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Fats that Heal & Fats that Kill

One of the most interesting results was finding out I belong to Haplogroup U which according to Wiki:

"Haplogroup U is found in approximately 11% of native Europeans and is held as the oldest maternal haplogroup found in that region. In a 2013 study, all but one of the ancient modern human sequences from Europe belonged to maternal haplogroup U, thus confirming previous findings that haplogroup U was the dominant type of Mitochondrial DNA (mtDNA) in Europe before the spread of agriculture into Europe and the presence and the spread of the Indo-Europeans in Western Europe."

Since all my ethnicity also came back as Western Europe, mostly Irish, British, Scandinavian, it confirmed for me that I'm on the right track by following the Paleo/Primal/LCHF way of eating

I already knew that just from the increasing health benefits I've experienced over the last 4 years, but was good to have it confirmed in black and white
 
Galja said:
At some point, they stopped selling flaxseed oil in the health food stores of the US which was our primary source for linoleic

As flax is dead cheap to grow and even has a rather short growing cycle, it would seem a no brainer to up the industry
Click to expand...

The author Udo Erasmus who is a Canadian, set up a manufacturing strategy for EFAs some time back. His supplements made principally from flax oil as a core ingredient are made in strictly controlled conditions for light, heat and oxygen. You can review them at his site www.udoerasmus.com


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Oh wow that's a new one on me. Must try it


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The Promethease report has excellent links to most of the research (including the 2 you mention) involved with each SNP. Sometimes so many references it's overpowering at times.
 
In Chapter 32 "Fat Consumption and Daily Requirements", the author refers to 1979 US figures which indicate the average citizen consumed 135 pounds (61kg) of fats that year, about 168grams per day. The fat consumed was made up of:

34% saturated
40% monounsaturated
15% polyunsaturated (w6) fatty acids

The info did not distinguish EFAs from non-essential, altered, denatured, and toxic polyunsaturates.

W3 intake was completely ignored.

The amount of EFAs left in their natural state after hydrogenation, exposure to destruction by light, air and food prep (both commercially and in the home) will be lower, and some of this may be unavailable to our body because saturated and monounsaturated long-chain fatty acids, trans, and sugars present in the diet interfere with EFA functions.

Interestingly, fat consumption has been increasing by about 1 pound per person per year up to the printing of this edition in 1993. I wonder if this has continued?

Nutrition Review indicated that fat consumption in other countries was considerably lower than the classic Western daily consumption:

Thailand 27gpd

Philippnes 30gpd

Japan 40gpd

Taiwan 45gpd

Denmark 160gpd

NZ 155gpd

UK 142gpd

US 168gpd

Canada 142gpd

People in the nations consuming a low-fat diet have a lower incidence of fatty degeneration, and people in the high-fat nations have a high incidence of fatty degeneration......Emmmmm....do we believe the extrapolation of that last statement?





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Galja said:
Here is the CDC summary

http://www.cdc.gov/nchs/fastats/diet.htm

Now, on public TV they had mention that transfat consumption has dramatically dropped but can't find confirmation of that
Click to expand...

I believe that trans fat inclusion is now illegal in the US, although providing it is under 0.5%, the legislature has allowed this level to be classified as "no trans".


@Oldvatr, will probably be able to fill in the gaps on this, as I am not sure about the UK status.


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There are currently no UK legal requirements for food manufacturers to label trans fats...This means you need to check ingredients lists for hydrogenated fats or hydrogenated vegetable oils.

Trans fats in the USA are not yet banned, and manufacturers have about 3 years to implement their removal or replacement by fully saturated varieties.
In 2012 the UK Government decided that there will be no legal action to remove transfats in UK manufactured foods. The FSA has stated that the level of TFA in UK foods is considered to be safe and no action is required. A voluntary Code of Conduct is informally being discussed between manufacturers, but it will not be binding

Most UK supermarket retailers have taken steps to remove TFA from their Own Brands, and Sainsbury is the only one so far that has achieved this. Wikipedia has an interesting coverage on this, so I am not going to copy it here,
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@Indy51

Don't know if you can answer this, but I am very curious about what an average no of polymorphisms that increase risk of Type 2 would be. Have you come across that? Or any information about what numbers are found in people already with T2?

Obviously, I am just being lazy, because I could probably find this out myself, but am wondering if you already know, and can save me the research.
 
Sorry, no I haven't run across that information. I was judging by the average of other SNPs I had for other diseases - the one that came closest to Type 2 was 11 for macular degeneration (and there's a family history of that, though none for Type 2 that I know of).

A lot also depends on the state of the research and how many studies have been done for specific diseases, eg. I know a lot of research has been done on macular degeneration. I figure a lot must have been done on prostate cancer as I came up with heaps of SNPs for that - thankfully I'm female so presumably don't have to worry about it

And of course the research is evolving and changing all the time - also research into specific diseases depends very much on funding, etc.
 
Learned something brand new to me this morning from my new text book.

It's called GAS (General Adaptation Syndrome).

This was developed in the 1940's by a medical doctor and researcher by the name of Hans Selye, whose specialism was Stress. He focused on both Positive stress (essentially things of which you have control) and Negative stress, those issues in life over which you are unlikely to have control.

During many years of research and careful observation Selye, identified one single unified underlying adaptive mechanism which deals with all kinds of stress and this is GAS which has 3 distinct stages:

1. Alarm Reaction: the candidate displays, restlessness, nervousness, "jitters" and other non-specific and non-directed behavioural sign of agitation.

2. Resistance: this follows Alarm Reaction and is essentially where our internal resources, mainly bio-chemical at the root of physiological and psychological responses endeavour to cope via Resistance. If the inner resources are sufficient to overcome the stress, we ADAPT (the A in GAS) and recover.

3. Exhaustion: If stress is greater than our Adaptive resources, exhaustion occurs. The most noticeable organ changes at this stage include enlarged stress-fighting (adrenal) glands and atrophied (shrunken) immune system (lymph and thymus). Diseases of Adaptation include:

High BP, water retention, arthritis, heart enlargement, strokes, ulcers, kidney problems, allergies, diabetis, neuro probs and cancer

Interestingly, these disease symptoms resemble symptoms of Essential Fatty Acids (EFA) deficiency.





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IMHO this is nothing new, It is the classic 'fight or flight' response to stress. Andrenalin is released which blocks insulin, and opens up the cells to energy release. The symptoms described cover everything under the sun, and are also generally recognised as standard side effects of diabetes. So is it chicken or egg? Does diabetes trigger adrenalin release as insulin resistance, or does prolonged stress cause diabetes? The article is describing observed reactions, but does not address the root causes.

Edit to Add: Personally, when I have GAS, my symptoms are somewhat different LOL
 

I'll summarise his conclusions re control later on today


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Selye, identified within each organism a sort of "life battery". His two poles of the battery were Good Oils and Proteins. Oils rich in EFAs, and sulphur rich proteins: oils containing many slightly negatively charged cis-double bonds and proteins containing many slightly positively charged sulphydryl groups. Between the two life poles runs our life currents, produced by the metabolism of carbohydrates and other molecules, flow when the circuit of essential nutrients is complete.

More stress requires more oils and proteins (as well as minerals and vitamins); less stress requires less. Whenever the demand by our body for good oils, protein and cofactors exceeds that supplied by our foods, our body begins to run down, and we slowly develop deficiency as reserves are used up. Deficiency leads to weakness, then sickness. The severity of the sickness depends on the severity of the deficiency. We then need rest, time to replenish our resources, and good nutrition for the low supplies.

So, Proteins and Good Oils are the two most abundant substances in our cells, we find them together in cell membranes, in lipoproteins that carry fats and cholesterol in our blood and in membranes of sub cellular organelles. They form the main structures and functional components of our entire body and so are the key biochemical armoury to deal with stress, and specially negative stress on a day to day basis.


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Another Rhonda Patrick interview, this time with one of the most respected lipid researchers in the US, Dr Ron Krauss. Rhonda's precis of the interview follows:

"In this conversation, Ron and I discuss...
  • Changes in the availability of funding for good nutritional research.
    • "It's a fact that NIH, which is the major funder of biomedical research in the world, has basically pulled the plug on clinical research support as a general area of emphasis. The infrastructure for doing good nutritional studies, in particular, has relied on a mechanism that is now being withdrawn." - Dr. Ronald M Krauss
  • The important difference between consumption of dietary cholesterol, which has a negligible influence on heart disease risk, and cholesterol produced endogenously in the body (which can be a marker of risk, depending on a complete profile).
  • The good, bad and the ugly of LDL-lowering drugs known as statins and much more.
  • What differentiates fructose from fruit versus fructose as an added sugar, namely: speed of absorption, presence or absence of other beneficial compounds (fiber, micronutrients, polyphenols, etc.), and differences in dose.
  • How LDL (low-density lipoprotein), and particularly the ApoB protein inside of LDL, is needed to transport cholesterol, triglycerides, and fatty acids throughout the bloodstream in order to deliver them to other tissues in the body that may need them.
  • What small, dense LDL particles are, how they form, what effect eating saturated fat versus refined carbohydrates have on LDL particle size and heart disease risk and more generally what the main risk factors for heart disease are.
  • The functional difference between large, buoyant LDL particles and small, dense LDL particles and introduces us to the traits of what he terms "atherogenic dyslipidemia." These traits consist of:

1. High levels of small, dense LDL cholesterol.

2. Low levels of HDL cholesterol.

3. High levels of triglyceride-rich lipoproteins (very-low-density lipoproteins or "VLDL") and their remnants.
  • How small, dense LDL particles increase the risk of atherosclerosis. There is only one ApoB protein per LDL particle, which is what enables ApoB to be a surrogate blood biomarker for LDL particle number.
  • How access to the ApoB protein can become obscured due to conformation changes in the small, dense LDL particles. As the size of the particle decreases, this conformation change reduces the ability for the particle to bind to the LDL receptor and be recycled by the liver.
  • How VLDL particles, the precursor to LDL, demonstrate an interaction with LPS (also known as endotoxin, a component of bacterial cell membranes), and how it's possible that some of the negative associations with this particle size may be a result of their simply being in the blood stream longer: this gives them a greater opportunity to undergo inflammatory transformations.
  • This part is especially exciting to me because it may be an interesting link by which gut health (where much of the bacteria and immune cells in the body are located) and the importance of controlling inflammation to cardiovascular health.
  • How saturated fat appears to increase the larger, more buoyant LDL particles, which do not have the same robust correlation to heart disease risk that the smaller, more dense particles do. Dr. Krauss also takes the stance that consumption of saturated fat does not have as strong of a link to heart disease risk as previously suggested by others, and may be less relevant except in the case of what he termed "hyper-responders." These "hyper-responders" have gene polymorphisms that cause them to respond differently to saturated fat.
  • How increased carbohydrate consumption, especially simple sugars may have been an unintended consequence of the push for low-fat diets, and how this increased traits associated with atherogenic dyslipidemia: namely, a shift from the larger, more buoyant LDL particles to the smaller, more dense LDL particles.
  • Broadly, the differences between the various types of lipoprotein particles, including very-low-density lipoproteins (VLDL), and high-density lipoprotein (HDL) and what their roles are in the body."
 
@KevinPotts thanks for your many chapter summaries that resulted in interesting conversations here. I'm coping with a cold at the moment, and this was a nice distraction tonight.
 
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