@yerrag

That general view of some peaters about lipolysis that you quoted in your reply probably stems from a misinterpretation of what Ray said about it. The emphasis he places on inhibiting lipolysis is in the context of too much PUFA stored in the tissues, which becomes less and less necessary as you become “PUFA depleted”. After that, inhibiting lipolysis becomes more of a therapeutic tool to be used in appropriate contexts, such as in some pathologies.

He even mentions that in healthy people (especially children) stress hormones are only produced in the amount needed because free saturated fatty acids serve as negative feedback, not allowing them to rise beyond what is necessary.

In good health, especially in children, the stress hormones are produced only in the amount needed, because of negative feedback from the free saturated fatty acids, which inhibit the production of adrenalin and adrenal steroids, and eating protein and carbohydrate will quickly end the stress. But when the fat stores contain mainly PUFA, the free fatty acids in the serum will be mostly linoleic acid and arachidonic acid, and smaller amounts of other unsaturated fatty acids. These PUFA stimulate the stress hormones, ACTH, cortisol, adrenaline, glucagon, and prolactin, which increase lipolysis, producing more fatty acids in a vicious circle. In the relative absence of PUFA, the stress reaction is self limiting, but under the influence of PUFA, the stress response becomes self-amplifying.

This misinterpretation is probably one of the bases for the idea that moderately high insulin several times a day is beneficial (because it inhibits lipolysis and increases glucose oxidation). I don't particularly consider insulin to be a “stress hormone”, but high insulin several times a day and for long periods is obviously a bad sign; insulin plays an “enhancing” role and not the main role.

Keto diets, a very low fat and/or very low protein diet, exercise, ACV before meals, walking after meals, and other similar tools aimed at reducing insulin are only necessary if metabolic dysfunction is already present. Is it good to have these options available with the constant attacks on our health? Yes, but the more miraculous a therapeutic tool is, the more likely it is that your health isn't as good as you think.

@Ancap

How is your sun exposure in summer compared to winter? Assuming nothing else changes...

If we use hibernating animals as an example, one of the reasons these animals develop insulin resistance and become “diabetic” is the absence of sunlight, since the sun is 50%+ infrared light and it stimulates the mitochondria. In a natural environment, the increasing absence of sunlight makes them prone to increased blood glucose (and insulin), and the less exposure to sunlight, the greater the response to carbohydrates.

A 15 min exposure to 670 nm light reduced the degree of blood glucose elevation following glucose intake by 27.7%, integrated over 2 h after the glucose challenge. Maximum glucose spiking was reduced by 7.5%.
Light stimulation of mitochondria reduces blood glucose levels

Whenever possible I like to eat outdoors, or stay outdoors after meals. On days when I can't, I always “simulate” this study and eat with the “chicken lamp” turned on towards me.

@alex155 But it has the same effect as taking t3 and t4, as long as you take it it will suppress the thyroid until you stop, at least that's what the studies say.

@alex155

I remember seeing that there's 1 or 2% T4 in iodocasein, Ray said that it's possible to consume some when you boil oysters in milk (I don't actually remember if it got to the point of boiling).

Iodine has other interactions that can be interesting too. Saturating the double bounds of PUFAs with iodine (and this can happen naturally inside the body) converts them into something closer to a saturated fat. Linoleic acid is converted into tetraiodostearic acid, oleic acid is converted into diiodostearic acid...

PRESS, M. (1974). CORRECTION OF ESSENTIAL FATTY-ACID DEFICIENCY IN MAN BY THE CUTANEOUS APPLICATION OF SUNFLOWER-SEED OIL. The Lancet, 303(7858), 597–599. doi:10.1016/s0140-6736(74)92653-1

@LucH said in New study says increased circulating levels of O6 PUFA arachidonic acid is fasting's mechanism for lowering inflammation (30 Jan 2024):

Hi,
Thanks for posting but I won’t take these studies for granted findings. Deductions are no valid arguments, for me, here. Why?
Main points in the first study:

• AA reduces inflammasones (it turns down the activity of the NLRP3 inflammasome in cell culture and in mouse).
• We already know fasting improves brain biology. Of course if we fast 24 H after a meal of 500 K/cal, it will induce lipogenesis, and thus fat that has been stored, often AA, supposed to be pro-inflammatory because training a cascade reaction. We make a statement but we don’t know how or why in some ways.
  But we know too that very long PUFAs depress the system and the thyroid if prolonged.
  The only interesting thing in this first study is the conclusion, not oriented:
• “There could be a yin and yang effect going on here, whereby too much of the wrong thing is increasing your inflammasome activity and too little is decreasing it,” said Professor Bryant. “Arachidonic acid could be one way in which this is happening.”

You can basically abolish the “brain improvements” of fasting just by consuming tryptophan, even if you don't consume anything else.

We found that adding back carbohydrate or fat did not affect Dietary Restricted(DR)-induced memory retention of mice in the NOR test (Fig 2A), indicating that these constituents do not limit memory performance during DR. In contrast, addition of protein to the DR diet attenuated DR-induced memory performance, bringing it back to alevel comparable to that for AL mice (Fig 2A). We next determined which amino acid affected memory function in this context....

Our results demonstrated that adding back tryptophan, but not glutamate, cysteine, or tyrosine, attenuated DR-induced memory retention (Fig 2B). Tryptophan alone is thus limiting for memory retention during DR. Although adding back carbohydrate and fat, but not protein or individual amino acids, significantly increased the body weight of DR mice (S2A and S2D Fig), none of these dietary manipulations affected general locomotor activity or total time spent on object exploration, compared to either the AL or DR group in the open field test or NOR test, respectively

I'm not sure what they were trying to see in relation to NSAIDs like aspirin, but they inhibit COX-1/2, for them to decrease the level of AA they would have to inhibit Phospholipase A2, which is the enzyme that releases AA from the membrane to be processed by COXs.

It wouldn't be surprising to see a negative feedback mechanism in relation to AA levels in an isolated variable like the one in this study, and there are other ways in which AA can influence this, after all, an increase in AA means more substrate for other things. I remember Travis commenting on AA influencing PPARδ and it also participates in inflammation, so maybe it's responsible for the negative feedback? haha

These findings indicate that PPARδ agonists have the potential to suppress the inflammatory response that triggers atherosclerosis

Some of Travis' mentions of Phospholipase A2:

Han starts off his article quite appropriately by mentioning phospholipase A₂. This is a real enzyme, and can cleave arachidonic acid from membrane phospholipids in vitro. It cannot do this at low lipid concentrations, but once a micelle is formed it will stick to it and start cleaving. The cell membrane is presumed to be similar to a phospholipid micelle. Phospholipase A₂ can cleave phosphotidylethanolamine, but needs to be anchored to phosphotidylcholine to do so. It will not anchor to an in vitro micelle composed exclusively of phosphotidylethanolamine.

By the way, another thing that Click mentioned in X in relation to a possible anti-inflammatory mechanism of fasting is the very restriction of methionine, which is a component of COX-2. One might expect a reduction in inflammation just by restricting some amino acids, on top of restricting other elements that can contribute.

@Insomniac said in I remember Ray Peat saying he used to eat lowish carb. Does anyone know around what age he switched to favoring carbs/sugar?:

@TexugoDoMel Thank you. That's the quote I remembered. I doubt I ever read he ate 50% calories as fat.

But 35 percent is just slightly less than a standard American diet. I remembered him talking about making food from coconut oil like he was at least experimenting with high saturated fat diets.

I think he was only low fat for a few years.

Perhaps because english isn't my first language, the first time I read this quote, especially the “little less fat, maybe 30 to 35%” part, I interpreted it as “little less fat, maybe 30 to 35% less”.

The few times I've seen him comment on his diet, he didn't seem to be eating all that much fat

That's all I remember

"Sugar helps the liver to make cholesterol, switching from starchy vegetables to sweet fruits will usually bring cholesterol levels up to normal. If the fat is mostly saturated, from milk, cheese, butter, beef, lamb or coconut oil, I think it's usually o.k. to get about 50% of the calories from fat, but since those natural fats typically contain around 2% polyunsaturated fats, I try to minimize my PUFA intake by having more fruit, and a little less fat, maybe 30 to 35%." -Ray Peat

Now I don't eat as much because I'm testing very low-fat, but I used to like to eat shredded coconut with sugar in a 1:1 ratio, especially before going to the gym. I never had any problems.

There are some studies saying that uncoupling protects the muscles, so I imagine it's something related. I think it's common knowledge that DNP seems to preserve a lot of muscle mass even if you lose a lot of weight (compared to fat loss with ozempic for example). When protein is restricted there is an increase in T3, uncoupling, brown fat... So this could be one of the reasons, but I don't know if it would preserve it for long

Low protein has twice as much t3