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.
Posts made by TexugoDoMel
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RE: Is it safe to eat raw coconut meat, ground dehydrated or a coconut butter?
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RE: Mice fed a 0% protein diet for a week lost nearly 20% of their body mass
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
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RE: PUFA Depletion
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
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RE: "Glucose Loading" protocol, a la Dr Stephens - A Critique
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
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RE: Its been 3 weeks now since I started to eat ultra low PUFA
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.
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RE: Most "Peaty" ways to recover
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
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RE: Mead Acid production even in the presence of other PUFAs
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.
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Mead Acid production even in the presence of other PUFAs
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.
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RE: Carnivore / keto and steroids
I've never looked that deeply in this context, but cortisol is just one of the hormones involved in glucose regulation.
The hormones glucagon, glucocorticoids and adrenaline are all increased in catabolic states and may work in concert to increase protein breakdown in muscle tissue and to increase amino acid uptake in liver for gluconeogenesis.
Although glucagon is regarded as a major hormone that activates gluconeogenesis during fasting, fasting-induced gluconeogenesis is reduced in adrenalectomized mice, an effect that is restored by treating mice with GC [ 40 – 42 ]. In fact, glucagon-, epinephrine-, or cyclic AMP(cAMP)-induced gluconeogenesis are all attenuated in adrenalectomized mice. Giving GC to adrenalectomized mice restores the ability of these hormones to induce gluconeogenesis. Thus, GC play a “permissive” role promoting the optimal ability of these hormones in gluconeogenesis.
So if cortisol is not close to 0, and their bodies are already adapted to a high level of fatty acid oxidation and they are maintaining a constant flow of ketones, it is unlikely that they will experience severe hypoglycemia since ketones are glucose sparing.
ketogenesis can be upregulated by hormones such as glucagon, cortisol, thyroid hormones, and catecholamines by causing a more significant breakdown of free fatty acids, thus increasing the amount available to be used in the ketogenic pathway. However, insulin is the primary hormonal regulator of this process.
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RE: Most "Peaty" ways to recover
Basically everything Peat says to keep the metabolism healthy is good for bringing the body back to that state after training, with the exception of aspirin, which is considered to be detrimental to gains due to its effect on prostaglandins.
In particular, I like to drink plenty of low-fat or skim milk/kefir after a workout, use red/infrared light (sun is better) and finish with a buteyko/CO2 bath.
CO2 seems to be a great addition post-workout, as it increases the number of mitochondria (PGC-1α), angiogenesis (VEGF) and O2 availability to the tissues.
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On the studies mentioned in episodes 53 and 64 of Generative Energy podcast
In episode 53 of “Generative Energy Ray talks about a study in which scientists took EFAD rats and threw them against the furniture, but even after that the scientists were unable to observe any damage. Ray also mentioned this in the interview with Tucker Goodrich and David Gornoski
Furthermore, in episode 64 of Generative Energy (Life | Energy | Estrogen | Fibrosis | Calcification | Process Theology | Altruism with Ray Peat), haidut comments on studies of EFAD rats regenerating wounds without any scarring.
I couldn't find it, does anyone have these studies? I don't know if @haidut has kept the one about the scar in efad
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Mead Acid, desaturases and accelerating PUFA(EFA) depletion
“The enzyme that produces the Mead fatty acid is strongly inhibited by PUFA seed oils (less strongly by fish oils), and so the presence of the Mead acid in the tissues is taken as evidence that the animal is suffering damage resulting from the absence of PUFA. The Mead acid happens to have some valuable anti-inflammatory effects, and is associated with many biological advantages, but research in that direction is prevented by the lack of funding.” Ray Peat
When Ray mentions the ability of EFAs to suppress the production of Mead Acid, he is talking about the effects they have on desaturases, and although ω-3 has the ability to suppress Mead acid this would probably only happen if ingested in large quantities, the biggest reason for the increase in Mead acid production is ω-6 restriction.
So first of all, you should know that desaturases "add 1 double bound" and elongases "add 2 carbons". Let's take stearic acid as an example, it has an 18-carbon chain and because it is saturated it has no double bounds, so we classify it as 18:0. When it is used as a substrate by the enzyme ∆-9 desaturase (D9D) a double bound is added and it becomes 18:1, so stearic acid (18:0) has been converted into the monounsaturated oleic acid (18:1). The logic is similar for elongases, if 18:1 is used as a substrate by an elongase it would be converted into a 20:1 fatty acid.
To produce Mead's acid, oleic acid (18:1ω-9) is the substrate for the enzyme ∆-6 desaturase (D6D), which transforms it into 6-9-octadecadienoic acid (now 18:2ω-9) which then undergoes the effects of an elongase and is converted into 8-11-eicosadienoic acid (now 20:2ω-9). The last step after this is to pass through ∆-5 desaturase (D5D), converting it into Mead acid(5-8-11-eicosatrienoic acid) with 3 double bounds (20:3ω-9).
The strong inhibition of Mead acid production by EFAs is due to their affinity for the D6D enzyme. α-linolenic acid has priority, followed by linoleic acid and then oleic acid.
The increase of the affinity of the ∆6-desaturase from oleic to linoleic and α-linolenic acid, as well as the correlative increase of the rate of their desaturating reactions explain the predominance of the polyunsaturated acids of the linoleic family or α-linolenic family over the acids of the oleic family in animals fed a complete diet.
For this reason, I can only see two ways of producing Mead's acid in larger quantities:
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By elimination: As Ray suggests, eliminating "essential" fatty acids (focus on eliminating ω-6) from the diet and accumulated in the body, thus releasing D6D for oleic acid.
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By competition: A greater flow of oleic acid in "unusual" situations. Just eating more MUFA won't make you produce more Mead's acid (unless perhaps you were already depleted of EFAs), but there are studies on rats that show that fasting for 3 days and refeed even with an ordinary diet will make the level of Mead's acid rise. The supposed reason? Fasting partially suppresses the desaturases and there is an overcompensation in refeed, apparently for brief moments there is an insufficiency of EFAs and an abundance of MUFAs such as Oleic, available to desaturases.
Control(normal), control-induced(fasting+refeed)
Accelerating pufa depletion through desaturases
In addition to the affinity factor, different macros exert different effects on desaturases, which in theory makes it possible to accelerate EFA depletion by manipulating desaturases. If we consider cystic fibrosis(CF) as an example, Mead's acid is common and is not always due to super low levels of linoleic acid (although they are almost always low), but rather to an increase in the expression of desaturases.
CF: Among these abnormalities are increases in the levels of n-7 and n-9 fatty acids, particularly palmitoleate (16:1n-7), oleate (18:1n-9), and eicosatrienoate or mead acid (20:3n-9)
Work from our laboratory provided correlative data suggesting that these metabolic changes were due to increased expression and activity of fatty acid desaturases ( 23, 24 ). The current study demonstrates that treatment of CF cells with exogenous DHA reverses the metabolic changes by suppressing expression of these enzymes. Specifically, DHA decreases expression of 5- and 6-desaturases.
I found a study in which they accelerated "essential" fatty acid deficiency by inducing D9D, fasting for 3 days + 4 days of refeed.
Biochemical indicator of "essential" fatty acid deficiency is a triene:tetraene ratio (20:3n-9:20:4n-6) greater than 0.4, and below is the difference between EFAD (fat-free diet without fasting) vs EFAD-Induced (fasting+refeed with fat-free diet) over 3 weeks.
Comparing the two, EFAD has a T:T ratio of 1.55 while EFAD-induced has a ratio of 2.60. The former's ratio seems to be more influenced by the increase in Mead Acid (20:3) with almost 60% more compared to EFAD-Induced, which seems to have a high ratio due to the depletion of Linoleic (18:2) and Arachidonic (20:4). This T:T ratio doesn't reflect all the tissues in the body, so this highlight is from the serum.
Do you remember that different macros influence enzymes in different ways? So.
Example 1:
Obs.: G= Glucose, C = Casein, HCO = Hydrogenated coconut oil, SFO = Sunflower Oil.Example 2:
While fasting is not "peaty" I have the impression that a similar or superior result can be achieved with a protein restriction replacing these 3 days of fasting. Protein restriction seems to have the same effects on desaturases, combined with carbohydrate increasing D9D and low fat (close to 0 PUFA) might be better.
In monkeys:
In rats:
In the present work a time-course study with young rats fed on a low-protein diet was an original approach for protein restriction, providing evidence that ∆-9 desaturase activity is impaired, as indeed are ∆6 and ∆5 desaturase activities, during growth under such a dietary regimen.
The effects of this cyclical approach, which accelerates the depletion of EFAs, are more localized:
The mol% of 20 : 3(n - 9) in serum was not increased by ∆9 desaturase induction and the 20 : 3(n - 9) to 20 : 4(n - 6) ratio was only modestly increased. The effects of ∆9 desaturase induction were even more attenuated in tissues other than the liver.
The liver is not the only tissue that shows changes in fatty acid composition. It has been noted, however, that the extent of change is much more profound in liver during the limited 48 hr refeeding period. In Table 5 it is seen that adipose tissue (epididymal fat pad), heart tissue, and the remaining carcass also reflect the variations noted with liverr, but the extent of change is less in the period studied.
So I think you can still expect a general acceleration on a diet with <0.8% linoleic acid, since even those on the control diet produced a small amount of Mead's acid, I suppose that some of it is transported out of the liver and what would take 4 years could be reduced to less due to competition, who knows.
The above studies showed that the concentrations of other PUFAs, such as ARA, EPA and DHA, decreased due to their partial displacement by Mead Acid(MA). The results suggest that MA competes with other long chain PUFAs in PUFA metabolism, and that the presence of MA is not solely due to the decrease in ARA in patients with EFA deficiency. The competition of MA with other PUFAs, especially ARA, is a main mechanism underlying its various physiological and pathological activities, as described below.
Besides, considering that simple approaches can have this influence opens up new possibilities for experimentation: would restricting calories a little on restriction days also increase overcompensation in refeed? And if I use niacinamide/aspirin on restriction days to decrease de novo lipogenesis, what would be the effect?
References
DAVID W. ALLMA, DOROTHY D. HUBBARD, and DAVID M. GIBSON. "Fatty acid synthesis during fa t-free refeeding of starved rats"
Hui Gyu Park, Matthew G. Engel,Kyle Vogt-Lowell, Peter Lawrence, Kumar S. Kothapalli, and J. Thomas Brenna. "The Role of Fatty Acid Desaturase (FADS) Genes in Oleic Acid Metabolism: FADS1 Δ7 desaturates 11-20:1 to 7,11-20:2"
J B Lefkowith. "Accelerated essential fatty acid deficiency by ∆9 desaturase induction: dissociation between the effects on liver and other tissues".
CAROL A. INKPEN, ROBERT A. HARRIS and FORREST W. QUACKENBUSH. "Differential responses to fasting and subsequent feeding by microsomal systems of rat liver: 6- and 9-desaturation of fatty acids"
Rodolfo R. BRENNER "The oxidative desaturation of unsaturated fatty acids in animals"
María C. Marína, Héctor M. Pucciarellib, and María J.T. de Alaniza. "Liver Desaturase Activities and FA Compositionin Monkeys. Effect of a Low-Protein Diet".
Victoria Ayala, Alba Naudí, Alberto Sanz, Pilar Caro, Manuel Portero-Otin, Gustavo Barja, Reinald Pamplona. "Dietary Protein Restriction Decreases Oxidative Protein Damage, Peroxidizability Index, and Mitochondrial Complex I Content in Rat Liver"
Hiroshi Kawashima and Katsuhiko Yoshizawa. "The physiological and pathological properties of Mead acid, an endogenous multifunctional n-9 polyunsaturated fatty acid"
Sarah W Njoroge, Michael Laposata, Waddah Katrangi, Adam C Seegmiller. "DHA and EPA reverse cystic fibrosis-related FA abnormalities by suppressing FA desaturase expression and activity"
Kelly F Thomsen, Michael Laposata, Sarah W Njoroge, Obi C Umunakwe, Waddah Katrangi, Adam C Seegmiller. "Increased elongase 6 and Δ9-desaturase activity are associated with n-7 and n-9 fatty acid changes in cystic fibrosis"*
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RE: Methionine/Cysteine restriction increases longetivity AND energy expenditure
@Mauritio said in Methionine/Cysteine restriction increases longetivity AND energy expenditure:
@TexugoDoMel said in Methionine/Cysteine restriction increases longetivity AND energy expenditure:
The intermittent restriction I mentioned I did a long time ago, I think my calculations at the time didn't even reach 0.1% cysteine (I think it was close to 0.07%? I don't remember).
I calculated the amounts I eat at the moment and it comes down to both aorund 600mg of methionine and cysteine, which is exactly 0.12% of a 2000kcal diet, so Im spot on.
You could also use the 10.4mg/kg/d of the above mentioned human study, which was the most effective dose, which would give most people around 600-1000mg of cysteine and methionine per day each.
I have no idea how you would get to 0.07% , because this is definitely me trying. Like I only eat around 15g of cheese per day as a treat lol.
What saves me diet wise is ice cream. I found some flavors with less than 2g of protein per 100g and one even 0.8g/100g. Meat cravings are going down, but it does get tiresome to almost only eat sweet stuff.
Fruit, lots of potatoes, coconut, butter, rice, a bit of sugar... I don't have many cravings and I like potatoes a lot, so it's easy for me to stick to them, even on workout days.
But I haven't done continuous MR for a long time, I prefer intermittent MR, even if it's not as efficient, because I don't need to lose weight.
The only difference is that my calories are almost twice as much as yours hence the impact on the percentage
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RE: Methionine/Cysteine restriction increases longetivity AND energy expenditure
@Mauritio said in Methionine/Cysteine restriction increases longetivity AND energy expenditure:
BUT: all of that is with 0% Cysteine and that's the issue. As outlined in the posts above if we want to replicate these studies using 0 percent Cysteine, the best we can do is to lower methionine even further, so to mimic a 0.12% methionine + 0% Cysteine diet we have to consume less than 0.12% methionine ,because we do not consume 0% Cysteine and methionine can be converted to Cysteine. I'm not sure how much less we would have to consume, but it might be quite a bit.
You mentioned that 0.02% cysteine would already abolish these effects of MR, I think I missed it, I couldn't find the info. I found 0.5% and the minimum I found similar to what you said was 0.2%.
The intermittent restriction I mentioned I did a long time ago, I think my calculations at the time didn't even reach 0.1% cysteine (I think it was close to 0.07%? I don't remember).
That's an interesting study. 28% increase in life span is pretty good! And that's without restricting methionine. Although 8/12% glycine in the diet is a huge amount that's like 50g of glycine or 150g of gelatin. Not sure how the lower amounts of glycine did.
The aim is not to ingest the same amount, but to potentiate MR with a higher dose of glycine since it is impossible to simulate without a diet similar to the one in the laboratory.
There seem to be some studies on BCAA restriction having similar effects in relation to FGF21, there's even a study mentioning the relationship between BCAA and methionine
I didn't know about taurine, some people say that aspirin also blocks some of the absorption of methionine but I've never seen anything about it.
M and CysR+glycine+selenomethionine+taurine still seems to be the closest way to simulate these studies.
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RE: Methionine/Cysteine restriction increases longetivity AND energy expenditure
@Mauritio said in Methionine/Cysteine restriction increases longetivity AND energy expenditure:
@TexugoDoMel
Thanks! Thats the one I meant.
The results arent as encouriging as I hoped, but still good.They had two Intermittent methionine restricion (IMR) groups, both of them were fed 3 days of a methionine restricted diet followed by a low methionine diet for 4 days in case of IMR1 and a no methionine diet in case of IMR2. They had a continuously methionine restricted diet as a control group
In terms of health effects only IMR2 was really capable of keeping up with continous MR. IMR1 had benefits but not quite as much.
Unforuntely its not really possible for people to have a no methionine diet.
Plus, none of the groups ate any cysteine. And only 0.02% in the diet is able to remove the benefits of MR. So Im increasingly worried about cysteine, since in most of the animals studies on MR, it is 0, which is hard to replicate in humans.![96494e3c-4d15-49e7-b368-04cdbfc7f2a0-image.png](Something went wrong while parsing server response) <img src="https://onlinelibrary.wiley.com/cms/asset/5bc56635-0d01-43e0-baf4-fa08c37470ab/acel13629-fig-0001-m.png" alt="Details are in the caption following the image"/>
So continous MR does seem to be quite a bit superior to intermitten MR ,which can also be seen by the other data on liver and hormones in the study.
The longer you restrict methionine, the better.An interesting finding of the study was that alternating high and low methionine days had a similar effect as the 3-4 approach, which underlines the flexibility of this diet.
So if you feel have a good week ,you can have a high protein day once a week and if you have bad week 4 times a week and still get a lot of benefits.<img src="https://onlinelibrary.wiley.com/cms/asset/5bc56635-0d01-43e0-baf4-fa08c37470ab/acel13629-fig-0001-m.png" alt="Details are in the caption following the image"/>Considering:
Control - Total methionine availability: 0.86%
MR(continuous) - Total methionine availability: 0.12%
IMR1(4 days 0.86% and 3 days 0.12%) - Total methionine availability: 0.54%
IMR2 and IMR2-A(4 days 0.86% and 3 days 0%) - Total methionine availability: 0.49%And this study in which glycine mimics some of the effects of methionine restriction:
https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fasebj.25.1_supplement.528.2I see it differently, especially considering Travis' content from the old forum.
If the goal is to limit methionine in this intermittent style, just eliminating meat and eggs would make it very difficult for you to reach 0.86% on "high methionine days", even with a little meat (unless you overdo it). Most days, even though I like milk and low-fat fish, I don't even reach 0.4% methionine while maintaining more than 1g/kg of protein. So I imagine that on restriction days the effects would be similar even if you didn't consume 0%, but tried to keep it as close to 0 as possible.
Travis said that the reason for restricting methionine is because the amount of methionine reflects the amount of polyamines, which are responsible for proliferation/growth and are generally up-regulated in cancers. I even remember him commenting on a study that just adding polyamines in the presence of stem cells made them differentiate into adipocytes, since polyamines also up-regulate enzymes such as fatty acid synthase, PPAR-gamma, etc.
He also mentioned a way of limiting the use of methionine to create polyamines through substrate competition, which happens when you ingest selenomethionine (supplement or food). The body does not distinguish between methionine and selenomethionine, but selenomethionine cannot be used to create polyamines.
So, in my opinion, the closest thing to simulating studies like this one, even if we don't reach 0% on restriction days, would be:
1- On non-restriction days still restrict consumption of meat and eggs in general so as never to reach 0.86% methionine.
2- On restriction days try to keep as close as possible to 0% methionine, so focusing on fruit and vegetables, tubers and some fats for satiety would be best. To help even more on these days, supplement glycine and selenomethionine (brassicas, such as kale, have a higher concentration of selenomethionine, or take supplements).
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RE: Methionine/Cysteine restriction increases longetivity AND energy expenditure
@Mauritio said in Methionine/Cysteine restriction increases longetivity AND energy expenditure:
Does anybody know the study where they showed that eating low protein 3 times a week, bascially gave the same benefits on longevity as doing it full time? I ve seen that mentioned but havent found the actual study. That is the last thing on that whole topic that Im really interested in.
Apart from what's already in this topic mentioning 3 days of restriction (protein in general), there's this one about intermittent methionine restriction/IMR (3 days of restriction).
To the best of our knowledge, we show for the first time that IMR confers to male and female mice the beneficial metabolic effects previously reported for continuous MR. That is, as compared with control-fed mice, animals undergoing the more stringent of two IMR regimens (IMR2) benefit from reduced adipose tissue accumulation, protection against hepatosteatosis, improved glucose homeostasis, and altered circulating levels of IGF-1, FGF-21, leptin, and adiponectin. Despite a much shorter interventional period than continuous MR (only 3 days per week), not only is IMR capable of producing similar health benefits, but other aspects of this intervention are actually superior to classical MR.
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RE: r/RayPeat someone, along with their family, developed an ARA and DHA deficiency
There are few studies on PUFA deficiency in which the rats consume a good amount of food, most studies keep the nutrients below the requirement and the rats degenerate.
I saw a study in which rats developed the symptoms of PUFA deficiency when placed on a fat-free diet ad libitum, the symptoms were cured spontaneously as long as the diet continued ad libitum, and it was even theorized that the rats produced the essential fatty acids. There's another study in which they didn't even develop symptoms even with a high amount of Mead's acid, but the diet was ad libitum from the start.
Without him talking about the symptoms, we can't be sure. The skin problems of PUFA deficiency seem to be caused by the replacement of linoleic acid(18:2n-6) by oleic acid(18:1n-9). You need a degree of unsaturation to control water permeability, there's a study that rats don't suffer many symptoms of deficiency because they kept the humidity high, it seems to take a while for mead acid(20:3n-9) to take over
WHE = 90% humidty
Bearing in mind that saturated and hydrogenated fats accelerate the depletion of DHA, I believe that the deficiency of DHA is real and there is no other that can replace its function.
In rats, 0.26% of calories in ALA was enough to maintain the maximum concentration of DHA(in organs such as the brain) in adult rats, 0.4% in young rats(which means it's difficult to become deficient in DHA). I haven't looked to see if it can be translated to humans literally, as a few oysters would do the job.
Tokelauans(max 7g PUFA/day) of the past seemed relatively depleted of omega-6 and were relatively free of the diseases of today, I don't remember reading about any particular problem
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RE: The relation between vitamin B6 and the unsaturated fatty acid factor
"All of the 9 animals which received no essential fatty acid showed development of scaly paws within 2 weeks after the initiation of the ad libitum feeding...
It should be noted that in the 9 animals which received no source of linoleic acid scaliness of the paws disappeared spontaneously, and within 66 days from the start of ad libitum feeding these animals, all of which had shown this symptom, were completely cured. The other skin lesions, when present, cleared much earlier.
This spontaneous disappearance of skin lesions within several weeks and paw scaliness within 66 days was again observed in a similar experiment carried out later with approximately the same number of animals on fat free ration A"
https://journals.sagepub.com/doi/abs/10.3181/00379727-66-16128
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RE: Thyroid Log
Iodine is very important but remember that iodine displaces bromide and fluoride and can cause unpleasant symptoms precisely because of this. It's a good idea to adjust the amount of selenium too, as there's a good chance you'll feel unwell when supplementing with iodine if you're deficient in selenium.
You said here:
AFAIK, only T4 Can be converted into rT3.
You're right, but T3 can be converted to diiodothyronine.