High PUFA Diet Is Pro-aging, Diabetogenic, And Increases Cortisol

[Drareg]

This enzyme is very interesting,if 11B-HSD1 is increased by PUFA it would explain why many get such great effects from it,cortisol can make you feel great if you were leaning to the lower side of things,higher cortisol types may be the reason why some react terribly to high dose PUFA.

Aspirin down regulates this enzyme,Im starting to guess some people may have lo wish cortisol on this forum and it may be the reason we see some contradictory effects from substances like niacinamide,aspirin DheA and the like.

11B-HSD1 may explain water retention from aspirin,niacinamide and coffee some are getting.

 

[Danmcakes]

I got some heated comment after my first show with Danny. The comments were about PUFA increasing cortisol synthesis. I was told that there is no study showing such connection. Well, here is one. As you can see high PUFA diet (70% PUFA) increases expression of 11b-HSD1, which is the enzyme responsible for cortisol synthesis. Also, high PUFA diet had the same effects as aging but the effects were stronger in the high PUFA group.

High-fat diet intake accelerates aging, increases expression of Hsd11b1, and promotes lipid accumulation in liver of SAMP10 mouse. - PubMed - NCBI

"...Hsd11b1 mRNA levels in the 12C, 6F and 12F groups were 170, 114 and 218% of that in the 6C group, respectively, with a significant increase in the 12F group. Hence, the liver mRNA levels of Hsd11b1 and Rbp4 were increased by aging, and increased further by a high-fat diet. This suggests that a high-fat diet accelerates aging, and that hyperinsulinemia and lipid accumulation in the liver are promoted by increased expression of these genes."

"...Overall, our results show that intake of a high-fat diet accelerated aging, increased the expression level of Hsd11b1, increased insulin secretion, and promoted lipid accumulation in the liver of SAMP10 mice. This suggests that repression of Hsd11b1 mRNA level is important for prevention of diseases such as hyperinsulinemia and fatty liver caused by a high-fat diet and aging. Since the expression of these genes increases with aging, a long-term approach to repression of the genes is required, and this might be achieved through control of food intake."

Two of the most powerful supplements for suppressing 11b-HSD are DHEA and retinol (vitamin A). Animal studies show that DHEA as little as 5mg can inhibit 11b-HSD and dose of about 20,000 IU retinol can do the same.

I like the study, but not sure it actually is a high PUFA diet ...what I read was that they used "Quick Fat; CLEA Japan, Tokyo,Japan" which from what I can find appears to be beef tallow....do you have other information to confirm it is high PUFA? Much appreciated.

 

[Lucenzo01]

We know the RDA for vitamin A is inadequate. The RDA was designed to determine what would prevent death and malnutrition, not give you optimal health. The animals studies with vitamin A that I have seen so far all used upwards of 20,000 IU (human equivalent doses) daily as the "normal" levels of vitamin A required to ensure normal functioning and health of the animal. The human dose of 5,000 IU converted to various animal models would induce a deficiency in most of them. I guess it comes down to determining how much vitamin A each one of us needs. It may vary between person to person but it is probably higher than 5,000 IU daily for most people.

Great thread, Haidut. Do you think a person that has taken a round of accutane (for example, me) would need higher doses of vitamin A?

 

[haidut]

Great thread, Haidut. Do you think a person that has taken a round of accutane (for example, me) would need higher doses of vitamin A?

Possibly, since accutane will fool the body to think there is excess vitamin A and thus decrease levels of the retinol-binding protein. If you do take a higher vitamin A dose make sure you always combine with some vitamin E as even a small dose vitamin E protects from the toxicity of massive dose vitamin A (100K+ IU).

 

[Mito]

Serum copper and ceruloplasmin. You want serum copper to be normal and ceruloplasmin to be close to the upper range.

I’m not sure ceruloplasmin in the upper range is necessarily a good thing?

”There are two things that we know regulate ceruloplasmin apart from copper status. Number one is inflammation. In inflammation, we talked about in the last episode one of the goals is to sequester iron because you want to prevent pathogens from having access to free iron. So you ramp up ferritin and you ramp down the intestinal absorption of iron. You also want to kick into gear your number two way of sequestering iron, which is to load it up into transferrin. But transferrin production isn’t the limiting factor to get iron into transferrin. In a healthy state we always only have 30% to 40% of our transferrin capacity saturated. The limiting factor is going to be the ability of ceruloplasmin to get iron into the right form so that it can get into transferrin. So in response to inflammation, you don’t just ramp up ferritin and ramp down intestinal iron absorption. You also ramp up ceruloplasmin. That makes me wonder, do you also ramp up ceruloplasmin in response to oxidative stress like you do ferritin to once again help sequester free iron to prevent iron from causing oxidative stress. Are they analogous? I don’t know, but it wouldn’t surprise me.

But what I do know is that ceruloplasmin is also regulated by estrogen. The effect is relatively modest for natural variations in estrogen and pretty strong for supplemental estrogen.

But what we can say is that ceruloplasmin, yes, is an important marker of copper status to a point, but it can lose its specificity when we’re looking at inflammation and estrogen, and maybe, just maybe, also oxidative stress.

https://chrismasterjohnphd.com/2017/02/03/manage-copper-status/

 

[haidut]

I’m not sure ceruloplasmin in the upper range is necessarily a good thing?

”There are two things that we know regulate ceruloplasmin apart from copper status. Number one is inflammation. In inflammation, we talked about in the last episode one of the goals is to sequester iron because you want to prevent pathogens from having access to free iron. So you ramp up ferritin and you ramp down the intestinal absorption of iron. You also want to kick into gear your number two way of sequestering iron, which is to load it up into transferrin. But transferrin production isn’t the limiting factor to get iron into transferrin. In a healthy state we always only have 30% to 40% of our transferrin capacity saturated. The limiting factor is going to be the ability of ceruloplasmin to get iron into the right form so that it can get into transferrin. So in response to inflammation, you don’t just ramp up ferritin and ramp down intestinal iron absorption. You also ramp up ceruloplasmin. That makes me wonder, do you also ramp up ceruloplasmin in response to oxidative stress like you do ferritin to once again help sequester free iron to prevent iron from causing oxidative stress. Are they analogous? I don’t know, but it wouldn’t surprise me.

But what I do know is that ceruloplasmin is also regulated by estrogen. The effect is relatively modest for natural variations in estrogen and pretty strong for supplemental estrogen.

But what we can say is that ceruloplasmin, yes, is an important marker of copper status to a point, but it can lose its specificity when we’re looking at inflammation and estrogen, and maybe, just maybe, also oxidative stress.

https://chrismasterjohnphd.com/2017/02/03/manage-copper-status/

Good ceruloplasmin is what ensures copper is used and not toxic. You definitely do not want serum copper to be high. And yes chronically elevated ceruloplasmin can mean trouble. It is a biomarker for lymphoma, among other things.
Peat said he wants to see dietary guidelines driven by ceruloplasmin levels, and hinted it should be above the 50% for optimal health. Again, I did not say it should be high but that it should be in the upper range.

 

[Regina]

Good ceruloplasmin is what ensures copper is used and not toxic. You definitely do not want serum copper to be high. And yes chronically elevated ceruloplasmin can mean trouble. It is a biomarker for lymphoma, among other things.
Peat said he wants to see dietary guidelines driven by ceruloplasmin levels, and hinted it should be above the 50% for optimal health. Again, I did not say it should be high but that it should be in the upper range.

Do you have any ideas on how someone could safely tweak up their ceruloplasmin level? Thx!

 

[haidut]

Do you have any ideas on how someone could safely tweak up their ceruloplasmin level? Thx!

It usually rises with better metabolism. I think it is a good question for Peat as well. Especially a question to clarify his comments on how nutrition should be gauged/changed according to ceruloplasmin levels.

 

[Regina]

It usually rises with better metabolism. I think it is a good question for Peat as well. Especially a question to clarify his comments on how nutrition should be gauged/changed according to ceruloplasmin levels.

Thank you.

 

[ddjd]

This enzyme is very interesting,if 11B-HSD1 is increased by PUFA it would explain why many get such great effects from it,cortisol can make you feel great if you were leaning to the lower side of things,higher cortisol types may be the reason why some react terribly to high dose PUFA.

Aspirin down regulates this enzyme,Im starting to guess some people may have lo wish cortisol on this forum and it may be the reason we see some contradictory effects from substances like niacinamide,aspirin DheA and the like.

11B-HSD1 may explain water retention from aspirin,niacinamide and coffee some are getting.

you're definitely onto something here.

i experimented with T4 only, which actually increases 11B-HSD1 expression, like PUFA, and my normally bloated stomach shrank within 10 minutes, in fact it felt very anti-estrogenic. t3, niacinamide, aspirin, palmitic acid, have the opposite effect - huge water retention, bloating etc.