Since late 2016 we have entered the age of disclosures! Fasten your mental safety belt and enjoy the ride! Heretic

Wednesday, March 30, 2016

Vegetarian diet causes genetic adaptation that raises risk of heart disease and cancer

- which was found by an Indian/American study "Positive selection on a regulatory insertion-deletion polymorphism in FADS2 influences apparent endogenous synthesis of arachidonic acid" published in Mol Biol Evol (2016) doi: 10.1093/molbev/msw049 on March 29, 2016.

The study found a specific genetic adaptation to vegetarian diet that is detrimental to cardiovascular health and causes higher susceptability to cancer, due to enhanced production of arachidonic acid. Such adaption is not observed among populations consuming diets that are not exclusively plant-based.

From Wiki 
More discussion of the study can be found in:

Science Daily / Are we what we eat?
Evidence of vegetarian diet permanently shaping human genome to change individual risk of cancer, heart disease


In a new evolutionary proof of the old adage, 'we are what we eat,' scientists have found tantalizing evidence that a vegetarian diet has led to a mutation that -- if they stray from a balanced omega-6 to omega-3 diet -- may make people more susceptible to inflammation, and by association, increased risk of heart disease and colon cancer.

Daily Mail - Vegetarian diet 'raises risk of heart disease and cancer'


Vegetarianism over generations can result in genetic mutations which increase the risk of heart disease and cancer.
Researchers found a long-term vegetarian diet means populations are more likely to carry DNA that makes them vulnerable to inflammation.
The mutation is believed to make it easier for vegetarians to absorb necessary fatty acids from plants, but also boosts their production of arachidonic acid, which increases inflammatory disease and cancer.

Added 2/04/2016

This is an important study because it is not only describing statistical correlation which may or may not reflect the real causes, but it also described specific biochemical and genetical mechanisms underlying the effects they have observed. I am tempted to draw the following conclusions, some of them may be a bit stretched, some not. Time will tell.

1) The key factor in the chronic diseases are polyunsaturated fats - not the carbohydrates and not the other types of fats (for example not the mono-unsaturated or saturated fats).

2) Adaptation to a low fat plant based nutrition takes place over many generations of people, works through epigenetic mechanisms, predisposing such populations to efficiently process and convert the little amount of total and mostly polyunsaturated plant fat that they eat. This adaptation allows them to very efficiently convert the small amounts of vegetable oils they consume to some essential fatty acids required for the body, preventing malnutrition related deficiency diseases.

3) The same adaptation allowing low fat plant based food eaters to survive, causes chronic diseases risk once they add too much polyunsaturated fat into their diet, due to hyperactivity of metabolic pathway involving arachidonic acid and prostaglandins. The threshold is probably 5-10% of calories. This threshold applies to polyunsaturated fats of all kinds, including fish fat - BUT IT DOES NOT APPLY TO SATURATED FATS!

4) Both population groups - the one adapted to a low fat plant based diet and the one unadapted could safely consume larger amounts of saturated fats (i.e animal saturated fat, dairy fats, coconut fat etc) if they choose so, without a detriment to their health because saturated fats do not partake in the biochemical pathways involving arachidonic acid and prostaglandins.

5) Population adapted to low fat plant based diet should not consume more than a few percent (in total calories) of polyunsaturated fats such as vegetable oils (and fish oil!), otherwise the risk of chronic diseases increases.

6) Population not adapted to low fat plant based diet, not only can but should consume somewhat higher amounts of polyunsaturated fats including fish fat. How much would be OK and how high is too high? This is to be determined, I am not sure! This will ensure adequate supply of some essential polyunsaturated fatty acids, that their bodies cannot synthesize as efficiently as the adapted group! At the same time, the non-adaptation to low fat makes this group particularly well adapted to consuming larger amounts of polyunsaturated fish fat!

7) For the people who are not adapted to a low fat plant based diet, or those who tried it but could not or would not do it, I would say this: - a high animal fat diet will automatically make it low to moderate in polyunsaturated fats (suitable to both adapted and non-adapted) as long as you avoid using vegetable oils! If in addition, you avoid also consuming excessive amounts of carbohydrates then you will avoid other risk factors involving metabolic dysfunctions involving hyper-insulinemia and glucose overload.

8) Last but not least, I am directing this message to my vegetarian on-line friends and real life friends: - if you find yourself thriving on a low fat plant based diet then you are probably genetically adapted to it, therefore ABSOLUTELY avoid consuming more than a few % of daily calories in form of plant oils and fish (or fish fat)! Stay with it - it will probably work for you, however you most likely DO NOT NEED TO AVOID SATURATED FAT! You do not need to avoid meat, dairy and poultry either but watch out for the polyunsaturated contents of some animal fat! In this respect, if you wanted to add meat to your low fat plant based diet, you are probably better off adding beef rather than chicken or fish!


9) Limiting consumption of polyunsaturated oils, especially Linoleic Acid present in commercial vegetable oils, will likely reduce mitochondrial damage alleviating the risk of metabolic syndrome, even on a high carbohydrate diet. This is key point of the Cardiolipin hypothesis that postulates that the primary cause of metabolic syndrome is mitochondrial degeneration due to incorporation of the linoleic acid into cardiolipin molecules, which makes mitochondria exceedingly vulnerable to oxidative damage. Such oxidative damage may be triggered be glucose overload as in a high carbohydrate diet, or by other factors. This is a two step process the primary factor (a) being the linoleic acid making mitochondria vulnerable and in the second stage (b) carbohydrate overload (or other toxins) actually damages the mitochondria. For further details on Cardiolipin hypothesis read Tucker Goodrich comments under my previous post and this blog.
I thoroughly enjoyed this article by Dr. Kendrick, very much on the topic of polyunsaturated fats: "Greater Cholesterol lowering increases the risk of death" , I hope you too. Here are some quotes:

The original researchers who set up and ran the SDHS did not fully publish their data at the time (one can only speculate as to why this may be so). When this current group of researchers finally managed to get hold of the full data from the SHDS, it was found that replacing saturated fat with polyunsaturated fat did lower cholesterol, however:

and another one:

The Minnesota Coronary Experiment (MCE), a randomized controlled trial conducted in 1968-73, was the largest (n=9570) and perhaps the most rigorously executed dietary trial of cholesterol lowering by replacement of saturated fat with vegetable oil rich in linoleic acid.
Now, a few years later, the researchers who re-analysed the Sydney Diet Heart Study decided to try and find all the unpublished data from the Minnesota Coronary Experiment (MCE). (One can again only speculate as to why the original researchers did not reveal all of their data). The main points from this re-analysis were the following

* Though the MCE intervention lowered serum cholesterol, this did not translate to improved survival

* Paradoxically, MCE participants who had greater reductions in serum cholesterol had a higher, rather than lower, risk of death

Stan (Heretic)

Saturday, March 5, 2016

They tried really really hard...

.. to prove that cholesterol and eggs were supposed to be harmful, in the most recent Finnish study:

Associations of egg and cholesterol intakes with carotid intima-media thickness and risk of incident coronary artery disease according to apolipoprotein E phenotype in men: the Kuopio Ischaemic Heart Disease Risk Factor Study

I respect persistence, dedication, efforts and resources devoted by the world medical establishment to their long term goals. I believe that no civilian scientific project ever, in the history of science, commanded more time, efforts and money than attempting to prove Ancel Keys' cholesterol theory of the 1950-ties! Probably more so, if we include the R&D efforts by the pharmaceutical companies, than even the space programs.

Conclusion: Egg or cholesterol intakes were not associated with increased CAD risk, even in ApoE4 carriers (i.e., in highly susceptible individuals).

(Thanks JC for the link alert)