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.

Cold environment, ketogenic diet and longevity

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A new lead:
Feeling Cold May Add Years to Your Life

Living in cold and frigid temperatures may be worth while as new research shows possible benefits of cold air for humans. A research study done at the University of Michigan observed the effects of cold air on the gene receptor, TRPA-1. The TRPA-1 receptor channel can be found in the nerve and fat cells of nematodes, also known as roundworms. It was discovered that roundworms live significantly longer under colder environments because the cold air seems to start a domino effect beginning with the receptor that eventually leads to the activation of the DAF-16/FOXO, the gene linked to longevity.
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Due to this new research, the human body's receptors should ideally trigger the longevity gene when it comes into contact with cold air. The research also concluded that mice, which are also warm blooded mammals, can live longer when their body temperatures are lowered by 0.9 degrees Fahrenheit. It was measured that their lifespan can be lengthened by 20%. Warm blooded mammals can reduce their core body temperature by careful calories restrictions. However, these methods have not been practiced or studied with the human body. In addition to cold air, research shows that other factors, such as wasabi and mustard oil also act as triggers to this chain reaction.

Does ketogenic diet come in only as the pretext to consume wasabi and mustard? Not only, ketogenic diet stimulates production of methylglyoxal ["Methylglyoxal on Atkins... Uh oh!" , "Ketosis leads to increased methylglyoxal production on the Atkins diet."] which activates TRPA-1 [see "METHYLGLYOXAL ACTIVATES NOCICEPTORS THROUGH TRPA1..."]. Incidentally methylglyoxal also disrupts cancerous cells ["A brief critical overview of the biological effects of methylglyoxal..."]

More reading on the subject, and on Dr. Jack Kruse's Cold Thermogenesis ideas can be found in his blog.
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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:

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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.
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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.

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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.
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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!]
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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...