Tuesday, August 14, 2012

Egg yolk consumption almost as bad as smoking when it comes to atherosclerosis

Egg yolk consumption almost as bad as smoking when it comes to atherosclerosis

Thanks to Mark for alerting me to this press release.  Excerpts: 

"Surveying more than 1200 patients, Dr. Spence found regular consumption of egg yolks is about two-thirds as bad as smoking when it comes to increased build-up of carotid plaque, a risk factor for stroke and heart attack. The research is published online in the journal Atherosclerosis."

"The study also found those eating three or more yolks a week had significantly more plaque area than those who ate two or fewer yolks per week. "

"The mantra 'eggs can be part of a healthy diet for healthy people' has confused the issue. It has been known for a long time that a high cholesterol intake increases the risk of cardiovascular events, and egg yolks have a very high cholesterol content. In diabetics, an egg a day increases coronary risk by two to five-fold," says Dr. Spence, a Professor of Neurology at Western's Schulich School of Medicine & Dentistry and the Director of its Stroke Prevention and Atherosclerosis Research Centre (SPARC) at the Robarts Research Institute. "What we have shown is that with aging, plaque builds up gradually in the arteries of Canadians, and egg yolks make it build up faster - about two-thirds as much as smoking. In the long haul, egg yolks are not okay for most Canadians."
 Spence and co-author Jenkins had already previously published "Dietary cholesterol and egg yolks: Not for patients at risk of vascular disease"  in the Canadian Journal of Cardiology. 

171 comments:

Chris said...

Of course all this is a load of nonsense when you examine the study!

http://understandnutrition.blogspot.co.uk/2012/08/eating-egg-yolks-as-bad-as-smoking.html

supert0nes said...

Thank goodness I'm not Canadian.

In other news I'll keep eating the whole egg.

Al said...

Just another silly "survey" study, Don. I hope you are still eating eggs. At this rate, you won't have much left to eat soon.

Horacio said...

Impresive you publish such BS... Obviously you did not even read the study.... One blog less to read

Peter said...

Great study. I have great respect for Spence and Jenkins. Unfortunately the creationists of the food debate are back with their anti-science assaults as usual. Well, actually the attackers are simply creationists while opposing SAFA and dietary cholesterol link to heart disease. That's directly a step away from the Darwinian foundation of biomedical research.

"Spence says, he's looked at that research and accuses the egg industry of being selective about what it shares with the public.

"They're just like the tobacco industry," he sai".

"He said the culprit is the cholesterol found in the yolk, which is 237 mgs in a jumbo egg".

http://www.cbc.ca/news/canada/toronto/story/2012/08/14/wdr-egg-yolk.html

Chris said...

Peter. Look at the link I posted above. The study does not say this.

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

@Chris

no, I do not look at your link. It's the same carbage from the same people who claim Ancel Keys cherry-picked the data. Nothing I haven't seen already.

"He (Spence) added that the effect of yolk consumption was independent of sex, cholesterol, blood pressure, smoking, body mass index and diabetes".

http://www.thestar.com/living/article/1241782--egg-yolks-unhealthy-says-western-university-s-david-spence

Bog said...

@Chris

you watch this video, and get a overview of the analytical skills of the creatinonist/anti-science crew active in the food debate.

Primitive Nutrition 64: China Studies, Part III
http://www.youtube.com/watch?v=5uGYMKLXt2Y&list=PLCC2CA9893F2503B5&index=64&feature=plpp_video

Terry Hilsberg said...

Don and Peter,

A factual question. Did you actually read the published study, before you wrote the post (Don) or wrote your comments (Peter)?

LeonRover said...

This is an epidemiological study and exhibits and measures correlation.

As usual in these kinds of studies it demonstrates the bad effects of atherosclerosis on smoking and yolk eating.

So, Guys, reduce your athero, it will help you to stop smoking.

Slainte

healthy-longevity said...

This new study is consistent with the large number of experiments on non-human primates demonstrating that even small amounts of dietary cholesterol induces atherosclerotic lesions, without evidence of a threshold beyond which a lower intake does not provide additional benefit.1 2 3 Furthermore a study on humans showed that dietary cholesterol was associated with increased carotid intima-media thickness, a marker of atherosclerotic independent of other risk factors.4

Numerous prospective studies found that egg intake is associated with a significant increased risk of type 2 diabetes, and that egg intake is significantly associated with a significant increased risk of cardiovascular disease and all-cause mortality among diabetic participants.5 6 7 8

Several prospective studies have also found that dietary cholesterol is associated with a significant increased risk of all-cause mortality.9 10 11

Matt said...

Peter, you ought to look at the link. He reports that the study authors, remarkably, did not correct for age.

Charles Grashow said...

Normal Plasma Cholesterol in an 88-Year-Old Man Who Eats 25 Eggs a Day — Mechanisms of Adaptation

http://www.nejm.org/doi/full/10.1056/NEJM199103283241306

So why didn't this man die??

Charles Grashow said...

http://www.ncbi.nlm.nih.gov/pubmed/21427738

RESULTS:
During a median follow-up of 6.1 years, 91 new confirmed cases of CVD were observed. No association was found between egg consumption and the incidence of CVD (HR: 1.10, 95% confidence interval: 0.46-2.63) for the highest versus the lowest category of egg consumption after adjusting for age, sex, total energy intake, adherence to the Mediterranean food pattern and other cardiovascular risk factors. Results were robust to different analytical scenarios.

CONCLUSIONS:
No association between egg consumption and the incidence of CVD was found in this Mediterranean cohort

http://www.ncbi.nlm.nih.gov/pubmed/20633314

CONCLUSIONS:
We did not find a significant positive association between egg consumption and increased risk of mortality from CHD or stroke in the US population. These results corroborate the findings of previous studies.

http://www.zoeharcombe.com/2012/08/egg-yolk-consumption-carotid-plaque-bad-science/

Jimmy Gee said...

As I have said before - I visit this site for a good laugh every no and then - HA HA HA HA HA HA HA!! And of course we see Peter has chimed in to lend support - more HA HA HA HA HA HA HA HA HA!!

Charles Grashow said...

http://sg.sports.yahoo.com/blogs/shine-on/egg-yolks-almost-bad-arteries-smoking-study-172428591.html

Spence and his team gathered data from 1,231 patients at the London Health Sciences Centre. The average patient age was 62.

Scientists took ultrasound measurements of the carotid arteries — this is the artery system that supplies blood and oxygen to the head and neck as well as the brain — to determine the amount of atherosclerotic plaque found inside the small but vital vessels.

Patients also filled out a survey that determined a number of lifestyle factors, such as smoking habits and the frequency of egg yolk consumption.

Researchers quantified their data by multiplying the number of cigarettes smoked per day by the number of years a person smoked.

They did the same with the eggs by multiplying the number of eggs per day with the number of years a person ate them.

What researchers found was that after the age of 40, plaque in the carotid arteries increased anyway. But patients who smoked and ate egg yolks experienced an enormous spike in plaque buildup.

And while smoking proved to be the bigger plaque accelerator, egg yolk eaters showed two-thirds of the effect of the smokers group.

Karen Harvey, a nutrition officer with the Egg Farmers of Canada, tells QMI that the comparison between cigarettes and eggs is ridiculous.

"It goes without saying that smoking is considered one of the most harmful activities when it comes to your personal health and wellness," Harvey says.

This is pure BS - find a study that uses non-smokers

healthy-longevity said...

In all of the studies that Charles cited eggs were compared to all other sources of energy combined in populations that consume a universally low nutrient diet. In regards to this a research panel organised by Walter Willett asserted that:
For example, it may not be useful, as is usually done, to compare a specific food to all other sources of energy, which are usually mainly refined starches, sugars, red meat, and fat-rich dairy products in typical Western diets.1

In other words these studies suggest that eggs are just as disease promoting as the other nutrient poor foods consumed in Western diets.

The data from this single person that Charles cited had a LDL level of 3.68 mmol/l (142 mg/dl), which definitely cannot be considered optimal.2

Perhaps Jimmy always resorts to laughing because he finds it too difficult to argue with the cited studies.

Charles Grashow said...

@healthy-longevity

Please critique this

http://www.zoeharcombe.com/2012/08/egg-yolk-consumption-carotid-plaque-bad-science/

Bog said...

@Charles:

"The ability to detect an association between a dietary variable and disease require adequate interindividual variation in that dietary factor. This implies that the likelihood of detecting a risk associated with specific food or nutrient among homogenous population who are characterized by little variation in food or nutrient studied will be low"

Nutrition In Pediatrics, 4 (Textbook).

Charles Grashow said...

http://www.ncbi.nlm.nih.gov/pubmed/14601690

http://www.mayoclinicproceedings.org/article/S0025-6196(11)62710-9/fulltext

Effect of a high saturated fat and no-starch diet on serum lipid subfractions in patients with documented atherosclerotic cardiovascular disease.

Diet
An HSF-SA diet was prescribed for all patients; they were instructed to attempt to consume one half of all calories as saturated fat, primarily as red meat and cheese. Eggs and other low-fat forms of protein were allowed, regardless of cholesterol content. Fresh fruit and nonstarchy vegetables were prescribed in restricted amounts at each meal. Starch was forbidden. Dietary logs were used to encourage compliance with the intake of saturated fat and restriction of carbohydrates in all patients.

RESULTS:
In patients with atherosclerotic cardiovascular disease, mean +/- SD total body weight (TBW) decreased 5.2%+/-2.5% (P<.001) as did body fat percentage (P=.02). Nuclear magnetic resonance spectroscopic analysis of lipids showed decreases in total triglycerides (P<.001), very low-density lipoprotein (VLDL) triglycerides (P<.001), VLDL size (P<.001), large VLDL concentration (P<.001), and medium VLDL concentration (P<.001). High-density lipoprotein (HDL) and LDL concentrations were unchanged, but HDL size (P=.01) and LDL size (P=.02) increased. Patients with polycystic ovary syndrome lost 14.3%+/-20.3% of TBW (P=.008) and patients with reactive hypoglycemia lost 19.9%+/-8.7% of TBW (P<.001) at 24 and 52 weeks, respectively, without adverse effects on serum lipids.

CONCLUSION:
An HSF-SA diet results in weight loss after 6 weeks without adverse effects on serum lipid levels verified by nuclear magnetic resonance, and further weight loss with a lipid-neutral effect may persist for up to 52 weeks.

nothing91 said...

Matt,

"Peter, you ought to look at the link. He reports that the study authors, remarkably, did not correct for age."

LOL, this is the best comment yet. You want intellectual lightweights like Don and Peter to actually read a study before getting all giddy and declaring it a "great study"? What are you, nuts? :-)

Don said...

Charles,

"The patient's plasma lipid levels were normal: total cholesterol, 5.18 mmol per liter (200 mg per deciliter); LDL, 3.68 mmol per liter (142 mg per deciliter); and HDL, 1.17 mmol per liter (45 mg per deciliter). The ratio of LDL to HDL cholesterol was 3.15."

Yes, that is "normal" meaning common in modern nations. It does not mean it is optimal. LDL of 142 puts him in a high risk category.

"Although it would have been desirable to study this patient on a low-cholesterol diet as well as on his customary diet of 25 eggs per day, it was impossible to do so. Therefore, we compared his cholesterol metabolism with that of our other subjects who were being studied by the same techniques. The results explain in dramatic fashion the apparent paradox of an enormous dietary cholesterol intake and longevity to the age of 88 without clinically important atherosclerosis. The patient had extremely efficient compensatory mechanisms — namely, a marked reduction in the efficiency of cholesterol absorption, greatly increased synthesis of bile acids, and apparently reduced cholesterol synthesis relative to his cholesterol absorption."

In other words, he was an unusual case.

Have you heard of the Bell Curve? All human characteristics are distributed across a population in a predictable fashion.

For example, some people are very very short stature (e.g. 4' tall), some are very large stature (e.g. 7' tall), and most have an intermediate stature (e.g. 5' to 6' tall).

Similarly, some people can eat a lot of cholesterol with relatively minor or more delayed ill effect, in some even a small amount of dietary cholesterol has extremely rapid harmful effects, and for most people, the effects of dietary cholesterol lie between these extremes.

This man who ate 25 eggs per day with only minor effects is obviously among the low-responder population. It is foolish to conclude that we all respond likewise, especially when the paper you cite actually documents that others do not respond in the same fashion.

As for your HSF-SA diet report, have you noticed that the subjects were in active weight loss, i.e. on a hypocaloric diet?

And that absolutely no mention was made of the effect on the actual atherosclerosis in this abstact? That the authors did not report that this HSF-SA diet halted or retarded the progression of the atherosclerosis? That they chose to focus on blood lipids instead of the actual disease process? I suspect that means the the intervention DID NOT have a beneficial effect on the atherosclerosis, because if it did, they would be shouting it as loud as possible, not failing to mention it.

Don said...

A general comment,


Could one of you who defend egg yolks and attack this study please provide me with the evidence that dietary cholesterol is either beneficial to atherosclerosis (not only blood lipids) or even essential to human health?

In other words:

1) Provide me with a set of references to experiments showing that eating eggs reduces the build up of atherosclerotic plaque, i.e. that eating eggs and cholesterol helps heal arteries damaged by atherosclerosis.

The studies would look like this: A group of people with established atherosclerosis are randomized to be put on one of two diets, the control having no dietary cholesterol (i.e. vegan), and the other identical in all respects except that a portion of plant foods is replaced with an equicaloric portion of whole eggs. To be favorable to your defense of eggs, the study outcome would be that the people eating the eggs have a more rapid reduction of atherosclerosis than those eating no cholesterol.

2) Provide me with some evidence that dietary cholesterol is essential for human cardiovascular and general health.

Good luck!



Don said...

Chris and Matt,

Interesting, the url of the blog you refer to is

http://understandnutrition.blogspot.co.uk

Which implies that the blog is being written by someone in the United Kingdom, but the headline says:

"Through my research as a PhD student at North Carolina State, I've realized that there is a disconnect between scientific knowledge in the field of nutrition and the public's perception of what makes a "healthy" diet."

It just seems a little funny that someone supposedly residing in the U.S. to attend graduate school has a blog with a U.K. url. Not impossible, just a little odd.

In his blog, I find this:

"The group who ate the most eggs also smoked the most and had the highest rate of diabetes."

And this:

" According to their data, it seems that eating lots of eggs actually promotes a healthier cholesterol profile and lower body mass index."

First, egg consumption is associated with increased risk of diabetes, so the finding of more diabetes in people eating more eggs is consistent with a larger body of evidence.

Second, if the people who ate the most eggs also smoked the most (as this author claims), then lower body mass index could be attributed to the smoking (which is associated with lower body mass index).

Chris said...

Don

the .co.uk thing is dependent on the country you are in reading the blog. Your blog for example appears on my browser as http://donmatesz.blogspot.co.uk/2012/08/egg-yolk-consumption-almost-as-bad-as.html because I am in the UK

Don said...

The blogger also writes:

"Amazingly, the authors do not address this in their paper nor do they hypothesize on what mechanism is causing high egg consumption to increase plaque buildup."

Spence and Jenkins discussed all the mechanisms by which egg and cholesterol consumption (eggs are the richest dietary source of cholesterol) promotes plaque formation, which promotes hypertension and increases the risk of thromosis, in the article to which I linked in my post. Those include post-prandial impairment of endothelium, post-prandial induction of inflammation, and ingestion of oxidized cholesterol.

Finally, he offers an alternative hypothesis:

"Perhaps the eggs actually had a protective effect allowing those who ate the most eggs to withstand more plaque buildup and live the longer before having a stroke. Those individuals who ate the fewest eggs had a stroke an average of 14 years earlier than those who ate the most eggs. Perhaps if they would have been eating more eggs, they would have lived longer without a stroke."

So, why didn't Spence et al choose this interpretation? Probably because it is inconsistent with the bulk of research on egg or cholesterol consumption and cardiovascular disease, and there is no known plausible mechanism by which eating more eggs and cholesterol would be preventive for ischemic strokes (the type that occurs most frequently in Canadians/North America). This author doesn't even have a plausible mechanism to offer for his reinterpretation.

When scientists interpret data, they do it in the context of the body of research on the topic, and to justify their interpretation they have to provide evidence to support that interpretation. Since there is little or no evidence that eating eggs protects against ischemic stroke, while there is significant evidence that egg and cholesterol consumption promotes atherosclerosis which underlies ischemic stroke, Spence et al would have had a very difficult time justifying this author's interpretation rather than their interpretation.

Especially in light of studies like the Physician's Health Study which found "egg consumption was positively related to mortality, more strongly so in diabetic subjects."

http://www.ncbi.nlm.nih.gov/pubmed/18400720

Further, the claim that they did not correct for age seems odd since the abstract states:

"Plaque area in patients consuming <2 eggs per week (n = 388) was 125 ± 129 mm(2), versus 132 ± 142 mm(2) in those consuming 3 or more eggs per week (n = 603); (p < 0.0001 after adjustment for age). In multiple regression, egg-yolk years remained significant after adjusting for coronary risk factors."

http://www.ncbi.nlm.nih.gov/pubmed/22882905

Finally, the Spence et al abstract conclusion is:

"Our findings suggest that regular consumption of egg yolk should be avoided by persons at risk of cardiovascular disease. This hypothesis should be tested in a prospective study with more detailed information about diet, and other possible confounders such as exercise and waist circumference."


http://www.ncbi.nlm.nih.gov/pubmed/22882905

Chris said...

Mark Sisson has an interesting analysis of this too

http://www.marksdailyapple.com/are-eggs-really-as-bad-for-your-arteries-as-cigarettes

Even the NHS Choices website which is usually pretty anti fat, noted the following about the study:

http://www.nhs.uk/news/2012/08august/Pages/Eating-egg-yolks-as-bad-as-smoking.aspx

Conclusion

This study found that egg yolk consumption was associated with increased fatty build-up in the arteries of the neck, though this was small when compared to the build-up expected with age. This study has important limitations which mean that it cannot be concluded that egg yolks are as bad for you as smoking:
Average egg yolk consumption per week and duration was evaluated through a questionnaire response. These are only estimates and may include a considerable degree of inaccuracy. Consumption may vary over time. We also don’t know how these eggs were prepared (boiled, fried in oil, scrambled in butter, etc).
This wasn’t a trial, and so people are choosing the number of egg yolks they eat. People who ate more egg yolks may differ in other health and lifestyle factors from people who ate less, and this may account for their different artery build-up. For example, as the researchers rightly acknowledge, they did not thoroughly assess other dietary factors, exercise or waist circumference. It is possible that higher egg yolk consumption could be associated with less exercise and higher overall saturated fat intake – both well known risk factors for heart disease. The small changes in fatty build-up in the arteries seen with higher egg yolk consumption could have been accounted for by these other factors.
None of the participants in this study were reported to be suffering from heart disease and the heart arteries were not examined.
We do not know how or whether the extent of fatty build-up in the neck arteries was associated with build-up in the heart arteries.
This is a relatively small, select sample of people attending a vascular clinic in Canada, and further quality studies would be needed to better assess the question.
This study perhaps best supports the notion of all things in moderation. Eggs are a good source of protein in addition to other vitamins and minerals and most experts advise that they can form part of a healthy, balanced diet.
If you have been told you have pre-existing risk factors for heart disease, or other CVDs, your GP will be able to provide more detailed advice about a recommended diet.


This study has important limitations which mean that it cannot be concluded that egg yolks are as bad for you as smoking!

Don said...

Chris,

OK, my mistake on the UK thing. When I access his blog without the url you provided, it doesn't have the uk. I made the mistake because in the past I noticed that some sites maintained by people outside the U.S. do have identifiers for country of origin in their url that show up in my browser even though I have always accessed them from within the U.S.

Don said...

Chris,

Spence did not conclude that eggs were as bad as smoking; but that they were "almost" as bad as smoking, specifically that high egg yolk intake was associated with a plaque build up rate approximately 2/3 that of smoking.

I'm not sure why the NHS thinks they should have examined the heart arteries. Do they really think that atherosclerosis in the carotid would be less significant if it was not also found in the heart, or, further, that the body is so strange that atherosclerosis in the carotids could be ongoing without it also occurring in every other vulnerable artery?

Also, you quote them thus: "This study found that egg yolk consumption was associated with increased fatty build-up in the arteries of the neck, though this was small when compared to the build-up expected with age."

So, why do they expect atherosclerosis with aging? Of course the portion of the build up associated only with eggs will be smaller than the total, because eggs would not be the only factor promoting atherosclerosis.

Further, in western populations, it is commonly the case that when people are told to avoid fatty meats and eggs, they increase their intake of lean meats, which have higher cholesterol levels than fatty meats (mg/100 g) because cholesterol is present in cell membranes of muscle to a greater extent than in adipose tissue.

The real limitation of this study is alluded to by Bog, namely, everyone in this study population was eating the 'normal' western diet in some variation, so the variation in animal source food intakes is not sufficient to clearly see the effects of any food commonly consumed.

As I have said before, logically, to see the effects of dietary cholesterol on health clearly, you have to compare increments of cholesterol intake starting from zero. Comparing people who eat 200 mg per day to people who eat 400 mg per day is insufficient because a lot of biological phenomena are threshold phenomena, i.e. once you pass a certain threshold, further increases in the stimulus (e.g. dietary cholesterol) have little or no discernible effect because the threshold for effect has already been passed. Its like comparing people who smoke two packs per day to people who smoke 4 packs per day. Their risk of lung disease is probably similar. To see the effect of smoking you have to compare smokers to non-smokers. Just sot, to see the effect of cholesterol, you have to compare people who eat no cholesterol (or virtually no cholesterol) to people who consume various increments.

Jimmy Gee said...

@ healthy-longevity,

HA HA HA HA - who needs to argue with studies like this. Let's see, poor methods, impossible confounding, cigarettes and the authors have vested interest in the statin industry.

Very trust worthy I'd say.

healthy-longevity are you Don's next sycophant?

nothing91 said...

Don,

"Could one of you who defend egg yolks and attack this study please provide me with the evidence that dietary cholesterol is either beneficial to atherosclerosis (not only blood lipids) or even essential to human health?'

Haha, you're the best. As usual you're incapable of seeing anything in terms other than black and white. Nothing in your world can be in the middle: eggs are either good or bad, cholesterol is either good or bad. Good or bad, black or white.

Everyone who understands the uselessness of this study must believe that eggs are "beneficial to atherosclerosis". Some world you live in. :-)

Peter said...

Avoiding cholesterol is a no-brainer.

The plasma lipids, lipoproteins, and diet of the Tarahumara indians of Mexico

"The lack of relationship between dietary cholesterol and plasma cholesterol concentration in Americans with these relatively high intakes....Under conditions of similar high dietary intake the wide range of plasma cholesterol levels in Iowa children indicates the impact of genetic-metabolic factors in setting homeostatic level of the plasma cholesterol level and not the cholesterol in the diet as it is. When populations consuming low-cholesterol, low-fat diet are looked at the same perspective, a completely different pattern emerges".

"Apparently the level dietary cholesterol intake in the Tarahumaras is below the so-called treshold level above which differences in intake do not affect plasma-cholesterol concentrations. We suggest from various metabolic-studies that this treshold may well be in between 100-300mg/day of dietary cholesterol"

"...the finding of linear association of dietary cholesterol intake and plasma cholesterol concentrations in man further undergirds the evidence relating dietary factors to hypercholesterolemia and atherosclerotic coronary heart disease".

http://www.ajcn.org/content/31/7/1131.long

healthy-longevity said...

Perhaps if Jimmy had read the following paper, which is probably one of the best kept secrets among the cholesterol skeptics, he may realise that it is the cholesterol skeptics who cite studies that use some of the most ‘poor methods’.
Diet-heart: a problematic revisit

I cited a number of well controlled studies on non-human primates without these limitations that Jimmy referred to. Even small amounts of dietary cholesterol were shown to increase atherosclerosis without evidence of a threshold beyond which a lower intake did not provide additional benefit.
Intimal thickening in normocholesterolemic rhesus monkeys fed low supplements of dietary cholesterol.

Nothing91,
The belief that there exists such a thing as being in the ‘middle’ when it comes to food and heart disease is flawed. A decreased intake of one form of energy will generally lead to an increase of another, and therefore it is the substitution of different foods that determines the true risk of heart disease.
Major dietary protein sources and risk of coronary heart disease in women.

Jack LaBear said...

First of all, intima-media thickness is not atherosclerosis. "After systematically reviewing the evidence base for IMT, the United States Preventive Services Task Force found no support for its routine use in stratification of risk for people at intermediate cardiovascular risk."[Helfand M, Buckley DI, Freeman M, Fu R, Rogers K, Fleming C, Humphrey LL. (Oct 6 2009). "Emerging risk factors for coronary heart disease: a summary of systematic reviews conducted for the U.S. Preventive Services Task Force.". Ann Intern Med 151 (7): 496–507. PMID 19805772}.
Secondly, the 88 yo gentleman who eats 24 eggs a day is not an isolated case. I deliberately eat an average of 3000mg cholesterol a day, my TC is 185 ( on the low side for health and longevity, epimemiologically), I'm 55 and I have no sign of atherosclerosis.

The Humane Hominid said...

It's quite telling to me how everyone ignores healthy-longevity's point about the primate data. Based on homology, evolutionary theory would predict a similar effect in humans, and the burden of proof lies with those claim the contrary. Denial of the "lipid hypothesis" is an implicit denial of evolution. If it applies to other mammals, why shouldn't we expect it to be true of ourselves?

Charles Grashow said...

http://www.paleostyle.com/?p=2001

The real chimpanzee diet – Fat, Glucose, Protein and a little Fructose

In summary, the chimp diet is 50-55% fats, 24-29% glucose and 21% protein – not “one that contains high amounts of complex carbohydrates and only small amounts of fat” quite the opposite. Luckily for the chimps their diet has no resemblance whatsoever to the SAD diet and if analyzed properly may indeed show the way to “the healthiest human diet” – high in fats and moderate in protein, and carbs with some fruits included for old time’s sack.

Peter said...

@Humane Hominid

great point. That was also what I was saying all the way. This discussion could be as well seen between evolution vs. intelligent design. Science against religion.

I quote the Tarahumara papar once again:

"Since in the experimental dietary cholesterol is sine qua non for the development for the experimental atherosclerosis, especially among the sub-human primates, the finding of linear association of dietary cholesterol intake and plasma cholesterol concentrations in man further undergirds the evidence relating dietary factors to hypercholesterolemia and atherosclerotic coronary heart disease".

http://www.ajcn.org/content/31/7/1131.long

@Healthy Longevity,

great paper by Jeremiah Stamler, the Dairy Counsil managed to stir the debate a bit (Siri-Tarino & Co), however, for some reason, not even the authors of the paper took the message seriously. BTW Jeremiah Stamler was in the same conference where meta-analysis conpcept was introduced by the first time to public by Richard Peto (the same guy who sorted out China Study data. Stamler knew the concept very well and knew what he was talking about.

Harvards own Frank Hu on february2012, The co-author of the Siri-Tarino Meta-analysis

”Why is red meat harmful? “Saturated fat, which can lead to cardiovascular disease, is really just the beginning of the story,” explains Hu”

http://harvardmagazine.com/2012/01/a-diabetes-link-to-meat

Peter said...

@Nothing91

there's no middle ground for eggs.

Spence: (egg yolks) "shouldn't be regarded as an item suitable for human diets for anyone at risk for vascular disease, and you name me a Canadian that isn't".

http://nutritionfacts.org/video/egg-cholesterol-in-the-diet/

nothing91 said...

healthy-longevity,

"The belief that there exists such a thing as being in the ‘middle’ when it comes to food and heart disease is flawed."

Thanks for confirming how out-of-whack with reality your fundamental thought processes are. It explains so much. :-)

Peter,

"there's no middle ground for eggs."

It's too bad your beloved Tarahumara eat them regularly. Have you told them yet that they're killing themselves? I'm sure they'd be real interested in your black-and-white nutritional philosophy.

BTW, have you gotten around to actually reading this "Great study" yet? :-)

Jimmy Gee said...

@ Healthy-longevity-

Again H-l you are too funny. Using an "opinion" article to justify your statement "...probably one of the best kept secrets among the cholesterol skeptics..."

Healthy-longevity your beginning to sound like Peter and Bog, or maybe you are all one-in-the-same.

Jack LaBear said...

@Humane Hominid
You are absolutely correct. It's about evolution. Humans evolved eating a lot more fatty meat than other primates, especially people fron Northern Europe, like my ancestors.

Having said that, Barry Groves has pointed out that gorillas and other herbivors acyually get most of their calories from fat because the intestinal fermentation converts the cellulose into fatty acids, not glucose.
http://www.second-opinions.co.uk/should-all-animals-eat-a-high-fat-low-carb-diet.html

You can cite "studies" till you're blue in the face, but the fact remains that there is a large and growing community of LC eaters because they have enjoyed an improvement in their health and well being as a result and are not suffering from heart disease, but rather preventing it. Even myself with my 3000mg of cholesterol a day and my 81 yo German father who has lived on large amounts of butter, cheese, steak, cream, sausages etc. and has no signs of heart disease.
You're wasting your time here.

Jimmy Gee said...

@ Don

Per your comment:

"Could one of you who defend egg yolks and attack this study please provide me with the evidence that dietary cholesterol is either beneficial to atherosclerosis (not only blood lipids) or even essential to human health?"

The main issue responders are having with this post is the absurd pseudo-science published in the referenced article. It's no wonder that the state of research regarding diet and health (CHD or overall health) is so screwed-up. Equally damaging are the "hungry for news" media that dupe individuals into believing this type of study has any merit.

healthy-longevity said...

@Jack

Barry Groves, just like William Douglas, another member of the Weston A Price Foundation are frauds who deny that cigarette smoke contains carcinogens and is a cause of lung cancer, and even claim that smoking is health promoting.1 2

A meta-analysis of 108 randomized controlled trials of diet and various medical based lipid modifying interventions found that lowering LDL cholesterol significantly decreased the risk of coronary heart disease and all-cause mortality, while modifying HDL or triglycerides provided no clear benefit after controlling for LDL cholesterol.3 Therefore it is probably not coincidental that virtually every prospective study on diets higher in protein and often fat, primarily of animal origin at the expense of vegetable protein or carbohydrates were associated with an increased risk of cardiovascular disease mortality.4 5 6 7 8

@Jimmy,

Why is that virtually none of the cholesterol skeptics ever cite or challenge the findings of Jeremiah Stamler’s paper, which has been cited by major health authorities explaining why the meta-analysis funded by the National Dairy Association is flawed?9 Perhaps it is because they find it too difficult to argue with the fact that saturated fat was associated with a 32% increased risk of coronary heart disease mortality despite the inclusion of over-adjustments for dietary and serum lipids.

The Humane Hominid said...

@Charles and Jack

You're both missing the point entirely, in a couple of ways.

1) Your posts saying nothing about the physical mechanism of atherosclerotic lesion formation, or about the composition of plague. These things are well-studied and well-understood across mammalian taxa. Why would the things that cause it in other mammals not cause it in us?

2) You've both misunderstood basic evolutionary theory. Whether humans evolved eating more fat than other primates is irrelevant to whether it's healthy for us. Many adaptations carry negative consequences along with whatever advantages they provide (sickle-cell anemia, for instance). And even if it were true that humans are better-equipped to handle fat than other primates, that derived trait doesn't eliminate or negate 22 million years of hominoid biochemistry.

Jack LaBear said...

Part1
@Don
"Could one of you who defend egg yolks and attack this study please provide me with the evidence that dietary cholesterol is either beneficial to atherosclerosis (not only blood lipids) or even essential to human health?"

This question is a bit of a straw man since the argument being made is not that dietary cholesterol is beneficial to atherosclerosis, but rather that egg consumption does not cause heart disease.

But I'll take you up on studies suggesting that dietary cholesterol is beneficial to human health.

"Human babies fed breast milk receive a good deal of cholesterol, higher than that found in formula. Some studies indicate that adults who were breast-fed babies score higher on intelligence tests than adults who were fed formula... We found that depriving piglets of cholesterol in the first 4-8 weeks of life is associated with lower cholesterol levels in the brain of young adult pigs than if they had been cholesterol-supplemented in early life. This suggests that newborns have a metabolic need for dietary cholesterol in normal brain development." http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=91958

That is why the pork brains I eat have 3500mg cholesterol in 4oz.
It is well known that statins can cause memory impairment. It is not unreasonable to believe that dietary cholesterol may benefit adult brain health too.

A study showed that middle age people doing resistance training had greater strength gains the higher their blood cholesterol and the more cholesterol they ate. Sarcopenia and weakness leading to falls and hip fracture are a serious problem in seniors. Again, statins can cause muscle breakdown.
Riechman SE, et al. Dietary Cholesterol and Skeletal Muscle Hypertrophy with Resistance Training: A Randomized Placebo-Controlled Trial. FASEB Journal, 2008; 22: 962.13.
http://www.fasebj.org/cgi/content/meeting_abstract/22/1_MeetingAbstracts/962.13
The heart is a muscle, cholesterol is important to muscle function.

Smith-Lemli-Opitz Syndrome is an impaired ability to synthesize cholesterol. While full blown cases die in utero or early childhood, the genetic mutation that causes it is the most common genetic disorder in people of Central European descent, with up to 1 in 35 people being carriers. There is a study that relatives of SLOS patients (carriers) have double the rate of violent suicide as controls. i.e. it causes brain dysfunction that can lead to premature death. The only useful treatment for SLOS is supplemental cholesterol.
Lalovic A, Merkens L, Russell L, Arsenault-Lapierre G, Nowaczyk MJM, Porter FD, Steiner RD, Turecki G. Cholesterol Metabolism and Suicidality in Smith-Lemli-Opitz Syndrome Carriers. Am J Psychiatry. 2004; 161: 2123-2126.

There is also evidence that there is impaired cholesterol synthesis in Huntington’s disease:
Low plasma total cholesterol in patients with Huntington’s disease and first-degree relatives
Manolis Markianos, Marios Panas, Nikolaos Kalfakis, Demetrios VassilopoulosAthens University Medical School, Department of Neurology, Eginition Hospital, Vas. Sophias 74, Athens 11528, Greece

Jack LaBear said...

Part2

Broadening the scope of the discussion, dietary creatine is only found in animal food. A study assessing learning and memory found that giving vegetarians supplemental creatine improved IQ and performance on tests of brain functions, but a similar study on omnivores did not do so.
“To obtain maximal increase by supplementation,
we chose to examine the effect of oral creatine
monohydrate supplementation on young adults with vegetarian
diets, in whom creatine levels are lower than they
are in omnivores (Delanghe et al. 1989).”

Oral creatine monohydrate supplementation
improves brain performance: a double-blind,
placebo-controlled, cross-over trial
Caroline Rae1* , Alison L. Digney1, Sally R. McEwan1 and Timothy C. Bates2
1Discipline of Biochemistry, School of Molecular and Microbial Biosciences G08, The University of Sydney, Sydney,
NSW 2006, Australia
2Macquarie Centre for Cognitive Science, Macquarie University, NSW 2109, Australia

Rawson ES, Lieberman HR, Walsh TM, Zuber SM, Harhart JM, Matthews TC (September 2008). "Creatine supplementation does not improve cognitive function in young adults". Physiology & Behavior 95 (1–2): 130–4. doi:10.1016/j.physbeh.2008.05.009. PMID 18579168.

Carnitine is also only found in animal food. It is important for the health of heart muscle and for proper brain function. Indeed, acetyl carnitine has been used as a “smart drug”.

CoQ10, only found in meat, has as a supplement been shown to slow progression of Parkinson disease.

Carnosine, is found only in meat, and some studies have shown an anti-alzheimer’s effect, reducing damage from amyloid and improving cognitive decline. http://www.ncbi.nlm.nih.gov/pubmed/17522447
http://www.ncbi.nlm.nih.gov/pubmed/9928418
http://www.ncbi.nlm.nih.gov/pubmed/21423579
Carnosine is important to muscle and hence cardiac function.

Let me suggest that some people who avoid animal food may as a result be cognitively impaired due to their misguided dietary choices and that is the cause of the fuzzy thinking and pseudo-science that they present.

Charles Grashow said...

http://www.fathead-movie.com/index.php/2012/08/16/the-anti-egg-bad-scientist-strikes-again/

Spence added the effect of egg yolk consumption over time on increasing the amount of plaque in the arteries was independent of sex, cholesterol, blood pressure, smoking, body mass index and diabetes.

Excuse me, but did I just read that the artery-clogging effects of eggs were independent of cholesterol?!! The whole reason Dr. Spence has been warning us against consuming eggs is that they contain too much cholesterol. So is cholesterol the bad guy here or not?

Let me see if I can follow the logic so far: eating eggs doesn’t raise cholesterol levels in our bloodstreams, cholesterol was not a determining factor for plaque buildup in this study, but Dr. Spence doesn’t want us to eat eggs yolks because (as he’s been busy explaining to the media), eggs contain more than the recommended amounts of cholesterol.

http://www.sciencedirect.com/science/article/pii/S0021915012005047

Egg-yolk years remained a significant predictor of carotid plaque area after adjustment for sex, total cholesterol, pack-years of smoking, systolic blood pressure, diabetes and body mass index. (Age is incorporated into pack-years and egg-yolk years).

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

Ha ha ha that's a good one. Oh, you're serious.

As in, you seriously believe that this tripe qualifies as valid science, and that despite there being an uncountable number of confounding variables, the fact that the author decides that this one variable can be isolated as causing atherosclerosis (based on self reporting of egg intake after the fact!) is good enough for your rigorous approach to the scientific study of nutrition?

Ha ha ha! Oh, you're serious again.

I find this "war on cholesterol" absolutely hilarious. Here you are demonising a substance that is critical to cellular structure and cellular signalling, and is produced by the liver in greater quantities when dietary intake is reduced (underlining its importance, unless you believe that the liver is just plain dumb and doesn't realise it's killing it's host).

But because there is cholesterol present in atherosclerosis, well then of course! It's the cholesterol that causes the atherosclerosis. Let's just ignore that whole correlation is not causation thing and beat the lipid hypothesis drum to death!

Just one study here (there are many more) highlighting the critical role cholesterol plays in the body and the stupidity of trying to lower cholesterol levels - http://www.ibc7.org/article/journal_v.php?sid=31

"There is evidence that cholesterol in the brain plays an important role in the neurotransmitter release. A decrease of the cholesterol level severely hampers the activity of the membrane fusion machinery, thereby inhibiting the release. Meanwhile, the results from several clinical studies suggest that a low cholesterol level is linked to the dysfunction of some brain activities. Because the neurotransmitter release underlies the basic brain function, the combined results lead to a testable hypothesis that the cholesterol-lowering drugs may inhibit the neurotransmitter release at the synapse. Such inhibition of the release could result in impaired brain function for a limited group of people. A molecular basis for the hypothesis is discussed."

I'm guessing your cholesterol deficient diet may be hampering your thinking capacity if you believe that egg yolks are almost as bad as smoking.

I suggest you eat some eggs to restore your cognitive function.

Charles Grashow said...

http://www.westonaprice.org/blogs/cmasterjohn/2012/08/16/does-eating-egg-yolks-increase-arterial-plaque/

http://ageconsearch.umn.edu/bitstream/116427/2/6C-1_Hailu_Goddard.pdf

Jimmy Gee said...

@ Healthy-longevity:

Your reference is little more than another opinion piece. Look at the articles own acknowledgement of limitations:

".Remaining gaps in the evidence
. Our understanding of the reasons for changes in the behaviour
of both populations and individuals remains incomplete.
. The mechanisms whereby such changes in behaviour translate
into changes in disease patterns are also incompletely
understood.
. Auditing and studying the most effective preventive measures
is therefore challenging.
. More research into prevention of CVD is needed, starting
early in life or even during fetal development.
. It is uncertain whether CVD is merely deferred by preventive
efforts or if it of can be avoided completely.
. There is an ongoing need for a valid and accurate description
of CVD morbidity and mortality throughout the world."

I think your brain needs help - go eat a couple of eggs already!

Jimmy Gee said...

To all you egg-haters, it would do you good to read the article in the reference below. It reveals just how lame this study is.

http://www.westonaprice.org/blogs/cmasterjohn/2012/08/16/does-eating-egg-yolks-increase-arterial-plaque/

Swede said...

Don't worry folks. Don has only been vegan for about a year. Based on his past behavior, it takes him about 14 years before he realizes that he is eating like an idiot.

Check back in 13 years to see what the next dietary adventure will be. He will explain how he ignored and rationalized away all of the conflicting evidence.

Is there someone in your life who can slap you around so you pull your head out of your ass? A few years ago you would say there is no dietary need for glucose, and now eating any non-plant food will lead to certain early death. How old are you? People your age don't normally swing from one extreme to the other so readily.

This blog is also a source of humor for me, but I couldn't resist a comment here because you made such a ridiculous post, which it typical of those who hold extreme views and ultimately have trouble supporting them without resorting to insincere methods (although you yourself probably are convinced of the sincerity of this crap).

Bix said...

@healthy-longevity

I wanted to thank you for that link to the Rhesus monkey study. It was eye-opening!

Charles Grashow said...

http://healthcorrelator.blogspot.com/2012/08/the-2012-atherosclerosis-egg-study.html

The highest amount of plaque is at the far left of the plot. It is associated with the lowest LDL cholesterol quintile. (So much for eggs causing plaque via LDL cholesterol eh!?) What is happening here? Maybe egg consumption above a certain level shifts the size of the LDL particles from small to large, making them harmless. (Saturated fat consumption, in the context of a nutritious diet in lean individuals, seems to have a similar effect.) Maybe eggs contain nutrients that promote overall health, leading LDL particles to "behave" and do what they are supposed to do. Maybe it is a combination of these and other effects.

nothing91 said...

Lots of crickets out there from the folks who were originally all giddy about this study. Shocking. :-)

healthy-longevity said...
This comment has been removed by the author.
healthy-longevity said...

Thanks to Bix for their exelent post regarding a study that found that feeding small amounts of dietary cholesterol, the equivalent of only 86mg cholesterol (half a small egg) in a human diet of 2000kcal causes arterial lesions in rhesus monkeys.
http://fanaticcook.blogspot.com/2012/08/small-amounts-of-dietary-cholesterol.html

The critiques of this egg study ignore the results from hundreds of animal studies, including those carried out on nonhuman primates showing that dietary cholesterol induces atherosclerosis. They also failed to mention that most large studies found an association between dietary cholesterol and egg intake and an increased risk of cardiovascular disease and all-cause mortality among diabetic participants.

They also mention nothing in regards to the plausible mechanisms that these researchers previously reviewed in which dietary cholesterol can induce atherosclerosis and increase cardiovascular events:
The more important issue is the postprandial effects of consuming cholesterol, including egg yolk. Focusing on fasting serum cholesterol levels misses the bulk of the problem. Even though serum cholesterol rises very little after a meal, dietary cholesterol increases the susceptibility of LDL-C to oxidation, vascular inflammation, oxidative stress, and postprandial hyperlipemia and potentiates the harmful effects of saturated fat, impairs endothelial function, and increases cardiovascular events.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989358/
http://download.journals.elsevierhealth.com/pdfs/journals/0828-282X/PIIS0828282X10000292.pdf

It appears that the cholesterol skeptics are again trying to crunch raw data that they do not have access to. I recommend that people actually read the full paper, and in particular refer to Fig 1. which shows the association between egg-yolk years and carotid plaque produced by leading nutrition researchers and published in a prestigious peer-reviewed journal, rather than just referring to the imaginary data produced by the cholesterol skeptics.
http://www.scribd.com/doc/102849595/1-s2-0-S0021915012005047-main

Charles Grashow said...

TOTAL CHOLESTEROL LEVELS vs MORTALITY DATA from 164 COUNTRIES

http://www.goprimal.com.au/wp-content/uploads/2012/03/cholesterol-mortality-chart.pdf

Cholesterol in range 200-240 mg/dl <> Lowest all cause mortality

Lower cholesterol <> More infectious and parasitic diseases and possibly higher cardiovascular mortality

Charles Grashow said...

How do you separate the plaque caused by smoking from the plaque caused by smoking??

Don said...

Charles,

Re: TOTAL CHOLESTEROL LEVELS vs MORTALITY DATA from 164 COUNTRIES

Do you suggest that lower cholesterol causes more infections, parasitic diseases, and cardiovascular disease based on the correlation shown in this chart?

Assuming the data was correctly collected and plotted, can you think of any possible confounders present in this unadjusted data?

Charles Grashow said...

http://www.paleodigest.com/pd/?u=http://cosmopolitanprimalgirl.wordpress.com/2012/08/21/eat-the-whole-frickin-egg/

Three eggs a day keep the doctor away!

A recent review of the scientific literature published in Current Opinion in Clinical Nutrition and Metabolic Care clearly indicates that egg consumption has no discernible impact on blood cholesterol levels in 70% of the population. In the other 30% of the population (termed “hyperresponders”), eggs do increase both circulating LDL and HDL cholesterol.

You’ve probably been conditioned to believe that anything that raises LDL cholesterol (so-called “bad” cholesterol) should be avoided like the plague. But even the medical mainstream has come to recognize that all LDL cholesterol is not the same. It’s true that small, dense LDL particles have been linked to heart disease. This is primarily due to the fact that they are much more susceptible to oxidative damage than normal LDL cholesterol particles.

However, egg consumption increases the proportion of large, buoyant LDL particles that have been shown to be protective against heart disease. Egg consumption also shifts individuals from the LDL pattern B to pattern A. Pattern B indicates a preponderance of small, dense LDL particles (risk factors for heart disease), while pattern A indicates a preponderance of large, buoyant LDL particles (which protect us from heart disease). This is a good thing.

Don said...

"A recent review of the scientific literature published in Current Opinion in Clinical Nutrition and Metabolic Care clearly indicates that egg consumption has no discernible impact on blood cholesterol levels in 70% of the population."

If you take a bunch of people who already consume more than 200 mg of cholesterol daily and already have cholesterol levels above 150 mg/dL, and feed them more eggs/cholesterol, 70% of them don't have further increases in cholesterol.

This study falls again into the category of incorrect procedure. As I have said many times now, to find out how eating eggs/cholesterol affects blood cholesterol levels, you have to start with a baseline diet that has NO cholesterol at all. This is the only logical, scientific approach because almost all biological phenomena involve thresholds of stimuli.

She says we need dietary cholesterol. That's news to the National Academy of Sciences Food and Nutrition Board, which states:

"Given the capability of all tissues to synthesize sufficient amounts of cholesterol for their metabolic and structural needs, there is no evidence for a biological requirement for dietary cholesterol. "

http://www.nap.edu/openbook.php?record_id=10490&page=542

That document also states:

"There is much evidence to indicate a positive linear trend between cholesterol intake and low density lipoprotein cholesterol concentration, and therefore increased risk of coronary heart disease (CHD). A Tolerable Upper Intake Level is not set for cholesterol because any incremental increase in cholesterol intake increases CHD risk. "

But if you want to believe a blogger instead of a document produced by the National Academy of Sciences, have at it.

Peter said...

@Charles,

would you change your mind in regards to the importance of particle size in the light of this expert panel report? If you look at the table 1 in the report you'll see that particle size measurement is not recommended for any of the patient groups, why? It's irrelevant against the traditional LDL-C.

Clinical utility of inflammatory markers and advanced lipoprotein testing: Advice from an expert panel of lipid specialists (2011)

“All lipoprotein particles in the LDL fraction are atherogenic, independent of size”

http://www.lipid.org/uploads/300/Expert%20Panel%20Paper.pdf

John LaRosa is top cardiovascular researcher and the president of SUNY Downstate Medical Center (ranked as 8th best medical school in the US) and I think he has lot to say to us:

More evidence for lowering LDL to below 70 (2011)

"LaRosa, who wrote an editorial [3] accompanying Lee's study, expanded on his views to heartwire: "I used to be skeptical about the idea of trying to achieve very low cholesterol levels, but now I am more accommodating. As cholesterol levels are coming down, we are seeing much lower rates of bypass surgery and elective angioplasty. I think elective angioplasty will eventually disappear altogether."

"Chimpanzees eat very little fat. They have LDL levels in the range of 40 to 70, and they don't get atherosclerosis. He noted that levels of LDL below 70 are on a par with those of nonhuman primates who don't develop atherosclerosis, adding that, like these primates, humans were designed to be vegetarians. "Our dental anatomy suggests that we are not meant to be meat eaters. Animals that eat meat have sharp tearing teeth, while we have flatter teeth more similar to vegetarian animals. I believe humans are not anatomically or metabolically designed to be meat eaters, and because we do consume animal fat that's why we get atherosclerosis. Chimpanzees don't eat meat; they eat very little fat. They have LDL levels in the range of 40 to 70, and they don't get atherosclerosis. Maybe we wouldn't get atherosclerosis either if we had levels this low."

http://www.theheart.org/article/1290061.do

In regards to your remarks on epidemiology of cholesterol count, learn all about primitive ploys the cholesterol denialists/creationists wants us to fall for.

Primitive Nutrition 40: Playing Games with Your Heart, Part I
http://www.youtube.com/watch?v=APWxP1M160I&list=PLCC2CA9893F2503B5&index=40&feature=plpp_video

Peter said...

Continues...


Cholesterol measured at the end of the lifespan tells us very little, in fact, in the Western context low cholesterol at the end of the life-span usually conveys only bad news.

Many obese diabetics with hypertension have low LDL (although even they benefit from Statin theraphy).

Most of cardiovascular deaths occur to people who have already suffered a stroke, their LDL is low because they are on an aggressive lipid-lowering drugs, however it takes some time before the plaques in their intima starts to ease. When we adjust these co-founders or simply study young people a completely different pattern emerges.

Think about it a bit in terms of those lung-cancer patients who do not smoke, how do they got the lung cancer? They smoked their whole life until their doctor forced them to quit. How did the people who died with low cholesterol got their cholesterol low, did they follow healthy plant-based diets like people in Central-Africa have traditionally done? Low LDL is very beneficial on healthy people.

Relationship of baseline serum cholesterol levels in 3 large cohorts of younger men to long-term coronary, cardiovascular, and all-cause mortality and to longevity.

“These results demonstrate a continuous, graded relationship of serum cholesterol level to long-term risk of CHD, CVD, and all-cause mortality, substantial absolute risk and absolute excess risk of CHD and CVD death for younger men with elevated serum cholesterol levels, and longer estimated life expectancy for younger men with favorable serum cholesterol levels”.

http://www.ncbi.nlm.nih.gov/pubmed/10891962

Peter said...

Some astonishing epidemiology

1) "As to the risk factors in predominantly rural African populations in southern Africa, the principal dietary sources of energy were in the past and still are to an extent cereals (maize and kaffir corn or sorghum) and their products, wild spinaches, and a variety of legumes (cowpeas, sugar beans, Jugo beans), along with relatively low intakes of most vegetables and fruits and infrequent consumption of small quantities of milk and meat".

"Serum cholesterol levels of rural Africans in the past ranged from about 3.0 to 3.5 mmol/l and remain low. The range of mean serum cholesterol levels of urban Africans was 3.5 to 4.40 mmol/l and later increased to 4.0 to 5.0 mmol/l" (3 mmol/l = 116mg/dl)

Nutrition and Heart Disease Causation and Prevention Edited by Ronald Ross Watson and Victor R . Preedy

2) The epidemiology of coronary heart disease in South Africa

"Numerous reviews, past and present, have emphasised the rarity of coronary heart disease (CHD) in Africa. In 1960 in Uganda, CHD was considered to be 'extremely rare'.I In 1977, black Africans were described as being 'virtually free of hypertension and CHD'.' In the same year, at Enugu, Nigeria, over a 4-year period, not one patient out of 348 with cardiac disorders had the disease.3 In 1983, in the UK, a leading article entitled 'British and African hearts' underlined the tremendous contrast between the experience of CHD in the two population groups: From 1988 to 1993 in Zimbabwe, at Parirenyatwa Hospital, the main referral centre for the country, there was an annual average of 6 black patients with acute myocardial infarction.' Even at present, as concluded in a comprehensive review compiled in Nigeria,6 'CHD is still rare ... despite its increased incidence in recent years.' This rarity applies particularly to rural dwellers, as recently noted in Tanzania.'"

".....Soweto (which now has a population of 3 - 4 million), according to records of the Department of Cardiology at Baragwanath Hospital (3 200 beds), 35 blacks were diagnosed with CHD in 1992,51 in 1993, and 62 in 1994. However, of the latter number only 36 were Sowetans; the rest lived elsewhere.I' Clearly CHD remains very uncommon in urban blacks in South Africa. To afford perspective, it could be asked how uncommon CHD is in urban blacks, compared with its occurrence in Western populations? Of the population of Soweto, almost all attend Baragwanath Hospital when serious illness occurs. If it is assumed that all the 36 patients with CHD mentioned ultimately died from the disease, CHD would be responsible for only about 0.2% of the roughly 20000 deaths occurring annually in Soweto, an extremely low proportion even allowing for uncertainties. In Europe, in the Seven Countries Study,16 for those in the Mediterranean countries and inland the age-standardised 25-year CHD mortality percentages were 4.7% and 7.7%, respectively. The proportions reported for countries in Northern Europe and for the USA were far higher, namely 16.0% and 20.3%, respectively. These comparisons with Western populations underline the very low occurrence of CHD in urban blacks".

http://archive.samj.org.za/1999%20VOL%2089%20Jan-Dec/Articles/02%20February/4.2%20THE%20EPIDEMIOLOGY%20OF%20CORONARY%20HEART%20DISEASE%20IN%20SOUTH%20AFRICA.%20A.R.P.%20Walker.pdf

Charles Grashow said...

@Peter

"They compared outcomes among 1054 patients with LDL levels below 70 mg/dL at the time of their MI as to whether they were discharged on a statin or not."


SO - the patients in question had LDL levels BELOW 70mg/dL at the TIME OF THEIR MI!!

Explain that - LDL BELOW 70 at THE TIME OF THEIR MI!!

Also - why should people be put on multiple drugs - with all of the bad side effects - just to lower their LDL if the patients in the study HAD LDL below 70 already?



Charles Grashow said...

http://www.emildegomamd.com/home_htm_files/deGoma_StatinsinLowLDLCholesterolPatients.pdf

In a pooled
analysis of 4 large randomized trials of intensive versus
standard statin therapy, however, the mean LDL achieved
was only 75 mg/dL (range 65 to 81 mg/dL), and the effect of
achieving significantly lower values has not been described
prospectively.11 These studies have all included subjects with
clear cardiovascular disease or recent acute coronary syndromes,
whereas patients without documented coronary artery
disease have been omitted. Furthermore, although a clear
cardiovascular benefit can be attributed to statin therapy, total
mortality is not clearly reduced by aggressive lipid management,
and a trend toward increased noncardiovascular mortality
was described in the TNT trial.3 By extension, it is
possible that an even more aggressive statin regimen might be
associated with significantly more noncardiac death.

Charles Grashow said...

@Peter

What is your current LDL level and are you taking stains drugs?

If it is above 70 are you taking stain drugs?

If yes, what kinds and how much - if no why not?

The Humane Hominid said...

Peter,

It is useless to show evidence to creationists and deniers. Though it can sometimes be fun.

Charles Grashow said...

http://www.ajcn.org/content/81/2/380.full

Direct comparison of a dietary portfolio of cholesterol-lowering foods with a statin in hypercholesterolemic participants

Treatment goals in primary prevention include an LDL-cholesterol concentration <4.15 mmol/L (160 mg/dL) with no more than one risk factor and ≤3.4 mmol/L (120 mg/dL) with 2 or more risk factors. In the case of secondary prevention with established cardiovascular disease, an LDL-cholesterol concentration of 2.6 mmol/L (100 mg/dL) or less is advised (11). For primary prevention, drug therapy is recommended when diet has failed to reduce LDL-cholesterol concentrations to <3.4 mmol/L in persons with 2 or more risk factors or in persons who have a calculated 10-y CHD risk of 10–20% according to the Framingham cardiovascular disease risk prediction equation. Drugs are also advocated for high-risk persons or for those with established disease (secondary prevention)

Peter said...

Thanks for the tip HumaneHominid,

I feel like having fun:

Oxidized Omega6 does not oxidize LDL, but dietary cholesterol does. So much for the free-range eggs

The role of dietary oxidized cholesterol and oxidized fatty acids in the development of atherosclerosis (2005)
http://www.ncbi.nlm.nih.gov/pubmed/16270280

Consumption of eggs with meals increases the susceptibility of human plasma and low-density lipoprotein to lipid peroxidation
http://www.ncbi.nlm.nih.gov/pubmed/9001684

Dietary cholesterol increases the susceptibility of low density lipoprotein to oxidative modification
http://www.ncbi.nlm.nih.gov/pubmed/10704618

Dietary cholesterol increases the susceptibility of LDL-C to oxidation, vascular inflammation, oxidative stress, and postprandial hyperlipemia and potentiates the harmful effects of saturated fat, impairs endothelial function, and increases cardiovascular events.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989358/

Gluten-free vegan diet induces decreased LDL and oxidized LDL levels and raised atheroprotective natural antibodies against phosphorylcholine in patients with rheumatoid arthritis: a randomized study

http://arthritis-research.com/content/10/2/R34

Peter said...

Avoiding dietary sources of cholesterol is no-brainers for everyone apart from creationists

The effect of dietary cholesterol on macrophage accumulation in adipose tissue: implications for systemic inflammation and atherosclerosis.

http://www.ncbi.nlm.nih.gov/pubmed/19133410

Cholesterol oxides and carcinogenesis.
http://www.ncbi.nlm.nih.gov/pubmed/2061746



nothing91 said...

Charles,

You're posting a little too much evidence for these guys. Their black-and-white nutritional philosophy would be threatened if they actually read anything you're posting. I'd hate for you to make their heads explode. :-)

Quote Of The Year definitely goes to Peter: "Great study." LOL.

Peter said...

@Nothing

what do you mean with black & white thinking?

Incase you live in a eco-niche where calories are hard to access then, I guess, it makes sense to eat products of chicken ovulation.

I live in an eco-niche where I can purchase John McDougalls "starch solution" online and go to store and buy rolled oats, maize, amaranth, buckwheat, fresh fruits and veggies. What benefit dietary cholesterol would provide me? Your logic sounds like drug-merchants sales pitch to me, "a little bit of horse won't do no harm".

nothing91 said...

Peter,

"What benefit dietary cholesterol would provide me?"

There you go with the "benefits" talk again. You and Don are like two peas in a pod.

I just can't imagine what I mean by black-and-white thinking.

Jack LaBear said...

"What benefit dietary cholesterol would provide me?"

This anti cholesterol “research” being posted here supposedly in support of the smoking egg study is ridiculous because that study actually suggests the hypothesis that egg consumption is favorable to artery health.

The study was done by gathering a group of people who had already had a stroke and asking them to fill out a survey of how many eggs they had eaten. The most egregious problem with this study is that it was not corrected for age, since atherosclerosis rates increase with age. But actually there is useful information in that.
Let’s assume for the moment that there actually was a correspondence between reported and actual egg consumption. Those reporting the most egg consumption had their stroke at an average age of 70 years, while those reporting the least egg consumption had their stroke at an average age of 55 years. Although an observational study can’t prove cause and effect, the fact remains that those who ate the most eggs didn’t have a stroke until 15 years later than those who ate the least eggs. And obviously, none of the egg eaters had died of heart attacks, even though those who ate the most were 15 years older.

How the heck is this study supporting the hypothesis that eating eggs is bad for your arteries?
To me, this simply discredits all these anti dietary cholesterol studies cited above.

Yes, I agree with Peter – avoiding cholesterol is literally a no-brainer, or at least a seriously dysfunctional-brainer ;-)

Peter said...

@Jack LaBear

the so-called "refutals" by the creationists are ridiculous, to the dissapointment of the intelligent design crowd, Spence and Jenkins adjusted the age indeed.

"Plaque area in patients consuming <2 eggs per week (n = 388) was 125 ± 129 mm(2), versus 132 ± 142 mm(2) in those consuming 3 or more eggs per week (n = 603); (p < 0.0001 after adjustment for age). In multiple regression, egg-yolk years remained significant after adjusting for coronary risk factors."

As said, we have a great new study by Spence and Jenkins which adds to the body numerous other studies including primate models on the adverse effects of dietary cholesterol.

Jack LaBear said...

@Peter

I stand corrected about lack of adjustment for age.
So what you’re telling me is that despite higher age adjusted intima-media thickness (plaque area was not measured) in egg eaters, egg consumption correlated with protection from strokes. To the tune of quarter of a lifetime. Even in people with higher rates of smoking and diabetes. Adjustment for those factors adds even more weight to the 14 year higher age of the egg eaters' stroke occurrence.
Regarding the monkey studies, I’m reminded of a commenter on a different blog who believes that the only good exercise for people is hanging from tree branches. Never mind that it made his back ache!

Charles Grashow said...

http://www.drbriffa.com/2012/08/15/note-to-medical-researchers-correlation-does-not-prove-causation/

http://www.drbriffa.com/2010/11/05/still-no-good-evidence-that-eggs-cause-heart-disease-despite-what-some-may-say/

http://www.fathead-movie.com/index.php/2012/08/23/more-on-the-egg-yolk-study/

"Currently, however, serious doubts have been expressed over the relevance of these dietary components to cardiovascular disease.

That’s because they’re not relevant.

In the case of cholesterol much of the debate has been focused on the lack of clear consensus on whether egg consumption consistently raises serum cholesterol or impacts negatively on postprandial events, including vascular reactivity. Most importantly the association of egg consumption with CHD events in cohort studies has been inconsistent.

Well, there’s a reason the association of egg consumption with CHD has been inconsistent: eggs don’t cause heart disease. If they did, the association would be consistent. If the evidence supporting a hypothesis isn’t consistent, a good scientist assumes there’s something wrong with the hypothesis."

"Here’s the description of how the data was collected:

In earlier years, data on smoking and egg consumption were recorded by patients into a lifestyle questionnaire at the time of referral. Since 2000, when our referrals were scheduled on an urgent basis soon after transient ischeamic attacks or strokes, a more limited set of lifestyle questions were asked at the time the history was obtained. These data were entered, along with the history, medications, physical examination and recommendations into fields in the database, from which clinic notes were generated.

Hmmm … so the study participants were people who’d been urgently referred to a clinic after suffering a heart attack or stroke. Not exactly what I’d call a random sample of the population, or even a random sample of the elderly population. And if egg yolks cause cardiovascular disease, why were the study participants who consumed less than one egg per week referred to a clinic for people who’ve had a heart attack or stroke? Seems to me they should have been out playing golf and enjoying their plaque-free health, not seeking an urgent referral.

The responses for smoking and egg yolk consumption were used to compute pack-years of smoking (number of packs per day of cigarettes times the number of years of smoking) and egg-yolk years (number of egg yolks per week times number of years consumed). This was not done for alcohol consumption, licorice intake or exercise, because the textual responses were mainly not quantifiable (e.g. “quit drinking six years ago”, “plays golf twice a week”).

I guess I’ll have to ask my Canadian pals: Why is licorice intake considered a potential confounding variable in Canada? Do you eat enough of it to skew health outcomes? Granted, it’s been a long time since I did standup comedy tours in Canada, but I don’t remember noticing a lot of people up there chewing on licorice. Nobody ever walked up to me after a set and said, “Great show, eh! Can I buy you a licorice?”"

Charles Grashow said...

http://www.psychosomaticmedicine.org/content/62/2/205.full.pdf+html

Higher Prevalence of Depressive Symptoms in Middle-Aged Men With Low Serum Cholesterol Levels

Conclusions: Men with a lower cholesterol level (#4.5 mmol/liter) have a higher prevalence of depressive symptoms than those with a cholesterol level between 6 and 7 mmol/liter. These data may be important in the ongoing debate on the putative association between low cholesterol levels and violent death.


http://www.sciencedirect.com/science/article/pii/0140673693925569

Plasma cholesterol and depressive symptoms in older men

Depressive symptom scores correlated significantly and inversely with plasma cholesterol concentrations, even after adjustment for age, health status, number of chronic illnesses, number of medications, and exercise, as well as measured weight loss and change in plasma cholesterol in the previous 13 years. Our finding that low plasma cholesterol is associated with depressive symptoms in elderly men is compatible with observations that a very low total cholesterol may be related to suicide and violent death. Since cholesterol lowering in the general population is widely recommended, this observation warrants further investigation.


http://www.psychosomaticmedicine.org/content/59/5/521.long

Depressive Symptoms, Social Support, and Lipid Profile in Healthy Middle-Aged Women

Conclusions: Low cholesterol levels in middle-aged healthy Swedish women were associated with a higher prevalence of depressive symptoms and with lack of social support. These findings may constitute a possible mechanism for the association found between low cholesterol and increased
mortality, particularly suicide.


http://www.psychologytoday.com/blog/the-breakthrough-depression-solution/201106/low-cholesterol-and-its-psychological-effects


http://www.ncbi.nlm.nih.gov/pubmed/1627030

Serum cholesterol level and mortality findings for men screened in the Multiple Risk Factor Intervention Trial. Multiple Risk Factor Intervention Trial Research Group.

For intracranial hemorrhage, cholesterol levels less than 4.14 mmol/L (less than 160 mg/dL) were associated with a twofold increase in risk. A serum cholesterol level less than 4.14 mmol/L (less than 160 mg/dL) was also associated with a significantly increased risk of death from cancer of the liver and pancreas; digestive diseases, particularly hepatic cirrhosis; suicide; and alcohol dependence syndrome. In addition, significant inverse graded associations were found between serum cholesterol level and cancers of the lung, lymphatic, and hematopoietic systems, and chronic obstructive pulmonary disease.

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

@Charles

you should travel a bit more.

Do rural Asians with very low TC cholesterol levels,places such as Thailand appear to depressed and aggressive to you? Did depression and anti-social behavior reigned among the Tarahumara's?

RaCCG9: Cholesterol, Cancer, and Depression
http://www.youtube.com/watch?v=2sLp_vAz9KQ&list=PLDBBB98ACA18EF67C&index=21&feature=plpp_video

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

@Charles,

look carefully the primitivenutrion video above, you get the basics of epidemiology of depression. What do you think? Is depression rampant among Hunter-Gatherers with their ridiculously low TC cholesterol levels?

Swede said...

"look carefully the primitivenutrion video above, you get the basics of epidemiology of depression. What do you think? Is depression rampant among Hunter-Gatherers with their ridiculously low TC cholesterol levels?"

How can you diagnose depression from a video?

You vegans are quite spritely with your mental extrapolations!

Peter said...

@Swede

well why do you think there's all the rage about HG's in the first place? That's because their health status have been in many cases studied thoroughly by Western medical experts and anthoropologists.

HG's have very generally very low depression rates although they subjected to lot of stress. However, I don'trecommend the HG route.

I would suggest that anyone who follows paleo-diet in their own clean, parasite-free eco-niche take a potent daily statin (atorvastatin, or preferably rosuvastatin, judged bythe lipid responses many paleo-dieter get, you need a good share of lipid lowering, a daily apple won’t cut the deal anymore). How do the real primal/paleo people still living in their stone-age manages it? This comes to an important co-founder the appeal-to-primitivism -crew don’t talk about. Parasites! The primitive tribes all have them, and they have them a lot. What do they do, they eat up the LDL in your intima. Statins have less side-effects.

1) Role of cholesterol in parasitic infections
http://www.ncbi.nlm.nih.gov/pubmed/15882457

2) An anti-atherogenic effect of Schistosoma mansoni infections in mice associated with a parasite-induced lowering of blood total cholesterol.

“Observations on S. mansoni-infected conventional laboratory mice indicate that patent schistosome infections could be counteracting the effects of an atherogenic diet by modulating host lipid metabolism and inducing a reduction in blood total cholesterol concentrations”.

http://www.ncbi.nlm.nih.gov/pubmed/12458825

Charles Grashow said...

http://stroke.ahajournals.org/content/20/11/1460.full.pdf

Serum cholesterol and hemorrhagic stroke in the Honolulu Heart Program.

We found a significant inverse association between serum cholesterol and intracerebral hemorrhage after controlling for age and other risk factors.

The increased risk of hemorrhagic stroke was noted only for men with
serum cholesterol in the lowest quintile (<189 mg/dl). Further breakdown of men with low serum
cholesterol (<200 mg/dl) indicated that the risk of hemorrhagic stroke was highest for those with the lowest serum cholesterol (<160mg/dl). These findings
suggest a threshold effect. The inverse association was stronger for normotensive than for hypertensive men, although there was no statistical evidence for an interaction of blood pressure and
serum cholesterol.

In Japan and other Asian countries, however, the risk of stroke is as much as three times higher than in the United States, and hemorrhagic stroke may account for more than one third of all strokes. As the population's average serum cholesterol is low, the appropriate public health goal should be to
maintain optimal levels of serum cholesterol (probably around 200 mg/dl), which would not increase
the risk of either stroke or coronary heart disease.

Charles Grashow said...

@Peter - what is your total cholesterol, HDL and LDL? We are curioustYSAust

nothing91 said...

@Peter

You should travel a bit more.

Do the Tarahumaras, who we now know eat eggs regularly, suffer from high cholesterol? Did heart disease reigned among the Tarahumaras?

@Swede

"How can you diagnose depression from a video?"

He can barely go a single comment without linking to a primitive nutrition video. Ain't it cute? :-)

Ben said...

"Its complicated. The effect of any nutrient or food on human health depends on quality, quantity, and context of consumption.

I can no longer allow myself to fall into simplistic thinking like 'meat good, grains bad,' 'fats good, carbs bad,' and such.

Meat can have benefits in some quantities, qualities, and contexts, and cause harm in other quantities, qualities, and contexts.

Ditto for fats, carbs, grains, everything.

Done with nutritional dualism.

Everything is relative.

Anything can be medicine or poison, depending on quality, quantity, and context.'

Don Matesz in "Follow Up to Farewell to Paleo." Aug. 4, 2011

Charles Grashow said...

@Nothing91

They eat appx 2-3 eggs per week.

http://www.ajcn.org/content/31/7/1131.full.pdf

"The plasma cholesterol values for all subjects were very low, averaging 125 mg/dl: for children, 116 mg/dl and for adults, 136 mg/dl. Men and nonpregnant women had similar values. Of note were the higher plasma cholesterol levels of the pregnant and lactating women, 193 and 178 mg/
dl, respectively. Only 4% of the children had plasma cholesterol concentrations above 150 mg/dl; none was above 160 mg/ dl. Of the children 24% had plasma cholesterol
levels below 100 mg/dl. Only 4% of
the adults (both sexes, excluding pregnant and lactating women) had plasma cholesterol levels above 180 mg/dl, and two individuals
(1 .4%) had levels of 224 mg/dl and
251 mg/dl, respectively. Of the adults 26% had plasma cholesterol concentrations between 150 and 180 mg/dl, and 8% had levels of 100 mg/dl and below.

The major caloric sources of the Tarahumara diet were corn and beans. These foods contributed about 90% of the total calories. The remainder of the diet was almost completely derived from other vegetable sources. Meat was seldom eaten. The chief animal food product consumed with some regularity was eggs, averaging 2 per week."

http://www.ajcn.org/content/32/4/905.full.pdf+html

"From the dietary histories and field observations, it became clear that the Tarahumaras received the majority of their daily nutrients
(90% of total calories) from corn and beans (pinto bean variety). About 94% of the total daily protein intake was from vegetable
sources, only 6% being from animal
sources. Of the small amount of fat in the Tarahumara diet, 33% was from animal sources with the remaining 67% of vegetable
origin. Most ofthe fat in this diet was derived
from corn and beans, rich sources of linoleic acid and of plant sterols. Corn contributed the greatest amount of carbohydrate, fiber, and plant sterols to the diet. The cholesterol intake, which was very low compared to usual
United States intakes, was primarily from eggs, the consumption of which averaged two
to three per week for each individual. Other sources included small, infrequent servings of
meat, fish, poultry, dairy products, and lard."

Charles Grashow said...

@Ben

"Meat can have benefits in some quantities, qualities, and contexts, and cause harm in other quantities, qualities, and contexts."

Would love for Don to tell us the benefits of meat.

Ben said...

Has anyone else noticed that it is no longer possible to access the reams of research and literature once present on this blog prior to 2009?

And that any article supporting the consumption of anything but Don's current diet have disappeared altogether?

Certainly, it is Don's blog. So he can freely choose what he wants people to see. But if his new paradigm is so compelling, so well-researched and so irrefutable, why would he not allow us access to all the (bad?) studies he referenced prior to 2009?

The Humane Hominid said...

The Tarahumarans are known carriers of Ascaris and Giardia parasites, both of which reduce the host's lipid parameters.

-- "Results show that E. histolytica, E. dispar and G. lamblia cyst passers had significantly lower levels of total serum cholesterol (73.42 +/- 2.24 mg/dL), compared to levels in ALA cases (101 +/- 2.85 mg/dL) and in controls (166.26 +/- 2.02 mg/dL)."

-- "During larval ascariasis, as it appears, the metabolism of lipids is significantly disturbed. The changes are due to the break in liver function and, presumedly, changes in hormone secretion which are provoked by the presence of the parasite."

Peter said...

@Charles,

again, look for co-founders. Whenever you decide to spray the fodder of creationists remember to ask, how did the people who died prematurely got their cholesterol low.

Low cholesterol, mortality, and quality of life in old age during a 39-year follow-up

"More dispute has arisen regarding the association of low cholesterol and mortality in elderly persons. For example, in the Honolulu Heart Program (5) low cholesterol was associated with greater mortality risk. Obvious explanations for the association are intervening factors that both increase mortality risk and decrease the cholesterol level. In the nine-year follow-up of the Helsinki Aging Study, mortality risk was associated with both lowered cholesterol synthesis and lowered cholesterol absorption (20), which reflect terminal decline and lead to lower serum cholesterol levels. These associations are not identified, and the relationship between cholesterol and mortality becomes distorted unless the follow-up is long enough"

http://content.onlinejacc.org/cgi/reprintframed/44/5/1002

@Humanehominid

The cholesterol levels of Tarahumara's are something what is expected from a people that consume whole-food plant based diet (together with 2 eggs per week). Their TC cholesterol was on average 134mg/dl which is very good, but we've seen lower in rural China and Central Africa.

The intelligent design -crew make a big fuss about the two eggs the Tarahumara consumed per week. That has been the point all along. How could the researcher have established a dose-dependent linear association of dietary cholesterol to serum cholesterol had Tarahumaras not consumed any dietary cholesterol at all?

here's the money line from the Study:

"Since in the experimental dietary cholesterol is sine qua non for the development for the experimental atherosclerosis, especially among the sub-human primates, the finding of linear association of dietary cholesterol intake and plasma cholesterol concentrations in man further undergirds the evidence relating dietary factors to hypercholesterolemia and atherosclerotic coronary heart disease"

http://www.ajcn.org/content/31/7/1131.long

Charles Grashow said...

@Peter

http://www.health-heart.org/eve-not-adam.pdf

Why Eve Is Not Adam: Prospective Follow-Up in 149,650 Women and Men of Cholesterol and Other Risk Factors Related to Cardiovascular and All-Cause Mortality

Results: Patterns of cholesterol levels showed marked differences between men and women in relation to age and cause of death. The role of high cholesterol in predicting death from coronary heart disease could be confirmed in men of all ages and in women under the age of 50. In men, across the entire age range, although of borderline significance under the age of 50, and in women from the age of 50 onward only, low cholesterol was significantly associated with all-cause mortality, showing significant associations with death through cancer, liver diseases, and mental diseases.

http://circ.ahajournals.org/content/86/3/1046.full.pdf

Report of the Conference on Low Blood Cholesterol: Mortality Associations

http://circoutcomes.ahajournals.org/content/5/3/381.abstract

In male physicians, higher baseline HDL-C levels were associated with a lower risk of all-cause and CVD mortality before age 90.


Peter - what are your lipid levels? You've never answered this question.

Peter said...

@Charles,

The last my cholesterol was measured was five years ago when ate pretty much semi-prudent standard Western fare. As my doctor concluded, I have genetically very efficient cholesterol cleaning mechanism, I cannot recall my numbers but they were low even despite the fare I consumed back then. I have no family history with CHD either. I switched to plant-based eating three years ago. I'd be very surprised if my TC cholesterol would be over, let say 115, they can be even lower, not sure thought.

Anyways, you are a bit behind your times.

American Cancer Society

"Many epidemiologic studies published in the 1980s documented an association between low circulating cholesterol and higher overall cancer incidence and mortality. This association has been attributed to reverse causation, that is, undiagnosed cancer causing a reduction in cholesterol levels. Reverse causation is strongly supported by observations that cholesterol levels decline before cancer diagnosis and that associations between low cholesterol and cancer incidence and mortality weaken when the first few years of study follow-up are excluded. In addition, a meta-analysis of randomized trials of cholesterol-lowering statins found no effect on risk of cancer, although only short-term effects could be addressed due to the short duration of most trials".

http://cebp.aacrjournals.org/content/18/11/2805.full

besides statin trials, also today, we know that people who inherited ultra low LDL have lower occurance of cancers compared to the main population.

Low cholesterol on healthy people protects against cancer:

The Importance of LDL and Cholesterol Metabolism for Prostate Epithelial Cell Growth (June, 2012)

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0039445

Charles Grashow said...

Doesn't this sound yummy

http://thevegg.com/

http://www.paleopharm.com/say-cluck-you-to-the-food-police/

What’s in the Vegg?

Ingredients: Nutritional Yeast Flakes, Sodium Alginate, Kala Namak (black salt), Beta-Carotene. Blend contents with one liter of water. (For Vegg users who wish to not mix all at once, use this conversion: Blend 1 teaspoon of The Vegg powder with 1/4 cup water equivalent to about two to three yolks!)

For his next product, Shepheard is hatching a new concept: a whole Vegg with a fryable white.

The Humane Hominid said...

Peter,

Yeah, I figured that is the case with the Tarahumara.

Creationists make a big deal about the supposedly low lipid profiles of HG peoples who eat lots of meat and fat. The creationists never account, however, for the fact that most parasites that infect humans metabolize the host's cholesterol, inducing an anomalously-low lipid profile.

Parasites have co-evolved with us and our ancestor species for millions of years. The creationists always forget this, and look at HG health profiles in isolation.

Show me a HG culture with high fat diets & low blood lipids, and I can probably show you the lipid-eating parasite they're a carrier for.

Don said...

Ben,

If you were literally starving, having not eaten enough for at least several weeks, and for some reason, adequate plant foods were not available, some amount of meat might be medicine, i.e. better than starving to death.

The contexts in which meat would possibly act as medicine are extremely rare in modern industrialized nations.

In addition, in making that statement, I unfortunately failed to incorporate the Chinese medicine understanding of three classes of medicine, simply because it didn't occur to me to apply it to the question at the time.

The first class medicines are foods and herbs that have no side effects and do not cause illness in the short or long term, but instead only strengthen and purify the body; we can consume these every day without conscious restriction of quantity because our appetite will naturally control our intake to appropriate levels.

The second class includes any substance that is slightly toxic, enough to cause side effects and illness, usually not immediately, but over a period of time; we prescribe or use these slow poisons only when warranted by a specific illness, in small amounts, and only for a defined, relatively short period of time, i.e. until the disease is corrected. In Chinese medicine, it is the doctor's duty to get his patients off of such substances as soon as possible, to avoid causing a new illness.

The third class we call poison medicines, because they are acute poisons and can cause serious damage to the body in a very short time of use; we prescribe or use these only when warranted by a life-threatening illness for which there is no other known treatment that will kill the pathogen. Examples would include various antimicrobials and parasiticides, and purgatives or emetics (prescribed to rid the body of an even worse toxin).

Chinese medical ethics states that a physician should only use second or third class medicines if clearly warranted by the illness and there is no way to treat the illness quickly enough with first class medicines.

Regardless of what any particular individual Chinese physician, past or present, has believed, and regardless of what anyone thinks that Chinese medical texts tell us about animal flesh, eggs, and milk, contemporary biomedical research clearly indicates that animal flesh, eggs, and milk all clearly belong to the second class of medicine (i.e. slow poisons) when regularly consumed.

Grains, vegetables, fruits, seeds, and nuts all generally (i.e. in the vast majority of contexts) belong to the first class of medicines, the exceptions being that some items might be poisons for some individuals (i.e. in some contexts), e.g. wheat is poison for people having celiac disease (about 1 percent of the population).

In addition, I have since that statement re-embraced my natural empathy and chosen to follow and promote a dietary path that harmonizes with my highest (and libertarian, Daoist, and Confucian) value of not infringing upon, initiating aggression against, or causing harm to any sentient beings.

It goes something like this: I have the right to do whatever serves me, so long as I do not infringe on the natural rights and well-being of others. Eating animals clearly infringes on their natural rights.

If I no longer appear to agree with something that I said one year, one day, one hour, one minute, or even one second ago, it might be because I value learning and evolution of understanding and continue to broaden my awareness and seek truth and apply it in my life.

Charles Grashow said...

@Don

Are insects sentient beings?

Charles Grashow said...

@Don

you now have "chosen to follow and promote a dietary path that harmonizes with my highest (and libertarian, Daoist, and Confucian) value of not infringing upon, initiating aggression against, or causing harm to any sentient beings.'

The food that you consume is fertilized with animal products

http://cmg.colostate.edu/gardennotes/234.pdf

Organic fertilizers are made from a huge variety of naturally occurring elements such as bat guano, blood meal, bone meal, feather meal, and fish meal.

Blood meal is a dry, inert powder made from blood used as a high-nitrogen fertilizer and a high protein animal feed. It is one of the highest non-synthetic sources of nitrogen. It usually comes from cattle as a slaughterhouse by-product

Bone meal is a mixture of crushed and coarsely ground bones that is used as an organic fertilizer for plants and formerly in animal feed. As a slow-release fertilizer, bone meal is primarily used as a source of phosphorus.

Fishmeal can be made from almost any type of seafood but is generally manufactured from wild-caught, small marine fish that contain a high percentage of bones and oil, and is usually deemed not suitable for direct human consumption. The fish caught for fishmeal purposes solely are termed “industrial”.[3] Other sources of fishmeal is from by-catch of other fisheries and by-products of trimmings made during processing (fish waste or offal) of various seafood products destined for direct human consumption. Virtually any fish or shellfish in the sea can be used to make fishmeal, although there may be a few rare unexploited species which would produce a poisonous meal.

Feather Meal - Sourced from poultry slaughter, feather meal has fairly high nitrogen levels but is
slow to release the nitrogen

So - you are responsible for a great many sentient beings being killed regardless of your philosophy.

wHAT SAY YOU.



Swede said...

"In addition, I have since that statement re-embraced my natural empathy and chosen to follow and promote a dietary path that harmonizes with my highest (and libertarian, Daoist, and Confucian) value of not infringing upon, initiating aggression against, or causing harm to any sentient beings.

It goes something like this: I have the right to do whatever serves me, so long as I do not infringe on the natural rights and well-being of others. Eating animals clearly infringes on their natural rights."

We argued about this a few posts ago. You still eat plants. They are alive. Why is what you call "sentient" life more important than "non-sentient" life? Do animals have "natural rights" that plants cannot posses?

The sunflower seed that you crushed between your teeth will never bloom. The avocado you slashed open and threw the seed into the trash will never flourish. The fruit you eat, and then shit out the seed to be flushed down the toilet and exiled into the wasteland of sewage shall never grow. Yet you rationalize that since they are not sentient, then such is acceptable in your moral view.

gunther gatherer said...
This comment has been removed by the author.
gunther gatherer said...

Charles, anyone with a backyard garden knows you don't have to use animal products to fertilize your crops. And have you never heard of an organic farmer?

You are desperately trying to search for holes in Don's argument but in doing so you only belie your own when you paste link after link claiming that eating animals is necesssary for human health. It is obviously not, or vegetarians, vegans and fruitarians would not be thriving as they do. And ancestral tribes with plant-based diets wouldn't be so much healthier than the Eskimo.

Peter said...

@HumaneHominid,

I know. You brought this theme to the public (parasites and cholesterol metabolism). I learned about it through primitivenutrition. He gave credit to you.

Peter said...

@Gunter

In regards to Eskimos, Healthy Longevity has done some good job by illustrating the loopholes of the appeal-to-nature fallacy

Forks Over Knives and Healthy Longevity: Perhaps the Science is Legit After All

"In 1925, Kuczynski reported on the nomadic Kirghiz plainsmen, who habitually consume a diet with large amounts of meat and milk, and observed a high incidence of obesity, premature extensive atherosclerosis, contracted kidney, apoplexy and arcus senilis. Their urbanized counterparts who consumed a more varied diet however did not exhibit such severe vascular disease.I

In 1940, based on years of clinical practice and reviewing medical reports, Bertelsen who is considered the father of Greenland epidemiology stated in regards to the mortality patterns amongst the Greenland Inuit that:

...arteriosclerosis and degeneration of the myocardium are quite common conditions among the Inuit, in particular considering the low mean age of the population.

In 1904, Bertelsen proved the existence of cancer in the native Inuit, diagnosing a case of breast cancer. During the following decades researchers documented that the existence of cancer was exceedingly common among the Inuit despite their relatively short life expectancy.Consistent with Bertelsen’s findings, an Inuit predating western contact who was mummified around 1475, 450km north of the Arctic Circle was shown to have evidence of cancer, likely of the breast.18 It has also been documented that numerous preserved pre-contact Inuit who were mummified dating all the way back to 1,500 years ago had a severe degree of atherosclerosis, osteoporosis, and osteoarthritis, consistent with studies of Inuit living in the 20th century. Other evidence of poor health among the pre-contact Inuit includes iron deficiency anemia, trauma, infection, dental pathology, and children with downs syndrome and Perthes disease"

http://healthylongevity.blogspot.fi/2012/08/forks-over-knives-and-healthy-longevity_17.html

Ronald John Neal said...

Thanks for your info. Many are saying that egg yolks carry bad cholesterol. For me, there some truth about that. The thing is, moderation must be practiced in eating egg yolks.

manhattan weight loss

nothing91 said...

"So - you are responsible for a great many sentient beings being killed regardless of your philosophy."

+1

The great aspect of this debate is listening to people like Don inevitably talk about organic farming, as if 100% of the food they eat comes from 100% organic sources (yeah right). The reality is, they're killing -- just like everything else which eats.

It's almost like they have blinders on or something. :-)

gunther gatherer said...

Yet another lame excuse from the Confusionists: "Plants die when we eat them, therefore vegans are killers just like us."

Millions of bacteria die every minute when we breathe. So what? No one is saying death doesn't happen. Only that you don't have to make animal suffering the basis of your diet or culture. This is without even touching on the greenhouse gas effects of your dietary choices and your responsibility for the planet.

healthy-longevity said...
This comment has been removed by the author.
healthy-longevity said...

Bix produced a very informative post regarding a paper that found that feeding small amounts of cholesterol to non-human primates, "about 25.8 milligrams cholesterol (~86mg chol for a human eating 2000 kcal, about half a small egg)" induced arterial lesions despite only modest changes to fasting serum lipids.

These findings are consistent with other evidence suggesting that there is no threshold beyond which a lower intake of cholesterol does not provide additional benefit, and that the disease promoting effects of dietary cholesterol are at least partly independent of the effects on fasting serum cholesterol.1 2 3

Jack LaBear said...

@healthy-longevity

What part about the smoking egg study showing that those who ate the most eggs got the artery disease called stroke 15 years later than those who ate the least eggs don't you get?
Is it the egg part or the stroke part?

Jack LaBear said...

@Peter

As you doubtlessly know, rural Chinese have very low cholesterol levels. They also have the highest rates of suicide in the world.

You wrote about those cheerful non-aggressive Thais. How about self-aggression? Thailand has over twice the suicide rate as US.

Charles Grashow said...

http://en.wikipedia.org/wiki/Suicide_in_Japan

Suicide in Japan has become a significant national social-issue.[1][2] Japan has one of the world's highest suicide rates, and the Japanese government reported the rate for 2006 as being the ninth highest in the world.[3] 71% of suicides in Japan were male,[2] and it is the leading cause of death in men aged 20-44.[4][5]
Factors in suicide include unemployment (due to the economic recession in the 1990s), depression, and social pressures.[4] In 2007, the National Police Agency revised the categorization of motives for suicide into a division of 50 reasons with up to three reasons listed for each suicide.[6] Suicides traced to losing jobs surged 65.3 percent while those attributed to hardships in life increased 34.3 percent. Depression remained at the top of the list for the third year in a row, rising 7.1 percent from the previous year.[6]

http://en.wikipedia.org/wiki/List_of_countries_by_suicide_rate

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

@Healthy longevity

great papers, one of the best kept secrets of the Intelligent Design/cholesterol denialist -crew.

@Jack & Charles,

I bet the Japanese Kamikaze can also be explained by low cholesterol. Thanks for pointing this. Some cultural anthropologists might raise the shame-based culture of Asians as a powerfull explanation but that's only because they haven't consulted you guys.

Is suicide also common among those who have inherited very low LDL? How about rural Central-Africa?

1) "As to the risk factors in predominantly rural African populations in southern Africa, the principal dietary sources of energy were in the past and still are to an extent cereals (maize and kaffir corn or sorghum) and their products, wild spinaches, and a variety of legumes (cowpeas, sugar beans, Jugo beans), along with relatively low intakes of most vegetables and fruits and infrequent consumption of small quantities of milk and meat".

"Serum cholesterol levels of rural Africans in the past ranged from about 3.0 to 3.5 mmol/l and remain low"

Nutrition and Heart Disease Causation and Prevention Edited by Ronald Ross Watson and Victor R . Preedy

Peter said...

3mmol/l -3,5mmol/l = 116-135mg/dl

gunther gatherer said...
This comment has been removed by the author.
gunther gatherer said...

Suicide caused by low trigs? I don't see any hunter gatherers offing themselves in droves.

Better try another tack for your arguments, Charles and Jack. You are looking ridiculous now.

Your assignment is to look up Correlation and Causation and recite them aloud for our next class.

Jack LaBear said...

To all you folks who keep posting anti-cholesterol articles, I'm going to repeat myself:

What part about the smoking egg study showing that those who ate the most eggs got the artery disease called stroke 15 years later than those who ate the least eggs don't you get?
Is it the egg part or the stroke part?

How about an intelligent response that addresses the issue this time instead of more smarmy crap?

Do you know about the Black Swan principle in science? What we have here is a smoking Black Swan ;-)
The irony here is that Don himself posted a pro egg article in this case, you have Peter writing things like: "Great study. I have great respect for Spence and Jenkins". Well, is the study good or isn't it? Did the study find that the greater the "egg yolk years", the lower the TC and LDL, or didn't it? Is stroke a thrombotic disease or not?

Here is Don's comment on the above:
"So, why didn't Spence et al choose this interpretation? Probably because it is inconsistent with the bulk of research on egg or cholesterol consumption and cardiovascular disease" Black Swan, Don.
I'll give you another "probably": “Dr Spence and Dr Davignon have received honoraria and speaker’s fees from several pharmaceutical companies manufacturing lipid-lowering drugs, and Dr Davignon has received support from Pfizer Canada for an annual atherosclerosis symposium; his research has been funded in part by Pfizer Canada, AstraZeneca Canada Inc and Merck Frosst Canada Ltd.“ That is the same reason that the opinions of all these "expert panels" carry little weight for me. When you have these so called researchers find from their own study that stroke was delayed by 14 years and serum cholesterol was lowest in those who ate the most eggs, yet conclude with an anti-cholesterol paragraph that simply ignores the data, just follow the money. Or in the case of vegans also follow the "we're going to save the world by getting everyone else to be like us" politics to find the truth!

Charles Grashow said...

@Jack LaBear

+1

To Don and the other vegans on this blog - you've made the choice that eating vegan is the morally/ethically superior way to go. Don has said that even if you could prove that eating meat is healthier than his current diet he would refuse to do so. Therefore, no matter how many studies we supply that support the opposite point of view he and others here will ignore them because they have seen the light.

@The Humane Hominid - this is what you said

http://letthemeatmeat.com/post/6598992716/interview-with-a-vegan-paleontologist-the-humane

"No paleontologist or anthropologist doubts that hominins ate meat – and, during the Ice Age outside of Africa, probably quite a lot of it – or that doing so shaped our evolution, but we’re not obligate carnivores who evolved in high latitudes. We come from the African tropics, and the ancestors from whom we inherited the plan for our digestive and masticatory traits are generally considered to have been largely frugivorous. Some australopithecine fossils even show evidence of grass consumption."

"Fruigvory is our base gut adaptation, but it’s flexible enough to allow primates to digest meat, especially cooked meat. When our lineage adopted a greater degree of carnivory as a survival strategy, nature selected for those variations of the base “frugivorous” gut that were slightly better at meat-digestion. But just because we got better at eating meat, that doesn’t mean we got worse at eating fruits, seeds and foliage. We didn’t specialize to become obligate carnivores."

"In other words, modern human guts are adapted to a diet of soft, energy-dense foods, a condition they inherited from “frugivorous” ancestors but that accidentally also allows them to be better at digesting meat than other primates. To put it succinctly, H. sapiens are functionally omnivorous because of their frugivory, not in spite of it (a point that threatens to undo the whole debate before it even starts."

"In that debate, I’m arguing to a fellow vegan that a human “fruigvorous” adaptation doesn’t preclude an ability to be good at eating meat. If I were debating a carnist on the same point, I’d say that just because humans can digest meat, that doesn’t mean we “evolved to” do so; it just means we found a new use for a flexible trait common to “frugivorous” primates."

So - does this mean we've evolved to eat meat, fruits, vegetables, grains, etc? Would this mean this a conscious decision to avoid meat is going against our evolutionary past?

Charles Grashow said...

http://www.mayoclinicproceedings.org/article/S0025-6196(11)62710-9/fulltext

Effect of a High Saturated Fat and No-Starch Diet on Serum Lipid Subfractions in Patients With Documented Atherosclerotic Cardiovascular Disease


The HSF-SA diet resulted in decreases in body weight and calculated body fat in patients with ASCVD. These decreases were accompanied by decreased fasting serum glucose, insulin, and TG levels. An NMR spectroscopic assay of serum lipids showed no effect on total cholesterol level or the LDL and HDL subfractions in these patients who were treated with statins throughout the observation time. Patients with PCOS and RH monitored in clinical practice for longer periods also lost weight and had no changes in serum lipid levels despite receiving no lipid-lowering drug therapy.

Charles Grashow said...

Lets do it with drugs!

http://www.medscape.org/viewarticle/762711_transcript

Lowering LDL-Cholesterol and Novel Targets to Achieve New Levels

Every participant in the study had a baseline LDL-C level of approximately 124 to 132 mg/dL while receiving atorvastatin. On top of that, we added SAR236553/ REGN727. As you can see, there was a 5% reduction in LDL-C level on top of the atorvastatin with placebo, but with the every 2-week dosing regimen of 50 mg, 100 mg, and 150 mg of SAR236553/ REGN727, we lowered LDL-C levels 40%, 64%, and 72%, respectively. Whenever I talk to people about these results, they say, "Wow!" Can you imagine? Here you may have a 40% to 50% reduction already from the statin, you add this medication on top of it, and now you have gone down an additional 40% to 72%. Unbelievable, isn’t it?

Dr Steg: What level of LDL-C does that get people to in absolute terms?

Dr McKenney: The 50-mg dose lowered LDL-C to 64 mg/dL, the 100-mg dose lowered it to 43 mg/dL, and the 150-mg dose lowered it to a mean level of 34 mg/dL.

Charles Grashow said...

6Don, Don, Don

http://donmatesz.blogspot.com/2011/03/more-raw-truth-about-raw-vegan-diets.html

If you think man is by nature adapted to a raw vegan diet, how the hell do you explain his exodus from tropical paradise into ecosystems where meat was the only reliable food for at least half of the year?

How can an animal adapted to a diet consisting exclusively of tropical fruits and vegetables spread out from Africa all over the entire planet, even into ecosystems (e.g. the arctic) where meat is the only food available almost all year round?

A commenter on my last post in this series said eating 10 bananas every day is no problem. Since then I tried five in a day. It gave me the runs. Enjoy your bananas, but living on them is not, let's say, a-peel-ing to me.

Whenever someone tells me we don't have teeth designed for eating meat, I simply ask, "Have you ever sliced open your tongue or cheek with your own teeth?" If so, you have proven to yourself that human teeth can easily slice raw meat.

We don't need canines to eat meat, we only need shearing teeth. All of human teeth have a more carnivore form than other primates, and this change in human teeth first appears about 2.5 million years ago.

A recent study of the evolution of horses determined that evolutionary changes in tooth form such as this would require about one million years of dietary evolution. This means that in order for early humans to have sharper teeth by 2.5 million years ago, their ancestors must have been eating meat for at least one million years prior. No surprise then, that our earliest evidence for meat-eating, stone-tool wielding hominins dates to about 3.5 million years ago.

Meat--its been what's for dinner for at least 3.5 million years, and we have the teeth to prove it.

Don also said

http://donmatesz.blogspot.com/2011/03/more-raw-truth-about-raw-vegan-diets.html

Don said...
Grok,

No. We are biologically virtually identical to humans of 50K years ago. We may NOT be so similar to people of 1 million years ago, i.e. Homo erectus.

We are NOW Homo sapiens sapiens, a distinct species. The question is, "what is Homo sapiens sapiens adapted to?", NOT "what are the predecessors of Homo sapiens sapiens adapted to?".

The people of 50K years ago actually left us plenty of cave paintings showing us that they were hunters of large animals, not banana foragers.

We have plenty of evidence that we are not adapted to eating 'healthy whole grains,' written in our physiology.

If we are adapted to a low fat, banana based diet, I wonder why we even have a gall bladder?

Or how about the difference between human and Australopithecene teeth?

http://www.newscientist.com/article/dn4122-meat-eating-is-an-old-human-habit.html

You think we need these sharp, shearing teeth to eat bananas or whole grains?

No, they weren't 'ripe' by your definition. So, are you saying that in order to have a healthy vegan banana based diet, I have to eat only bananas at a specific level of ripeness? That we are adapted to a banana-based diet, but only if the bananas are at a specific level of ripeness? So that here we have an animals that is adapted to eating a diet consisting of 'ripe' bananas, but not somewhat ripe bananas?

I wonder how an animals could become so specialized in banana eating, but not tolerate bananas at all stages of ripeness?

And

Charles Grashow said...

Don said...
Chris,

You are right. Although the earliest evidence of grain consumption MIGHT be 20-30K years ago, grains didn't become staples, large enough part of diet to exert selective pressure, until about 12K, and that only in the Fertile Crescent area. At that time, most humans on earth still did not eat grain-based diets. Outside of that region, grain-farming has come even later, in some places (e.g. North America) not until about 1000 years ago, and when Europeans got here, there were still tribes not practicing agriculture, so that would mean some people only started eating grain-based diets in the last few hundred years. Even 12K years is not enough time to create significant genetic adaptations, especially since some of the diseases caused by grains (e.g. celiac) don't kill you before you have time to reproduce.

The Humane Hominid said...

Charles wrote:
So - does this mean we've evolved to eat meat, fruits, vegetables, grains, etc? Would this mean this a conscious decision to avoid meat is going against our evolutionary past?


It means this is, fundamentally, a stupid question.

Everything in nature changes, and nothing is optimized for our use. Even if hominins adapted to a diet with more meat, this by itself in no way implies that meat is healthy. If you think otherwise, then you have a cartoon understanding of evolution.

The point of the passage you quoted is that the fact we use a given trait for a given purpose does not mean the trait arose FOR that purpose, or BECAUSE of it. Most traits possessed by any organism are not adaptations to their particular circumstances, but inheritances that have either proved non-deleterious or have been co-opted for new uses. The classic example is feathers on birds. They enable birds to fly, but that's not what they're "for." Feathers pre-date flight by tens of millions of years. They're a trait that arose in response to other selective pressures, and later got co-opted.

There's good evidence that the changes in human-lineage diets were a consequence rather than the cause of the craniofacial and dental traits you cite. Specifically, they're likely caused by a mutation in the MYH16 gene, which codes for masticatory muscle robusticity in primates.

In other words, the changes came first, forcing the mutants born with them to find a solution compatible with their new morphology, or go extinct. That solution, in part, was possibly greater carnivory than other hominoids, but the jury is still out. In any case, the argument you lot tend to make -- that meat-eating led to these changes -- gets natural selection backwards. It borders on Lamarckism.

And even if you were right -- even if Homo adapted specifically to meat-eating -- this adaptation would only be a modification to older hominoid traits, not a nullification of them. A mechanical ability to eat meat better than other primates does not automatically make meat-eating healthy for us as individuals. In all likelihood, it would remain as bad for our long-term health as it is for that of the non-human primates, and continue to have the same atherogenic effects on us that it has on them. This is because nature is conservative, and would therefore only make changes that were adequate to the challenge, not perfect for them. A tweak to the teeth here, maybe, a twist to the gut there, but the underlying biochemistry would remain homologous with other hominoids. Natural selection doesn't care about your longevity or quality of life. It just wants you to make babies. If some mechanical tweaks in favor of meat-eating gave you the ability to survive on the savannah long enough to do that, then nature wouldn't mess with anything else about you. You'd just end up with a trait that improves your reproductive fitness, but still destroys your long-term health.

To put it bluntly, it's possible for humans to be adapted to meat-eating, and for meat-eating to still be bad for us. Which is why it's a stupid question.

Ben said...

According to the CDC (http://www.cdc.gov/nchs/data/dvs/lead1900_98.pdf), in 1900 the leading causes of death had cancer and heart disease at only about 13%. Today, they are expected to cause about 50% of all deaths.

Of course, life expectancy was lower then, but this was mainly a symptom of the greater chance that children would die rather than specific diseases.

So, did 19th Century Americans eat a lot less meat and dairy? Did they eat a more vegetarian diet? Or did it have more to do with activity levels and the fact that more food was local, homemade, without preservatives and pesticides, etc.?

nothing91 said...

Jack,

"Well, is the study good or isn't it? Did the study find that the greater the "egg yolk years", the lower the TC and LDL, or didn't it? Is stroke a thrombotic disease or not?"

Only the parts of the study which support their black-and-white view of nutrition are "great". The rest they just ignore.

This is, of course, the only way a person can maintain such an absolutist stance on something as complex and intricate as nutrition -- ignore contrary evidence. Don and Peter are experts at it. :-)

healthy-longevity said...

I’m not sure why those people who ignore everything that I said somehow think that they are in a position to refer to Don and Peter as being ignorant.

The cholesterol skeptics often claim that this cholesterol paradox observed in cross-sectional studies refutes evidence from hundreds of carefully conducted feeding trials that have firmly established the relation between diet, including dietary cholesterol and serum lipids. This paradox may largely be explained by dietary changes, as was observed in the Chicago Western Electric Company study below:

Dietary lipids and serum cholesterol level: change in diet confounds the cross-sectional association.

Shekelle RB, Stamler J, Paul O, Shryock AM, Liu S, Lepper M.

In the Chicago Western Electric Company study, diet was assessed at the initial examination, in 1957-1958, of 1900 middle-aged men and again at their second examination about one year later. At the first examination, lipid composition of the diet, as summarized by a score based on the formula of Keys, Anderson and Grande, was positively associated with level of serum cholesterol. Between the first and second examinations, however, hypercholesterolemic men were more likely than others to have reduced intake of dietary saturated fatty acids and cholesterol. As a result, at the second examination the cross-sectional linear association between the diet score and serum cholesterol concentration was significantly positive for men with initial levels of serum cholesterol less than 250 mg/dl, significantly negative for men with initial levels of 250 mg/dl or higher and not significantly different from zero for all men together. The bias introduced by change in diet among hypercholesterolemic men differs importantly from bias due to unreliability of measurement and to interindividual differences in intrinsic level of serum cholesterol, because it can produce statistically significant but spurious correlations.

Jack LaBear said...

"Health-longevity",

It is only a paradox from the view of your your paradigm.

Charles Grashow said...

http://www-bcf.usc.edu/~stanford/chimphunt.html

The Predatory Behavior and Ecology of Wild Chimpanzees

"At Gombe, we now know that chimpanzees may kill and eat more than 150 small and medium sized animals such as monkeys, wild pigs and small antelopes each year."

Don said...

"The cholesterol skeptics often claim that this cholesterol paradox observed in cross-sectional studies refutes evidence from hundreds of carefully conducted feeding trials that have firmly established the relation between diet, including dietary cholesterol and serum lipids. "

It seems that for the cholesterol skeptics, epidemiological evidence is junk when it suggests that dietary or elevated serum cholesterol is harmful (e.g. China study). When this happens, they chant "correlation is not causation."

On the other hand, they seem also to believe that epidemiological evidence can trump controlled feeding trials when a particular report of epidemiogical evidence seems to them to suggest dietary and high serum cholesterol are harmless. When they see this type of report, they seem to forget that correlation does not establish causation.


Healthy-Longevity, I am not sure why they can't understand your point that what a species does as a matter of fact (e.g. chimps killing and eating animals) does not establish that the species is physiologically adapted to that practice.

Perhaps this will help:

Humans can and do smoke tobacco. Millions do every day, every year. Probably humans smoke hundreds of millions of cigarettes every year. This doesn't serve as evidence that humans are physiologically adapted to smoking tobacco.

Simply, an individual of any species, and even large numbers of members of any species, can adopt a behavior that is incompatible with the animal's basic physiology, and thereby incur disease.

The Humane Hominid said...

Din wrote: Simply, an individual of any species, and even large numbers of members of any species, can adopt a behavior that is incompatible with the animal's basic physiology, and thereby incur disease.

It's more than that, Don! A whole species can actually adapt to a situation that's incompatible with their basic physiology, and it will remain incompatible with their basic physiology, despite the adaptation. And the adaptation itself can come with pretty severe burdens, too.

Look at sickle cell anemia and the various thalassemias. They're adaptations to malaria, but still have pretty devastating consequences, especially for recessive homozygotes. But the traits are retained because they provide a measure of resistance to an even more devastating selection pressure. Nature did not engineer a perfect solution; it just jerry-rigged an adequate one.

So it could very well be true that H. sapiens adapted to more meat than other primates. But that still doesn't make meat good for us.

Charles Grashow said...

@Peter

You said - "More evidence for lowering LDL to below 70 (2011)

"LaRosa, who wrote an editorial [3] accompanying Lee's study, expanded on his views to heartwire: "I used to be skeptical about the idea of trying to achieve very low cholesterol levels, but now I am more accommodating. As cholesterol levels are coming down, we are seeing much lower rates of bypass surgery and elective angioplasty. I think elective angioplasty will eventually disappear altogether."

"Chimpanzees eat very little fat. They have LDL levels in the range of 40 to 70, and they don't get atherosclerosis. He noted that levels of LDL below 70 are on a par with those of nonhuman primates who don't develop atherosclerosis, adding that, like these primates, humans were designed to be vegetarians. "Our dental anatomy suggests that we are not meant to be meat eaters. Animals that eat meat have sharp tearing teeth, while we have flatter teeth more similar to vegetarian animals. I believe humans are not anatomically or metabolically designed to be meat eaters, and because we do consume animal fat that's why we get atherosclerosis. Chimpanzees don't eat meat; they eat very little fat. They have LDL levels in the range of 40 to 70, and they don't get atherosclerosis. Maybe we wouldn't get atherosclerosis either if we had levels this low."

BUT


http://www-bcf.usc.edu/~stanford/chimphunt.html

The Predatory Behavior and Ecology of Wild Chimpanzees

"At Gombe, we now know that chimpanzees may kill and eat more than 150 small and medium sized animals such as monkeys, wild pigs and small antelopes each year."


SO - chimpanzees DO EAT MEAT - yet according to you they have LDL between 40-70

But Don said

"Healthy-Longevity, I am not sure why they can't understand your point that what a species does as a matter of fact (e.g. chimps killing and eating animals) does not establish that the species is physiologically adapted to that practice."

Very Very confusing

The Humane Hominid said...

@ Charles
SO - chimpanzees DO EAT MEAT - yet according to you they have LDL between 40-70

Hardly surprising, since chimps share many lipid-eating parasites with humans.

Very Very confusing

Well, maybe you should learn about evolution. It'll make sense to you then.

Adaptations aren't necessarily healthy. If they give you a slight edge in reproductive success, they will be preserved, even if they hurt you in other ways.

Peter said...

@Charles,

like HumaneHominid pointed out there's important co-founders that are neglected by creationists/intelligent desing -folk.

You can also be sure that chimps do not entertain themselves with steaks, eggs and other animal products on every meal they touch four-five times a day. Their overall diet pattern is vegeterian dominated by fruits.

Charles Grashow said...

@Don

http://www.birminghamchinesemedicine.co.uk/diet.html

http://www.birminghamchinesemedicine.co.uk/practitioners.html

General advice on diet in Chinese Medicine is guided by the importance of maintaining a strong Spleen and avoiding the development of Damp. A preventative diet would therefore emphasise:

relatively large amounts of grains, including rice, bread, pasta (rice is particularly good because it is easily digested and slightly encourages urination, which helps to reduce Dampness) or other complex carbohydrates eg potatoes.


relatively large amounts of lightly cooked vegetables.


moderate amounts of fruit (if there is a digestive weakness then stewed fruit might be better, and concentrated fruit juices are to be avoided).


moderate amounts of animal protein (beef, pork, lamb, chicken, fish, seafood) and eggs. (Most people would be OK with 2 oz meat 3-4 times a week)


very moderate amounts of dairy products (cheese, milk, cream, butter), oils and refined sugars. The more the person is affected by Dampness, the less of these should be consumed.


spices (eg pepper, ginger, cinnamon, nutmeg, mace, cardamom, cloves) have a warm and pungent quality, hence they assist digestion and help to reduce Dampness. Garlic is very good for the same reason.

SO - animal products are allowed in small amounts.

What say you Don.

Jack LaBear said...

Alright, it is time to deal with this "creationists/intelligent design -folk" bullshit.
The fact that you not so cleverly attempt to ad hominem all people who don't agree with your point of view as being grossly deluded and unscientific is just evidence that you don't have any logical leg to stand on.

I can play that game too. LaRosa et al:
"Our dental anatomy suggests that we are not meant to be meat eaters"
What is "meant to be" supposed to mean? Divine intent? That phrase is a tell-tale sign of a supernatural belief.

Charles Grashow said...

BTW - I'll bet that Don will be on the 30 bananas a day diet by sometime next year

Check out his wife's blog with the banana photos.

http://thefoodway.blogspot.com/2012/08/the-last-two-days-we-upped-our-fruit.html

Jack LaBear said...

"Blue jays are largely vegetarian birds. Most of their diet is composed of acorns, nuts, and seeds..."

Therefore, although eagles survive on their all meat diet long enough to reproduce, they would be much healthier if they also ate a vegetarian diet composed of acorns, nuts, and seeds. After all, they are both birds!

That's about how meaningful are these primate studies cited above by the "meant to be" folks.

Charles Grashow said...

http://ajcn.nutrition.org/content/80/5/1175.full?ijkey=87bd7ab2417a32a9ca32b1a83c2d63a8266b0f43

Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women

Conclusions: In postmenopausal women with relatively low total fat intake, a greater saturated fat intake is associated with less progression of coronary atherosclerosis, whereas carbohydrate intake is associated with a greater progression.

http://high-fat-nutrition.blogspot.com/search/label/Arteriosclerosis%20and%20saturated%20fat

http://ajcn.nutrition.org/content/80/5/1175/T1.expansion

On the raw data a high intake of saturated fat didn't quite reverse the women's arteriosclerosis, but after modeling it did. Modeling appears to involve adjusting your results to estimate what the values would have been if your patients didn't smoke, didn't have diabetes, didn't eat cholesterol (gasp) etc.

Glancing through the patient characteristics in table 1 you can see why adjustment might be needed.

Look at smoking. The high saturated fat group had the highest percentage of smokers and a hugely higher pack-years value (34 pack-years) than any other group (all below 18). They boozed the most, ate most trans fats and pooped the least fibre. They may even, wait for it, have eaten an egg a day! On the plus side they obviously had the highest HDL cholesterol and lowest triglycerides, because they also ate the least carbohydrate.

If you had to describe this group in one word it would have to be "naughty". These naughty people did all the WRONG things (according to the AHA) and, after adjustments, began the reversal process of their IHD. Thumbing your nose at the AHA, even in this mild manner (by my standards), looks to be good for you.

The lowest saturated fat group had the highest carbohydrate intake, let's call them the Goody Goodies. They made excellent progress as coronary bypass fodder.

The Humane Hominid said...

@ Jack La Bear:

Nope, dead wrong. Nice straw man, though.

An argument from our side equivalent to the straw man you've constructed would be "lions and cows are both mammals, therefore lions should be vegetarian." But that's clearly not what we're saying at all.

Blue jays and eagles may both be "birds," but they are members of completely different bird lineages who had to overcome very particular selection pressures. They are about as homologous to each other within the "birds" as lions and cows are within the mammals.

Our argument -- or at least, mine, since I don't presume to speak for Don or healthy-longevity -- is a lot more specific than "lions and cows are both mammals..."

The point isn't that lions and cows are both mammals, but that humans are nested within the hominoid clade, and as such share a great deal of physiology, biochemistry, anatomy, and morphology with other members of this particular group of primates.

Evolution predicts that the shared derived features of a clade will affect all members of that clade in similar ways, because of their recent common ancestry. It predicts that the things which induce atherosclerosis in other hominoids probably do so in us, and for the same reasons. The same lipid-eating parasites that co-evolved with them also did so with us, and therefore have similar effects on us.

This isn't about what we're "meant" to do; such talk is meaningless in biological terms. It's about what trade-offs our shared derived hominoid features impose on us.

This is why primate studies -- especially those that focus on the hominoids -- are relevant, and why they undermine the paleo/creationist diet paradigm. To argue that humans aren't burdened by highly similar trade-offs as other hominoids is to argue that evolutionary theory has no predictive power. It is a denial of evolution, implicitly rejecting what it explicitly seeks to co-opt.

If humans aren't hominoids, then evolution is false. Your argument implicitly denies this hominoid heritage, and it therefore rejects evolution itself. That's why it's appropriate to call your position creationist.

nothing91 said...

Jack,

"Alright, it is time to deal with this "creationists/intelligent design -folk" bullshit."

Actually I think we were all having fun ignoring it. That's why they keep mentioning it over and over again -- they're just trying, desperately, to get a rise out of someone. They're basically 50% troll, 50% clueless nutritionists. :-)

The Humane Hominid said...

Oops, I forgot to mention Peter. I don't presume to speak for him, either.

Sorry, Peter.

Peter said...

@HumandeHominid

Your postulation was top-snotch. I whole heartedly agree. I, in fact, wrote the following already in my first contribution to this thread:

"Great study. I have great respect for Spence and Jenkins. Unfortunately the creationists of the food debate are back with their anti-science assaults as usual. Well, actually the attackers are simply creationists while opposing SFA and dietary cholesterol link to heart disease. That's directly a step away from the Darwinian foundation of biomedical research".

It's been clear to me since day one that we are dealing with religious, anti-science fanatics here. Paleo dietary philosophy = Intelligent Desing. I wouldn't mind critisism directed for Spence and Jenkins had they established something revolutionary in their new study, but since they only confirmed what is to be expected, I cannot but perceive the critisism as religious denialism.

Jimmy Gee said...

I think all of these vegan comments are laughable. This level of defense over an article with serious flaws really illustrates the depths that militant vegans go to. If you want to be a vegan - be a vegan - just show people you have half-a-brain and admit that this study is ridiculously flawed. So many others (without ties to the statin industry) see this study for what it is - biased as well as poorly executed.

Charles Grashow said...

http://nutsci.org/2012/08/15/scrambled-messages-about-eggs/

http://nutsci.org/2010/04/23/the-incredible-egg/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2386667/

Charles Grashow said...

nutritional advice per the new Don

http://donmatesz.blogspot.com/p/primal-diet-guide.html


Eat


1. Whole cereal grains and whole grain products (rice, bread, pasta, pastries, etc.) and grain-like seeds of dicot plants (quinoa, amaranth, buckwheat, teff, etc.
2. Legumes (beans and peas, including soy and peanuts)
3. Vegetables, herbs, and spices, including roots, bulbs, stems, leaves, fungi (mushrooms), and algae (sea vegetables) mostly cooked.
Emphasize green leafy vegetables because these have the highest nutrient density of any foods, including a high protein content.
Eat as wide a variety as possible.
Proper cooking increases net nutrient delivery.
4. Fruits and berries

Condiments

In no particular order. Be sparing with use of the nuts, seeds, olives, and avocados if you wish to lose body fat.

1. Nuts and seeds (almonds, coconuts, walnuts, hazelnuts, pecans, brazil nuts, macademias, pumpkin, sesame, sunflower, hemp, etc.)
2. Whole olives and avocados
3. Herbs and spices.
4. Plant-sourced sweeteners, including cane sugar, maple syrup, rice syrup, agave syrup, etc.
5. Salt
5. Traditionally fermented soy products: soy sauce, miso, tamari, etc.

Supplements

1. Vitamin B12 or foods fortified with vitamin B12.

In modern circumstances, a vegan diet has only one nutritional weakness, a shortage of vitamin B12, which has arise due to modern agricultural and sanitation practices that destroy the vitamin B12 producing microbes that would in nature colonize the soil and enrich plants and water with vitamin B12. Thus, modern vegans should take steps to ensure vitamin B12 intake through fortified foods or supplements.

To get adequate vitamin D, everyone should get regular moderate sun exposure.

Occasional

1. Refined grain products

Avoid

1. All types of fish, eggs, poultry, dairy products, and red meat, and products thereof (lard, tallow, butter, etc.) no matter the feeding strategy.
2. Separated fruit or nut oils (olive, avocado, coconut, palm, almond, etc.), oil seeds and seed oils (corn, safflower, sunflower, sesame, hemp, etc.)
3. Any food to which you have an allergic reaction.

Jack LaBear said...

@ nothing91

I stand corrected ;-)

Jack LaBear said...

Gunther-Gatherer said

"Your assignment is to look up Correlation and Causation and recite them aloud for our next class."

I did better than that and will recite a class on interventional studies attempting to show CVD benefit by lowering saturated fat.

First, Don challenged us to find a single study showing CVD benefit for eating cholesterol. I pointed out that the smoking egg study met that criterion, but that was just observational. The studies that I am going to present out loud manipulated saturated fat and most will agree that cholesterol is present in animal fat. So here is an interventional one:

Frantz et al (1989). Test of effect of lipid lowering by diet on cardiovascular risk. The Minnesota Coronary Survey
Outcome: After 4.5 years, no reduction in cardiovascular events or total deaths from the treatment diet, with a non-significant trend towards a benefit to a high saturated fat diet. Results observed despite a 14.5% reduction in cholesterol levels in the experimental group.
• Overview: 4.5 year, double-blind, randomized trial in 6 Minnesota state mental hospitals and one nursing home involving 4,393 men and 4,664 women, examining effects of a lipid lowering diet on heart disease.
• Main Points: Intervention: 38% fat diet (9% Saturated fat, 15% polyunsaturated fat, 14% monounsaturated, 166 mg cholesterol); Control diet: 39% fat diet (18% saturated fat, 5% polyunsaturated fat, 16% monounsaturated fat, 446mg cholesterol) Intervention group cholesterol levels decreased 14.5% and were stable for the entire study. Control and intervention foods were indistinguishable from each other.
• Comments: Rare double blind dietary clinical trial. Average total time in hospital for each subject was 384 days. The number of person years observed was 9,538, with 5,903 of these years continuously for more than 2 years and 2,495 for more than 4 years. Cholesterol diet did not seem to be effective, although average hospital stay was only 1 year.

Notice that the control diet had almost 3 times as much cholesterol (280mg/day more), and the intervention group had 14.5% lower cholesterol, yet there was a “trend towards a benefit to a high saturated fat diet”.

This one showed a trend for all cause mortality benefit for a high saturated fat and high cholesterol diet, despite the fact that the control group smoked more and had less hypertension treatment:

Frantz et al (1989). Test of effect of lipid lowering by diet on cardiovascular risk. The Minnesota Coronary Survey
Outcome: After 4.5 years, no reduction in cardiovascular events or total deaths from the treatment diet, with a non-significant trend towards a benefit to a high saturated fat diet. Results observed despite a 14.5% reduction in cholesterol levels in the experimental group.
• Overview: 4.5 year, double-blind, randomized trial in 6 Minnesota state mental hospitals and one nursing home involving 4,393 men and 4,664 women, examining effects of a lipid lowering diet on heart disease.
• Main Points: Intervention: 38% fat diet (9% Saturated fat, 15% polyunsaturated fat, 14% monounsaturated, 166 mg cholesterol); Control diet: 39% fat diet (18% saturated fat, 5% polyunsaturated fat, 16% monounsaturated fat, 446mg cholesterol) Intervention group cholesterol levels decreased 14.5% and were stable for the entire study. Control and intervention foods were indistinguishable from each other.
• Comments: Rare double blind dietary clinical trial. Average total time in hospital for each subject was 384 days. The number of person years observed was 9,538, with 5,903 of these years continuously for more than 2 years and 2,495 for more than 4 years. Cholesterol diet did not seem to be effective, although average hospital stay was only 1 year.

Jack LaBear said...

Ad-Hominid wrote; “You are dead wrong”

That’s funny, I don’t feel dead.
I’m 55 years old, I eat 3000mg cholesterol a day, My TC is 185, HDL 85, trigs 50 and I have the delusion I’m not dead and actually feel great. What’s up with that?
Wait, I forgot. I’m a creationist, so I must be in Heaven!
Well, guess I don’t need to worry about what to eat anymore.

“Clades as constructs.
In cladistics, the clade is a hypothetical construct based on experimental data.”
I believe I have presented some pretty good experimental data.

“Cladistics, either generally or in specific applications, has been criticized from its beginnings. Decisions as to whether particular characters are homologous, a precondition of their being synapomorphies, have been challenged as involving circular reasoning and subjective judgements.”

Hmmm, circular reasoning and subjective judgements. Why does that sound so familiar?

Don said...

Humane Hominid,

Thanks for not speaking for me, and I completely agree with the central point:

"...that humans are nested within the hominoid clade, and as such share a great deal of physiology, biochemistry, anatomy, and morphology with other members of this particular group of primates."

Jack,


Most of the cholesterol in animal tissues is in the muscle, not the fat, because cholesterol is part of muscle cell membranes.

The study you cite replaced animal fats with vegetable oils, in order to maintain similar fat intakes (38-39%). Thus, at most it shows an undesirable effect of a diet high in vegetable fats even in the presence of a reduced cholesterol intake.

What did the authors of the original study say? Here it is:

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CCsQFjAB&url=http%3A%2F%2Fatvb.ahajournals.org%2Fcontent%2F9%2F1%2F129.full.pdf&ei=xB1BUM2TI-GyyAGv1oGoBg&usg=AFQjCNGJYY0JflJQGLj8QmH0GcoBMt85kQ

Don said...



In their abstract:

"For the entire study population, no differences
between the treatment and control groups were observed for cardiovascular events,
cardiovascular deaths, or total mortality. A favorable trend for all these end-points
occurred In some younger age groups."

How did they make this blinded?

"Products that
proved particularly useful were filled milk and ice cream, a
whole egg substitute, soft margarine, whipped topping,
filled cheese, low fat ground beef with added vegetable
oil, and filled sausage products."

They also say:

"When the study was initiated, we suspected that any
favorable outcome would be confined to the younger
participants in most of whom severe atherosclerosis would
not yet be present. It also seemed likely that a fair length
of time would be required for the diet to exert an effect. In
two recently reported drug trials, the Lipid Research Clinics Primary Prevention Trial67 and the Helsinki Heart
Study,8 2 years were required before favorable trends
appeared. Therefore, it is of some interest to look for
trends in persons on the diets for at least 2 years who fell
in the age ranges chosen for those studies (35 to 59 and
45 to 55 years old, respectively). Such an analysis is
presented in Table 6. If total time in hospital including
multiple admissions is counted in arriving at the numbers
on the diets for more than 2 years, only one more death
and no more cardiovascular events are identified in the 35
to 59 year age group. In men younger than 50 years, there
were three events and two deaths in the treatment group.
In the control group, there were 11 events and 12 deaths."

"Although this study did not show a statistically significant
reduction in cardiovascular events or total deaths
from the treatment diet, the authors suspect that it might
have shown such a reduction if the period of treatment
had been longer in persons in the age range likely to
benefit. We included persons of all ages, both men and
women, with an average cholesterol concentration of 207
mg/dl, compared to about 290 mg/dl for the participants in
the Helsinki and Upid Research Clinics trials. When the
study was first proposed, very lengthy stays in mental
hospitals were common. By the end of the initial 3-year
pre-treatment observation period, the practice of vigorous
drug treatment and early discharge to the community was
in full swing."

"Table 6, in which the analysis is confined to persons
on diet for at least 2 years and in the age groups chosen for recent drug trials, shows some favorable trends, but
the numbers are far too small to achieve statistical
significance."

So the study has a major problem admitted by the authors, which is that people were not continuously on the study diet, but intermittently as they were not continuously hospitalized. Further, most of the people weren't on the diet long enough to produce a benefit. Finally, when the authors limited analysis to the people who were on the diet at least 2 years, the trend was toward a benefit of the intervention, despite the intervention being high in refined foods and fats.

A good example of how a piece of research is incompletely presented and somewhat twisted by "skeptics" to support their views.

Don said...

Check out Table 2 in Frantz et al and you will also see that the intervention diet supplied about 95-100 g protein per day, and 1.2 g calcium; which means that the intervention group was getting plenty of reduced-fat milk and egg products, containing plenty of animal protein. The intervention was primarily accomplished by reducing intake of egg yolks and milk fat, while allowing 166 mg of cholesterol from meat, which is about 4 ounces of meat daily. This was not a plant-based intervention, it was an attempt to reduce heart disease risk by substituting modified milk, egg, and meat products for the usual. They were "filled" with vegetable oils.

The Humane Hominid said...

@Jack,

Cut-n-pastes from Wikipedia, in an effort to hand-wave away an entire field of study they clearly do not understand, is also a classic creationist tactic.

The Humane Hominid said...

I believe I have presented some pretty good experimental data.

Belief is irrelevant, Jack. If you have experimental data demonstrating that humans are not hominoid primates, I suggest you get your work published at PLOSOne, or in Nature, or in a physical anthropology journal. Or, just contact your local university.

There's a Nobel Prize in your future!

Jack LaBear said...

MRFIT Research Group (1982). Multiple Risk Factor Intervention Trial (MRFIT)
Outcome: After 7 years, mortality from CHD was 17.9 deaths per 1,000 in the intervention group, and 19.3 per 1,000 in the control group, a non-significant difference of 7%. Total mortality rates were 41.2 per 1,000 in the intevention group and 40.4 per 1,000 in the control group, also not significantly different.
• Overview: Randomized primary prevention trial testing effects of multi-factor intervention on mortality from coronary heart disease (CHD) in 12,866 high-risk men aged 35-57, in which men were randomized to either the special intervention (SI) or the usual care (UC) for a mean time of seven years
• Main Points: The Special intervention (SI) consisted of: stepped-care treatment of hypertension, counseling for cigarette smoking, and dietary advice for lowering blood cholesterol levels. The dietary advice consisted of: reducing saturated fat intake to less than 10% of calories (later changed to <8%), dietary cholesterol intake < 300mg (later changed to < 250mg). Usual care (UC) consisted of their usual source of healthcare in their community.
• Comments: One of the largest clinical trials ever examining dietary interventions and CHD. There were 2 other major co-contaminant interventions — hypertension treatment and smoking cessation. After 2 years on the cholesterol lowering diet blood cholesterol in the SI and UC groups decreased by 10 mg/dL and 3.4 mg/dL respectively. After 6 years, the mean levels were reduced by 12.1 mg/dL and 7.5 mg/dL. This decrease was 50% less than the researchers hoped for. However, with blood pressure medications, smoking cessation counseling, and a decrease in blood cholesterol levels, it is surprising that there were no significant CHD differences between the groups.

There have been 2 interventional studies that meet the following criteria:
1) The only significant intervention involved a reduction in fat and saturated fat and an increase in polyunsaturated fats
2) They ask the question: does this diet reduce heart disease? (defined as heart attacks or death from heart disease)

Women’s Health initiative (2006) – 48,835 women, 8 years, no significant difference between intervention and control.

Diet and Reinfarction trial (1989) – 2,033 men, 2 years, no significant difference between the groups given and not given fat and fiber advice. No significant differences in ischaemic heart disease between intervention and control (intervention was only advice in this trial)

Before you accuse me of cherry picking studies, how about a meta-analysis from one of your beloved expert panels?

In 2009, the Cochrane Collaboration, an international not-for-profit organization, published a meta-analysis of clinical trials that either reduced or modified dietary fat for preventing cardiovascular disease. Twenty-seven studies met the inclusion criteria, and no significant effect on total mortality (RR = 0.98, 95% CI: 0.86-1.12) or cardiovascular mortality (RR = 0.91, 95% CI: 0.77-1.07) was found between the intervention and control groups

Is that loud enough for you Gunther?

Jack LaBear said...

Don Wrote,

Jack,

Most of the cholesterol in animal tissues is in the muscle, not the fat, because cholesterol is part of muscle cell membranes.

Me:
The study says that cholesterol intake in the intervention group was 166mg/d and in the control group it was 446mg/d.

Jack LaBear said...

Don Wrote,

Jack,

Most of the cholesterol in animal tissues is in the muscle, not the fat, because cholesterol is part of muscle cell membranes.


Me:
The USDA nutrient database says that raw beef fat contains 99mg cholesterol/100g while raw beef chuck contains 67mg colesterol/100g

Charles Grashow said...

http://www.update-software.com/BCP/WileyPDF/EN/CD002137.pdf

The WHOLE 218 page study!

Authors’ conclusions

The findings are suggestive of a small but potentially important reduction in cardiovascular risk on modification of dietary fat, but not reduction of total fat, in longer trials. Lifestyle advice to all those at risk of cardiovascular disease and to lower risk population groups, should continue to include permanent reduction of dietary saturated fat and partial replacement by unsaturates. The ideal type of unsaturated fat is unclear.


Plain Language Summary

Cutting down or changing the fat we eat may reduce our risk of heart disease

Modifying fat in our food (replacing some saturated (animal) fats with plant oils and unsaturated spreads) may reduce risk of heart and vascular disease, but it is not clear whether monounsaturated or polyunsaturated fats are more beneficial. There are no clear health benefits of replacing saturated fats with starchy foods (reducing the total amount of fat we eat). Heart and vascular disease includes heart attacks, angina, strokes, sudden cardiovascular death and the need for heart surgery. Modifying the fat we eat seems to protect us better if we adhere in doing so for at least two years. It is not clear whether people who are currently healthy benefit as much as those at
increased risk of cardiovascular disease (people with hypertension, raised serum lipids or diabetes for example) and people who already
have heart disease, but the suggestion is that they would all benefit to some extent.

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

@Jack,

you sources are not well-focused interventions. In the WHI-trial f.ex, the intervention group, those who received the 20-min counselling and no monitoring, took 3/4 of their protein from animal sources. They also had equally low-fiber intake, 16g per day. There was no difference in LDL in the intervention group next to the control group. It was the same carnivoric, low-fiber dietary context.

Jack LaBear said...

Peter,

Your criticism is too focused. There are many studies with the same result, including the Cochrane Collaboration meta-analysis.

healthy-longevity said...

The Corchrane Collaboration found a 14% lower risk of cardiovascular events in the fat modification group, for which subgrouping suggested that this reduction was related directly to the effect on serum total and LDL cholesterol and TG, and a duration of at least two years. The lack of reduction of cardiovascular events in the reduced fat group could largely be explained by a much smaller reduction in serum and LDL cholesterol, suggesting a lack of sufficient dietary changes or adherence to the dietary recommendations.

Jeremiah Stamler provided a more informative description of the results of the WHI in his editorial that is simply ignored by virtually all cholesterol skeptics, as perhaps they find it too difficult to explain why saturated fat was associated with a 32% increased risk of CHD mortality despite the inclusion of over-adjustments for dietary and serum lipids which would have attenuated this finding.

“This section discusses the Women's Health Initiative Trial uncritically, without attention to key aspects or implications of design and findings. That trial primarily explored the effects of low total fat on breast and colon cancer, not the effects of improved dietary lipid composition on CHD; reported improvements in dietary lipid composition by the intervention group were small; improvements in total and LDL cholesterol, BP, and so forth were miniscule or nil, yielding nonsignificant effects on CHD (predictably)—eg, for a combined “hard” CHD endpoint [in women without baseline cardiovascular disease (CVD) history], the hazard ratio for the intervention group was 0.94 (95% CI: 0.86–1.02). As Howard et al have noted, “Trends toward greater reductions in CHD risk were observed in those with lower intakes of saturated fat or trans fat or higher intakes of vegetables/fruits.” The investigators concluded that “more focused diet and lifestyle interventions may be needed to improve risk factors and reduce CVD risk”. This inference is concordant with extensive data that show CHD rates lower by 90% and life expectancy years longer for the small minority of adult Americans with favorable levels of the 4 readily measured diet-dependent major CHD risk factors [total cholesterol, BP, body mass index (BMI), glycemia/diabetes] and nonsmoking status.”
http://ajcn.nutrition.org/content/91/3/497.full

A meta-analysis of 108 randomized controlled trials of diet and various medical based lipid modifying interventions found that lowering LDL cholesterol significantly decreased the risk of coronary heart disease and all-cause mortality, while modifying HDL or triglycerides provided no clear benefit after controlling for LDL cholesterol.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/

Perhaps if the cholesterol skeptics did not have such a sevre case of confirmation bias, it would be relatively easy to find numerous examples of them describing the results of the two major papers I provided links to, as well as demonstrating that they do not always change the topic when presented with these findings.

Charles Grashow said...

If the goal is to lower LDL levels to the lowest levels possible (<70 or <50) why not go on an all fruit diet - ala Douglas Graham 80-10-10?


Fruitarian Blood Work

to convert mmol/l to mg/dl
http://en.mte.cz/conversion.php?mmol=1.4&mg=&count_it=1

http://eatfruitfeelgood.com/2010/06/14/blood-test-results-in/

total cholesterol = 66.6
ldl cholesterol (calculated) = 29.88
hdl cholesterol -= 25.02
cholesterol/hdl ratio = 2.66
triglycerides = 25.56

http://livingonfruit.blogspot.com/2011/02/my-personal-blood-test-results-released.html

total cholesterol = 82.8
ldl cholesterol = 46.8
hdl cholesterol = 25.2
cholesterol/hdl ratio = 3.27
triglycerides = 16.2

http://eatmorerawfoods.com/2012/05/blood-test-results-on-low-fat-raw-vegan-diet-2012/

Here are LDL levels below 50 and total cholesterol 80 or below

Why not try an N=1 experiment - get lipid levels checked and go on this type of diet for 6 months to a year and then retest your lipids?

Charles Grashow said...

LOW Cholesterol: The Risks, Dangers & The Reality

http://metabolichealing.com/key-integrated-functions-of-your-body/cardiovascular/low-cholesterol-the-risks-dangers-and-the-reality/

"Low Cholesterol & Autoimmune Disease

Numerous studies on various autoimmune diseases note the prevalence of low cholesterol values in autoimmune processes. THIS study reveals that total cholesterol and LDL were significantly decreased in the 5 years before RA diagnosis.
Other studies such as THIS one cites the prevalence of low cholesterol is Sjrogren's. THIS study identifies low cholesterol in type 1 diabetes. THIS study identifies low cholesterol, LDL and lipid values in Crohn's Disease.
The implication that I derive from these correlations is that because cholesterol is anti-inflammatory, decreases in cholesterol production is associated with a higher susceptibility to oxidative stress, infections, inflammation and free radical damage. To say that an autoimmune patient suffers from these is an understatement."

"Low Cholesterol, Toxicity & Infections

Cholesterol is an essential component for bile synthesis. Bile contains conjugated toxins from the liver's detoxification pathways. Inadequate bile production is strongly associated with toxicity and liver distress.
Studies such as THIS have shown that LDL cholesterol has the capability of reducing pathogens and infectious bacteria. Endotoxins from gram negative bacteria bind to LDL particles. When bound to LDL, they are inactivated. Additionally, when endotoxins are bound to LDL, the toxins are unable to trigger the production of pro-inflammatory cytokines such as TNF-a. Therefore if there is insignificant cholesterol and LDL, a person may be at an increased risk for infection"

Charles Grashow said...

@Don

So you wrote this

TUESDAY, JUNE 14, 2011
Farewell To "Paleo"

Yet on 8/12/2011 - two months AFTER SAYING FAREWELL TO PALEO you ate this

http://donmatesz.blogspot.com/2011/08/some-recent-meals.html

On August 12, I had the meal below. Two grass-fed beef burgers, one raw and one cooked, about 8 ounces total.

On August 22
A couple hours later, I had the plate below with about 4 ounces of leftover cod

Later that same day I had two plates of food. The first has a ~4 ounce turkey burger under that pile of wilted onions

Then I had the second plate: another turkey burger and onions

SO - 2 months after quitting paleo you were eating RAW MEAT!!

Don said...
eimearrose,

I only eat raw grass-fed meat from two suppliers. I won't eat grain-fed meat raw, because grain-fed carries more pathogens, including multiple antibiotic resistant pathogens.

http://donmatesz.blogspot.com/2011/04/conventional-meat-may-contain-mar.html


I purchase it frozen (freezing kills some pathogens). I typically put raw garlic, cumin, chili powder, and a small amount of olive oil in the meat and let it marinate a while before eating it. I don't think there is any special benefit to eating raw meat, in fact research suggests the meat protein is less digestible when raw, but I just like some raw meat now and then.
August 25, 2011 4:10 PM

Don said...
Soccer Guro,

I need ~2500 kcal per day typically, but don't always hit that mark. My macronutrient ratios fluctuate a bit depending on whether I eat more nuts/olives/avocados or more starch/fruit in any day, but it ranges around about 15-20% protein, carbs fluctuating from 35-50% and fats from 30-45%, mostly from nuts, olives, and avocados. Carbs are from 225 g to 300 g per day, but I find the high end a bit much to digest (volume) from whole foods.
August 25, 2011 6:51 PM

SO - now 1 year later you're going to a raw food/fruit diet

Sounds like a very confused person to me!



Liz said...

GOD I have NO IDEA what to eat to be healthy, or healthier. There is so many contradicting evidence. What do you do? WHAT DO YOU DO!! I've been eating mainly lots of spinach, leafy greens, rice,peppers,jalapeño, tomatoes, small amounts of whole bread and high fiber pasta, beans, cabbage, some chicken, fruit, some oatmeal, some tubers, organic olive oil in small amounts, small amounts of soy meat, this week I was experimenting with boiled eggs. I feel not good. My energy is bad, im still somewhat overweight, my chest annoys me, Definitively slow elimination. I dont know what to do. Will I have to experiment? Why in the world havent we come to a conlusion to something so vital like.. NUTRITION. omg