Malhotra's Study from India (1960) 19 times more animal fat 7 times less heart disease

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"Epidemiology of ischaemic heart disease in India with special reference to causation.", S L Malhotra, Br Heart J. 1967 Nov; 29(6): 895–905. Old study but very memorable. S.L. Malhotra analyzed statistics of 1.15M employees of India Railways from 88 Railway company owned hospitals for the employees and their families. He found that the Southern employees consumed 19 times less animal fat than the Northern India, smoked 1/10-th of the cigarettes, ate less sugar - and had 7 times higher rate of ischaemic heart disease!

animal fat is low cardio vascular risk, carbs are high risk

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A 2016 Czech study of 42 European countries

"Food consumption and the actual statistics of cardiovascular diseases: an epidemiological comparison of 42 European countries", by Pavel Grasgruber,* Martin Sebera, Eduard Hrazdira, Sylva Hrebickova, and Jan Cacek; Food Nutr Res. 2016; 60: 10.3402/fnr.v60.31694.

Quote:

The mean consumption of 62 food items from the FAOSTAT database (1993–2008) was compared with the actual statistics of five CVD [CVD=Cardio-Vascular Disease] indicators in 42 European countries. Several other exogenous factors (health expenditure, smoking, body mass index) and the historical stability of results were also examined.
...

The most significant dietary correlate of low CVD risk was high total fat and animal protein consumption.

Additional statistical analyses further highlighted citrus fruits, high-fat dairy (cheese) and tree nuts. Among other non-dietary factors, health expenditure showed by far the highest correlation coefficients.

The major correlate of high CVD risk was the proportion of energy from carbohydrates and alcohol, or from potato and cereal carbohydrates. Similar patterns were observed between food consumption and CVD statistics from the period 1980–2000, which shows that these relationships are stable over time.

...
Our results do not support the association between CVDs and saturated fat, which is still contained in official dietary guidelines. Instead, they agree with data accumulated from recent studies that link CVD risk with the high glycaemic index/load of carbohydrate-based diets. In the absence of any scientific evidence connecting saturated fat with CVDs, these findings show that current dietary recommendations regarding CVDs should be seriously reconsidered.
...

Low cholesterol levels correlate most strongly with the proportion of plant food energy in the diet (r=−0.87, p less than 0.001 in both sexes) and with sources of plant carbohydrates represented by items such as % PC CARB energy (r=−0.87 in men, r=−0.83 in women; p less than 0.001) (Fig. 2), % CA energy (r=−0.85 in men, r=−0.81 in women; p less than 0.001), and cereals (r=−0.74 in men, r=−0.73 in women; p less than 0.001). Smoking correlates quite strongly with lower cholesterol as well, but in men only (r=−0.62, p less than 0.001).

Remarkably, the relationship of raised cholesterol with CVD risk is always negative, especially in the case of total CVD mortality (r=−0.69 in men, r=−0.71 in women; p less than 0.001)

Most interesting is the discussion section at the end of the paper:

Discussion

Raised cholesterol correlates negatively with CVD risk

The results of our study show that animal fat (and especially its combination with animal protein) is a very strong predictor of raised cholesterol levels. This is in accordance with the meta-analyses of clinical trials, which show that saturated animal fat is the major trigger of raised cholesterol (6, 16). Interestingly, the relationship between raised cholesterol and CVD indicators in the present study is always negative. As shown in Figs. 3 and ​and Supplementary Figs. 1 and 2, this finding is visually less persuasive in the case of CVD mortality, where factors such as the quality of healthcare come to the foreground, but it is quite unambiguous in the case of women's raised blood pressure.

The negative relationship between raised cholesterol and CVD may seem counterintuitive, but it is not at variance with the available evidence. The largest of the recent worldwide meta-analyses dealing with cholesterol and CVD risk (17) observed a positive relationship between raised cholesterol and CVD mortality at younger ages, but this association gradually started to reverse in seniors, where the number of deaths is the highest. In fact, the relationship between raised cholesterol and stroke mortality in seniors was slightly negative. Both this study and other studies dealing with blood profiles of patients hospitalised with CVD events (18–22) demonstrate that low HDL (high-density lipoprotein associated) cholesterol (around ~1.0 mmol/L), or high total cholesterol: HDL-cholesterol ratio are the best indicators of CVD risk. Total cholesterol is usually normal or slightly elevated (4.5–5.5 mmol/L), and hence it cannot serve as a predictor of CVD events. Some other authors also point to high plasma triglycerides (which correlate with low HDL-cholesterol levels) (23), or to the ratio between triglycerides and HDL-cholesterol (24) as another useful risk indicators.

In this context it is important to note that saturated fat is not only the key trigger of high total cholesterol, but even high HDL-cholesterol and LDL (low-density lipoprotein associated)-cholesterol (16). Saturated fat also decreases triglyceride levels, but the total cholesterol: HDL-cholesterol ratio remains stable. The main sources of saturated fatty acids are red meat and milk products (whole fat milk, cheese, butter) (see Supplementary Table 1). Therefore, in Europe, where the consumption of animal products is the highest in the world, we can assume a strong connection between total cholesterol and HDL-cholesterol. Understandably, this relationship may not be so strong outside Europe and it may also vary depending on the individual diet. This could explain regional and individual differences in the relationship between total cholesterol and CVD risk.

Although the concurrent increase of LDL-cholesterol levels is often taken out of context and used as an argument against the intake of saturated fats in dietary recommendations (25), saturated fat is primarily tied to the less dense, large LDL particles (26), whereas cardiovascular risk is connected with the denser, small LDL particles (27), which accompany carbohydrate-based diets. There is also no evidence that the reduction of saturated fat intake (on its own) would decrease CVD risk (28). On the other hand, it is true, that so far, there is no clear evidence that saturated fat would be beneficial for the prevention of CVD. The only possible exception among the sources of saturated fat is dairy (29–31).

Major correlates of high CVD risk

Carbohydrates

The results of our study show that high-glycaemic carbohydrates or a high overall proportion of carbohydrates in the diet are the key ecological correlates of CVD risk. These findings strikingly contradict the traditional ‘saturated fat hypothesis’, but in reality, they are compatible with the evidence accumulated from observational studies that points to both high glycaemic index and high glycaemic load (the amount of consumed carbohydrates × their glycaemic index) as important triggers of CVDs (1, 32–34). The highest glycaemic indices (GI) out of all basic food sources can be found in potatoes and cereal products (Supplementary Table 2), which also have one of the highest food insulin indices (FII) that betray their ability to increase insulin levels.

The role of the high glycaemic index/load can be explained by the hypothesis linking CVD risk to inflammation resulting from the excessive spikes of blood glucose (‘post-prandial hyperglycaemia’) (35). Furthermore, multiple clinical trials have demonstrated that when compared with low-carbohydrate diets, a low-fat diet increases plasma triglyceride levels and decreases total cholesterol and HDL-cholesterol, which generally indicates a higher CVD risk (36, 37). Simultaneously, LDL-cholesterol decreases as well and the number of dense, small LDL particles increases at the expense of less dense, large LDL particles, which also indicates increased CVD risk (27). These findings are mirrored even in the present study because cereals and carbohydrates in general emerge as the strongest correlates of low cholesterol levels.

The authors discuss the reason behind the origin of the now discredited cholesterol-heart disease hypothesis prompted by Ancel Keyes' ‘Seven Countries Study’:

Discrepancy in the old statistics: The root of the ‘saturated fat hypothesis’?

The paradoxical results of our historical comparison (men's statistics from 1980 and 1990) have an interesting analogy in the ‘Seven Countries Study’, which stood behind the current ‘saturated fat paradigm’. The authors of this longitudinal ecological research, finished in the early 1980s, concluded that men's CHD [CHD=Coronary Heart Disease] mortality in seven countries correlated positively with high blood pressure, high cholesterol, and high saturated fat intake, but the relationship of high blood pressure and high cholesterol with men's stroke mortality (in 12 cohorts from six countries) was strongly negative (54). Because CHD mortality was the central CVD [CVD=Cardio-Vascular Disease] indicator in this study, we think that the authors did not pay sufficient attention to this discrepancy and they contented themselves with the fact that stroke mortality was positively associated with high blood pressure at the individual level. Ironically, in the following decades, the ecological relationship of CHD with risk factors completely reversed.

...Second, the effect of increased longevity in highly developed countries, after the eradication of serious infectious diseases after World War II, led to a temporary epidemic of CVDs, which also coincided with rapidly improving living standards and the increasing consumption of animal food. Because of the chronic nature of CVDs, this dietary change may have brought health benefits only after several decades and as a result, the relationship of CVD indicators to animal products has reversed with a certain delay (Supplementary Figs. 42–47). In the eastern half of Europe, this phenomenon started to fully manifest only very recently (possibly in combination with heavy alcohol drinking), which led to the increase of CVD rates.

The obvious fallacy of the ‘saturated fat hypothesis’ can be demonstrated by the example of France – a country with the highest intake of animal fat in the world and the second lowest CVD mortality (after Japan) (56). In fact, if we use a limited sample of 24 countries (without the former republics of USSR, Czechoslovakia and Yugoslavia, and Luxembourg), a summary mean of food consumption from the last half-century (1961–2008) produces very similar results like the mean for the period 1993–2008 (Table 4), reaching r=0.82 between % CA [CA=carbohydrates] energy and raised blood pressure in women.

A short summary of the paper can be read in the following article:

New study finds wheat and carbs biggest risk for heart disease, red meat and saturated fat has no direct effect

Telomere length correlates with red meat consumption

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Blog article:

Unexpected relationship between Red Meat Diet and PBMC Telomere Length, Sep 28, 2016 1:30:54 AM / by Stacy Matthews Branch, DVM, PhD

Update 15-Jan-2020

500% extension for C.Elegans by TOR and Insulin IIS signaling modification:
Pathways that extend lifespan by 500 percent identified Discovery of cellular mechanisms could open door to more effective anti-aging therapies, Date:January 8, 2020, Mount Desert Island Biological Laboratory

Quote:

The new research uses a double mutant in which the insulin signaling (IIS) and TOR pathways have been genetically altered. Because alteration of the IIS pathways yields a 100 percent increase in lifespan and alteration of the TOR pathway yields a 30 percent increase, the double mutant would be expected to live 130 percent longer. But instead, its lifespan was amplified by 500 percent.

Reference:

"The relationship between peripheral blood mononuclear cells telomere length and diet - unexpected effect of red meat.", Kasielski M, Eusebio MO, Pietruczuk M, Nowak D., Nutr J. 2016 Jul 14;15(1)

Fig.1 from the paper above.

Mount Desert Island Biological Laboratory. "Pathways that extend lifespan by 500 percent identified: Discovery of cellular mechanisms could open door to more effective anti-aging therapies." ScienceDaily. ScienceDaily, 8 January 2020.

Jianfeng Lan, Jarod A. Rollins, Xiao Zang, Di Wu, Lina Zou, Zi Wang, Chang Ye, Zixing Wu, Pankaj Kapahi, Aric N. Rogers, Di Chen. Translational Regulation of Non-autonomous Mitochondrial Stress Response Promotes Longevity. Cell Reports, 2019; 28 (4): 1050 DOI: 10.1016/j.celrep.2019.06.078

Optimal sodium is 3-5g/day and potassium above 2g/day

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- in order to minimize the risk of cardio-vascular disease. This is based on thew recent study:
"Joint association of urinary sodium and potassium excretion with cardiovascular events and mortality: prospective cohort study", by Martin O’Donnell et al., BMJ 2019; 364

These guidelines are significantly higher than the existing WHO recommendations.

Fig 3

Heat map of risk for composite of cardiovascular events or death showing lowest risk in region of moderate sodium intake 3-5 g/day and higher potassium intake and highest risk in region of extremes of sodium excretion and low potassium excretion. The reference hazard for these hazard ratios was set at a value of sodium daily excretion/intake of 5.00 g and potassium daily excretion/intake of 2.25 g (median excretion of sodium and potassium), marked as X. The overlaid lines represent joint distribution quartiles; each region contains a quarter of the analysed participants. r=0.34

Meat-and-greens diet reported to cure rheumatoid arthritis

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These are just personal reports here below, from 3 people, not a study. Exactly, why no studies?

From Twitter

Quote:

"All I eat is meat and greens, no carbohydrates"

Jordan Peterson cures an unspecified autoimmune disorder, psoriasis, gastric reflux, and gum disease, his 30-ty years old daughter Mikhaila cures a very severe form of rheumatoid arthritis (2 joint replacement at age 16) on an initially a "chicken-and-broccoli" diet (enhanced by other meats since).


Update:

Hunter-gatherers diets are low to moderate in carbohydrates

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Reposted from Frédéric Leroy‏ @fleroy1974

The meatans

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Carnivore "vegans"

Wiki Steak

Quote:

They mock vegans and eat 4lb of steak a day: meet 'carnivore dieters'
An extreme, all animal-based diet is gaining followers in search of heightened productivity, mental clarity, and a boosted libido. But experts express doubts

Instagram: shawnbaker1967At 51 years of age I am well aware of the tremendous evidence that demonstrates maintaining as much lean muscle mass as possible is necessary to mitigate the risks of cardiovascular disease and promotes excellent metabolic health-I remain incredibly insulin sensitive with a fasting insulin of just 2.6 and maintain extremely low levels of inflammation with a hsCRPof on 0.6 and also have very low triglycerides levels of only 54- also my VO2max is also among the best in the world for my age based on my rowing capacity- it is the entire system and its overall function that best indicate health!

Potatoes and cereals are heart disease risk while dairy, fat and meat are good for you

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- says the new study: "FOOD CONSUMPTION AND THE ACTUAL STATISTICS OF CARDIOVASCULAR DISEASES: AN EPIDEMIOLOGICAL COMPARISON OF 42 EUROPEAN COUNTRIES" .

Results: ...The most significant dietary correlate of low CVD risk was high total fat and animal protein consumption. Additional statistical analyses further highlighted citrus fruits, high-fat dairy (cheese) and tree nuts. ... The major correlate of high CVD risk was the proportion of energy from carbohydrates and alcohol, or from potato and cereal carbohydrates.

Conclusion: Our results do not support the association between CVDs and saturated fat, which is still contained in official dietary guidelines. Instead, they agree with data accumulated from recent studies that link CVD risk with the high glycaemic index/load of carbohydrate-based diets. In the absence of any scientific evidence connecting saturated fat with CVDs, these findings show that current dietary recommendations regarding CVDs should be seriously reconsidered.

(CVD stands for "Cardio Vascular Disease")

by Cecilia Bleszynski (C) 2017

The first graph published in the paper:

is the most interesting in conjunction with the rest of the results, showing that the high consumption of animal fat and protein correlates very well with high blood cholesterol level and at the same time (see for example Fig.4 and 7) the high cholesterol and high consumption of animal fat and protein correlate consistently and strongly with the low cardiovascular and other diseases' risk! That is yet another nail to the coffin of the cholesterol-heart hypothesis and an indication that the blood cholesterol correlation with cardiovascular disease (+ or -) is secondary and spurious while the primary risk factor appears to be related to the carbohydrate contents of the diet! Note that some of the graphs refer to women some for men but the actual correlation factors are similar for men and momen (see Table 1) with the exception of correlations involving BMI and smoking which are opposite for women and men (that is another interesting subject).

Most of the results point consistently and strongly, see for example Fig.10 towards the carbohydrates contents of the diet as being the strongest positive correlator with the cardiovascular disease risk, where as the animal and most plant fats correlate most negatively (that is being protective) against cardiovascular disease, see Table 1, with the notable exception of sunflower oil which correlates strongly and positively with the CVD.

It is also interestingly to notice a strong linear correlation graph with very low data scatter, between the prevalence of raised blood glucose and consumption of carbohydrates plus alcohol ('CA' variable), on Fig.9:

Although diabetes risk was not directly measured in the study, Fig.9 appears to indicate that diabetes risk may be steeply correlated to the total consumption of carbohydrates plus alcohol, and strongly inversely correlated with the consumption of animal fat and protein (see Table 1). For example an increase of the dietary carbohydrate+alcohol contents from 42% to 68% seems to increase the prevalence of high blood glucose (and thus probably diabetes risk as well) by a factor of 3!

The overall results of this study are also remarkably consistent with the original China Study data as published on the Oxford University web site and  discussed on this blog (see my previous posts).

The study is also discussed in the following journalistic article:

"Potatoes and cereals are health risk, while dairy is good for you, says new study".

Fat and cholesterol-heart disease theory - worldwide hoax perpetrated by American Sugar Association!

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This is now official, documents found and published! If one thinks about the implications, scale and the length of time, it would probably not be surprizing if this were followed by some some serious Crime Against Humanity type investigation against the officials that were involved, and named!

NY Times: How the Sugar Industry Shifted Blame to Fat

The sugar industry paid scientists in the 1960s to play down the link between sugar and heart disease and promote saturated fat as the culprit instead, newly released historical documents show.

The internal sugar industry documents, recently discovered by a researcher at the University of California, San Francisco, and published Monday in JAMA Internal Medicine, suggest that five decades of research into the role of nutrition and heart disease, including many of today’s dietary recommendations, may have been largely shaped by the sugar industry.

“They were able to derail the discussion about sugar for decades,” said Stanton Glantz, a professor of medicine at U.C.S.F. and an author of the JAMA Internal Medicine paper.

The documents show that a trade group called the Sugar Research Foundation, known today as the Sugar Association, paid three Harvard scientists the equivalent of about $50,000 in today’s dollars to publish a 1967 review of research on sugar, fat and heart disease. The studies used in the review were handpicked by the sugar group, and the article, which was published in the prestigious New England Journal of Medicine, minimized the link between sugar and heart health and cast aspersions on the role of saturated fat.

...

In 1965, Mr. Hickson enlisted the Harvard researchers to write a review that would debunk the anti-sugar studies. He paid them a total of $6,500, the equivalent of $49,000 today. Mr. Hickson selected the papers for them to review and made it clear he wanted the result to favor sugar. Harvard’s Dr. Hegsted reassured the sugar executives. “We are well aware of your particular interest,” he wrote, “and will cover this as well as we can.”

JAMA paper: Sugar Industry and Coronary Heart Disease Research
A Historical Analysis of Internal Industry Documents

Abstract

Early warning signals of the coronary heart disease (CHD) risk of sugar (sucrose) emerged in the 1950s. We examined Sugar Research Foundation (SRF) internal documents, historical reports, and statements relevant to early debates about the dietary causes of CHD and assembled findings chronologically into a narrative case study. The SRF sponsored its first CHD research project in 1965, a literature review published in theNew England Journal of Medicine, which singled out fat and cholesterol as the dietary causes of CHD and downplayed evidence that sucrose consumption was also a risk factor. The SRF set the review’s objective, contributed articles for inclusion, and received drafts. The SRF’s funding and role was not disclosed. Together with other recent analyses of sugar industry documents, our findings suggest the industry sponsored a research program in the 1960s and 1970s that successfully cast doubt about the hazards of sucrose while promoting fat as the dietary culprit in CHD. Policymaking committees should consider giving less weight to food industry–funded studies and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development.

...
RESULTS

SRF’s Interest in Promoting a Low-Fat Diet to Prevent CHD

Sugar Research Foundation president Henry Hass’s 1954 speech, “What’s New in Sugar Research,”12 to the American Society of Sugar Beet Technologists identified a strategic opportunity for the sugar industry: increase sugar’s market share by getting Americans to eat a lower-fat diet: “Leading nutritionists are pointing out the chemical connection between [American’s] high-fat diet and the formation of cholesterol which partly plugs our arteries and capillaries, restricts the flow of blood, and causes high blood pressure and heart trouble… if you put [the middle-aged man] on a low-fat diet, it takes just five days for the blood cholesterol to get down to where it should be… If the carbohydrate industries were to recapture this 20 percent of the calories in the US diet (the difference between the 40 percent which fat has and the 20 percent which it ought to have) and if sugar maintained its present share of the carbohydrate market, this change would mean an increase in the per capita consumption of sugar more than a third with a tremendous improvement in general health.”12

The industry would subsequently spend $600 000 ($5.3 million in 2016 dollars) to teach “people who had never had a course in biochemistry… that sugar is what keeps every human being alive and with energy to face our daily problems.”12

...

The SRF’s vice president and director of research, John Hickson, started closely monitoring the field.15
In December 1964, Hickson reported to an SRF subcommittee15 that new CHD research was a cause for concern: “From a number of laboratories of greater or lesser repute, there are flowing reports that sugar is a less desirable dietary source of calories than other carbohydrates, eg,—Yudkin.”15 Since 1957, British physiologist John Yudkin16 had challenged population studies singling out saturated fat as the primary dietary cause of CHD and suggested that other factors, including sucrose, were at least equally important.17,18

Hickson proposed that the SRF “could embark on a major program” to counter Yudkin and other “negative attitudes toward sugar.”15 He recommended an opinion poll “to learn what public concepts we should reinforce and what ones we need to combat through our research and information and legislative programs” and a symposium to “bring detractors before a board of their peers where their fallacies could be unveiled.”15 Finally, he recommended that SRF fund CHD research: “There seems to be a question as to whether the [atherogenic] effects are due to the carbohydrate or to other nutrient imbalance. We should carefully review the reports, probably with a committee of nutrition specialists; see what weak points there are in the experimentation, and replicate the studies with appropriate corrections. Then we can publish the data and refute our detractors.”15

In 1965, the SRF asked Fredrick Stare, chair of the Harvard University School of Public Health Nutrition Department19 to join its SAB as an ad hoc member.20 Stare was an expert in dietary causes of CHD and had been consulted by the NAS,1 National Heart Institute,21 and AHA,22 as well as by food companies and trade groups.19 Stare’s industry-favorable positions and financial ties would not be widely questioned until the 1970s.23

....

SRF Funds Project 226: A Literature Review on Sugars, Fats, and CHD
On July 13, 1965, 2 days after the Tribune article, the SRF’s executive committee approved Project 226,31 a literature review on “Carbohydrates and Cholesterol Metabolism” by Hegsted and Robert McGandy, overseen by Stare.10 The SRF initially offered $500 ($3800 in 2016 dollars) to Hegsted and $1000 ($7500 in 2016 dollars) to McGandy, “half to be paid when you start work on the project, and the remainder when you inform me that the article has been accepted for publication.”31 Eventually, the SRF would pay them $650032 ($48 900 in 2016 dollars) for “a review article of the several papers which find some special metabolic peril in sucrose and, in particular, fructose.”31

Diets higher in protein are associated with lower adiposity and do not impair kidney function

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Another myth bites the dust. It appears protein-kidney scare was a BS all along...

The recently published paper:

Diets higher in animal and plant protein are associated with lower adiposity and do not impair kidney function in US adults

Conclusions: Diets higher in plant and animal protein, independent of other dietary factors, are associated with cardiometabolic benefits, particularly improved central adiposity, with no apparent impairment of kidney function.

They finally proved correlation between saturated fat and heart disease...

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... and it is inverse!

From Wiki

In case you missed it, see the study link and the post on Diet Doctor.  See also an interesting post on the High Fat Hep-C Diet blog.  In a nutshell:

Each additional 5% of saturated fat (SFA) contents was associated with 17% lower risk of ischemic heart disease (IHD)  : Hazard Ratio 0.83 +/- 0.1.

RESULTS:
During 12 y of follow-up, 1807 IHD events occurred. Total SFA intake was associated with a lower IHD risk (HR per 5% of energy: 0.83; 95% CI: 0.74, 0.93). Substituting SFAs with animal protein, cis monounsaturated fatty acids, polyunsaturated fatty acids (PUFAs), or carbohydrates was significantly associated with higher IHD risks (HR per 5% of energy: 1.27-1.37). Slightly lower IHD risks were observed for higher intakes of the sum of butyric (4:0) through capric (10:0) acid (HRSD: 0.93; 95% CI: 0.89, 0.99), myristic acid (14:0) (HRSD: 0.90; 95% CI: 0.83, 0.97), the sum of pentadecylic (15:0) and margaric (17:0) acid (HRSD: 0.91: 95% CI: 0.83, 0.99), and for SFAs from dairy sources, including butter (HRSD: 0.94; 95% CI: 0.90, 0.99), cheese (HRSD: 0.91; 95% CI: 0.86, 0.97), and milk and milk products (HRSD: 0.92; 95% CI: 0.86, 0.97).

Interestingly, equal-caloric substitution of 5% of SFA in the diet with:

•  any carbohydrate type (low GI, medium GI or high GI),
•  mono-unsaturated fats,
•  polyunsaturated fats,
•  animal protein,

- correlated positively with IHD, while substitution of SFA with vegetable protein correlated negatively! (Correlation calculations were corrected against known confounding factors such as age, sex, BMI, waist circumference, educational level, physical activity level, smoking status, alcohol intake, energy-adjusted intakes of cholesterol, fiber, and vitamin C.

Stan (Heretic)

The Skinny on Fat by Credit Suisse

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A better title would have been "Money and greed trump medical lies and stupidity"
I shall better be kind to the bankers, some of them are on our side!
 8-:)

Credit Suisse Investor's report   (a short summary titled The Real Skinny on Fat is available on The Financialist page) concludes that saturated and monounsaturated animal fat is healthy and was unjustifiably blamed for the health problems that were in fact more likely caused by the overconsumption of vegetable polyunsaturated  oils and carbohydrates.  The institute's report is thus    advising to invest in natural food producers selling product rich in saturated fats.  

Low fat diets are useless - new study

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... a recently published study has found.   The Telegraph article  on the same topic:
Cut out carbs, not fat if you want to lose weight, Harvard study finds

Wiki Cereal

 The analysis of 53 studies, involving 67,000 dieters found who cut back on fat were two and a half pounds heavier after a year than those who embraced a “low carb” approach.

...
Dr Deirdre Tobias at Bingham's Division of Preventive Medicine said: "Despite the pervasive dogma that one needs to cut fat from their diet in order to lose weight, the existing scientific evidence does not support low-fat diets over other dietary interventions for long-term weight loss." "In fact, we did not find evidence that is particularly supportive of any specific proportion of calories from fat for meaningful long-term weight loss.” The study found low carbohydrate diets were the most successful.

Human brain size is shrinking!

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From uncyclopedia.

Human brain (average 1100 to 1300cm^3) seem to have deteriorated at least in size, in the last couple of hundred thousands years.   How does that decline translate to intelligence?  Not sure but I would speculate that it probably does correlate!

As to the cause, anthropologists seem to be rather in agreement that nutrition may have had something to do with that.  Humankind seemed to have regressed from very healthy nomadic lifestyle based on hunting and fishing to a settled one based on farming and consuming starchy plant based food.  Which correlated with the deterioration of physical health, body size and brain size.  [add refs later]

According to this research.  Neanderthal did not have to use fire to cook their exclusively animal based meals.  My thought is that they must also have consumed plenty of DHA from animal brains and spinal cords, together with all the fats to grow and feed their very large brains of average volume 1600 cm^3 (some sources give bigger estimates) .   Ability to use fire gave Cro-Magnon (average brain volume 1500 or 1600 cm^3) an advantage when game became scarce and food versatility became useful, by the end of the last ice age.
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US to drop anti-cholesterol food guidelines!

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Cholesterol in food is "no longer a concern"!   It is now OK to eat bacon and eggs!

From Commons.Wiki 

U.S. may lower cholesterol's level of threat to health: report

WASHINGTON (Reuters) - A U.S. advisory panel reviewing national dietary guidelines has decided to drop its caution against eating cholesterol-laden food, the Washington Post reported on Tuesday.

At a December meeting, the Dietary Guidelines Advisory Committee discussed its decision to no longer deem cholesterol a "nutrient of concern," according to the Washington Post.
...

What happened to those scientists and medical doctors who, for many decades have been signing and propagating the anti-cholesterol guidelines?  I wonder, what could be the overall health damage estimate, caused by those recommendations, to date?
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Are some diets "mass murder"?

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Recently published paper in BMJ, of the title above:

BMJ 2014; 349 doi: http://dx.doi.org/10.1136/bmj.g7654 (Published 15 December 2014)

Wiki 

Quotes:

Jean Mayer, one of the "greats" of nutrition science, said in 1965, in the colourful language that has characterised arguments over diet, that prescribing a diet restricted in carbohydrates to the public was "the equivalent of mass murder."1 Having ploughed my way through five books on diet and some of the key studies to write this article, I’m left with the impression that the same accusation of "mass murder" could be directed at many players in the great diet game. In short, bold policies have been based on fragile science, and the long term results may be terrible.

...

An analysis of the data from the Seven Countries Study in 1999 showed a higher correlation of deaths from heart disease with sugar products and pastries than with animal products.13 John Yudkin from London had since the late 1950s proposed that sugar might be more important than fat in causing heart disease,4 but Keys dismissed his hypothesis as a “mountain of nonsense” and a “discredited tune.” Many scientists were sceptical about the saturated fat hypothesis, but as the conviction that the hypothesis was true gripped the leading scientific bodies, policy makers, and the media in the US these critics were steadily silenced, not least through difficulty getting funding to challenge the hypothesis and test other hypotheses.

...

It might be expected that the powerful US meat and dairy lobbies would oppose these guidelines, and they did, but they couldn’t counter the big food manufacturers such as General Foods, Quaker Oats, Heinz, the National Biscuit Company, and the Corn Products Refining Corporation, which were both more powerful and more subtle. In 1941 they set up the Nutrition Foundation, which formed links with scientists and funded conferences and research before there was public funding for nutrition research.

...

Recognising that the fat hypothesis was falling apart, some scientists, particularly Walter Willett, professor of epidemiology at Harvard (whom I’ve also met), began to promote the Mediterranean diet, which comes in many forms but is essentially lots of fruit, vegetables, bread and grains (including pasta and couscous), little meat and milk, and plenty of olive oil. Such a diet is much easier to eat than a low fat diet, and a combination of vested interests, including the International Olive Oil Council and a public relations company Oldways, which promoted the diet, has—together with the natural seductiveness of the Mediterranean region—made the diet popular. But the science behind it is weak, as a Cochrane review found,20 and some of the evidence comes from R B Singh, whose research is suspect.21

Last but not least and somewhat related to the above topic,  some science fun stuff. Enjoy!

The Demise of Science? Hundreds of Computer Generated Studies Have Been Published in Respected Scientific Journals.

Suddenly and mysteriously, protein no longer leaches calcium from bones!

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Surely, all the past warning by vegans against consuming too much proteins, as being bad for bones, especially animal proteins, must have been based on something?  Something must have happened in the environment...


Recently published:

Biomarker-calibrated protein intake and bone health in the Women's Health Initiative clinical trials and observational study

Quotes [my comments added in square brackets]:

Abstract
Background: The effects of dietary protein on bone health are controversial.

[Really? I was under an impression that it has all been 'proven' long ago by a scientist from Cornell...]

Conclusions: Higher biomarker-calibrated protein intake within the range of usual intake was inversely associated with forearm fracture and was associated with better maintenance of total and hip BMDs.

These data suggest higher protein intake is not detrimental to bone health in postmenopausal women.

[This is using double-negative form to weaken a perceived impact of the statement. Under 'normal' circumstances, a scientist would have simply stated: "We found that eating more protein improves bone density and reduces probability of some types of bone fractures in postmenopausal women"]

Heretic

(P.S. Thanks JC for the link!)

Do statins or low fat diets cause osteoporosis?

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New study: "Association Between Myocardial Infarction and Fractures: An Emerging Phenomenon."

Most interesting is this, quote:

...substantial temporal variations were noted (
1979 to 1989: hazard ratio, 0.81 ...
1990 to 1999: hazard ratio, 1.47 ...
2000 to 2006: hazard ratio, 1.73 ...
...
Trends were similar regardless of age, sex or fracture site. Conversely, the overall hazard ratio for death in MI cases versus controls did not change materially...

The only obvious factor that was different in the first decade (blue - less osteoporosis following a MI event) as opposed to the second and third decade of the study (red - more osteoporosis!) is the common usage of statin drugs! Perhaps a popularity of the low fat high carbohydrate diets in treating MI patients (the so-called AHA diet) may be another factor distinguishing the red from the blue decades.

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Update 16-July-2011

Another recent study found on Dr.McDougall forum, linking bone underdevelopment with malnutrition, in this case a lack of dairy products:

Thin Bones Seen In Boys with Autism and Autism Spectrum Disorder

Quotes:

The boys in the study who were on a casein-free [READ DAIRY-FREE (added by H.)] diet had the thinnest bones. In fact, the 9 boys who were on a casein-free diet had bones that were 20 percent thinner than normal for children their age. Boys who were not on a casein-free diet showed a 10 percent decrease in bone thickness when compared to boys with normal bone development.

The study authors wrote that bone development of children on casein-free diets should be monitored very carefully. They noted that studies of casein-free diets had not proven the diets to be effective in treating the symptoms of autism or ASD.

As a side note from my own experience. It reminds me that a nurse examining children at my school in the Eastern Europe, 1960-ties (I was around 12) told us that many, about a half had unusually thin but long bones in their hands and different elbow joints, as compared with the medical reference books that she used. Those children had normal food intake, were rather well fed. I always wondered what was causing the difference and that the same factor affecting bone development may have also affected the risk of autism! What was that factor? We didn't eat breakfast cereals nor drank pop. We ate a high carb medium fat diet not much different from that of the 1930-ties or before. Definitely more sugar - sugar became very cheap in the 1960-ties, and margarine became the new "health" "food" of the day plus vegetable oils became a popular cooking fat substitute in the 1970-ties. Sugar was very expensive before WWII in Poland due to special sugar tax, then became completely unavailable during German occupation 1939-1945 and then became cheap afterwards. What else other than sugar could have done the damage?

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Study: add more carbs be more hungry!

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A new study: "A Paleolithic diet is more satiating per calorie than a Mediterranean-like diet in individuals with ischemic heart disease"

What is remarkable about it, is that the patients felt more satiated and thus ate automatically 24% less by their own choice, and the only major difference between the two tested diets was the amount of carbohydrates (grains)! Everything else was very similar.

Think about it: both groups eat some typical basic foodstuff, then just let one group add 82g more carbohydrates (grains!) plus 13g more fat (oil) per day and what is the main result? - THEY FEEL MORE HUNGRY!

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No benefit of veg and fruit consumption in t2 diabetes!

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 Fig 4 Hazard ratios for incidence in diabetes type 2 for highest versus lowest intake of fruit and vegetables combined. Weights are from random effects analysis

Newly published meta-study in BMJ:

Fruit and vegetable intake and incidence of type 2 diabetes mellitus: systematic review and meta-analysis

Quote:

Results Six studies met the inclusion criteria; four of these studies also provided separate information on the consumption of green leafy vegetables. Summary estimates showed that greater intake of green leafy vegetables was associated with a 14% (hazard ratio 0.86, 95% confidence interval 0.77 to 0.97) reduction in risk of type 2 diabetes (P=0.01). The summary estimates showed no significant benefits of increasing the consumption of vegetables, fruit, or fruit and vegetables combined.

I have to add a comment:
   There is only one supposedly significant, positive correlation found in this study - the one with green veg (hazard ratio 0.86).  It is possible [but see also (*)] that the significancy results from pooling four separate studies together. When you look at the individual studies on FIG5 : three are only marginally positive, that is their error estimates touch 1.0, while one large study [39] (Women’s Health Study) shows the hazard ratio of 1.0 which indicates no effect.

This paper  [37] (Nurses' Health Study data) is also interesting because it is one of the largest and longest of its kind. Again, no benefit overall from vegetable consumption and miniscule benefit from greens alone. It also shows this interesting graph:

Note (*): There is a discrepancy in the data. The resulting hazard ratio may also turn out to be not statistically significant for green vegetables, since the overall P=0.18 as per FIG.5 while at the same time it is written as P=0.01 in the abstract for the same result. Given the wide spread 0.77-0.97, my guess is that the abstract figure of 0.01 may be a typo, but I am not 100% sure.