Saturated Fat Allows Bacteria To Translocate

[Captain_Coconut]

In Mice, so why not in Humans?? We already know SFA increases postprandial serum LPS in humans, I doubt it is the only thing getting through. I think bacterial translocation and the dormant blood biome is at the root of many diseases.

Effects of Dietary Fat Profile on Gut Permeability
and Microbiota and Their Relationships
with Metabolic Changes in Mice

https://onlinelibrary.wiley.com/doi/pdf/10.1002/oby.21122

“Effect of dietary fat profile on gut permeability and bacterial translocation
Transepithelial resistance of the colon of HFD-sat mice was 26% lower than that of CTRL (P < 0.05). The HFD-n6 and CTRL groups did not differ, whereas HFD-n3 tended to increase transepithelial resistance (64.3 6 2.8 Ohm cm22 vs. 52.7 6 1.5 Ohm cm22 for CTRL; P 5 0.11; Figure 3A). Bacterial DNA content in the mesen- teric fat [as a surrogate marker of bacterial translocation (13)] of HFD-sat mice trended higher (2-fold; P 5 0.12), whereas HFD-n6 and HFD-n3 groups did not differ, from CTRL (Figure 3B). Repre- sentative DGGE of the bacterial content in the mesenteric fat of HFD-sat mice revealed a banding pattern distinct from that of CTRL or fecal microbiota from HFD-sat mice (Figure 3C). The closest relatives for most DGGE bands found in HFD-sat mesenteric
fat samples were typical commensals including Akkermansia and members of Lachnospiraceae.”

 

[Captain_Coconut]

Mesenteric fat as a source of C reactive protein and as a target for bacterial translocation in Crohn's disease

The prevalence of gut translocation in humans. - PubMed - NCBI

 

[Kartoffel]

You would think it's not so hard to find a saturated fat that is actually high in saturated fat

"high saturated fat (60%kcal from fat, of which 34% was saturated fatty acids)"​

 

[Captain_Coconut]

[Intestinal bacterial translocation in patients with biliary tract diseases]. - PubMed - NCBI

A nested case-control study on dietary fat consumption and the risk for gallstone disease. - PubMed - NCBI

The preliminary experimental and clinical study of the relationship between the pigment gallstone and intestinal mucosal barrier. - PubMed - NCBI

Higher triglycerides = higher risk of gallstones = more bacterial translocation.

 

[CLASH]

This has really become a witch hunt....

 

[Kartoffel]

This has really become a witch hunt....

Yeah, he is obsessed with the idea that saturated is really bad, and tries to make all sorts of weird connections. He should change his name to Captain_Peanut or Captain_Soybean

 

[michael94]

Why so mean

 

[Captain_Coconut]

Why so mean

LOL. It is just a natural defense mechanism for people who are afraid to earnestly consider evidence that does not support their current comfort zone.

 

[Makrosky]

I think the most important thing about these captain coconut posts is to remember one thing : don't forget to test your assumptions from time to time. And I don't mean theoretically. Try going low sat fat and increase non-harmful PUFAs and see what happens. Maybe you get a big surprise.

 

[TeaRex14]

Witch hunt would be putting it strongly. There is a lot of merit to the idea of reducing total fat intake, this would inherently include a reduction in dietary saturated fats. But the reason why I say the science isn't settled on this issue is because it becomes impossible, quite literally speaking, to increase dietary saturated fats without also increasing dietary unsaturated fats. The two are linear, and when you increase the consumption of one you're inherently increasing the consumption of the other. Also there's the fact if saturated fats are inherently bad for us, then carbohydrate would also have to be bad. Because any carbohydrate we ingest that isn't used immediately, or converted into glycogen, gets converted into saturated fatty acids. This is why it's crucial to realize that circulating free fatty acids, regardless of their degree of saturation, is more harmful then the inherent consumption of any particular fatty acid.

 

[Kartoffel]

Why so mean

That's not mean, just a little jibe. And I think he has more than earned it for his deliberate attempt to spread misinformation about saturated fat wherever he can. He has seen the studies showing that saturated fat reduces bacterial transloaction, cures cirrhosis, and other LPS-related diseases, and yet continues to ignore them. He ignores any counter evidence, and then accuses his oppnents of not considering evidence, while I have replied in detail to everything he cited. He doesn't even read most of these papers he posts, otherwise he would have noticed that the high-saturated fat diet in this paper is 35% and probably contained almost as much 18:2 as the high-n6 diet. They don't even disclose the fats they used.

Here is a study showing the complete opposite, even with ethanol. Just look for A.A. Nanjii to find more evidence that completely dismisses Captain_Soybeans theories.

Saturated and Unsaturated Dietary Fats Differentially Modulate Ethanol-Induced Changes in Gut Microbiome and Metabolome in a Mouse Model of Alcoholic Liver Disease

 

[Kartoffel]

But the reason why say the science isn't settled on this issue is because it becomes impossibly, quite literally speaking, to increase dietary saturated fats without also increasing dietary unsaturated fats.

You make a good point. That's why they use high-"saturated" fat diets as in this study, with only 35% saturated fat. They know that this is bull****, and that it would be easy to use a real saturated fat such as beef, coconut, cocoa or butter. Even palm oil is more saturated than whatever they used in that study. But they use it anyway because they already know that real saturated fat doesn't work to get the results they want as dozens of publications have already demonstrated it to be protective against LPS.

 

[michael94]

That's not mean, just a little jibe. And I think he has more than earned it for his deliberate attempt to spread misinformation about saturated fat wherever he can. He has seen the studies showing that saturated fat reduces bacterial transloaction, cures cirrhosis, and other LPS-related diseases, and yet continues to ignore them. He ignores any counter evidence, and then accuses his oppnents of not considering evidence, while I have replied in detail to everything he cited. He doesn't even read most of these papers he posts, otherwise he would have noticed that the high-saturated fat diet in this paper is 35% and probably contained almost as much 18:2 as the high-n6 diet. They don't even disclose the fats they used.

Here is a study showing the complete opposite, even with ethanol. Just look for A.A. Nanjii to find more evidence that completely dismisses Captain_Soybeans theories.

Saturated and Unsaturated Dietary Fats Differentially Modulate Ethanol-Induced Changes in Gut Microbiome and Metabolome in a Mouse Model of Alcoholic Liver Disease

Good points and all but I don’t think mice have the same sort of problems with fat digestion that some 20 year old + humans do. I can understand how prolonged stress would make one intolerant to fats simply due to not being able to digest the fat or say, handle the LPS properly. And I don’t think that’s easy to replicate in a mouse model with an acute toxin

 

[TeaRex14]

You make a good point. That's why they use high-"saturated" fat diets as in this study, with only 35% saturated fat. They know that this is bull****, and that it would be easy to use a real saturated fat such as beef, coconut, cocoa or butter. Even palm oil is more saturated than whatever they used in that study. But they use it anyway because they already know that real saturated fat doesn't work to get the results they want as dozens of publications have already demonstrated it to be protective against LPS.

That may very well be the case. Anecdotally, I always feel better when I consume predominantly saturated fats. Grassfed beef, gum free dairy products, coconut oil, etc. Maybe it's because I just find foods containing larger portions of saturated fat to taste better, lol. When you think of high PUFA foods like oils, nuts, seeds, fatty fishes they all taste like crap to me.

 

[Captain_Coconut]

Witch hunt would be putting it strongly. There is a lot of merit to the idea of reducing total fat intake, this would inherently include a reduction in dietary saturated fats. But the reason why I say the science isn't settled on this issue is because it becomes impossible, quite literally speaking, to increase dietary saturated fats without also increasing dietary unsaturated fats. The two are linear, and when you increase the consumption of one you're inherently increasing the consumption of the other. Also there's the fact if saturated fats are inherently bad for us, then carbohydrate would also have to be bad. Because any carbohydrate we ingest that isn't used immediately, or converted into glycogen, gets converted into saturated fatty acids. This is why it's crucial to realize that circulating free fatty acids, regardless of their degree of saturation, is more harmful then the inherent consumption of any particular fatty acid.

Carbs converted to SFA are not the same as ingesting SFA.

The first study I posted shows the effect of the 3 main fats. We see SFA is the one that raises translocation. While many dietary fats will be a more mixed composition, this does not mean somehow postprandial endotoxin and translocation from SFA is neutralized, sure it may dampen it to have other fats mixed. We have a choice we can make on how much we are getting of each fat, cut out beef and coconut and we basically get very little sfa. I think dietary SFA is fine in moderation, if one is already sick eating a tablespoon of coconut oil is stupid, I learned the hard way and wanted to find out why this happened, like I have said in the past I had great success with coconut oil when I was younger. The difference is I was a 22 bmi then, but more recently I went from a 25 to 26 bmi simply by increasing coconut oil and limiting all pufa below 5 grams daily. The effect depends on ones state of current health, it is not one size fits all.

 

[Vinero]

You should post this in the vitamin A thread @Captain_Coconut. This is relevant to the people who are on the low vitamin A diet, since we are limiting all saturated fats, and experimenting with MUFAs and PUFAs.

 

[Kartoffel]

Good points and all but I don’t think mice have the same sort of problems with fat digestion that some 20 year old + humans do. I can understand how prolonged stress would make one intolerant to fats simply due to not being able to digest the fat or say, handle the LPS properly. And I don’t think that’s easy to replicate in a mouse model with an acute toxin

You can of course assume that rat study results don't fully apply to humans, but the same results have been obtained with pigs that have a digestive tract that is much more similar to ours. Studies in humans have also shown that saturated fat protects the liver and lowers baseline serum endotoxin. All the studies are posted in the big saturatd fat-endotoxin thread.

Effects of coconut oil on glycemia, inflammation, and urogenital microbial parameters in female Ossabaw mini-pigs

The first study I posted shows the effect of the 3 main fats.

No it doesn't. Tell me what saturated fat has 35% saturated fatty acids?

 

[CLASH]

@Makrosky
I did the low fat thing in many iterations for close to 3 years.... low fat, super low fat, low fat with coconut oil, low fat with butter, low fat with olive oil, low fat with beef tallow, low fat with all sugar, low fat with mostly starch, low fat with a mixture of both sugar and starch, low fat with fruit only, low fat using granulated sugar, low fat higher order protein, low fat lower protein. I dont think n-3 or n-6 are “non-harmful” so I’m not sure what you are recommending here...

There are numerous people on this forum who suffer with low libido, psychological issues, gut issues and hormonal issues on a ray peat inspired low fat diet.... I have found that my issues, which were similar to these were greatly resolved with a higher fat diet from MUFA and SAFA sources. Plus, there is a host of research supporting my experience.... People on this forum continue to beat thier heads against the wall, attempting to go low fat to avoid PUFA and when they have an issue going even lower fat is often recommended in the echo chamber and the person often reports feeling better for 2 days before getting worse. I have watched the iteration over and over. Now @Captain_Coconut tries a diet with 30% coconut oil, which is known to irritate the gut, and gets a bad response. Then he proceeds to quote rat studies and guinea pig studies (studies that often arent even using high safa diets or are confounded with a simultaneous high PUFA intake), both animals that dont neccesarily eat high fat diets in thier natural state, and short term human studies involving obese and type 2 diabetics who get an increase in post prandial endotoxemia in the short term, (which is conflicting in the studies as to whether it even causes an inflammatory response) while in the long term studies as posted by @Kartoffel and my self shows benefit to somehow frame saturated fatty acids as to be avoided. This is even continued when the studies he posts are refuted. I’m all for having an open mind and would love to have a discussion of the mechanisms, but dumping studies with a negative bent and then claiming saturated fat is bad on weak evidence and without an overlying context seems a bit questionable. Especially in light of the fact that it was all inspired by a bad experience with a 30% coconut oil diet....

Even more to this if saturated fat is so terrble how are people doing well on keto, losing weight and seeing a decrease in thier digestive issues? How are they managing thier autoimmune disease, which seem to be largely gut microbiota related? Why would animals concentrate it in thier milk? Why would the majority of large mammals have the bulk of thier diets as saturated/ monounsaturated fatty acids? Why does the body convert carbohydrate to them? Why do populations around the world celebrate these fat sources and prize them as food? Why do populations that relied on high fat diets not have obesity, diabetes if these fats promote endotoxemia which in @Captain_Coconut’s model is causative in these? Why do they not have chronic infections in thier fat stores? I dont see the overlying context, all i see is cherry picked studies and an attempt to find a cause to his experience with a 30% coconut oil diet which is already well known to cause gut issues....

Most importantly why are all these people on the ray peat forum eating low fat diets becoming fatter, having lower libidos, getting anxiety and mental issues and complaining of gut issues?

@TeaRex14
Fatty acids are always being circulated and oxidized.
Ratio of PUFA to calories and to SAFA and MUFA as well presence of adequate carbohydrate intake seems to be more important than strict limiting, although overall limiting seems to be important. PUFA can be sufficiently limited even on a high fat diet. Plus going very low PUFA makes the diet very restricted, hard to see how it is so optimal if it was difficult for most populations to have even adhered to it. There has to be more to the picture, especially considering that PUFA restriction doesnt seem to be solving many peoples issues here. Edward J. Edmonds has a post showing that with low amounts of exogenous LCFA froms MUFA and SAFA the body retained PUFA even in the presence of SAFA from MCT and especially on low fat diets. His hypothesis was the LCFA spared glucose so that the liver could glucoronidate the PUFA and excrete it.
26 - The Bitter Citizen - Linoleic Acid - The Last Breath

 

[Makrosky]

@Makrosky
I did the low fat thing in many iterations for close to 3 years.... low fat, super low fat, low fat with coconut oil, low fat with butter, low fat with olive oil, low fat with beef tallow, low fat with all sugar, low fat with mostly starch, low fat with a mixture of both sugar and starch, low fat with fruit only, low fat using granulated sugar, low fat higher order protein, low fat lower protein. I dont think n-3 or n-6 are “non-harmful” so I’m not sure what you are recommending here...

There are numerous people on this forum who suffer with low libido, psychological issues, gut issues and hormonal issues on a ray peat inspired low fat diet.... I have found that my issues, which were similar to these were greatly resolved with a higher fat diet from MUFA and SAFA sources. Plus, there is a host of research supporting my experience.... People on this forum continue to beat thier heads against the wall, attempting to go low fat to avoid PUFA and when they have an issue going even lower fat is often recommended in the echo chamber and the person often reports feeling better for 2 days before getting worse. I have watched the iteration over and over. Now @Captain_Coconut tries a diet with 30% coconut oil, which is known to irritate the gut, and gets a bad response. Then he proceeds to quote rat studies and guinea pig studies (studies that often arent even using high safa diets or are confounded with a simultaneous high PUFA intake), both animals that dont neccesarily eat high fat diets in thier natural state, and short term human studies involving obese and type 2 diabetics who get an increase in post prandial endotoxemia in the short term, (which is conflicting in the studies as to whether it even causes an inflammatory response) while in the long term studies as posted by @Kartoffel and my self shows benefit to somehow frame saturated fatty acids as to be avoided. This is even continued when the studies he posts are refuted. I’m all for having an open mind and would love to have a discussion of the mechanisms, but dumping studies with a negative bent and then claiming saturated fat is bad on weak evidence and without an overlying context seems a bit questionable. Especially in light of the fact that it was all inspired by a bad experience with a 30% coconut oil diet....

Even more to this if saturated fat is so terrble how are people doing well on keto, losing weight and seeing a decrease in thier digestive issues? How are they managing thier autoimmune disease, which seem to be largely gut microbiota related? Why would animals concentrate it in thier milk? Why would the majority of large mammals have the bulk of thier diets as saturated/ monounsaturated fatty acids? Why does the body convert carbohydrate to them? Why do populations around the world celebrate these fat sources and prize them as food? Why do populations that relied on high fat diets not have obesity, diabetes if these fats promote endotoxemia which in @Captain_Coconut’s model is causative in these? Why do they not have chronic infections in thier fat stores? I dont see the overlying context, all i see is cherry picked studies and an attempt to find a cause to his experience with a 30% coconut oil diet which is know to cause gut issues....

Most importantly why are all these people on the ray peat forum eating low fat diets becoming fatter, having lower libidos, getting anxiety and mental issues and complaining of gut issues?

Hey Clash! I think I didn't explain myself well. You can read whatever studies you want in either direction but the definite answer is how you feel when implementing a strategy. A "wide feel" if you know what I mean. It is not a temporary burst of energy or something like that. At this point anyone that has been on the forum for some time is knowledgeable enough to detect these kind of things that seem to be good at the beginning but can lead to bad consequences. For non-harmful PUFA I mean something like EVOO.

Personally, I haven't tried it so metodically as you but I feel better when I do a bit of saturated fat a day : from small ammounts of dairy (butter, cheese or milk) and the rest is EVOO. No sat fat at all or only sat fat is not good for me. That's what I mean with my comment, people should try on their own body (which is unique) the hypothesis. I tried high sat fat, no good. I tried avoiding sat fat, not good either. If the mantra repeated on this forum is that all PUFA is bad (which is not) then nobody will try a different approach, and CCoconut posts elicit at least the idea that is worth trying it. That's all I said.

I also think discussing studies is very intelectually stimulating but there are so many factors at play that no one should be blindly following them to implement a strategy on fat intake and LPS stuff.

 

[Alpha]

It's not a proper study to lump fatty acids into categories like saturated and unsaturated. Post a study that shows any one FA and it's effects in certain measurements.

I'm also assuming the other variables are controlled for like types of food and macro breakdown.