Lipids and thyroid activity

[RRM]

Benefits are so relative. Metabolism turns up when PUFA intake is low. So, that it is logical that you need more vitamins too. So comparing rats or people that are deficient in the PUFAs without an adaption to the increased nutritional needs is not the right way to investigate this matter.

A vast percentage of the studies showing the beneficial effects of PUFAs,
are actually about (supplemental intake) increasing their intake beyond normal/minimal intake.

Metabolism turns up when PUFA intake is low.

Maybe not.
"Compared with saturated fatty acid intake, n-6 PUFAs reduce liver fat and modestly improve metabolic status (in obese subjects), without weight loss. A high n-6 PUFA intake does not cause any signs of inflammation or oxidative stress." Bjermo H et al

"hamsters were fed either a PUFA-rich diet or a diet rich in saturated fatty acids (SFAs) for 6-10 wk .... Respirometry revealed no effect of diet on whole-animal or mass-specific resting metabolic rate or on lower critical temperature."Pannorfi R et al

"Long chain n-3 PUFA supplementation has been shown to reduce obesity in rodents ... Human intervention trials indicate potential benefits of Long chain n-3 PUFA supplementation for reducing obesity" Buckley JD et al

Maybe you mean metabolism is increased when PUFA-deficient?

[overkees]

AA is the precursor for PGE2

But AA also stimulates IL-6 production via PGE2:
“Here, we show that PGs are able to induce IL-6 synthesis in a human astrocytoma cell line. PGE1 and PGE2, but not PGD2 and PGF2 alpha, led to a rapid and transient induction of astrocytic IL-6 mRNA, followed by IL-6 protein synthesis. Furthermore, PGE2 potentiated IL-1 beta-induced IL-6 mRNA synthesis”
http://www.ncbi.nlm.nih.gov/pubmed/9850935

PGE2 increases SOCS, but IL-6 increases SOCS too:
It appears that all three different SOCS are increased rapidly in response to IL-6 in vitro and in vivo.
http://europepmc.org/abstract/MED/9202125
SOCS3 production is increased by PGE2 in breast cancer cells. Breast cancer cells appear to be STAT indepent (STAT proteins are normally the ones responsible for SOCS production), so this proves the PGE2 involvement in the increase in SOCS3.
http://www.ncbi.nlm.nih.gov/pubmed/17636039
“PGE2 treatment causes upregulation of SOCS3 expression independently of STAT activation.”
http://mend.endojournals.org/content/21/10/2516.short

Excessive SOCS production leads to leptin resistance (and SOCS deficiency in the opposite: weight loss and increased insulin sensitivity):
“Excessive SOCS-3 activity in leptin-responsive cells is therefore a potential mechanism for leptin resistance, a characteristic feature in human obesity.”
http://www.ncbi.nlm.nih.gov/pubmed/10514492
“Moreover, the Socs3-deficient mice were resistant to high fat diet–induced weight gain and hyperleptinemia, and insulin-sensitivity was retained.“ http://www.nature.com/nm/journal/v10/n7/abs/nm1071.html
“Our study establishes that SOCS3 upregulation alone in Pomc neurons is sufficient to cause leptin resistance and obesity.” http://diabetes.diabetesjournals.org/co ... /db09-1024

Too much IL-6 messes up the thyroid:
“We conclude that the low T3 syndrome in nonthyroidial illness is associated with high serum IL-6 levels.” http://www.ncbi.nlm.nih.gov/pubmed/8263160
“IL-6 in vivo would be capable of inhibiting the synthesis and release of T4 and, to a greater extent, T3 from the thyroid gland. “
http://www.ncbi.nlm.nih.gov/pubmed/8895357

“Serum IL-6 values in NTI patients were negatively correlated with serum FT3 values (r = 0.56, p < 0.001), and positively correlated with serum rT3 values” http://www.ncbi.nlm.nih.gov/pubmed/7930379

Leptin and the thyroid:
“Circulating leptin concentrations are inversely correlated with rT3, suggesting that leptin decreases result in increased conversion of T4 to rT3, perhaps accounting for the weight loss associated decreases in T4 and T3 despite unchanged serum TSH “ http://jcem.endojournals.org/content/87/5/2391.full.pdf

High PUFA diet and the thyroid:
High fat diet on rats (Lard + soybean oil, High PUFA). owever, alteration in the activity of deiodinases led to increased production of rT3, which likely prevented the increase of T4 and T3 in the circulation. This combined with reduced spontaneous physical activity must have functioned as an important mechanism that limited energy expenditure, ultimately favoring fat accumulation and the development of obesity in rats fed a HF diet. http://endo.endojournals.org/content/151/7/3460.long
"The high-PUFA diet promoted weight gain: it caused excess weight to be retained at a lower calorie intake."
http://www.ncbi.nlm.nih.gov/pubmed/5008 ... stractPlus

omega 3 and leptin resistance (can’t figure this one out yet):
“We conclude that n-3 PUFA induces peripheral leptin resistance via an increase in the expression of hypothalamic occludin, reducing paracellular transport of leptin into the brain.”
http://www.ncbi.nlm.nih.gov/pubmed/16054080

About the metabolism issue:
“the observed increase in resting metabolic rate produced by using coconut oil to create an essential fatty aciddeficiency, is partly the result of increased heat production in the brown adiposetissue. The weight of that fat decreased by 28%, while its ability to produce heatincreased 690/0”
http://www.ncbi.nlm.nih.gov/pubmed/2573473
"Binding of unsaturated fatty acids to Na+,K+-ATPase leading to inhibition and inactivation," http://www.ncbi.nlm.nih.gov/pubmed/2159804
"Uncoupled respiration on glutamate, malate or succinate was also affected by treatment with EPA. With liver mitochondria isolated from rats that had been treated with a omega-3 fatty acid in the fasted state, the respiratory rates were lower than those observed with mitochondria isolated from control rats. "
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1219333/
We show that PUFA-deficient cells display an increase of phosphorylation efficiency, a higher mitochondrial ATP/ADP-Pi ratio being maintained despite the lower delta psi.
http://www.ncbi.nlm.nih.gov/pubmed/11460926

[RRM]

About the metabolism issue:

None of these sources support your claim that metabolism is increased at low PUFA intakes.
Source number 1 an 4 are about PUFA-deficiency
(with a growth shortfall of 21%!)
Source number 2 is about the effect of PUFA on ATPase.
Source number 3 is about the blood-lipid lowering effects of omega-3 fats.
"When the level of EPA in mitochondrial phospholipids was enhanced by dietary EPA given to fed rats,
... the mitochondrial rates of respiration were found to be higher ...
Our data suggest that treatment of rats with polyunsaturated fatty acids,
in particular the omega-3 EPA, increases fatty acid degradation".

Your source number 3 actually confirms what was found in a number of studies:

"Long chain n-3 PUFA supplementation has been shown to reduce obesity in rodents"
... enhanced fat oxidation and energy expenditure and reduced fat deposition Buckley JD et al

"The n-3 fatty acids replaced the n-6 fatty acids in tissue lipids and reduced synthesis of '2 series' prostaglandins in addition to causing lower weight gain" Cunnane SC et al

"Rats fed dietary fats rich in 20- and 22-carbon polyenoic fatty acids deposit less fat and expend more energy at rest than rats fed other types of fats
...dietary fish oil reduces fat deposition by increasing the expression of mitochondrial uncoupling proteins
and increasing fatty acid oxidation by the less efficient peroxisomal pathway." Baillie RA et al

"Fish oil in a high lard diet prevents obesity, hyperlipemia, and adipocyte insulin resistance in rats" Hainault I, et al

"Omega-3 PUFA of marine origin reduce adiposity in animals fed a high-fat diet." Ruzickova J et al

The only study with opposite results was one in diabetic rats, because here the omega 3 fats prevented adipose tissue inflammation. Todoric J et al

[overkees]

Well, that is all about omega 3. The way I see it now is that omega 3 works on the short term as a medicine and you will get the reported results, however it operates as a sort of anti omega 6 and it is better to have no omega 6 to begin with.

The classical examples are the rats in the experiments in the early 30s and 40s that were used to prove 'essentiality' of the omega 6 fatty acids. The rats were fad only sugar and no EFAs. The EFAD rats had sky high metabolism. But it might have more to do with the absence of omega 6 and the presence of sugar than with PUFAs in general. All the thyroid studies seem to relate to IL-6, PGE2 and TNF-alpha and these are all highly related to omega 6 metabolism.

So we might conclude, for now: Omega 6 and its derivatives lower metabolism.

[Kasper]

The classical examples are the rats in the experiments in the early 30s and 40s that were used to prove 'essentiality' of the omega 6 fatty acids. The rats were fad only sugar and no EFAs. The EFAD rats had sky high metabolism. But it might have more to do with the absence of omega 6 and the presence of sugar than with PUFAs in general. All the thyroid studies seem to relate to IL-6, PGE2 and TNF-alpha and these are all highly related to omega 6 metabolism.

So we might conclude, for now: Omega 6 and its derivatives lower metabolism.

It's all about AA derivatives right ?



I've been studying this topic a little bit, but I think it is a little bit more complicated as you represent it here.
It is a long time ago, so maybe I'm talking nonsense here.
I found for example that only if AA is released from the membranes (by phospholipase A), those PGE2, PGD2 etc. can cause problems.
This would mean that you can have very much AA in your membranes and still no problems.

Another thing is, this is all about AA, but most omega-6 are not in this form, but in the form of LA.
LA can be converted to AA, but LA can also be converted to GLA or DGLA, which doesn't seem to cause problems.

In the end, I came to this conclusion that it is more about inflammation than about omega-6.
When the body is inflamed it releases AA from the membranes which gets converted to PGD2/PGE2 etc.
So this is more about all sources of inflammation. I don't know if LA consumption for example significantly increases AA in the membranes.
But then still, in balding scalps PGD2 is higher than normal, and PGE2 is lower than normal. Why is that ? Both come from AA, but ratios are different.
With the thyroid PGE2 is more a problem (apperently). Candida could play a role here as well:

Candida albicans produces lipid metabolites that are functionally similar to host prostaglandins. These
studies, using mass spectrometry, demonstrate that C. albicans produces authentic prostaglandin E2 (PGE2)
from arachidonic acid. Maximal PGE2 production was achieved at 37°C in stationary-phase culture supernatants
and in cell-free lysates generated from stationary-phase cells.

[overkees]

Alot of pathogens seem to ride on the AA release flow. And this is indeed the problem. More on this later. If there is nothing to activate it, there will be no problems. However, it might be easier to prevent the heavy inflammation reaction caused by too much AA.

It is like your body is attacking a robber in a quiet village with a nuclear bomb, instead of just calling the police.

So..... one might say adress the inflammation and not the fatty acids. However, if I look at the reports of people who are on a omega 6 elimination diet (you will still get +2-4 g a day even if you are really extreme) and no fatty fatty fish. They all report a change in wound healing. The wound gets much less red and the wound seems to get a rubbery membrane around it instead of the hard layer that people usually get. Alot of inflammation diseases dissapear after a couple of months.

It takes 2 years on a very strict protocol to let the body use the mead acids instead of the omega3s and omega6s, if you do fasting and are very lean and didn't eat alot of n3s and n6s this will be alot shorter. It has been proven that normal amounts of olive oil don't interfere with the mead acid production and that fish oils are the least worst dietary omegas that inhibit the desaturase enzymes that are involved. So... RRM might already have a substantial amount of these omega 9s in his blood. I do remember him saying he also had this other type of wound healing, which is a clear indication of the mead acid presence. Unbelievable xD. I think however if he lowers the fish and adds in the grass fed beef he will be of even better.

Now egg yolks are high in omega6, so I would limit consumption to about 3-4 max a day (I believe this is also the amount RRM eats).

[RRM]

Metabolism turns up when PUFA intake is low.

Maybe not. .... (articles)

Well, that is all about omega 3.

Then PLEASE dont say "PUFA".
You really need to be more accurate when making statements.

So we might conclude, for now: Omega 6 and its derivatives lower metabolism.

No, you conclude something AFTER you have proven it first.

[overkees]

No, you conclude something AFTER you have proven it first.

The thyroid and PUFA connection is clear cut and to me is a proof that you want to avoid eating too much PUFAs, and that the amounts of the SAD are way to high and off limits. What is too much to me is, when I compare it with other traditional diets, above 2% of the total calories in the diet. Fish for its EPA can have therapeutic properties in larger and should be regarded as a medicine.

[RRM]

The thyroid and PUFA connection is clear cut

I have shown you that it is not what you presented it to be.
That the statement "Metabolism turns up when PUFA intake is low" is simply incorrect.

[overkees]

Okay, let me rephrase that: Omega 6 fatty acids, opposed to saturated fatty acids, inhibit thyroid functioning.
This can't be said about omega 3s, but it needs to be researched if this is due to the modulating and competitive effects they have on omega 6 metabolism.

Therefore it seems to me that it would be logic to limit the omega 6 consumption (out of traditional and evolutionary viewpoints) to not more than 2% of daily calories.

[RRM]

Omega 6 fatty acids ... inhibit thyroid functioning

What studies show exactly that?

it would be logic to limit the omega 6 consumption to not more than 2% of daily calories

Based on what data, exactly?

Total omega-6 in % of energy present

33.4% Brazil nuts
10.2% Egg yolk
8.0% Avocado
8.0% Olive oil
3.3% Salmon
2.2% Tuna
1.7% Mackerel
1.7% Macadamia nuts
1.7% Coconut oil
1.1% Oranges
0.6% Orange juice
0.3% Banana
0.2% Honeydew
0.2% Beef
0.1% Mango


Total omega-6 in % of total fat

37.3% Brazil nuts
25.9% Oranges
19.2% Banana
14.5% Orange juice
13.0% Honeydew
12.6% Egg yolk
8.4% Avocado
8.0% Olive oil
5.5% Salmon
4.1% Beef
3.5% Tuna
2.9% Mackerel
2.0% Mango
1.8% Macadamia nuts
1.7% Coconut oil

Suppose you need 3000 kcal daily, a diet of 150 g. salmon, 50 g. olive oil, 5 bananas and the rest OJ,
would supply you with 2.0% omega-6 / total energy.
Replacing salmon with yolks and Including a handful of Brazil nuts and 2 avocadoes would yield 7.9% omega-6 / total energy.