, which are a huge concern in their own right.

And if it is so plainly obvious that atherosclerosis is mostly caused by things that have nothing to do with LDL concentration, which it is, why do people still think that LDL is the most important thing ever? Why not just make the drugs or better yet the high grade nutritional supplements to combat the real causes and stop prescribing statins and speculating over whether or not small increases in the amount of LDL traveling through the blood is worth reinventing your life over? That is just anchoring on one little unproven detail You’re the one advising people to give up nutritious foods that have beneficial nutrients that plants don’t, it’s not like if there really was something wrong with meat then people would be wise to eliminate it, there is much good and there are problems with every food to some extent if you really look at it. Even if I hadn’t debunked so many supposed mechanisms by which meat kills you, that still wouldn’t make eating it reckless and dangerous because of what you give up when you don’t eat it. http://evolutionarypsychiatry.blogspot.ca/2012/09/turboboost-your-brain-eat-meat.html How many supplements should I take to prevent deterioration of health, mood and intellect because I eliminated a food that I thought was bad for me? Last time I checked even the health conscious vegetarians were dying at a similar rate to meat-eaters (except in the Seventh Day Adventists' studies... which are kind of dubious).

Anyway good chatting with you all. Make corrections to what I have said if you want and I'll read them but not respond because I don't think I have anything more to say.

Anonymous said...

Ah yes, more assertions Peter. High LDL AND getting atherosclerosis, well then, that solves everything, vegan diets for all. There is no way to have LDL of 100 without a vegan diet, right? I did address that in my most recent posts above your last one, I hope you benefit from it. I have learned much.

Peter said...
This comment has been removed by the author.
Anonymous said...

*not that there is no way, I have an LDL of 105 (oh noes, I need to drop it quick!) and Gary Taubes has pretty low LDL http://garytaubes.com/2011/04/before-sugar-were-talking-about-cholesterol/ But suppose it was a higher, it wouldn't necessarily be bad, just to clear up my position. I'm certainly not arguing that we all need to obsess over getting our LDL as low as possible by any means necessary.

Anonymous said...

So do you mean that LDL-lowering is no longer a business? You're just grasping at straws, fixating on the fact that I said statin when LDL-lowering isn't going away and is still profitable. If statins are gone that doesn't undo the shame and guilt for having them all this time, does it?

Peter said...
This comment has been removed by the author.
Peter said...


You are a joke. The last valid patent for a statin (atorvastatin) expired last year. Statins make as much money as aspirins do these days. As said, you are basically on the same boat with the with 9/11 conspiracy crew, holocaust deniers and creationists. Good luck with that!

"The most commonly used statins are off patent, which means the drug companies no longer have any financial incentive expanding the market. It's the medical community who is pushing for wider use of statins since they are convinced by the evidence this will reduce heart attacks and strokes in the future"

--Peter Weissberg, British Heart Foundation

Maybe, just maybe the "normal" LDL levels observed in people living in Western societies that are +200% above to what is physiologically normal are not healthy. You surely understand that blood-pressure or BMI that is 200% above to what is biologically normal is not healthy.

Cholesterol Treatment Trialists’ (CTT) Collaborators. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. Lancet 2012;380:581–90.


Jane said...

You are missing something really important: autophagy. All that oxidative damage should be repaired. You need to look at which nutrients are important in autophagy. Hint: manganese and magnesium.

Healthy Longevity said...

Williams, 1908 referred to the cancer rates of another nomadic population that lived predominantly or organic pasture raised animal foods:
“Cancer is commoner in Argentina which comprises the pampas region inhabited by the Gauchos, who for months subsist entirely on beef, and never touch salt than in other parts of South America. On the other hand, among the natives of Egypt, who are of vegetarian habits, and consume immense quantities of salt, cancer is almost unknown”

These findings are consistent with those of major modern studies such the report from the World Research Fund showing that red meat is a major risk factor for cancer and that dietary fiber provides significant protection, but raises questions as to whether the wheat centered plant based diet of the Egyptians provides protection against salt sensitive cancers. In regards to the cancer rates among the different populations of Egypt, Williams also stated:
“These include the Berberines and the Sudanese, who are all Mussulmans, and live almost entirely upon vegetarian diet. Cancer is fairly common, however, among the Arabs and Copts, who live and eat somewhat after the manner of Europeans.”

In the controlled feeding trials I cited that found that heme iron induced NOCs and DNA adducts in the digestive tract, the researchers used red meat that was cooked at a low temperature to ensure that the findings were not confounded by cooking methods. Indeed a high red meat higher fiber diet resulted in less DNA adducts than the high red meat lower fiber diet, but still resulted in excess DNA adducts compared to the higher fiber vegetarian group.

Stabby’s claims that adding a few dietary supplements will turn the body into a plate of armour that undoes all the damaging properties of cholesterol, saturated fat and heme iron reminds us of the fairy tale “The Emperor’s New Clothes”. Stabby simply presents us with invisible fittings that he claims is a bulletproof plate of armour and asks us to take a quantum leap of faith to assume that eating large quantities of heme iron and saturated animal fat potentially at the expense of a lower intake of whole plant foods will provide significant protection against chronic diseases. He also simply claims that the results from the meta-analysis of 108 randomized controlled trials showing that lowering LDL significantly lowers the risk of coronary heart disease and all-cause mortality, independent of non-lipid effects of specific drugs and the mechanism by which LDL is lowered, was simply made up of studies forged by the industry. Stabby is a classic example of a denialist that will look under every pebble to make up some sort of excuse and refuses to consider the overwhelming preponderance of evidence presented before him.

I already cited a paper explaining how the limitations of the studies comparing vegetarians and non-vegetarians would likely have resulted in biasing the true relationship towards null, which is especially true for the Health Food Shoppers Study. As the researchers stated:
“it is noteworthy that the absence of a strong meat-mortality association in the Health Food Shoppers Study came from a design where meat intake was estimated from a nonquantitative item on whether a subject was vegetarian. A validity assessment of the survey used in this study indicated that self-reported vegetarian status on a questionnaire was a poor marker (ie, 34% of those indicating vegetarianism on a questionnaire did consume meats) of actual meat intake”

Atherosclerosis has not only been observed in pre-contact Inuit, but also in virtually all major autopsy studies of Inuit dating from early contact up until modern time, where there was much less of an impact of other unfavourable environmental factors such as smoky living conditions. Again, there are over 100 hundred experiments demonstrating that dietary cholesterol induces experimental atherosclerosis in a variety of species, including non-human primates. This would undoubtedly partly explain the findings of atherosclerosis in the Inuit and the nomadic populations.

Themovape said...

Does it take many years for high blood pressure to cause heart attack ? I'm sixteen year old overweight female , I think I have heart disease , I've had a EKG done .. Normal but my blood pressure goes up sometimes . I also have shortness of breath and I'm tired a lot , it's been five months since I had the ekg.


Themovape said...

Food that is tasty has all kinds of additives in different forms.Some of those are sugar, salt, other seasonings, chemical flavor enhancers, chemicals that are preservatives etc. I love this kind of article.Very nice!

Themovape said...

Stabby is a classic example of a denialist that will look under every pebble to make up some sort of excuse and refuses to consider the overwhelming preponderance of evidence presented before him.