Friday, March 15, 2019

Tucker on omega six PUFA

While I've been day dreaming about antiporters at the origin of life Tucker has been busy. I guess most people reading here would read Tucker anyway but just in case not, here's the link

Response to Gary Taubes on Omega-6 Fats (Seed Oils) and Obesity

Personally I have no issue with the two concepts being complementary. Carbohydrate in quantities which get glucose past the liver will drive up systemic insulin. Omega six (and 18C omega three) fatty acids will make adipocytes hyper-respond to the obesogenic signal of elevated systemic insulin. Fat (largely dietary sourced) is then lost in to adipocytes. Loss of this fat is the equivalent of not having eaten it, so you are left hungry. It's the old weight gain causes hunger paradigm. I like it.



ctviggen said...

Like you, I think they are complementary. I also think they can operate separately. I got fat eating tons of carbs (and some fat), but not PUFAs. Tucker had effects from PUFAs. I think we're on opposite ends of the spectrum, but there's a large group in the middle who are not.

raphi said...


Tucker Goodrich said...

Thanks, Peter!

Hap said...

and what about the signalling effects and primary toxicity of N6 metabolites? Effects on innate immune response?

M said...

Both CNN and Fox News are telling me that the cholesterol in eggs will give me a heart attack. We are now in 2019. WTH.

Passthecream said...

Tucker that is a very interesting essay and fascinating cultural archaeology where you have gone way beyond Taubes' viewpoints but I do favour Peter's narrative. The idea that coconut and O3 oils can be protective against the harms of 06 oils is
puzzling if an adulterated lard with 40% cottonseed oil but presumably 60% of real lard is still harmful?

Reading of the difficulty of removing the toxin gossypol from cottonseed however makes me wonder if either gossypol residues or contaminants from the purification process could be responsible for much of the harm.


Gossypol is very nasty with a wide spectrum of effects and you can imagine commercial interests then (and now!) not taking much care over it especially when destined for the bargain end of the market. Likewise the erucic acid in rapeseed oil or some of the highly sought after phenolic flavour compounds in extra virgin olive oil that give it a sharp, peppery taste. Fresh e.v.o. tastes disgusting to my palate.

I am old enough to remember an article in New Scientist discussing the harms of rapeseed oil as a common contaminant in low priced olive oil. The marketing seems to have skipped over this. I also remember buying tins of sardines in 'sild' oil ie cottonseed. That's all your Xmases at once.

Passthecream said...

A correction, it turns out that sild is a type of fish used mostly for its oil. But definitely there were sardines in cottonseed oil.

karl said...

Taubs should be able to see that concentrated seed oils were not really pushed until the early 1960s. The data is out there.

We do have groups where the introduction lagged - When I was first in the Philippines in 1986 people bought lard or coconut oil to cook in - I did not observe T2D body types. Latter in 1995 - the introduction of seed oil was starting. Today T2D is exploding there with cheap seed oil in the stores - even the poor are getting fatter.

One could do studies based on the introduction of concentrated seed oil and incidence of T2D - but it does not fit the false narratives pushed by the grant system.

I wonder if Taubs has ever seen this set of graphs:

The change really happened in the 1960's - Taubes?

Taubs seems like his is not aware of the low level FADH2:NADH ratios that have been discussed here. I've also not seen where he has written or talked about LPL(LipoProtein Lipase) or HSL(Hormone-Sensitive Lipase) - so I'm guessing he just isn't aware of this stuff:

My current narrative is that it is a one-two punch - inappropriate insulin sensitivity of adipose tissue caused by high PUFA consumption - causing over storage of fat - leading to hunger that is easily fed with a cheap carb diet. High carbs (particularly fructose) fuels de-novo lipogenesis (DNL) - with insulin sensitive adipose tissue ready to store ever more fat. (I'm quite aware that my narrative may not be quite correct or complete (not everyone seems to get fat on this diet).)

Combine that with false narratives pushed about "healthy fats", "essential fats", and we have the perfect storm - a pandemic of T2D.

Fred Lander said...

MY first ever major weight gain, about 40 lbs. could not be explained for several years as it did not even occur to me that those big boxes of Splenda could have any negative impact. I had, in the meantime, adopted large amounts of coconut oil for cooking , and in 5 months 35 lbs. just disappeared, without any effort at all. Then, the weight loss stopped and my appetite came back. Then, it occurred to me, that I had run out of coconut oil several weeks before, and then did a search in pubmed. Ahaaaaa! It was all in the literature and I just had to look, but also a nice blind experiment!
Ivor Cummins interviewed Tucker Goodrich about a month ago:
I am looking into Dr. Gerhard Spiteller's hypothesis that the furan fatty acids are the benefit of eating oily fish, not the omega3. This may have been covered before.
"6.7.2. Furan fatty acids (F-acids) are potent radical scavengers
The w-3 PUFAs like w-6 PUFAs, are characterized by
the oxygen-sensitive common structural element
CH=CH CH2 CH=CH . Based on this structural element w-3
PUFAs are as sensitive to oxygen as w-6 PUFAs, and therefore,
are prone to peroxyl radical attack.[108] Thus, the CHD-protecting
characteristic of marine food must be based on other factors.
Marine animal fat, besides typical w-3 fatty acids, contains
powerful radical scavengers, antioxidant furan fatty acids (FChem.
acids).[109] F-acids can efficiently quench LPO.[110] Interestingly,
the radical-scavenging properties of fish-meal require the presence
of free F-acids.[111] The observation, that only free F-acids
are physiologically active, is in agreement with the experience
that fatty acids become only active after liberation from esters,
for example, phospholipids caused by cellular structural alterations.[
15–17, 33]"
" The Action of Peroxyl Radicals, Powerful Deleterious Reagents,
Explains Why Neither Cholesterol Nor Saturated Fatty Acids Cause
Atherogenesis and Age-Related Diseases "
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