Showing posts with label fat - omega 6 sceptic/dangers. Show all posts
Showing posts with label fat - omega 6 sceptic/dangers. Show all posts

7.10.11

Fish oil, misuse & inflammatory disease - Rob Wolf

Fish Oil

Ahhh…fish oil. A whole industry built around supplying us with something that should be a natural part of our food supply. Prior to the 1970’s meat and dairy in the United states was still grass fed so we received ample amounts of the main constituents of fish oil, EPA and DHA, as part of our normal diet. With the adoption of grain feeding our cattle and the use of seed and vegetable oils heavy in the short omega 6 fat (linoleic acid) we have witnessed a dramatic shift away from the essential fatty acid profile we’d expect to see from an ancestral diet of ~1-1 or 2-1 N-6/N-3 to more than 10-1.

The health implications of this shift have not been great. The N-6 family tends to produce “pro-inflammatory” cellular signaling, while the N-3 family tends to produce “anti-inflammatory” signaling. This is a simplification but it get’s the idea across. More accurately, with excessive N-6 we see cellular signaling profiles that tend to promote pathology including cancer, autoimmunity and glucose dysregulation. I see this more like a band or orchestra playing out of tune than too much of one thing vs another thing, but the fact remains folks likely get too much of the short form of N-6 fats. My early solution (and the solution of many other people including Barry Sears, Charles Poliquin and number of other folks) was to front load the system with large amounts of N-3 fats in the form of fish oil to “balance” the intake of N-6 fats. I mentioned a formula in my book for figuring out your fish oil dose and my pals at Whole9 put up a nifty calculator to help you figure out not only how much fish oil you needed overall, but also how damn many capsules that meant depending upon your product of choice.

These recommendations were born several years ago when I was still working for CrossFit, trying to sneak in as much paleo-pseudoscience as I could between polishing the brass of the magical, 40-30-30 Zone.  Given the relatively low protein recommendation of the Zone, combined with moderate to low carbohydrate levels, the only thing left to recommend to hard charging athletes was to ramp up fat intake, and what better fat to use than nuts and seeds? Portable, cheap, yummy. Also, 36-DD heavy in linoleic acid. No worries I thought, we’ll just “balance” things out with more fish oil. Well, by looking at performance parameters and blood work it became clear we still had inflammatory issues that were far from optimum. Some digging in the literature and review of the basic metabolic pathways showed that linoleic acid intake tends to squash the anti-inflammatory outputs of our EPA/DHA supplementation. Recommendations were tweaked to get fat from sources low(er) in linoleic acid such as coconut and pastured butter and we observed improvements in performance and various blood parameters including C-reactive protein and fasting insulin levels.

Eventually the Zone was canned and folks were told to get protein and carb intake up to levels that matched activity. Things REALLY improved!

But I was still of the opinion that fairly high dose fish oil was beneficial to folks with significant systemic inflammation and health issues. The recommendation was to take a fairly large amount of fish oil for a few weeks, then titrate that down to a maintenance level. The thinking here was that we could send a large “anti-inflammatory” signal to the system and get the Titanic steering away from the proverbial iceberg. Some folks (smarter than myself like Chris Kresser) had different ideas on this. Chris liked limiting linoleic acid and keeping EPA/DHA to low-ish levels, mainly from food, with perhaps a few grams per day of supplemental fish oil. What I had not initially considered is signaling, be it anti or pro-inflammatory is a cell by cell affair, and this is based largely on the make-up of fatty acids in our cell membranes. In an inflamed, sick, standard American diet model, individuals have a significant overabundance of linoleic acid in their cell membranes. The idea of front loading more EPA/DHA to change the fatty acid profile of our cells is great until you run into the brick-wall of our metabolic machinery. Cell fatty acid turnover cannot be “goosed” from behind like shoving a bungee jumper off a bridge. Fatty acid turnover has a rate limiting step that is not “substrate limited.” Or, in non-geek-speak more fish oil will not make the process go faster. Instead we need to limit the intake of linoleic acid, keep a decent intake of EPA/DHA, but we need not, and in fact should not hammer that dosage, as we will see when we look at oxidative stress and free-radical chemistry.

When we talk about “inflammation” we must consider two basic elements:

1-The immune system (in this case mainly the innate, non-adaptive immune system made up of macrophages, leukocytes and neutrophils…we’ll largely ignore (for today) the adaptive immune response which is involved in autoimmunity)

2-The various cell-signaling components that tell the immune system what to do. Now, almost everyone has heard of oxidative damage, free radicals, antioxidants and the like.

In chemistry we characterize reactions in a number of ways, with most synthetic reactions involving the shuffling of an electron pair between one atom or molecule and another atom or molecule. This is like a banjo-playing square-dance! Fun, safe, predictable. Another type of reaction that we must consider in biological systems, particularly the immune system, is free radical chemistry. In this situation we see a single electron running amuck. This is more akin to a mosh-pit at a punk concert. In the technical parlance free radicals can “fuck-shit-up.”

The innate immune system makes good use of free radicals when battling bacteria, viruses and parasites. If an immune cell comes in contact with something deemed to be a foreign invader the cell will tend to engulf the item, then release a dose of free-radicals that likely will kill the cell, but will also (hopefully) take out the pathogenic interloper in a Kamikaze style mission. As you recall, inflammation involves not only the immune system but also the cellular signaling components such as prostaglandins, leukotriens and a host of other goodies. In the pro-inflamed state the signaling is effectively “high allert.”

The immune cells are ramped up and just looking for a fight.  As such, there is a tendency for the immune cells to get a little spastic and attack things they should not. As a consequence, we are subjected to an elevated level of oxidative stress. This is to be expected when fighting a cold or bacteria, but it portends doom when it is an outgrowth of endotoxemia (intestinal permeability, bacterial overgrowth) and elevated systemic inflammation from a diet and lifestyle that is throwing too many of the wrong switches. Now, this is a pretty bad scenario as it is, but if we have large amounts of polyunsaturated fats (like those in fish oil, seed and similar oils) in our system things can go from bad to worse.

Polyunsaturated fats are HIGHLY oxidizable. Linseed oil (refined FLAX oil actually…), if added to paper or rags and left open to the air, can get enough reaction going to combust. This is possible because polyunsaturated fats under go what is called a “chain propagative” reaction. Throw one teensy electron into a cell membrane full of polyunsaturated fats and you can witness a mountain of damage. This is why an individual with significant systemic inflammation would do well to limit polyunsaturated fats (particularly linoleic acid) as they are already experiencing oxidative stress. High levels of polyunsaturated fats in the cell membranes will not help things. This oxidative stress issue pops up in other, unlikely spots that can mask problems which otherwise are ascribed a therapeutic effect. Fish oil supplementation has been associated with decreased blood triglyceride levels. Folks savvy to the underpinning of insulin resistance know that elevated triglycerides are an indicator of insulin resistance, so any intervention that lowers triglycerides should be a good thing. Well…in the digestive process all nutrients must be broken down, passed through the gut lining and eventually make their way to the liver.

Fats are released out of the liver in the form of LDL’s, VLDL’s and the like, but they are tested in the liver for oxidative stress potential. If the package is made up of oxidized lipids (lipid peroxides) the batch is scuttled and the liver attempts to degrade the contents of the sample to prevent damage to the rest of the body. The liver is willing to take this hit as it has a large capacity for regeneration, but as with alcoholic cirrhosis, it does take an ass-kicking.  While this chaos ensues in the comfy confines of the liver, our blood triglycerides go down, apparently a good thing, but this is a completely different mechanism of action relative to decreased triglycerides stemming from improved insulin/leptin sensitivity. This is a long-winded way of saying it’s time to revisit our fish-oil recommendations.

 

So, what should I do?


1-LIMIT linoleic acid!! You’d think after I jumped up and down about his for the past 1500 words that it would be obvious, but I just wanted to make sure we are clear on this. Nuts, seeds, corn, safflower, sunflower and similar seed oils are “no bueno.”
 
2-Limit linolenic acid form things like flax, hemp, chia etc. I’d prefer you get the bulk of your N-3’s in the ready made forms of EPA/DHA and your N-6’s as aracidonic acid.  The conversion of linolenic acid to EPA/DHA is inefficient and overall exposes up to a greater oxidative potential as you must consume MORE total polyunsaturated fats to get the goods. I know there are some folks that recommend these short chain fats. Do whatever you like but this is what makes sense to me.

3-Try to get the bulk of your EFA’s (both N-3 and N-6) from grass fed meat, and perhaps pastured dairy in the form of butter. BUT that’s expensive!! I know Buttercup, I know. Do your best. Sardines, mackerel and similar fish are also great sources.

4-Supplement with 2-4 grams of EPA/DHA heavy oils from fish oil, fermented cod liver oil (god help me…that stuff is NASTY, but Chris Kresser loves the stuff) or vegetarian sourced DHA from algae. The DHA can retro-convert to EPA, so no problems there. Which should it be, 2 or 4 grams? If you are “big” take 4. If you are little, take 2. If you do not know if you are big or little, please disavow all knowledge or the paleo diet and adopt veganism. Please.

At the end of the day I think these recommendation support our best understanding of the science and it seems to reflect clinical findings. It also simplifies things to a great degree. Many a client has balked at the high-dose fish oil that has been part of my and other folks recommendations. I think there are some great supplements for specific purposes (adaptogens, creatine and a few other goodies) but where food is concerned, food seems to be best. Shocker. Similarly, there are not shortcuts to health and wellness, just better information and feedback so we can make better decisions.



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8.7.11

Are Nuts And Seeds Healthy?

Are Nuts And Seeds Healthy?
....brief review by Paleo Diet Lifestyle

Conclusion

We learned that even if they are often loaded with vitamins and minerals, most nuts and seeds should be kept to a minimum on a healthy diet for a few main reasons:
  • Most nuts contain lectins that can irritate the gut lining;
  • Most nuts also contain phytic acid that bind to minerals and blocks their absorption;
  • Most nuts are very high in total polyunsaturated fat and in omega-6 fat, two things that should be keept to a minimum;
Nuts like walnuts and pine nuts are some of the worst ones in terms of fatty acid profile.  A few deserve a special mention though:
  • Macadamia nuts, high in monounsaturated fat, healthy even in high amounts;
  • Chestnuts, starchy and very low in polyunsaturated fat, beneficial as a source of healthy carbohydrates;
  • Brazil nuts, high in omega-6 and total PUFA, but also extremely high in selenium and probably useful in small amount to get adequate amounts selenium;
We also learned that we can make the nutrients in nuts and seeds more bioavailable and mitigate the antinutrient properties in them by soaking them in salty water overnight.

2.7.11

Ray Peat - evils of unsaturated fatty acids


Discusses links between unsaturated fatty acids (UFA) and:
  • hypothyroidism
  • heart disease
  • immunosuppression
  • cancer
  • brain dysfunction (via UFA peroxidation)
  • obesity

Notable mentions:
  • nutrition in fish heads
  • 600 day half life of dangerous UFA in human tissue
  • theory that there is no essential dietary fatty acids for humans

1.7.11

Eat Fat Get Thin - Catalyst: ABC TV Science

Catalyst: Eat Fat Get Thin - ABC TV Science
Narration
And Tony's theory is, if you have LOW Omega 3, your membranes will be more sluggish - slowing metabolism down.
This may be the key to why the modern diet makes us fat - and if it is, it's not just that we're eating too much.
Tony believes we've slowed our metabolisms down by eating food with the wrong balance of fats.
We've moved away from the Omega 3 rich hunter gatherer diet we evolved with towards a diet dominated by another fat: omega 6.

Professor Tony Hulbert
Back in hunter gatherer times ... the balance between omega 3 and omega 6 was more one to one, whereas nowadays it's much more biased towards the omega 6, So sometimes up to 30:1... more omega 6 than omega 3.

Narration
Omega 6 comes from seeds and grains, and is particularly high in the kinds of vegetable oils we rely on in the western world. The most common oil in processed food, Soy oil is almost 90% omega 6.
And we haven't just changed our diet, we've also changed the diet of the animals we eat. We're increasingly feeding them Omega 6 rich grain,
dramatically reducing the Omega 3 content of the meat.

Professor Tony Hulbert
The meat we eat if it's been pasture fed it's got a much better balance of omega 3's relative to omega 6's - about 40% to 60%. If it's fed grain it'll be about 20% omega 3 to 80% omega 6.

Narration
Tony believes that this reliance on Omega 6 at the expense of Omega 3 will put us at risk of many of the diseases of the modern world.

Professor Tony Hulbert
If the omega 3 is too low your omega 3 in your membranes will be low, you're more likely to become insulin resistant, develop uh... obesity and various other uh... cardiovascular diseases that arise from that and also uh... other diseases like depression uh... seem to be associated with not enough omega 3 in your cell membranes.
and:

http://www.uow.edu.au/research/proflectureseries/UOW009451.html
http://www.uow.edu.au/health/healthsciences/mrc/Members/UOW039108.html
http://www.uow.edu.au/science/biol/biolschoolstaff/UOW057175.html

Unsaturated vegetable oils toxic - Ray Peat Phd

Coconutoil.com - UNSATURATED VEGETABLE OILS: TOXIC


SUMMARY 
  • Unsaturated fats cause aging, clotting, inflammation, cancer, and weight gain.
  • Avoid foods which contain the polyunsaturated oils, such as corn, soy, safflower, flax, cottonseed, canola, peanut, and sesame oil.
  • Mayonnaise, pastries, even candies may contain these oils; check the labels for ingredients.
  • Pork is now fed corn and soy beans, so lard is usually as toxic as those oils; use only lean pork

  • Fish oils are usually highly unsaturated; "dry" types of fish, and shellfish, used once or twice a week, are good

  • Avoid cod liver oil.
  • Use vitamin E.
  • Use coconut oil, butter, and olive oil

  • Unsaturated fats intensify estrogen's harmful effects.

27.6.11

PUFA essential nutrient, or toxic? - by Ray Peat Phd

Unsaturated fatty acids: Nutritionally essential, or toxic?

A R T I C L E
by Ray Peat Phd

Unsaturated fatty acids: Nutritionally essential, or toxic?



In 1929 George and Mildred Burr published a paper claiming that unsaturated fats, and specifically linoleic acid, were essential to prevent a particular disease involving dandruff, dermatitis, slowed growth, sterility, and fatal kidney degeneration.

In 1929, most of the B vitamins and essential trace minerals were unknown to nutritionists. The symptoms the Burrs saw are easily produced by deficiencies of the vitamins and minerals that they didn't know about.
 
What really happens to animals when the "essential fatty acids" are lacking, in an otherwise adequate diet?

25.6.11

Vegetable Oils and Heart Disease : A Closer Look

Precious Yet Perilous
Written by Chris Masterjohn Phd

Vegetable Oils and Heart Disease : A Closer Look
 
Six randomized, controlled trials specifically testing the effect of the substitution of polyunsaturated vegetable oils for animal fats on heart disease have been published.64-69

The first randomized, controlled trial of dietary fat substitution was published in 1965. Substitution of corn oil for animal fat and carbohydrate doubled the number of major cardiac events. The results were not quite statistically significant, meaning there was a slight possibility they were due to chance. The researchers 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.”64
A second trial found that replacing animal fats with polyunsaturated vegetable oils increased mortality by 39 percent. Rather than considering the possibility that the lipid hypothesis might be false, the investigators concluded that “men who have had myocardial infarction are not a good choice for testing the lipid hypothesis.”66

Three other such trials found either no effect,65, 67 or a small increase in mortality in the group consuming vegetable oil, which was not statistically significant.68

The longest study on the effect of vegetable oil ever conducted was the Wadsworth Veterans Administration Hospital Study.69 The researchers randomized over four hundred men who were long-term inpatients to one of two dining halls. One hall used butter and the other used a mix of vegetable oils. The study was double-blinded and lasted over eight years. The researchers took care not to reuse the vegetable oil after cooking but took no such precautions with the butter, resulting in butter that was very deficient in vitamin E.74 There were also twice as many heavy smokers and 60 percent more moderate smokers in the butter group. The group consuming butter had 50 percent more cardiovascular deaths. The group consuming vegetable oil, however, had more atherosclerosis than the control group and in the last few years of the study began experiencing a marked increase in the risk of cancer. Total mortality was slightly higher among those consuming vegetable oil, but the difference was not statistically significant.

There are two remarkable findings about this study. Even though cardiovascular deaths were lower in the vegetable oil group, atherosclerosis slightly increased. This clearly disproves the hypothesis that vegetable oils decrease the accumulation of atherosclerotic plaque by decreasing cholesterol levels. It further suggests that had there been an equal distribution of smokers between groups and had the control group received adequate vitamin E, vegetable oil may have proven to markedly increase the accumulation of atherosclerotic plaque as well as the risk of cardiovascular mortality. The fact that cancer began rising in the vegetable oil group in the last few years of the study—again, despite the heavy rate of smoking and deficient intake of vitamin E in the control group—suggests that the full extent of the ravages of oxidative stress and inflammation caused by vegetable oils takes at least five years to develop. A longer study may have shown a much greater risk of mortality in the vegetable oil group. These six studies clearly show that vegetable oils are not capable of reducing total mortality and strongly suggest that they may raise the risk of heart disease and cancer.

The Perils of PUFA: Oxidative Stress (broken glass analogy)

Precious Yet Perilous
Written by Chris Masterjohn Phd
September 22 2010 15:02

The Perils of PUFA: Oxidative Stress

In 1985, the lipid researcher Hugh Sinclair gave a pre-banquet speech on his seventy-fifth birthday before the Second International Congress on Essential Fatty Acids, Prostaglandins and Leukotrienes in London, in which he described the deleterious effects of one hundred days on an “Eskimo diet” of seal blubber and undeodorized mackerel oil. He went on the diet to measure his bleeding time because the weather during a recent trip with several colleagues to northwestern Greenland had curtailed him from measuring the bleeding times of real Eskimos. Despite a daily supplement of vitamin E, his blood and urine levels of malondialdehyde (MDA)—a product of the oxidative destruction of PUFA (see Figure 3d)—rose to fifty times the normal level. Although MDA causes birth defects, Sinclair was not worried about having “misshapen offspring” because his sperm had disappeared.31
Sinclair’s experience illustrates one of the unique dangers of all essential fatty acids, regardless of their class—their vulnerability to oxidative stress.

fall10-masterjohnfigure3Figure 3. Oxidative Stress and the Shattering of Delicate PUFAs
Compounds with unpaired electrons, called free radicals, are capable of
stealing electrons from, or “oxidizing,” PUFAs. PUFAs are uniquely vulnerable
to oxidation because they are the only fatty acids with two or more double
bonds, and it is the carbon that lies directly between two double bonds that
is vulnerable to oxidation at physiological temperatures. In the figure, a lipid
peroxyl radical (LOO) steals an electron and a hydrogen atom from a PUFA.
b. Having stolen the electron and hydrogen atom, the lipid peroxyl radical becomes
a lipid peroxide (LOOH). The addition of oxygen to the oxidized fatty
acid forms a new lipid peroxyl radical that can oxidize another PUFA (LH).
c. There are now two lipid peroxides, one shown in its chemical structure and
one abbreviated as LOOH. The newly oxidized fatty acid (L•) can now continue
the chain reaction.
d. Many of these oxidized fatty acids will continue to degenerate into smaller
compounds, like a glass that shatters into many pieces. One such compound,
malondialdehyde (MDA), is shown in the figure. MDA is particularly dangerous
because it can leave the membrane and damage proteins, DNA, and
other important cellular structures. This process can be likened to the shattering
of delicate glass, which results in a mess of dangerous shards that must be
properly cleaned up.

Oxidative stress, or lipid peroxidation, shown in Figure 3, can be thought of as the destruction of structurally and functionally important molecules within the body, beginning with the shattering of PUFAs. PUFAs, in this sense, are like delicate glass. Glass performs many useful functions: we use it to protect ourselves and our property from the assaults of raging storms, for the utensils from which we eat and drink, to see when our vision fails, to examine complex specimens whose details we cannot otherwise distinguish with the naked eye, and in many other more sophisticated examples of modern technology. At the same time, glass is delicate and can shatter. When glass shatters, it invariably leaves behind a mess of dangerous shards. Anyone who breaks a glass on their kitchen floor knows to clean up the shards immediately, lest they or their family cut their feet by walking on them. Likewise, when PUFAs shatter they leave behind shards such as MDA, which are capable of damaging proteins, DNA and other structurally and functionally important components of our cells.
The best way to avoid shattering glass is to be careful with how one uses, cleans and stores it. Nevertheless, the danger of breaking glass will increase simply by having too much of it around. Likewise, the consumption of excess PUFAs increases oxidative stress even when the oils are fresh and properly cared for. Consumption of fresh, non-oxidized DHA, EPA or omega-3-rich perilla oil increases markers of oxidative stress in rats.58 Rats fed 30 percent of their diet as corn oil have double the rate of lipid peroxidation, half the aerobic capacity, and 42 percent lower glycogen stores in their heart tissue compared to rats fed an equal amount of coconut oil.59 A randomized, doubleblind, placebo-controlled trial likewise showed that six grams per day of fish oil increased lipid peroxides and MDA in healthy men, regardless of whether they were supplemented with 900 IU of vitamin E (see Figure 4).60
Sinclair might have better replicated the “Eskimo diet” had he sought the guidance of an Eskimo. Arachidonic acid is necessary for sperm production, and the liberal consumption of glands and other organs rich in arachidonic acid may protect the Inuit and Aleut peoples from the high levels of EPA they obtain from fatty fish and marine oils.31 There may be other components of their traditional diets that limit the vulnerability of PUFAs to oxidative stress, such as antioxidants like coenzyme Q10, lipoic acid, and preformed vitamin A found abundantly in organ meats, or other unknown factors. Human studies have generally used alpha-tocopherol, a form of vitamin E, to protect against the oxidation of fish oils within the body, but supplements of pure alpha-tocopherol suppress levels of gamma-tocopherol, a different form of vitamin E with a unique spectrum of antioxidant protection. Some of the main oxidants in human blood, moreover, are water-soluble so PUFAs require water-soluble antioxidants such as vitamin C for protection. Exactly which components of the traditional Inuit diet best protected them from their high intake of fish oils is unclear, but Sinclair’s experience demonstrates the danger of attempting to replicate a particular peculiarity of one group’s traditional diet without replicating the diet as a whole.

fall10-masterjohnfigure4Figure 4. Fish Oil Increased in Lipid Peroxides and MDA in Humans While Vitamin E Had No Effect
A double-blind, randomized, placebocontrolled trial compared six weeks of supplementation with six grams per day of omega-3 fatty acids from menhaden fish oil to supplementation with six grams per day of olive oil, with or without 900 IU per day of vitamin E as synthetic alpha-tocopherol, in healthy men. For each group, the bar on the left represents the change in lipid peroxides, and the bar on the right represents the change in MDA. Asterisks indicate a statistically significant increase over the course of the six weeks. Fish oil supplementation caused a significant increase in lipid peroxides while MDA and vitamin E had no effect. Adapted from the data in reference 60.

Are omega 3 and omega 6 as healthy as they want us to believe?

Uploaded by on May 5, 2010
 
Ever since 1955 and especially after 1970 the use of poly-unsaturated fatty acids, like in sunflower oil, soy oil, flax oil and canola oil has increased strongly. As from 1955 and especially after 1970 the number of cases of overweight and diseases of civilization has strongly increased.

too much omega-6, not enough omega-3 - making us sick

How too much omega-6 and not enough omega-3 is making us sick

Death by vegetable oil

So what are the consequences to human health of an n-6:n-3 ratio that is up to 25 times higher than it should be?
The short answer is that elevated n-6 intakes are associated with an increase in all inflammatory diseases – which is to say virtually all diseases. The list includes (but isn’t limited to):
  • cardiovascular disease
  • type 2 diabetes
  • obesity
  • metabolic syndrome
  • irritable bowel syndrome & inflammatory bowel disease
  • macular degeneration
  • rheumatoid arthritis
  • asthma
  • cancer
  • psychiatric disorders
  • autoimmune diseases
The relationship between intake n-6 fats and cardiovascular mortality is particularly striking. The following chart, from an article entitled Eicosanoids and Ischemic Heart Disease by Stephan Guyenet, clearly illustrates the correlation between a rising intake of n-6 and increased mortality from heart disease:
landis graph of hufa and mortality
As you can see, the USA is right up there at the top with the highest intake of n-6 fat and the greatest risk of death from heart disease.

Omega 6 - damages mitochondrial - Ray Peat

Food-junk and some mystery ailments: Fatigue, Alzheimer's, Colitis, Immunodeficiency. Carrageenan

On a typical diet, tissues progressively accumulate linoleic acid, and this alters the structure of mitochondrial cardiolipin, which governs the response of the mitochondrial enzymes to the thyroid hormone. 

This process is especially evident in the female liver. In the “autoimmune” diseases, such as lupus, there are typically antibodies to cardiolipin, as if the body were trying to reject its own tissues, which have been altered by the storage of linoleic acid. The altered mitochondrial function, which is involved in so many symptoms, can become part of a vicious circle, with endotoxin and estrogen having central roles, once the stage has been set by the combination of diet, stress, and toxins.

23.6.11

Omega-6 displaces Omega-3 - Dr. Bill Lands

"Dr William E.M. Lands (born July 22, 1930) is an American nutritional biochemist who is the world's foremost authority on essential fatty acids. Lands graduated from University of Michigan in 1951 and served on the faculty there from 1955 to 1980. He then moved to University of Illinois (1980-1990) and subsequently the National Institutes of Health (1990-2002), where he served as the Senior Scientific Advisor to the Director of the National Institute on Alcohol Abuse and Alcoholism.
Lands is credited for discovering the beneficial effects of balancing the effects of excess omega-6 fatty acids with dietary omega-3 fatty acids. The effect of essential fatty acids on formation of hormones is documented in his book, "Fish, Omega-3 and Human Health." University of Michigan's Department of Biological Chemistry endowed a Lectureship in honor of William E.M. Lands."