Saturated fats in a meal and Endotoximia

[salvio]

I wasn't sure in which section put this but I'm curious:

[PDF] Impact of dietary fat on gut microbiota and low-grade systemic inflammation: mechanisms and clinical implications on obesity | Semantic Scholar

It is believed that high-fat diets and SFA consumption should be avoided, and MUFA and omega-3 PUFA intake should be encouraged in order to regulate gut microbiota and inflammation, promoting body weight/fat control. Abstract Dietary fat strongly affects human health by modulating gut microbiota...

www.semanticscholar.org

Can saturated fats increse Dysbiosis and endotoxemia? Is is possible revert it?

The article says that the problem are FFA in the colon so I suppose that if the energy intake of meal isn't to high and to the colon arrives a low energy plop the ploblem shouldn't be so strong.

What do you thing about?

 

[Korven]

I could be wrong here, but I think the idea that "high fat diets = bad for gut health" comes from mice studies where they feed the mice junk food diets high in PUFA. This doesn't mean that healthy foods such as milk, meat and eggs causes dysbiosis in humans.

Saturated fats causing endotoxemia and systemic inflammation has been debunked several times on this forum, it's a mechanism to detox LPS. Lots of people reverse autoimmune issues on diets high in saturated fats.

 

[salvio]

I could be wrong here, but I think the idea that "high fat diets = bad for gut health" comes from mice studies where they feed the mice junk food diets high in PUFA. This doesn't mean that healthy foods such as milk, meat and eggs causes dysbiosis in humans.

Saturated fats causing endotoxemia and systemic inflammation has been debunked several times on this forum, it's a mechanism to detox LPS. Lots of people reverse autoimmune issues on diets high in saturated fats.

io want to precise that I only want to discuss about it cause I've found these:

Eucaloric Ketogenic Diet Reduces Hypoglycemia and Inflammation in Mice with Endotoxemia - PubMed

Dietary strategies to alter the immune response to acute inflammation have the potential to improve outcomes in critically ill patients. A eucaloric ketogenic diet (EKD), composed predominantly of fat with very small amounts of carbohydrate, can provide adequate caloric support while minimizing...

pubmed.ncbi.nlm.nih.gov

Postprandial serum endotoxin in healthy humans is modulated by dietary fat in a randomized, controlled, cross-over study

High-fat diets may contribute to metabolic disease via postprandial changes in serum endotoxin and inflammation. It is unclear how dietary fat composition may alter these parameters. We hypothesized that a meal rich in n-3 (ω3) fatty acids would ...

www.ncbi.nlm.nih.gov

"
In conclusion, our results demonstrate that the composition of dietary fat, but not a meal’ s percent calories from fat, is significant in determining postprandial changes in blood endotoxin concentration in healthy adults in vivo.

So it looks like that the amount of carbs and the amount of meal determine in increasing of endotoxins in the gut cause if the meal is low cals low carbs shouldn't increase LPS in bloodstream a lot.

I found the full article and I'd like to have your opinion about:

(PDF) Postprandial serum endotoxin in healthy humans is modulated by dietary fat in a randomized, controlled, cross-over study

PDF | Background High-fat diets may contribute to metabolic disease via postprandial changes in serum endotoxin and inflammation. It is unclear how... | Find, read and cite all the research you need on ResearchGate

www.researchgate.net

I'm trying to find this:

Eucaloric Ketogenic Diet Reduces Hypoglycemia and Inflammation in Mice with Endotoxemia.​

I'm curious to get if in single meal with a bit of fruits I can reduce LPS adsorbition.

 

[Korven]

io want to precise that I only want to discuss about it cause I've found these:

Eucaloric Ketogenic Diet Reduces Hypoglycemia and Inflammation in Mice with Endotoxemia - PubMed

Dietary strategies to alter the immune response to acute inflammation have the potential to improve outcomes in critically ill patients. A eucaloric ketogenic diet (EKD), composed predominantly of fat with very small amounts of carbohydrate, can provide adequate caloric support while minimizing...

pubmed.ncbi.nlm.nih.gov

Postprandial serum endotoxin in healthy humans is modulated by dietary fat in a randomized, controlled, cross-over study

High-fat diets may contribute to metabolic disease via postprandial changes in serum endotoxin and inflammation. It is unclear how dietary fat composition may alter these parameters. We hypothesized that a meal rich in n-3 (ω3) fatty acids would ...

www.ncbi.nlm.nih.gov

"
In conclusion, our results demonstrate that the composition of dietary fat, but not a meal’ s percent calories from fat, is significant in determining postprandial changes in blood endotoxin concentration in healthy adults in vivo.

So it looks like that the amount of carbs and the amount of meal determine in increasing of endotoxins in the gut cause if the meal is low cals low carbs shouldn't increase LPS in bloodstream a lot.

I found the full article and I'd like to have your opinion about:

(PDF) Postprandial serum endotoxin in healthy humans is modulated by dietary fat in a randomized, controlled, cross-over study

PDF | Background High-fat diets may contribute to metabolic disease via postprandial changes in serum endotoxin and inflammation. It is unclear how... | Find, read and cite all the research you need on ResearchGate

www.researchgate.net

I'm trying to find this:

Eucaloric Ketogenic Diet Reduces Hypoglycemia and Inflammation in Mice with Endotoxemia.​

I'm curious to get if in single meal with a bit of fruits I can reduce LPS adsorbition.

There was a good discussion on this topic in this thread: Dairy = Essential Or Deadly? . You might find it interesting!

Also you probably want to check out CLASH's posts on saturated fat and endotoxin.

 

[salvio]

There was a good discussion on this topic in this thread: Dairy = Essential Or Deadly? . You might find it interesting!

Also you probably want to check out CLASH's posts on saturated fat and endotoxin.

The link about references isn't reachable.

 

[salvio]

To be honest I noticed some strange data in the fats used.

For instance teh high saturated fats use an huge amount of lauric acid whereas low-fat diet uses a dominance of MUFA, the ration n-6/n-3 is very different in the n-3 and n-6 tests.

I created an excel-sheet to better analyze the percentage of various fats in the study and the first thing I noticed that the LPS induction follow the same insulin resistance pattern of this study:

Distinctive postprandial modulation of beta cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids - PubMed

The data presented here suggest that beta cell function and insulin sensitivity progressively improve in the postprandial state as the proportion of MUFAs with respect to SFAs in dietary fats increases.

pubmed.ncbi.nlm.nih.gov

So MUFA/SFA ratio increase insulin sensibility (maybe cause decrease LPS translocation and not only for glucose FFA competition? Who knows). Notice that when the amount of fat is high even MUFA and PUFA create the same problem with insulin.

And: Acute metabolic response to high-carbohydrate, high-starch meals compared with moderate-carbohydrate, low-starch meals in subjects with type 2 diabetes - PubMed

Where if you eat a little of sugar from fruit and eat fats insulinemic response it's lower (and maybe translocation of LPS?) and that justifies a meal where a low amount of carbs and a moderate-high amount of SFA can't create problems as occurring in ketogenic diets.

Another question should so the dynamic balance or the in-out of energy between two meals, it's enough to pass from a very cold environment to one at 20 degrees to see BMR to decrease at 20%, for example the gut adsorption different temperature:

[Influence of environmental temperature on absorption of xylose in fasting animals] - PubMed

The A. have studied 28 pairs of rats; 17 pairs received 1,1 g of soya oil; 7 pairs were starved. The partners were kept; one at the environmental temperature of 6 degrees C, the other at 30 degrees C. After a night, all rats were tested for xylose absorption. Xylose intestinal absorption in the...

pubmed.ncbi.nlm.nih.gov

Effect of fasting on the intestinal absorption of D-glucose and D-xylose in rats in vivo - PubMed

The present study was planned to elucidate the role of fasting on the intestinal absorption of monosaccharides particularly--glucose and xylose in inbred female albino rats. Rats (weighing 250-300 grams) were divided into three groups. One group of rats served as control while the other two were...

pubmed.ncbi.nlm.nih.gov

It look like the more someone needs of energy the more he/she/it will adsorb it by gut and vice versa.

So the explication could be that cause SFA can be used as ready energy fuel (as glucose) the body in diminished adsorption when the energy balance is a constant positive or positive for too meals, and so the small gut can decrease adsorption allowing free FFA to reach Colon and letting LPS translocation.

 

[salvio]

However it's true that Chylomicrons are powerful ant inflammatory molecules.

Abstract​

Chylomicrons (CM) can bind endotoxin (lipopolysaccharide [LPS]), forming CM-LPS complexes, and protect against endotoxic shock and death in rodent models of gram-negative sepsis. The liver appears to play a central role in this process, as demonstrated by the increased uptake of LPS by this organ. We examined the effect of CM on the uptake and cellular response to injected 125I-LPS by hepatocytes and hepatic nonparenchymal cells. Whereas CM increased the uptake of LPS by both hepatocytes and Kupffer cells, the increase was proportionately greater in hepatocytes than Kupffer cells. Importantly, CM-LPS complexes inhibited inducible nitric oxide synthase (iNOS) mRNA expression and NO production in Kupffer cells and endothelial cells, reducing mRNA levels by 45% to 50% as compared with LPS alone. CM-bound LPS also reduced NO production by hepatocytes in response to cytokine stimulation. Lastly, CM-LPS complexes yielded a concentration-dependent inhibition of LPS-induced tumor necrosis factor alpha (TNF-alpha) production by Kupffer cells in vitro. These data indicate that the mechanism by which CM protect against endotoxicity may involve an increased uptake of LPS by hepatocytes. Moreover, uptake of CM-bound LPS by liver cells attenuates the capacity of these cells to respond to proinflammatory stimulation. These results highlight important anti-inflammatory properties of CM.

Chylomicrons alter the hepatic distribution and cellular response to endotoxin in rats - PubMed

Now question is: are the short chain fatty acids a problems?