I'm Done Looking For A Method To Lower Body Fat Without Caloric Restriction

[raypeatclips]

Yes, it's true. @raypeatclips Endotoxin absorption increase with saturated fat and decrease with unsaturation. This is normal, because the saturated fat is transporting the endotoxin via chylomicrons to the liver for detoxification. Fats that don't stimulate chylomicrons, such as medium chain fats, won't increase the absorption of endotoxins.

Edit: I noticed you said saturated fat transport the endotoxin for detoxification, yes I agree with that, so that is a positive of saturated fat in the diet, and should be included. Yet you don't want saturated fat in the diet?

Do you have any scientific proof to back this up, other than the study posted above that unfortunately uses a cream containing carageenan and polysorbate 80? (I really wish it hadn't because I want answers to this too.)

Peat has been saying for years that saturated fat helps with endotoxin, and I'm willing to believe it isn't, if you have some sort of proof to back up what you are saying.

Your posts remind me of tyw's from years ago, have you been inspired by him?

 

[raypeatclips]

@Salmonamb

Studies Peat has referenced before

Protective Effects of Medium-Chain Triglycerides on the Liver and Gut in Rats Administered Endotoxin

"Gut permeability to horseradish peroxidase was about 30 U/L in the corn oil group (Fig. 4). In rats given MCTs, values were decreased significantly compared with the corn oil group. Gut permeability was increased about threefold in the corn oil group after LPS administration. This increase was blunted by about 70% by MCT administration."

"Inflammation, focal necrosis, and hemorrhagic change were observed after LPS administration in the corn-oil group. MCTs prevented these pathologic changes significantly."


Dietary saturated fatty acids down-regulate cyclooxygenase-2 and tumor necrosis factor alfa and reverse fibrosis in alcohol-induced liver disease i... - PubMed - NCBI

"The data indicate that a diet enriched in saturated fatty acids (groups 3 and 4) effectively reverses alcohol-induced liver injury, including fibrosis. The therapeutic effects of saturated fatty acids may be explained, at least in part, by reduced endotoxemia and lipid peroxidation, which in turn result in decreased levels of TNF-alpha and Cox-2."


Effect of dietary linoleate content on the metabolic response of rats to Escherichia coli endotoxin. - PubMed - NCBI

"Coconut oil completely abolished the responses to endotoxin. "

 

[Hans]

Do you have any scientific proof to back this up

Saturated fat is a TLR4 agonist https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3413240/

Saturated fat increases endotoxin absorption, omega 6 is neutral and omega 3 decreases endotoxin absorption. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5097840/
"The test meal was a porridge made with quick-ready oatmeal (Hy-Vee Supermarkets, Ames, IA) prepared with water according to the manufacturer’s instructions. To this oatmeal, 1) coconut oil (Spectrum, Lake Success, NY), 2) olive oil (Crisco, Orville, OH), 3) grapeseed oil (Pompeian, Baltimore, MD) or 4) fish oil (Carlson, Arlington Heights, IL) was added in order to provide each of the four test meals a unique macronutrient (Table 2) and fatty acid profile (Table 3). 60 g ± 17 g of hard-boiled egg (Crystal Farms 6 peeled hard-boiled eggs ready-to-eat, Lake Mills, WI), 201 g ± 26 g of fat-free skim milk (HyVee fat free skim milk, Des Moines, IA), and 184 g ± 33 g of orange juice (Tropicana Pure Premium No Pulp, Bradenton, FL) were served with the porridge. The participants were required to eat the test meal in its entirety within 15 min of serving."

"Comparison of the mean endotoxin values of the three high fat diets to the low fat diet did not yield a statistically significant (p < 0.05) difference suggesting that absolute fat intake does not influence post-prandial endotoxemia." So the type of fat does not increase or decrease endotoxin production from a meal.

"Notably, the higher-fat test meals, in which each meal provided 35 % of calories from fat, were not different from the low-fat meal (20%) in their effect on postprandial serum endotoxin (data not shown). This suggests that in an isoenergetic series of meals, a higher percentage of fat does not differentially alter postprandial serum endotoxin concentration." Looks like not only the type, but neither the quantity reduces endotoxin production.

"Although serum endotoxin was found to increase after a saturated fatty acid rich meal or decrease after an n-3 PUFA enriched meal, markers of in vivo inflammation were unaffected." The study just shows that saturated fat increases the absorption of endotoxins moreso than omega 6.

PUFAs and endotoxins both increase gut permeability which could cause endotoxin leaking into the body, but this says nothing about endotoxin absorption. I agree MCT and SFAs in general are protective. The endotoxin absorption property of SFAs isn't bad, because it actually aids in endotoxin detoxification and is healing to the liver. Some people just get an immune response to this effect, and is then best to go low SFA and consume low endotoxin producing foods, until their health improves. Only PUFAs can cause lipid peroxidation and oxidative stress.

I think Tyw does good research, but that doesn't mean I agree 100% with him about everything. I like to do my own research to come to my own conclusions, and that is what I believe everyone should do.

 

[Braveheart]

+1 This was me. I didn't realise how calorifically dense saturated fat is, so in my mind I was eating much less than I actually was. I wonder if this is the reason for so much weight gain on the Peat diet. I'd advise everyone to track every calorie you eat, at least for a few days, in order to better understand it. Also a few cokes can add excess calories on top of an already good amount of calorie meal.

You are correct about tracking...I'm in disbelief over how many here are trying to do this without good tracking...

 

[Jon]

Yes, it's true. @raypeatclips Endotoxin absorption increase with saturated fat and decrease with unsaturation. This is normal, because the saturated fat is transporting the endotoxin via chylomicrons to the liver for detoxification. Fats that don't stimulate chylomicrons, such as medium chain fats, won't increase the absorption of endotoxins. It's just that some peoples immune systems can't handle the endotoxins and reacts badly to it. In general I think it's best to eat the least gut irritating and endotoxin producing food, even if you eat lots of saturated fat or not. Like you probably know, endotoxin increases gut permeability, contributes to insulin resistance, diabetes, weight gain, organ inflammation and damage, increase in serotonin, etc.



Yes a very low fat diet will not work for everyone, and might just work for the minority. It depends on what kind of fat you have in your adipose tissue. Most people have mostly unsaturated fat, so it will make the deficit even more stressful (lipid peroxidation, etc.). The lower I take my fat, the better I generally feel. More energy, satiety, glucose tolerance, no sleepiness after a carb meal, etc. I might experiment with higher fat intake later on because fat do make food taste better and stuff like eggs are a great source of nutrients as you say. I actually notice, when going very low fat that my muscle are harder, more vascular and I'm rarely hungry. My bodyfat drops pretty quick (not lbs quick, but to the eye) even though my deficit is not that big. I also notice that my libido isn't reduced, but might actually be increasing.
Fat free rats are actually immune to diabetes, many cancers and are extremely resilient to many stressors. PUFAs are really the driving force for disease and aging.
I don't think mobilizing lots of fats are stressful, because it's excessive beta-oxidation that are, dare I say causing, diabetes, and not excessive lipolysis (but it obviously contributes). When fats flood the mitochondria, most fats only undergo semi beta-oxidation because the TCA and electron transport chain cannot keep up. This leads to a buildup of lots of semi oxidized lipid fragments, which are most likely prone to oxidation by the ROS. These fats accumulate in the cell leading to an increase in intracellular fat, which further interfere with normal cellular function. So I think as long as the body is able to completely oxidize and/or excrete the fats via glucuronidation, and neutralize the ROS, it won't be as stressful. It's the excessive beta-oxidation that mainly leads to problems. Researchers found that when blocking beta-oxidation, it restored insulin function and glucose oxidation, even in the presence of lots of intracellular fat (which are linked to insulin resistance and diabetes).



True. I guess I was just initially surprised that I am losing fat at 2500 calories without much exercise, because in the past I cut on 2000 calories and weight trained like 5-6 times a week, plus extra cardio lol. Fat loss was fast then, but I won't say that it's slower now. Maybe I was putting myself in such a stress state back then that my weight loss was actually slowed down.
I feel that at 2500 calories the stress isn't accumulating yet, but might if I increase my activity level.
William Brown ate 2500 calories with 2g of fat for 6 months, and his weight dropped from 69kg to 62kg in three months, after which his weight remained stable. He wasn't even active as far as I know. So low fat will definitely speed up the metabolism, if someone can tolerate it.

I want to add that, the more PUFAs someone eats, the more their cardiolipin will become unsaturated with linoleic acid, which is very easily damaged by the free radicals from complex I and III. The linoleic acid creates HNE, which is about 1000 times more reactive than superoxide, and can actually leave the cells and do damage systematically. This leads to a rapid loss in cardiolipin, degradation of electron transfer chain complexes and reduction of mitochiondrial function. The electron transport chain can literally not work without cardiolipin. Replacing the linoleic with oleic acid (made from de novo lipogenesis) in the cardiolipin, protects it from oxidative stress, and so also mitochondrial function. So although saturated fats create more ROS and thus insulin resistance than PUFAs, it will not contribute to lipid peroxidation, mitochondrial destruction, and diabetes as PUFAs would. So many reasons to avoid PUFAs.

All good reasons to watch fat closely no matter your health goals. Ive never thought that a high fat diet was a good thing, at 146lbs and 14% bf I only eat 37g of fat a day usually in the neighborhood of 4g pufa, 25g sfa, 8g mufa. So I definitely don't practice getting in high fat.

It would be very interesting if the bad effects i and others feel from vlf were in fact pufa being oxidized from bodyfat stores but somewhat hard for me to swallow just because of how pronounced they are and how akin it is to just being in a deep calorie deficit. None the less very interesting, thanks for the explaination.

 

[raypeatclips]

Saturated fat is a TLR4 agonist Saturated fatty acids activate TLR-mediated proinflammatory signaling pathways

Saturated fat increases endotoxin absorption, omega 6 is neutral and omega 3 decreases endotoxin absorption. Postprandial serum endotoxin in healthy humans is modulated by dietary fat in a randomized, controlled, cross-over study
"The test meal was a porridge made with quick-ready oatmeal (Hy-Vee Supermarkets, Ames, IA) prepared with water according to the manufacturer’s instructions. To this oatmeal, 1) coconut oil (Spectrum, Lake Success, NY), 2) olive oil (Crisco, Orville, OH), 3) grapeseed oil (Pompeian, Baltimore, MD) or 4) fish oil (Carlson, Arlington Heights, IL) was added in order to provide each of the four test meals a unique macronutrient (Table 2) and fatty acid profile (Table 3). 60 g ± 17 g of hard-boiled egg (Crystal Farms 6 peeled hard-boiled eggs ready-to-eat, Lake Mills, WI), 201 g ± 26 g of fat-free skim milk (HyVee fat free skim milk, Des Moines, IA), and 184 g ± 33 g of orange juice (Tropicana Pure Premium No Pulp, Bradenton, FL) were served with the porridge. The participants were required to eat the test meal in its entirety within 15 min of serving."

"Comparison of the mean endotoxin values of the three high fat diets to the low fat diet did not yield a statistically significant (p < 0.05) difference suggesting that absolute fat intake does not influence post-prandial endotoxemia." So the type of fat does not increase or decrease endotoxin production from a meal.

"Notably, the higher-fat test meals, in which each meal provided 35 % of calories from fat, were not different from the low-fat meal (20%) in their effect on postprandial serum endotoxin (data not shown). This suggests that in an isoenergetic series of meals, a higher percentage of fat does not differentially alter postprandial serum endotoxin concentration." Looks like not only the type, but neither the quantity reduces endotoxin production.

"Although serum endotoxin was found to increase after a saturated fatty acid rich meal or decrease after an n-3 PUFA enriched meal, markers of in vivo inflammation were unaffected." The study just shows that saturated fat increases the absorption of endotoxins moreso than omega 6.

PUFAs and endotoxins both increase gut permeability which could cause endotoxin leaking into the body, but this says nothing about endotoxin absorption. I agree MCT and SFAs in general are protective. The endotoxin absorption property of SFAs isn't bad, because it actually aids in endotoxin detoxification and is healing to the liver. Some people just get an immune response to this effect, and is then best to go low SFA and consume low endotoxin producing foods, until their health improves. Only PUFAs can cause lipid peroxidation and oxidative stress.

I think Tyw does good research, but that doesn't mean I agree 100% with him about everything. I like to do my own research to come to my own conclusions, and that is what I believe everyone should do.

Interesting, thank you for posting!

 

[JustAGuy]

All good reasons to watch fat closely no matter your health goals. Ive never thought that a high fat diet was a good thing, at 146lbs and 14% bf I only eat 37g of fat a day usually in the neighborhood of 4g pufa, 25g sfa, 8g mufa. So I definitely don't practice getting in high fat.

It would be very interesting if the bad effects i and others feel from vlf were in fact pufa being oxidized from bodyfat stores but somewhat hard for me to swallow just because of how pronounced they are and how akin it is to just being in a deep calorie deficit. None the less very interesting, thanks for the explaination.

I personally don't feel any negatives whatsoever from eating very low fats. Averaging about ~15g a day from grains/lean meat/vegetables.

 

[Jon]

I personally don't feel any negatives whatsoever from eating very low fats. Averaging about ~15g a day from grains/lean meat/vegetables.

Interesting. But that's with sufficient calories to maintain weight, yes?

It may make sense too with your particular level of leaness that you don't experience much stress at maintenance calories vlf being that you're ectomorphic. You may have low pufa stored in general which is pretty awesome if that's the case! but I still think with a deficit comes stress no matter your macro make up.

 

[walker_in_aus]

Hello
I wanted to create a calorie deficit by increasing my metabolism on a high calorie diet, but so far it has been a failure, or I'm eating too much. Aspirin as discussed here, and 1,200mg daily of caffeine(aside from many other things that ramp up my metabolism/thyroid) was a failure as well. My only option is to lower calories.
Also, I think implementing this, with this would make it quite safe.

Aspirin can inhibit fatty acid oxidation. It's very good for protecting general health this way, but it can definitely slow down "fat loss"

 

[JustAGuy]

Interesting. But that's with sufficient calories to maintain weight, yes?

It may make sense too with your particular level of leaness that you don't experience much stress at maintenance calories vlf being that you're ectomorphic. You may have low pufa stored in general which is pretty awesome if that's the case! but I still think with a deficit comes stress no matter your macro make up.

Yes, effect of fats doesn't matter if I am maintaining or bulking or cutting. I just always feel better if I eat less fats and add more carbs. If I am cutting I can go lower calories (aka: cut faster) and feel the same as I did in higher calories with less fats.
I have been higher BF (close to 20% maybe?) for a period in the past in high school, ate tons of crap (pufa oils in foods, fried stuff) so for sure there must've been some PUFA.
It just feels like I feel better on the same amount of calories if I remove fats and add carbs. Even if I am eating 40g fat and I lower it to 20g fat and add more carbs I feel quite a noticeable energy boost from it.
It feels like fats cause my carbs to "work less well" for some reason.
I am for sure an ecto, 6'6 tall and only have a wrist circumfence of 6.2 inch.
Totally agree deficit = stress, I always notice less stress tolerance from working out in a deficit. I balance this out with things like less CNS intensive rep ranges (more 15-20, less 8-12). And using machines instead of freeweights, more isolation less compound (do 1h machine rows vs doing both hands simultaneously, more rest times etc.)

 

[Hans]

Another reason vlf works so well for some but not for others, is become of racial differences in de novo lipogenesis (DNL). In this study for example, caucasians have higher DNL than African-Americans. Racial differences in in vivo adipose lipid kinetics in humans
The further people lived from the equator, the more PUFAs they consume and the less they had to rely on making PUFAs (Mead acid) themselves through DNL. So someone with an ancestry far from the equator, might not do so well on a vlfd.
And the closer to the equator, the less PUFAs people consumed, and the more they had to rely on making PUFAs themselves, and these people do better on a vlfd.

 

[cyclops]

Yes, effect of fats doesn't matter if I am maintaining or bulking or cutting. I just always feel better if I eat less fats and add more carbs. If I am cutting I can go lower calories (aka: cut faster) and feel the same as I did in higher calories with less fats.
I have been higher BF (close to 20% maybe?) for a period in the past in high school, ate tons of crap (pufa oils in foods, fried stuff) so for sure there must've been some PUFA.
It just feels like I feel better on the same amount of calories if I remove fats and add carbs. Even if I am eating 40g fat and I lower it to 20g fat and add more carbs I feel quite a noticeable energy boost from it.
It feels like fats cause my carbs to "work less well" for some reason.
I am for sure an ecto, 6'6 tall and only have a wrist circumfence of 6.2 inch.
Totally agree deficit = stress, I always notice less stress tolerance from working out in a deficit. I balance this out with things like less CNS intensive rep ranges (more 15-20, less 8-12). And using machines instead of freeweights, more isolation less compound (do 1h machine rows vs doing both hands simultaneously, more rest times etc.)

Out of curiosity, what is your current body fat% and weight?

 

[JustAGuy]

Out of curiosity, what is your current body fat% and weight?

180lbs, bf% like 7-8% or something, can't pinch fat anywhere basically.

 

[Ron J]

I didn't have glycine left so I had to consume pork rinds, but now that I have glycine, my low fat diet(10%) starts today. I'll lower niacinamide to 750mg in about 3-4 days because I usually mix most powdered supplements in a large container, instead of wasting time taking them one by one, day after day.

 

[Jon]

Another reason vlf works so well for some but not for others, is become of racial differences in de novo lipogenesis (DNL). In this study for example, caucasians have higher DNL than African-Americans. Racial differences in in vivo adipose lipid kinetics in humans
The further people lived from the equator, the more PUFAs they consume and the less they had to rely on making PUFAs (Mead acid) themselves through DNL. So someone with an ancestry far from the equator, might not do so well on a vlfd.
And the closer to the equator, the less PUFAs people consumed, and the more they had to rely on making PUFAs themselves, and these people do better on a vlfd.

Dude just want to say that through your explanations of what happens down the electron transport chain in reguards to each of the substrates on topic in the thread: https://raypeatforum.com/community/...e-and-spatial-memory.25064/page-3#post-360765
I have become more convinced of the efficacy for vlf over a more balanced diet for rehabilitating a compromised metabolism.

It makes sense now as to why it works while eating sufficient calories to prevent an energy deficit.

So we can safely say that vlf is best for rehabbing METABOLISM but it's use should not be geared towards FAT LOSS?

Would it make more sense that once fat loss ensues while on vlf that this is a sign you have raised metabolism and it would be a good idea to methodically increase calories to stop weightloss in order to maintain new found metabolism? Perhaps after eating this calorie level for awhile, you could think about a moderate deficit on a balanced macro ratio, consisting mainly of glucose (starch) and saturated fats? This should hypothetically prevent the cells from being flooded with too much energy while transitioning out of a deficit back to normal calories and preserve the metabolism restored by vlf prior to deficit, does this sound like a good layout for implementing EACH dieting strategy?

 

[Jon]

@Salmonamb I should also add/pose the suggestion that starch should be the primary fuel source on vlf and fruit and fructose only enough to represent micros? This sound good?

 

[Terma]

I didn't have glycine left so I had to consume pork rinds, but now that I have glycine, my low fat diet(10%) starts today. I'll lower niacinamide to 750mg in about 3-4 days because I usually mix most powdered supplements in a large container, instead of wasting time taking them one by one, day after day.

Honestly, no offense but when I posted on this thread I assumed you'd covered basics like not taking 1500mg niacinamide/day.

750 is still way too much (RP never told people to use this much), and mixed like that unless the powders all look different you have no way of knowing it's evenly distributed. I'd take max 50mg/day in weight loss and that's mostly if low protein (no supplementation necessary if high protein, lean meats are high in both NAD and TRP already).

What benefits do you get from it? Most likely you could get them from something else less intrusive, although if it's from the benzo-like calming effect or such, similars like well benzos also interfere with weight loss.

 

[Ron J]

Honestly, no offense but when I posted on this thread I assumed you'd covered basics like not taking 1500mg niacinamide/day.

750 is still way too much (RP never told people to use this much), and mixed like that unless the powders all look different you have no way of knowing it's evenly distributed. I'd take max 50mg/day in weight loss and that's mostly if low protein (no supplementation necessary if high protein, lean meats are high in both NAD and TRP already).

What benefits do you get from it? Most likely you could get them from something else less intrusive, although if it's from the benzo-like calming effect or such, similars like well benzos also interfere with weight loss.

I knew Peat's recommendation, but perhaps I got carried away and went with 1,500mg, probably thinking that it was alright long-term. If 750mg interferes, I'll simply lower it until I get results.

 

[Terma]

Well, I don't blame you for not having read every single thread, but it happens to be the worst culprit from everything I can determine. Neither Vit E nor Glycine (unless high doses) should affect metabolism quite as much, and Glycine is more controversial I'd say [not very likely to be a problem]. Even Aspirin is part of the popular ECA stack, and may lower cortisol despite its other effects.

Most of the other threads on this forum are ignoring the strong relation between the methylated NNMT product N-methylnicotinamide and obesity - this could be the very core of the issue (rather than simply "inhibiting lipolysis"). The best you could hope for in this case is that Glycine + Vit A consume most of the methyl rather than NNMT, but I don't know if the cells actually work this way, and if thyroid is working, the thyroid partially keeps Glycine + Vit A from doing that, so I tend to think, no.

 

[Terma]

The Aspirin, as part of the ECA stack, could in fact be a promoter of the strategy I described earlier, which is to limit Cortisol while boosting Norepinephrine (achieved by the E and C part).