Dairy fat could PREVENT a heart attack

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Dairy fat from milk, butter, and cheese could actually PREVENT a heart attack SEPTEMBER 21,2021

“Many studies have relied on people being able to remember and record the amounts and types of dairy foods they have eaten, which is especially difficult given dairy is commonly used in a variety of foods,” says study co-author Dr. Matti Marklund from Uppsala University, in a statement.
“Instead, we measured blood levels of certain fatty acids, or fat ‘building blocks’ that are found in dairy foods, which gives a more objective measure of dairy fat intake that doesn’t rely on memory or the quality of food databases,” Dr. Marklund continues. “We found those with the highest levels actually had the lowest risk of CVD.”
... Researchers assessed dairy fat consumption in the group of Swedish 60-year-olds by measuring blood levels of a particular fatty acid. This substance generally appears in dairy foods and is therefore useful in reflecting intake of dairy fat. Study authors tracked the group for an average of 16 years to see how many had heart attacks, strokes, and other serious circulatory events. They also looked at how many died from any cause during this time.
The CVD risk was lowest for those with high levels of the fatty acid, coming from a high intake of dairy fats. The results remained the same after accounting for factors including age, income, lifestyle, dietary habits, and other illnesses. Moreover, those with the highest levels had no increased risk of death from all causes.

Reference
"Biomarkers of dairy fat intake, incident cardiovascular disease, and all-cause mortality: A cohort study, systematic review, and meta-analysis", Kathy Trieu , et al., PLOS MEDICINE, Published: September 21, 2021

Denise Minger's different kinds of magic

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I love her presentation!

Probably not true!

Who is a bastard who wrote "why"?

Magic rocks!   :)

I highly recommend to listen to her video. She is reviewing some old studies showing therapeutic effects of the very low fat high carbohydrate diets (VLFHC). Low fat means well below 10% preferably about 2%. When I begun my high fat low carb experiment back in 1999, which grew into my ongoing lifestyle nutrition to this day, I was aware that the very low fat natural food diet has been successfully used in halting progression of coronary heart disease and MS. I was familiar about Pritikin and Dr. Swank work. Prior to 1999 I was experimenting with vegetarian nutrition but I found it unpalatable, unless a sufficient amount of fat was added. More than 10%. So for me finding dr. Kwasniewski's Optimal Diet was a "gift from God", or I should say a gift from a friend of mine (Andrew S.)! Kwasniewski's Optimal Diet is high animal fat low carb diet (HFLC). After noticing back then that the VLFHC diets have some therapeutic property, I had many questions (i.e. "question everything"). One of them is about the long term viability and the side effects. Like with every therapy, there may be side effects. Are there side effects of VLFHC diets? How do people do on such nutrition scheme fare in the long term? Longevity issue? Longevity with a robust health or not so well? The same question can also be asked about any other diet, including the HFLC diet.

Unlike most other low carb promoters at that time (1970-ties - 1990-ties), dr. Kwasniewski did acknowledge that a high carbohydrate diet may also be healthy, quoting Japanese rice based diet as an example. He also insisted that, on such a diet (1) fat intake must be limited to abut 10% and (2) a sufficient amount of (lean) protein must be consumed. Insulin sensitivity is very high on such a diet because the intake of fat is very low but the pancreatic insulin secretion is medium. Insulin cannot be too low, due to carbohydrate-based metabolism. Typically it amounts to about 20-30 iu per day, based on my understanding and from reports by t1 diabetics (quoting from memory so verify this before you requote me!)

Dr. Kwasniewski also noticed, based on his patients record, that a particular proportion of macronutrients, consisting of about 35-45% of fat (by calories) and about 45-35% of carbohydrates is particulary unhealthy and makes people prone to developing diabetes and atherosclerotic heart disease. Kwasniewski also noticed that it causes a peculiar form of neuro-degeneration for people in their 40-ties and 50-ties manifesting itself in form character disorder (psychopathy). He called that dietary zone "dangerous middle zone". Pancreatic insulin secretion has to be very high (typically 40-60 iu/day or more) on such a diet in order to overcome the insulin insensitivity induced by the high fat intake.

He also noticed that as soon as you up the total fat intake to above 50% of calories then these pathological effects gradually subside and the diet becomes healthy again, even therapeutically healthy. The widely popular diet he publicized in the 1980-ties, arrived at the macronutrient proportions P:F:C (Protein to Fat to Carbohydrates) in gram per day per 1kg of ideal body weight of 1:3-3.5:0.8 to 1:2-2.5:0.5 . This typically works out at way over 60% (typ about 85%) of fat by calories. Notice that fat has 9kcal/g, glucose 4.5kcal/g and protein 3.5kcal/g (or less if used anabolically). Interestingly, Kwasniewski also found that his patients with coronary heart disease begun reversing and recovering. So his patients with many autoimmune disease such as asthma, rheumatoid arthritis, MS, IBS, and other - also recovered on his diet! Even though the HFLC diet is the exact opposite of the VLFHC diet, it nevertheless produced surprisingly similar (if not greater) therapeutic effects! Notice that the insulin sensitivity (and the effect of fat upon it) becomes irrelevant due to very low intake of carbohydrates. Kwasniewski quoted insulin requirement at this point, to be about 6-10 iu/day. How did he measured it? By observing his type 1 diabetic patients!

What Denise Minger has done, is rediscovering and publicizing that fact that there are 2 dietary zones that have therapeutic properties, not just one diet!

What I would disagree with, is her presumption that the VLFHC diet would:

- "results in healthier gut microbiome long term"

There is not proof or comparison studies done for VLFHC vs HFLC on that, while there is enough reports indicating the long term gut flora deterioration among vegans (I would put refs to Dr. Stanley Bass and Dr. Gian-Cursio reports on Natural Hygienists).

- "may do best for ApoE4 carriers"

No proof either, other than high serum cholesterol which does not always translate to a health risk, except for people eating in the dangerous middle zone.

- "may be able to restore and heal glucose tolerance which does not happen on the high fat..."

This is not true based on my personal observation. Initially yes, HFLC diet did not restore my glucose tolerance, it only allowed my body to bypass the issue by not showering my body with the excess carbohydrates. Whenever I tried to eat a little bit more than 50g of carbohydrates in a day, I would inevitably come to regret it! Carb-headache and nausea. Beer was especially bad for me. However, after about 2 years I noticed that I was able to increase that limit and add more than previously and after about 6-7 years I noticed that my carbohydrates tolerance has been totally restored! For example I can now consume a high carb dinner if I have no other choice without any adverse side effects. I don't do it often, but it is nice to know that my metabolism has completely been restored. I suspect it has to do with the mitochondrial regeneration. It takes about 7 years to regrow and renew most of our muscular tissues from our stem cells. I also found it that initially I had to watch not only the total carbohydrates intake, but I also had to limit the overall caloric intake from fat as well. Initially the total limit was about 1800kcal. Believe it or not that is actually perfectly sufficient for an adult leading an active life on the high fat diet, without any problems (I was 43 in 1999 when I begun HFLC and I weigh 64k, 173cm height) It was as if my metabolic channels were impaired for both macronutrients, for carbs as well as for fat, except the metabolism of fat, being more effective, allowed me to live better and have more energy in spite of the limitations. Again, that restriction is no longer applicable and lifted itself after about 7 years.

Stan (Heretic) Bleszynski

salt and cardiovascular risk debunked

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It was a fake theory! Fake - I like this word.

A Canadian study, just published in The Lancet:
Urinary sodium excretion, blood pressure, cardiovascular disease, and mortality: a community-level prospective epidemiological cohort study
Andrew Menteet al., VOLUME 392, ISSUE 10146, P496-506, AUGUST 11, 2018

Quote:

The association between mean sodium intake and major cardiovascular events showed significant deviations from linearity (p=0.043) due to a significant inverse association in the lowest tertile of sodium intake (lowest tertile <4.43 g/day, mean intake 4.04 g/day, range 3.42-4.43; change -1.00 events per 1000 years,...

Sodium intake was associated with cardiovascular disease and strokes only in communities where mean intake was greater than 5 g/day.

Halite (rock salt) from the Wieliczka salt mine,

Note: "inverse" association means that lower sodium INCREASES the rate of disease. In this case the cutoff threshold for the inverse relation is about 4g per day. The recommended daily dose of sodium by the fake (I love it) medical authorities is about 2g/day. Also, the usage of the unit "minus one event per 1000 years" has to be interpreted such that statistically there is one event less than the average, per 1000 patients per year rather than having to wait 1000 years for one patient event.

Read also here:

Salt not as damaging to health as previously thought, says study

Quote:

The study suggests that very low levels of salt could lead to more heart attacks and suggests that moderate salt consumption may be protective.
...
The World Health Organization recommends cutting sodium intake to no more than 2g a day - the equivalent of 5g of salt - because of the link to increased blood pressure, which is in turn implicated in stroke.

Carbohydrates are killing us

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"Carbohydrates are killing us"
By Eric Thorn - (cardiologist affiliated with the Virginia Hospital Center)- Sunday, July 8, 2018

Quote:

Consider a report published last year in The Lancet that studied nutrition among more than 135,000 people across 18 different countries — making it the largest-ever observational study of its kind. The researchers found that people who ate the least saturated fat — about the same amount currently recommended for heart patients — had the highest rates of heart disease and mortality. Meanwhile, people who consumed the most saturated fat had the lowest rate of strokes.

Identify what is bad for you ... (Wiki Bacon)

Reference study:

Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study

American Heart Assoc. recommendations gave its own president heart attack!

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American Heart Association President Suffers Heart Attack at 52

Good article by Dr. Mercola. I like the fact that he is not mincing the words.

Story at-a-glance

• John Warner, cardiologist and president of the American Heart Association (AHA), recently suffered a heart attack in the middle of a health conference at the age of 52
• In all likelihood, Warner followed AHA recommendations, many of which can actually worsen or cause heart disease
• AHA supports ample grain consumption and recommends eating harmful fats such as canola, corn, soybean and sunflower oil, both of which are known to cause and/or contribute to cardiovascular problems
• Good heart health starts with your diet — what you eat and when you eat. A powerful treatment for heart disease is to work your way up to an intermittent fasting schedule where you’re fasting for 20 hours a day
• When you do eat, make sure you eat real food, and consider a cyclical ketogenic diet, high in healthy fats, low in net carbs with moderate protein. Once you’re comfortable with this intermittent fasting schedule, start doing a monthly water only fast, working your way up to multiple days

Many AHA Recommendations Worsen Heart Health

In all likelihood, Warner followed AHA recommendations, many of which are actually recipes for heart disease disaster. Of the foods scientifically proven to cause heart disease and clogged arteries, excess sugar and industrially processed omega-6 vegetable oils, found in nearly all processed foods, compete for space at the top the list. And what kinds of foods does the AHA recommend to protect your heart?

Not only does it support ample grain consumption, it also recommends eating harmful fats such as canola, corn, soybean and sunflower oil.5 “Blends or combinations of these oils, often sold under the name ‘vegetable oil,’ and cooking sprays made from these oils are also good choices,” the AHA says. Meanwhile, the association still insists saturated fats are to be avoided.

Just this past summer the AHA shocked health experts around the world by sending out a worldwide advisory6 saying saturated fats such as butter and coconut oil should be avoided to cut your risk of heart disease, and that replacing these fats with margarine and vegetable oil might cut your heart disease risk by as much as 30 percent. Overall, the AHA recommends limiting your daily saturated fat intake to 6 percent of daily calories or less.7

This is as backward as it gets, and if Warner was following this long-outdated advice, it’s no wonder he suffered a heart attack. In fact, it is to be expected. As noted by American science writer Gary Taubes in his extensive rebuttal to the AHA’s advisory,8 with this document, the AHA reveals its longstanding prejudice — and the method by which it reaches its flawed conclusions.

In short, the AHA simply excluded any and all contrary evidence. After this methodical cherry-picking, they were left with just four clinical trials published in the 1960s and early ‘70s — the eras when the low-fat myth was born and grew to take hold. The problem is nutritional science has made significant strides since then, and a number of significant studies have firmly disproven the hypothesis that saturated fat causes heart disease, finding no association whatsoever.

Low-salt diet increases insulin resistance in healthy subjects

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Interesting study:


Low-salt diet increases insulin resistance in healthy subjects.
Garg R1, Williams GH, Hurwitz S, Brown NJ, Hopkins PN, Adler GK., Metabolism. 2011 Jul;60(7)

From Wiki Salt

Quote:

Abstract
Low-salt (LS) diet activates the renin-angiotensin-aldosterone and sympathetic nervous systems, both of which can increase insulin resistance (IR). We investigated the hypothesis that LS diet is associated with an increase in IR in healthy subjects. Healthy individuals were studied after 7 days of LS diet (urine sodium < 20 mmol/d) and 7 days of high-salt (HS) diet (urine sodium > 150 mmol/d) in a random order. Insulin resistance was measured after each diet and compared statistically, unadjusted and adjusted for important covariates. One hundred fifty-two healthy men and women, aged 39.1 ± 12.5 years (range, 18-65) and with body mass index of 25.3 ± 4.0 kg/m(2), were included in this study. Mean (SD) homeostasis model assessment index was significantly higher on LS compared with HS diet (2.8 ± 1.6 vs 2.4 ± 1.7, P < .01). Serum aldosterone (21.0 ± 14.3 vs 3.4 ± 1.5 ng/dL, P <  .001), 24-hour urine aldosterone (63.0 ± 34.0 vs 9.5 ± 6.5 μg/d, P < .001), and 24-hour urine norepinephrine excretion (78.0 ± 36.7 vs 67.9 ± 39.8 μg/d, P < .05) were higher on LS diet compared with HS diet. Low-salt diet was significantly associated with higher homeostasis model assessment index independent of age, sex, blood pressure, body mass index, serum sodium and potassium, serum angiotensin II, plasma renin activity, serum and urine aldosterone, and urine epinephrine and norepinephrine. Low-salt diet is associated with an increase in IR [insulin resistance]. The impact of our findings on the pathogenesis of diabetes and cardiovascular disease needs further investigation.

Saturated fat does not clog the arteries

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Saturated fat does not clog the arteries: coronary heart disease is a chronic inflammatory condition, the risk of which can be effectively reduced from healthy lifestyle interventions FREE
Aseem Malhotra1⇑, Rita F Redberg2,3, Pascal Meier4,5

Quote:

Coronary artery disease pathogenesis and treatment urgently requires a paradigm shift. Despite popular belief among doctors and the public, the conceptual model of dietary saturated fat clogging a pipe is just plain wrong. A landmark systematic review and meta-analysis of observational studies showed no association between saturated fat consumption and (1) all-cause mortality, (2) coronary heart disease (CHD), (3) CHD mortality, (4) ischaemic stroke or (5) type 2 diabetes in healthy adults.1 Similarly in the secondary prevention of CHD there is no benefit from reduced fat, including saturated fat, on myocardial infarction, cardiovascular or all-cause mortality.2 It is instructive to note that in an angiographic study of postmenopausal women with CHD, greater intake of saturated fat was associated with less progression of atherosclerosis whereas carbohydrate and polyunsaturated fat intake were associated with greater progression.3

Study contradicts official guidelines promoting low salt intake

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Another mainstream medical theory bites the dust! Just like with the cholesterol-and-fat bull..t in the past - it will be interesting to find out what has gone wrong and who did it!   :)

Higher sodium intake associated with lower blood pressure.

PUBLIC RELEASE: 25-APR-2017
Low-sodium diet might not lower blood pressure
Findings from large, 16-year study contradict sodium limits in Dietary Guidelines for Americans

Quotes:

Chicago (April 25, 2017) - A new study that followed more than 2,600 men and women for 16 years found that consuming less sodium wasn't associated with lower blood pressure. The new findings call into question the sodium limits recommended by the current Dietary Guidelines for Americans.

Lynn L. Moore, DSc, associate professor of medicine at Boston University School of Medicine, will present the new research at the American Society for Nutrition Scientific Sessions and annual meeting during the Experimental Biology 2017 meeting, to be held April 22-26 in Chicago.

"We saw no evidence that a diet lower in sodium had any long-term beneficial effects on blood pressure," said Moore. "Our findings add to growing evidence that current recommendations for sodium intake may be misguided."

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

High cholesterol does not cause heart disease new research finds...statins waste of time

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From US FDA

High cholesterol 'does not cause heart disease' new research finds, so treating with statins a 'waste of time'


Quote:

13 JUNE 2016 • 1:01AM
Cholesterol does not cause heart disease in the elderly and trying to reduce it with drugs like statins is a waste of time, an international group of experts has claimed.
A review of research involving nearly 70,000 people found there was no link between what has traditionally been considered “bad” cholesterol and the premature deaths of over 60-year-olds from cardiovascular disease.
Published in the BMJ Open journal, the new study found that 92 percent of people with a high cholesterol level lived longer.
Lowering cholesterol with medications is a total waste of time
Professor Sherif Sultan, University of Ireland
The authors have called for a re-evaluation of the guidelines for the prevention of cardiovascular disease and atherosclerosis, a hardening and narrowing of the arteries, because “the benefits from statin treatment have been exaggerated”.

Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review


Quote:

Abstract
Objective It is well known that total cholesterol becomes less of a risk factor or not at all for all-cause and cardiovascular (CV) mortality with increasing age, but as little is known as to whether low-density lipoprotein cholesterol (LDL-C), one component of total cholesterol, is associated with mortality in the elderly, we decided to investigate this issue.
Setting, participants and outcome measures We sought PubMed for cohort studies, where LDL-C had been investigated as a risk factor for all-cause and/or CV mortality in individuals ≥60 years from the general population.
Results We identified 19 cohort studies including 30 cohorts with a total of 68 094 elderly people, where all-cause mortality was recorded in 28 cohorts and CV mortality in 9 cohorts. Inverse association between all-cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance; in seven cohorts, no association was found.
Conclusions High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.

Eating too little salt may increase your risk of a heart attack or stroke claims new research

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Daily Mail On-Line article:

Eating too LITTLE salt may INCREASE your risk of a heart attack or stroke, claims controversial new research

Wiki Salt

Nutritional heresy strikes back, some quotes:

The research was carried out by investigators at McMaster University and Hamilton Health Sciences.
They analyzed more than 130,000 people across 49 countries, focusing on whether the relationship between sodium (salt) intake and death, heart disease and stroke differs in people with high blood pressure compared to those with normal blood pressure.
Their findings showed that regardless of whether people have high blood pressure, low-salt intake is linked to a greater incidence of heart attacks, stroke, and deaths compared to average intake.
...

Dr Mente said that this suggests that the majority of individuals in Canada and most countries are consuming the right amount of salt.
He added that targeted salt reduction in those who are most susceptible because of hypertension and high salt consumption may be preferable to a population-wide approach to reducing sodium intake in most countries except those where the average sodium intake is very high, such as parts of central Asia or China.

He added that what is now generally recommended as a healthy daily ceiling for sodium consumption appears to be set too low, regardless of a person's blood pressure level.
'Low sodium intake reduces blood pressure modestly, compared to average intake, but low sodium intake also has other effects, including adverse elevations of certain hormones which may outweigh any benefits,' Dr Mente said.

'The key question is not whether blood pressure is lower with very low salt intake, instead it is whether it improves health.'

Dr Martin O'Donnell, a co-author on the study and an associate clinical professor at McMaster University and National University of Ireland Galway, said: 'This study adds to our understanding of the relationship between salt intake and health, and questions the appropriateness of current guidelines that recommend low sodium intake in the entire population.'

The study was funded from more than 50 sources, including the PHRI, the Heart and Stroke Foundation of Canada and the Canadian Institutes of Health Research.

-----

Reference:

A.Mente et al., The Lancet, 20/05/2016, "Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies"


Please note that the medical authorities have again been caught issuing inaccurate, perhaps harmful nutritional guidelines for half a century based on what appears to be the "treating the numbers" paradigm and experts' opinions rather than based on science. Is nobody responsible for the misconduct?

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)

LDL cholesterol doesn't matter!

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According to this study (Framingham data):

Increased Small Low-Density Lipoprotein Particle Number

Compared with participants without the MetSyn [Metabolic Syndrome], those with the MetSyn had a higher CVD [Cardio Vascular Disease] event rate. However, among participants with the MetSyn, CVD rates were similar for groups with an elevated versus a lower number of small LDL particles (defined by the sex-specific median).

Conclusions— Small LDL particle number is elevated in the MetSyn, increases with the number of MetSyn components, and most prominently is correlated with triglycerides and HDL-C. Whereas increased small LDL particle number identified the MetSyn with high sensitivity, a higher small LDL particle number was not associated with greater CVD event rates in people with the MetSyn.

Putting it in simple terms: the common misconception that LDL correlates with cardio-vascular disease was caused by bad math! LDL correlated with MetSyn and MetSyn correlates with CVD.  Medical establishment leaders with insufficient mathematical training  incorrectly believed that correlation supposedly follows the "The law of syllogism"  (i.e. if LDL → MetSyn and MetSyn → CVD then LDL → CVD) - BUT IT DOES NOT!

 That study simply proved it by finding that in the sub-population of people who already had MetSyn, the number of small LDL particles did not matter!    Cholesterol theory is very dead and thoroughly debunked, case closed!  Fire them all and move on, next myth please...
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Useless low fat dietary guidelines by governments, no scientific justification!

.

Open Heart/BMJ just published a meta-study:

Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis

Objectives National dietary guidelines were introduced in 1977 and 1983, by the US and UK governments, respectively, with the ambition of reducing coronary heart disease (CHD) by reducing fat intake. ...

Conclusions

Dietary recommendations were introduced for 220 million US and 56 million UK citizens by 1983, in the absence of supporting evidence from RCTs.

Discussion
The main findings of the present meta-analysis of the six RCTs [Randomized Controlled Trials] available at the time of issuing dietary guidelines in the US and UK indicate that all-cause mortality was identical at 370 in the intervention and control groups. There was no statistically significant difference in deaths from CHD. The reductions in mean serum cholesterol levels were significantly higher in the intervention groups; this did not result in significant differences in CHD or all-cause mortality.
It is a widely held view that reductions in cholesterol are healthful per se. The original RCTs did not find any relationship between dietary fat intake and deaths from CHD or all-causes, despite significant reductions in cholesterol levels in the intervention and control groups. This undermines the role of serum cholesterol levels as an intermediary to the development of CHD and contravenes the theory that reducing dietary fat generally and saturated fat particularly potentiates a reduction in CHD.
...
There was best practice, randomised controlled trial, evidence available to the dietary committees, which was not considered and should have been. The results of the present meta-analysis support the hypothesis that the available RCTs did not support the introduction of dietary fat recommendations in order to reduce CHD risk or related mortality. Two recent publications have questioned the alleged relationship between saturated fat and CHD and called for dietary guidelines to be reconsidered.31 ,32 The present review concludes that dietary advice not merely needs review; it should not have been introduced.

Actual data from the publication:

References and links:

http://www.zoeharcombe.com/blog/

Interestingly, the original studies at that time produced similar similar conclusions of non-supporting the reduction of dietary fat.  The following quotes are from Zoë Harcombe's blog (one of the main author of the above quoted study):

The studies’ own conclusions.  These are the verbatim conclusions from each of the studies:

1965 Rose Corn and olive oil: “It is concluded that under the circumstances of this trial corn oil cannot be recommended as a treatment of ischaemic heart disease. It is most unlikely to be beneficial, and it is possibly harmful.” (ref 9)

1965 Research Committee Low-fat diet: “A low-fat diet has no place in the treatment of myocardial infarction” (ref 10) [heart attack].

1968 MRC soya-bean oil: “There is no evidence from the London trial that the relapse-rate in myocardial infarction is materially affected by the unsaturated fat content of the diet used.” (ref 11)

1969 Dayton LA Veterans study: “Total longevity was not affected favorably in any measurable or significant degree… For this reason, and because of the unresolved question concerning toxicity, we consider our own trial, with or without the support of other published data, to have fallen short of providing a definitive and final answer concerning dietary prevention of heart disease.” (ref 12)

1970 Leren Oslo Diet Heart study: “Epidemiological studies have demonstrated several factors associated with the risk of developing first manifestations of coronary heart disease. Blood lipids, blood pressure and cigarette smoking are such risk variables… In spite of the small numbers this observation lends some support to the view that the multi-factorial approach is the best way to the solution of the coronary heart disease problem.”(ref 13)

1978 Woodhill Sydney Diet Heart Study: “Survival was significantly better in the P [control] Group.” “It must be concluded that the lipid hypothesis has gained little support from secondary intervention studies.” (ref 14)
...

Salt intake not correlated with mortality

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New study and one more medical myth demolished:

Dietary Sodium Content, Mortality, and Risk for Cardiovascular Events in Older Adults

Wiki

Quote:

Results  The mean (SD) age of participants was 73.6 (2.9) years, 51.2% were female, 61.7% were of white race, and 38.3% were black. After 10 years, 881 participants had died, 572 had developed CVD, and 398 had developed HF. In adjusted Cox proportional hazards regression models, sodium intake was not associated with mortality (hazard ratio [HR] per 1 g, 1.03; 95% CI, 0.98-1.09; P = .27). 

Statins review paper

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"Nuclear explosion" is probably a better term than review!

Source Wiki

"The Ugly Side of Statins. Systemic Appraisal of the Contemporary Un-Known Unknowns" by Sherif Sultan and Niamh Hynes published in Open Journal of Endocrine and Metabolic Diseases, 2013, 3, 179-185.

The whole text is well worth reading in its entirety! Some quotations:

From the Abstract:

A comprehensive review of Pubmed, EM-BASE and Cochrane review databases was undertaken for articles relating to cardiovascular primary prevention and statin side effects with the aim of harmonising their roles within contemporary clinic practice. Particular attention was paid to large-scale randomised controlled trials on contemporary cardiovascular pharmacotherapies and their specific adverse effects on metabolic pathways which feature prominently in cardiovascular primary prevention and regenerative programmes.

There is a categorical lack of clinical evidence to support the use of statin therapy in primary prevention. Not only is there a dearth of evidence for primary cardiovascular protection, there is ample evidence to show that statins actually augment cardiovascular risk in women, patients with Diabetes Mellitus and in the young. Furthermore statins are associated with triple the risk of coronary artery and aortic artery calcification.
...

Utmost Medical Tragedy.

We seem to have fallen into the marketing trap and ignored the niggling side effects with regard to the HMG-CoA reductase inhibitors [1]. The only statin benefit that has actually been demonstrated is in middle aged men with coronary heart disease. However, statins were not shown to best form of primary prevention. Aspirin, as a form of primary prevention decreases the risk for total cardiovascular events and nonfatal Myocardial Infarction over any other factor [5]. In actual fact, high cholesterol levels have been found to be protective in elderly and heart failure patients and hypo-cholestereamic patients had higher incidence of intra-cerebral bleeds, depression and cancer [1].

The statin industry, with all of its spin-off, is a 20-billion-a-year industry. We are observing the revealing of the utmost medical tragedy of all times. It is unprecedented that the healthcare industry has inadvertently induced life-threatening nutrient deficiency in millions of otherwise healthy people. What is even more disparaging is that not only has there been a failure to report on these negative side-effects of statins, there has actually been active discouragement to publish any negative studies on statins.

Statins induce diabetes.

The US Veterans affair healthcare system study on 15 million veterans in 10 hospitals in Southern USA concluded that statins affect fasting and postprandial glucose level by inducing a state of hyperglycaemia in diabetic as well as non diabetic patients [12]. This relationship between statin use and rise in glucose level is independent of age and use of aspirin, beta blockers and angiotensin-converting enzyme inhibitors. Furthermore, a sub-analysis of the JUPITER study showed that statin therapy can induce full blown type 2 diabetes in women [13]. This was astonishingly shown in the sub study of PRO-VE-IT TIMI 22, in which there was a significant increased risk of developing HBA1c > 6% in both diabetics and non diabetics [14]. Moreover Huptas et al. have demonstrated that statin therapy can induce a state of insulin resistance [15].
...
Statins manipulate glucose metabolism as a consequence of inhibitory effects on adipocytes. They induce insulin resistance through reduction in insulin-stimulated glucose uptake with a strong impact on glycaemic control in non obese patients.
...
Preiss et al. [19] demonstrated, in a pooled analysis of data from the five major statin trials, an increased incidence of new onset diabetes with statin therapy and provided evidence of a dose dependent association.

Statins accelerate arterial calcification.

The Confirm registry had shocked the scientific world with the strongest evidence that statin use is associated with an increased prevalence and extent of coronary plaques calcification [32]. Ironically for a drug which was marketed to lower the risk of cardiovascular disease, the confirm registry identified a strong association of statin use to the progression of coronary artery plaque features. Moreover, Statin use was correlated with a greater incidence of severe coronary artery stenosis as well as increase in the numbers of coronary vessels developing obstructive coronary artery disease. Furthermore, statin use was linked to an increase in the prevalence and extent of mixed calcific plaque. Five prospective studies have borne witness to the fact that statin therapy does not induce any coronary calcium regression and evolution of coronary calcium continues regardless of statin treatment[33,34]. The Veteran Affairs Diabetes Trial [35] established that statin consumption was linked to accelerated progression of Coronary Artery Calcification (CAC) in participants with Type 2 Diabetes Mellitus without previous coronary artery disease, despite the fact that statin users had significantly lower and nearly optimal LDL-cholesterol levels.

------

Updated 5-Oct-2013, press news by Irish Independent:

"HSE gags surgeon after cholesterol drug claims"

A LEADING vascular surgeon [Sherif Sultan], whose research review concluded cholesterol-lowering medicines may do more harm than good for many otherwise healthy people, has been gagged by the Health Service Executive. ...

It's the olive oil not veggies!

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"Primary Prevention of Cardiovascular Disease with a Mediterranean Diet" NEJM, February 25, 2013

A total of 7447 persons were enrolled in this Spanish study (age range, 55 to 80 years). Three groups: (1) control diet, (2) Meditteranean Diet with Nuts, and (3) Meditteranean Diet with Extra Virgin Olive Oil.

Significantly less cardiovascular events and death in group (2) and (3) (P=0.009 and 0.02) but only group (3) showed a noticeable (P=0.11) reduction of death from all causes.

Fig.1 from the Spanish study.

Please notice no reduction of death from all causes in the nuts group!

To me this study is a clear endorsement of the type of fatty acids characteristic of olives, as being unequivocally healthy, while nuts may lower one risk while increase some other.

Why were nuts as good as extra virgin olive oil (EVOO) for cardio but not as good in terms of total death?  Was there some other  cause of death that was positively correlated with nuts (but not with EVOO), which neutralized the benefit of eating nuts for cardio-vascular health?   I am guessing here but it is quite possible that polyunsaturated fat from nuts may have contributed to cancer risk whereas the mono-unsaturated and saturated fats from the olive oil did not!  

See also NYT article.

Study: double mortality after replacing animal fats with vegetable fats

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Also a mystery of some "missing data" etc. I am reposting this quote from Barry Groves' blog:

Quote:

...
The new research, published online in the British Medical Journal, was carried out by experts from the US Government’s National Institutes of Health in Maryland. They recovered missing data from a study in the 1960s involving 458 men aged 30-59 who had suffered a heart attack or angina. Using modern statistical methods to compare death rates, they found there was no evidence of the benefit of replacing saturated fats with omega-6 linoleic acid, found in vegetable fats. In fact, they said replacing the animal fats with polyunsaturated fatty acids (PUFAs) from vegetable fats increased risk of death in those patients with cardiovascular disease. Those who increased their intake of the “healthy” fats over three years were almost twice as likely to die. The omega-6 linoleic acid group in the study had a higher risk of death from all causes (62 per cent), as well as from cardiovascular disease (70 per cent) and coronary heart disease (74 per cent), compared to others. Linoleic acid is present in high amounts in some commonly used vegetable oils such as corn, sunflower, safflower and soya bean.
...

The study was published in BMJ on the 5-Februsary 2013: "Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis" (pdf)

More quotes (from the study, the highlights and the capitalized comments in [] brackets are mine):

Advice to substitute vegetable oils rich in polyunsaturated fatty acids (PUFAs) for animal fats rich in saturated fatty acids (SFAs) has been a cornerstone of worldwide dietary guidelines for the past half century.1 When this advice originated in the 1960s, PUFAs were regarded as a uniform molecular category with one relevant biological mechanism—the reduction in blood cholesterol.1 2 Omega 6 (n-6) linoleic acid (LA) was the best known dietary PUFA at the time.

...

Diet intervention
The intervention group received instructions to increase their PUFA intake to about 15% of food energy, and to reduce their intake of SFA and dietary cholesterol to less than 10% of food energy and 300 mg per day, respectively.10 To achieve these targets, intervention participants were provided with liquid safflower oil and safflower oil polyunsaturated margarine (“Miracle” brand, Marrickville Margarine). Liquid safflower oil was substituted for animal fats, common margarines and shortenings in cooking oils, salad dressings, baked goods, and other products, and was also taken as a supplement. Safflower oil polyunsaturated margarine was used in place of butter and common margarines.

Control
The control group received no specific dietary instruction. However, some participants began substituting polyunsaturated margarine for butter after their coronary event.33 Because the research team made no effort to alter the PUFA or SFA content of control diets, such dietary changes were allowed to continue.
...
In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit. These findings could have important implications for worldwide dietary advice to substitute omega 6 linoleic acid, or polyunsaturated fats in general, for saturated fats.[IF THEY HAD BEEN PUBLISHED RATHER THAN GONE MISSING, AT THE TIME, FOURTY YEARS AGO!]
...
Increased all cause mortality in the safflower oil group was reported in 1978,10 although deaths due to cardiovascular disease and coronary heart disease were not reported by group.[BECAUSE THE DATA WENT MISSING!] Clinical outcomes for cardiovascular disease and coronary heart disease have been considered to be more relevant than all cause mortality when evaluating the evidence base25 and formulating dietary guidelines.26 Therefore, previous meta-analyses of PUFA intervention trials and risk of cardiovascular disease25 27 28 have been incomplete because they were not able to include these missing data from the SDHS. [SDHS=SYDNEY DIET HEART STUDY. CONCIDENTALLY, THE MISSING HEART MORTALITY DATA HAPPENED TO CONTRADICT, BY A LARGE FACTOR, THE EXPECTED OUTCOME! HAD THE HEART MORTALITY DATA NOT GONE "MISSING" FOURTY YEARS AGO, THE ENTIRE VEGETABLE OIL INDUSTRY WOULD PROBABLY NOT EXIST BY NOW!]

Interestingly, since the control group was found also shifting towards substituting all animal fats with vegetable oils and spreads, the degree of dietary change between the study group and the control group was most likely smaller than the nominal goal for PUFA intake increase to 15%. Yet, such a small difference of probably much less than 15% in PUFA (in absolute calories) have created a huge increase in cardiovascular disease, by about 70%. It indicates that the relative risk of cardiovascular disease rises proportionally to the absolute PUFA caloric intake, with a proportionality factor of about 5 or higher! (If the linear interpolation model holds true). Furthermore, an increase due to PUFA was even higher than an increase in cardiovascular mortality due to smoking (see Table 6)!

This high multiple factor seems to be confirm by the data from Table 5 indicating that for every 5% PUFA increase (in absolute energy%) the All cause mortality, the Cardiovascular disease mortality and the Coronary heart disease mortality increased by 31%, 35% and 26% respectively (relative risk factor).  This implies a proportionality factor of about 5-7.

 That is, for every 1% added Poly-Unsaturated Fatty Acids ( PUFA) in absolute calories % of the total, cardiovascular mortality INCREASED  by 5 to 7%. This is big news!

There is an even bigger news: Saturated fat is good for us! Table 5 exonerates the much maligned saturated fats from being implicated in heart disease (Dr. Ornish, please listen). For every 5% added saturated fat (in % of absolute total calories) the risk of mortality defined in the same categories as above DECREASED  by 30%, 28% and 28% respectively!  With the proportionality factor being also about 6, that is for every +1% of absolute saturated fat intake, mortality decreased by 6%!

This study has also neatly killed the second "bird" - the infamous cholesterol-heart disease hypothesis, quote:

As expected, increasing n-6 LA from safflower oil in the SDHS significantly reduced total cholesterol; however, these reductions were not associated with mortality outcomes (results not shown). Moreover, the increased risk of death in the intervention group presented fairly rapidly and persisted throughout the trial. These observations, combined with recent progress in the field of fatty acid metabolism, point to a mechanism of cardiovascular disease pathogenesis independent of our traditional understanding of cholesterol lowering.

It is interesting to observe the exact moment, around year 3.5 into the study on the graph Fig.2c below. I am speculating here, but a dramatic fall of mortality rates in both the intervention and in the control group coincidental with a sudden increase in quitting the study, may indicate a point when the participants and doctors realized that something is wrong and begun reverting to their previous diet. Butter, anyone?

Fig.2 (bottom) from the study.  

Notice how the number of deaths dropped to zero after year 3.5, and a dramatically higher rate of study-quitting by the patients. About 30 people used to leave the intervention group per year (out of which 5-16 were due to death) until year 3.5. Subsequently 49 and 36 patients quit but none died! There is probably more to be told that wasn't discussed in the paper, but the numbers reveal enough...

Lower LDL cholesterol = more heart failure death!

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Another fascinating paper caught by my friends from a vegan forum - and another chunk of the mainstream medical belief system imploding!  

Note (*)

68% more death in the group with LDL < 71mg/dL (1.8 mmol/L) compared with those > 130mg/dL!

New study "Low-Density Lipoprotein Levels in Patients With Acute Heart Failure" by 
Mark R. Kahn et al., 16 Oct 2012,  found strong rising trend towards higher and higher mortality with lower and lower LDL, in every subcategory of the heart disease etiology or statin/lack of statin treatment. For example, for the total mortality (multivariate statistical analysis), relative mortality risk increased monotonically with lowering of the LDL such as illustrated in the following table:

LDL (mg/dL)	Relative Mortality
> 130	1.0
101-130	1.16
71-100	1.25
< 71	1.68

(based on table III in the study)

The study showed a similarly increasing mortality risk with lower LDL, over time, illustrated by the following figures from the paper:

*)  Harvard Medical School building