@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

I don't think it's worth it, since it's only a “pseudo depletion”.

In animals, a diet where most of the fat was oleic acid depleted PUFAs (omegas-6 and omegas-3) faster than a diet with no fat or hydrogenated coconut oil.

If I were to try a diet for rapid depletion, it would be a low-fat one supplemented with stearic acid, since most of the stearic is converted to oleic by our delta-6 desaturase (high carbohydrates also increase its activity). The higher the ratio of Oleic to Linoleic the better

Carbohydrates alone raise serotonin through the effect that insulin has on amino acids, increasing the proportion of tryptophan in the blood in relation to other amino acids (which insulin removes from the blood). It would basically be the same if you supplemented tryptophan alone.

But although it seems that carbohydrates are a problem in this case, the real problem is the ratio of amino acids. If you consumed the same amount of sucrose but added some gelatin/collagen or even BCAAs, this effect on increasing serotonin would be abolished. This is even the basis for the “acute serotonin depletion” technique

John D. Fernstrom has several studies on amino acids ratio and serotonin

When plasma tryptophan is elevated by the injection of tryptophan or insulin, or by the consumption of carbohydrates, brain tryptophan and serotonin also rise; however, when even larger elevations of plasma tryptophan are produced by the ingestion of protein-containing diets, brain tryptophan and serotonin do not change. The main determinant of brain tryptophan and serotonin concentrations does not appear to be plasma tryptophan alone, but the ratio of this amino acid to other plasma neutral amino acids (that is, tyrosine, phenylalanine, leucine, isoleucine, and valine) that compete with it for uptake into the brain.

Fernstrom, J. D., & Wurtman, R. J. (1997). Brain Serotonin Content: Physiological Regulation by Plasma Neutral Amino Acids. Obesity Research, 5(4), 377–380. doi:10.1002/j.1550-8528.1997.tb00567.x

Choi, S., DiSilvio, B., Fernstrom, M. H., & Fernstrom, J. D. (2009). Meal ingestion, amino acids and brain neurotransmitters: Effects of dietary protein source on serotonin and catecholamine synthesis rates. Physiology & Behavior, 98(1-2), 156–162. doi:10.1016/j.physbeh.2009.05.004

The amount of studies producing EFA deficiency with fat-free or Hydrogenated Coconut Oil-added diets are the majority, but apparently not the fastest to deplete EFAs.

I posted a few days ago how Oleic acid (MUFA) accelerates EFA deficiency, in the simplest study below 0.8% linoleic and a 20:1 Oleic:Linoleic ratio accelerated depletion. Apart from macadamias, I don't know of anything that has a good OA:LA ratio and little PUFA or is pure Oleic, so I think supplementing with Stearic Acid may be even better, since it is well known and used and has no PUFA, it is also widely converted into Oleic Acid within the body (Rats on a diet rich in Oleic vs Stearic have basically the same amount of Oleic in the tissues).

It would be nice to do an OmegaQuant to see if the depletion is working.

@jamezb46

I usually control my breathing and do a few breath holds, maintaining between 85~90% SpO2 for a few minutes, I know it's not the best way to measure hypercapnia, but it's the most practical for me. Bag breathing is one option, a CO2 bath is another.

For a more localized effect, those who are more creative can create a "homemade paste" of CO2 (paste/hydrogel, baking soda and some acid) and seal the desired area for a few minutes. Animal studies have shown good results from doing this for 10 minutes over a few days.

In conclusion, our study demonstrates that the CO2 paste prevents excessive scarring and accelerates muscle regeneration. This may be due to the induction of an artificial Bohr effect, which leads to the upregulation of MyoD and myogenin, and the downregulation of IL-1β, IL-6, and TGF-β. The CO2 paste is inexpensive and non-invasive. Therefore, it may be the treatment of choice for patients with muscle damage. Further research should be conducted to confirm our findings.

@brad bloo co2 paste when

@thyroidchor27

I don't see a problem with a little olive oil, but if you want to tip the scales to the "peaty side", macadamia is probably a better option due to the Oleic:Linoleic ratio.

When I say PUFA in this article, I'm referring mainly to omegas-6, as they are responsible for most of what is known as essential fatty acid deficiency(EFAD). Omegas-3 deficiency causes other effects, which I won't cover here.

On Mead Acid(MA)

That MA is produced in large quantities in a state of Linoleic(LA)/Arachidonic(ARA) deficiency is already known (The other post in which I talk about this and mention a few more things can be found here), but what is little known is that MA also has the ability to deplete other PUFAs by competition, either by "metabolic pathways" or structurally (taking the place of other PUFAs in membranes).

Below is a table showing the proportion of fatty acids in plasma phospholipids in diets with different Mead:Linoleic ratios

Regardless of the proportions, the presence of LA in the diet seems to be the determining factor in the minimum levels of LA/ARA in phospholipids, but that's not what matters here, what we can see is that the increase in the proportion of MA affects the levels of LA/ARA as well, clearly demonstrating a competition between these PUFAs for the same positions in the membrane. MA(20:3 ω-9) is a "substitute" for ARA(20:4 ω-6), so the effects will be more noticeable at the ARA level than LA.

The conclusion seems to be the same:

Nice to know, but if MA is produced in large quantities only in EFAD, what relevance does it have for us? It's not as if there's a significant external source of MA.

Indeed, but considering that MA is produced from Oleic Acid (OA), I've been thinking for some time about the possibility of manipulating levels through diet. In theory, if the LA:ALA ratio, which is usually much higher than 1, hinders the conversion of ALA (even though it has priority compared to LA) to EPA/DHA, the same would be possible with the OA:LA ratio, favoring OA. I always thought it curious that MA was produced from OA but most studies only induce EFAD with a fat-free diet or hydrogenated coconut oil.

Does consuming more OA increase MA production?

Apparently yes. Below is the difference between the levels of MA derivatives in a diet rich in LA vs rich in OA:

Unfortunately in this study I didn't find the information on how much OA was in the high LA diet so I could get a better idea, but in this other study there are more details:

Influence of diets on MA(20:3 ω-9)

We saw before that the amount of LA is the biggest influence on MA limits, but take a look at the graph and compare it with the diets and their OA:LA ratios.

• Soybean Oil: 0.4
• Fish Oil: 13.3
• Lard: 4.6

Although Fish Oil(omega-3 has the aggravating factor of reducing Δ-6 desaturase) has the best OA:LA ratio, the amount of MA is still less than that of Soybean oil with 50% LA and a ratio of 0.4! OA seems to increase MA regardless of LA.

Is the presence of OA/MA able to help deplete EFAs?

Apparently, not only is it able to help, but it happens much faster than a fat-free or coconut oil diet.

SF(OA=14.2%/LA=75.5%) - CO(OA=2.63%/LA=0.45%) - OA(OA=69%/LA=3.54%)

Trienes* = Mead Acid(20:3 ω-9)

Within 21 days MA was found in the brain, liver and serum in the OA group, even though the diet with the lowest LA was CO.

After 90 days, the intensity of EFAD was greater in the OA group

Curiosity: Usually EFAD at these levels is enough to cause growth stunting, but apparently OA didn't have as much of this, at least in this study. Study with too little time to find out.

Other studies seem to confirm OA ability to increase MA independently of LA:

Others point to OA ability to interfere with LA levels:

Attention was thus focused on the possibility that oleic acid interfered with the normal utilization of some other component in coconut oil. As we were dealing with essential fatty acid deficiency symptoms, this component might be linoleic acid. Gas-liquid chromatographic analysis of coconut oil showed that it contained 1.5% of linoleic acid, furnishing about 20 mg. of linoleic acid per day per guinea pig. This amount, although small, can support almost normal growth without any deficiency symptoms as shown by feeding coconut oil alone. However, when comparatively large amounts of oleic acid are included in the diet, the animals no longer can utilize the small but significant amount of linoleic acid and deficiency symptoms are observed.

It may be possible that under these circumstances oleic acid competes with linoleic acid and acts as an inhibitor with some of the enzymes involved in arachidonic acid formation. If such is the case, metabolites of oleic acid would accumulate in the oleic acid-fed group. Eicosatrienoic acid, which is formed from oleic acid under conditions of fat deficiency, was found in the oleic acid-fed group and was absent in the other groups.

To produce MA, it seems that the amount of oleic matters in an "acute" way, and the limits and intensity with which it can increase seem to be defined by the OA:LA ratio at the moment.

The way I see it, for those who strive to deplete PUFA, there's no reason why someone can't reach this EFAD status or can't accelerate this state to happen in less than 4 years. Considering depletion as something that happens in a linear way is the reason many peaters find it impossible outside of laboratory environments.

REFERENCES

Cleland, L. G., Neumann, M. A., Gibson, R. A., Hamazaki, T., Akimoto, K., & James, M. J. (1996). Effect of dietary n-9 eicosatrienoic acid on the fatty acid composition of plasma lipid fractions and tissue phospholipids. Lipids, 31(8), 829–837.

Nada Birkic, Toni Azar, Krishna Rao Maddipati, Zeljka Minic & Christian A. Reynolds. Excessive dietary linoleic acid promotes plasma accumulation of pronociceptive fatty acyl lipid mediators

Mizunoya, W., Iwamoto, Y., Shirouchi, B., Sato, M., Komiya, Y., Razin, F. R., … Ikeuchi, Y. (2013). Dietary Fat Influences the Expression of Contractile and Metabolic Genes in Rat Skeletal Muscle. PLoS ONE, 8(11), e80152.

Menon, N. K., & Dhopeshwarkar, G. A. (1981). Essential fatty acid deficiency and lipid metabolism of the developing brain. Progress in Lipid Research, 20, 129–134.

Lowry, R. R., & Tinsley, I. J. (1966). Oleic and Linoleic Acid Interaction in Polyunsaturated Fatty Acid Metabolism in the Rat. The Journal of Nutrition, 88(1), 26–32.

Mohrhauer, H., Rahm, J. J., Seufert, J., & Holman, R. T. (1967). Metabolism of Linoleic Acid in Relation to Dietary Monoenoic Fatty Acids in the Rat. The Journal of Nutrition, 91(4), 521–527.