Endotoxin And Fat Consumption

[Amazoniac]

Is it? Why?

I don't know, I was just wondering because, as far as I know, most of the fat absorption occurs within the middle part of the small intestine and only the remnants by its end, which is the part that starts to have significantly more bacteria. Acidity also decreases up to a certain point along the intestines, and acidity encourages the growth of safer bacteria. I'm mentioning this because it would be unexpected for the body to have too much endotoxin being absorbed earlier than usual..

 

[tyw]

No dairy, no greens, but...but where do you get your calcium mister?

Soy and sardines it is

What are your thoughts on apple cider vinegar compared to normal white vinegar? Which is best?

I usually use Apple cider vinegar. No clue whether there is going to be a difference compared to other vinegars on the basis of health effects.

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I have no clue regarding links between glycine and endotoxin absorption from the small intestine.

I do not drink bone broth. Makes me bloated.

....

 

[Mito]

Soy and sardines it is

According to SELFNutritionData's database, the calcium content of sardines and soy is approximately 100 mg per 1 g (or more) of PUFA. To meet the RDA of calicium from those sources would mean at least 10 g PUFA/day? Do you really consume that much PUFA daily or do you just not get the RDA of calcium? Or are my calcium/PUFA ratios off?

 

[tyw]

According to SELFNutritionData's database, the calcium content of sardines and soy is approximately 100 mg per 1 g (or more) of PUFA. To meet the RDA of calicium from those sources would mean at least 10 g PUFA/day? Do you really consume that much PUFA daily or do you just not get the RDA of calcium? Or are my calcium/PUFA ratios off?

Firstly, I do not really bother with managing PUFA intake when overall fat is very low, especially when calories are not in surplus, and . "Very low" typically means 15g fat a day or below for me, which is pretty much the norm when I get to control my own food intake. "Calories not in surplus" seems to be the case for me, since I've typically been in slight weight loss for a few years, and weight stable for about 1.5 years now. Add to that my context whereby I'm likely 10% body fat, and PUFA consumption becomes even less of an issue.

Next, I have generally had low calcium intake through my life (except for a 2 year stint of high seafood consumption). Whether or not this is a genetic factor, I do not know, but there is reason to believe so. Paper 'Habitual dietary calcium intakes and calcium metabolism in healthy adults Chinese: a systematic review and meta-analysis' -- http://apjcn.nhri.org.tw/server/APJCN/25/4/776.pdf

In our previous paper, we reported a calcium requirement of 400-500 mg/d for Chinese adults between 18 and 60 years of age, which is much lower than that for Americans and Europeans.

Mean daily dietary intakes of calcium ranged between 288 and 948 mg. Subgroup analysis showed that average calcium retentions in four quartile groups were 45 mg/d, 18 mg/d, 85 mg/d and 163 mg/d, respectively.

All of them were on the right side of zero, that is, positive balance.

The Chinese adults pooled in the present study appear able to maintain a positive calcium balance with plant based diets at calcium intakes as low as 300 mg/d, via a possible adaptation in calcium metabolism to increase fractional calcium absorption and decrease calcium excretion in urine and faeces.​

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[beachbum]

I generally disagree with the idea of inherent "autoimmunity", but the fact that even 1mg of gluten can affect some of the worst coeliac patients, is probably indicative of a very fast, cascading systemic breakdown of communication between components induced by the initial stress of gluten .... The proline and glutamine in gliadin is powerful stuff.

What do you mean by proline and glutamine in gliadin is powerful stuff. In a good or bad way.

 

[Wagner83]

Paper (a) will elaborate on why PUFAs do not cause as big of a response -- they suppress the initial inflammatory cascade within intestinal cells. The pro-PUFA observer sees this as a "good thing", because "less inflammation bro".

This is faulty logic -- the pro-PUFA stance claims that suppressing the alarm bells (stuff like NF-kB and TNF-alpha) is equivalent to decreasing the harm caused by the objects that are raising the alarm in the first place. I will elaborate more in the "Personal interpretations" section below.​

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.

So do you think this study on orange juice is actually negative, similar to what you mentioned on PUFAs above ? Orange Juice Neutralizes The Proinflammatory Effect Of A HFHC Meal And Prevents Endotoxin Increase

 

[meatbag]

This is why ELF-EMFs that are below 1,000 Hz are very harmful. This is the shared resonance of many compounds (like Ca2+) that we use in biology, and ELF-EMF emitters like Power Lines push out 50-60Hz frequencies that are in the Earth's Natural Schumann band.

Hey Tyw (or anyone elese who knows :)),

Where are you getting that Ca2+ resonance value?

 

[haidut]

This is why ELF-EMFs that are below 1,000 Hz are very harmful. This is the shared resonance of many compounds (like Ca2+) that we use in biology, and ELF-EMF emitters like Power Lines push out 50-60Hz frequencies that are in the Earth's Natural Schumann band

Are you aware of the recent discussion on Reddit about the dangers of EMF and its mechanism of action? The proposed mechanism was activation of calcium channels, which I doubt is a coincidence considering the shared resonance you mentioned. I posted a few threads about this last year. Selenium seems to block the damage completely, as would calcium blockers of course.

 

[tyw]

The original source was Dr Robert O. Becker's book, 'The Body Electric'.

Since then, there have been many examples of experiments exposing cells to the "Calcium ion cyclotron resonance" frequency.

Just 2 Examples:
- Calcium ion cyclotron resonance (ICR), 7.0 Hz, 9.2 microT magnetic field exposure initiates differentiation of pituitary corticotrope-derived AtT20... - PubMed - NCBI
- Calcium ion cyclotron resonance (ICR) transfers information to living systems: effects on human epithelial cell differentiation. - PubMed - NCBI

And one overview (recommended reading):
- ELF fields and their effects on calcium homeostasis

NOTE: I do believe that these are "shared native bands", in the sense that such frequencies are part of the normal implementation of biology. Exposure of human-generated EMFs in these frequency bands should be seen as adding extra information to these endogenous systems. Whether or not the system is disrupted as a result -- whether exogenous EMF is truly "interference", or if it just harmless noise -- depends on unknown factors.

It is clear that extreme EMF sensitivity exists wrt ELF EMF, but the exact mechanisms are unknown. Viewing these exogenous ELF EMFs as communication interference within the body, is my current model for reasoning about any new information that comes up.​

As mentioned my original post, this is a clear disruption to the signalling machinery of various biological systems. Overall Impact is going to depend on exposure context. eg: SAR characteristics of emitter, penetration depth, which organ systems are involved, etc .....

I have not looked deeply into the mechanics of selenium. Any cursory knowledge I have on this topic specific to EMF revolves around muscular contraction studies, where it can bolster the contraction signal.

I do not expect selenium supplementation (beyond what is normal) to be helpful in the common context of EMF exposure -- ie: powerful radio transmitter next to head (cellphone). Too many factors to consider wrt selenium and the exposed organ in this context (the brain, to which selenium distribution is highly variable, and as such, highly endogenously regulated -- Anatomical regional differences in selenium levels in the human brain. - PubMed - NCBI).

The only true fix would be to either block entirely the ability of said EMF to penetrate important tissues, or to find a way to restore normal function of signalling machinery in the face of explicit disruptions. Elimination of calcium channel mechanics isn't the solution. A solution in the face of EMF is more akin to finding a way to implement or bolster endogenous cellular "checksums" and "error correcting codes". This is something that we do not know how to do in any reliable fashion in the context of EMF stress.

Hence, I still take the perspective that avoiding EMF emitters as much as possible is the safest course of action.

Hey Tyw (or anyone elese who knows :)),

Where are you getting that Ca2+ resonance value?

Are you aware of the recent discussion on Reddit about the dangers of EMF and its mechanism of action? The proposed mechanism was activation of calcium channels, which I doubt is a coincidence considering the shared resonance you mentioned. I posted a few threads about this last year. Selenium seems to block the damage completely, as would calcium blockers of course.

 

[raypeatclips]

Are you aware of the recent discussion on Reddit about the dangers of EMF and its mechanism of action? The proposed mechanism was activation of calcium channels, which I doubt is a coincidence considering the shared resonance you mentioned. I posted a few threads about this last year. Selenium seems to block the damage completely, as would calcium blockers of course.

Do you know what amount of selenium is needed to protect against EMF damage? Thank you.

 

[mattyb]

I didn't have time to read the whole thread yet, but I'm curious what you all & @tyw think are the most effective antibiotics (or antibiotic-like substances) at killing bacteria in the small intestine.

Also, any idea how much your theory's action applies to small intestine vs large intestine?

The most effective are conjugated bile salts. It's how the body naturally regulates small intestine bacterial populations.

If you have SIBO, best thing you can do is get bile salts flowing. Curcumin/tumeric can be used to increase bile flow - but you must make sure you don't have any large gallstones, as this can cause the stones to obstruct the biliary ducts (very dangerous). Increasing dietary fat consumption will enhance bile flow as well. - likely one of the antibacterial mechanisms of a ketogenic diet.

 

[haidut]

Do you know what amount of selenium is needed to protect against EMF damage? Thank you.

Peat was asked and said "200mcg daily for a week and then either 100mcg daily or eating more seafood".

 

[meatbag]

The original source was Dr Robert O. Becker's book, 'The Body Electric'.

Since then, there have been many examples of experiments exposing cells to the "Calcium ion cyclotron resonance" frequency.

Just 2 Examples:
- Calcium ion cyclotron resonance (ICR), 7.0 Hz, 9.2 microT magnetic field exposure initiates differentiation of pituitary corticotrope-derived AtT20... - PubMed - NCBI
- Calcium ion cyclotron resonance (ICR) transfers information to living systems: effects on human epithelial cell differentiation. - PubMed - NCBI

And one overview (recommended reading):
- ELF fields and their effects on calcium homeostasis

NOTE: I do believe that these are "shared native bands", in the sense that such frequencies are part of the normal implementation of biology. Exposure of human-generated EMFs in these frequency bands should be seen as adding extra information to these endogenous systems. Whether or not the system is disrupted as a result -- whether exogenous EMF is truly "interference", or if it just harmless noise -- depends on unknown factors.

It is clear that extreme EMF sensitivity exists wrt ELF EMF, but the exact mechanisms are unknown. Viewing these exogenous ELF EMFs as communication interference within the body, is my current model for reasoning about any new information that comes up.​

As mentioned my original post, this is a clear disruption to the signalling machinery of various biological systems. Overall Impact is going to depend on exposure context. eg: SAR characteristics of emitter, penetration depth, which organ systems are involved, etc .....

I have not looked deeply into the mechanics of selenium. Any cursory knowledge I have on this topic specific to EMF revolves around muscular contraction studies, where it can bolster the contraction signal.

I do not expect selenium supplementation (beyond what is normal) to be helpful in the common context of EMF exposure -- ie: powerful radio transmitter next to head (cellphone). Too many factors to consider wrt selenium and the exposed organ in this context (the brain, to which selenium distribution is highly variable, and as such, highly endogenously regulated -- Anatomical regional differences in selenium levels in the human brain. - PubMed - NCBI).

The only true fix would be to either block entirely the ability of said EMF to penetrate important tissues, or to find a way to restore normal function of signalling machinery in the face of explicit disruptions. Elimination of calcium channel mechanics isn't the solution. A solution in the face of EMF is more akin to finding a way to implement or bolster endogenous cellular "checksums" and "error correcting codes". This is something that we do not know how to do in any reliable fashion in the context of EMF stress.

Hence, I still take the perspective that avoiding EMF emitters as much as possible is the safest course of action.

 

[Kartoffel]

I finally found a paper that looked at long-term endotoxin levels in humans consuming different types and quantities of fat and wanted to share it here. Essentially all of the rat studies show that PUFA cause endotoxemia, and damage the liver while SAT reduces it, and protects the liver from any LPS. Yet, all the human studies seem to show that SAT (coconut oil in particular) seems to aggravate endotoxemia. The problem with all the studies is that they only look at a single meal, and observe postprandial LPS levels. They all find that SAT increase them while PUFA even lower them compared to control low-fat diets.
Lopez-Moreno et al. finally conducted a long-term intervention study and fed people different diets for 12 weeks. They either provided a high-fat diet rich in SAT, a high-fat diet rich in MUFA, or two control low-fat diets (one enriched with n-3). As all the other studies before they found that the SFA-diet increased postprandial LPS. The interesting thing are the fasting levels for LPS. In accordance with the theory that postprandial LPS levels are higher after consuming SFA because they kill bacteria, but will otherwise lower the potential for LPS production, fasting levels were only half in the SFA group. As I see it, this confirms that SFA do not aggravate endotoxemia, and are likely to lower the total burden from systemic endotoxins in humans.

Sci-Hub | Effect of Dietary Lipids on Endotoxemia Influences Postprandial Inflammatory Response. Journal of Agricultural and Food Chemistry, 65(35), 7756–7763 | 10.1021/acs.jafc.7b01909

 

[haidut]

I finally found a paper that looked at long-term endotoxin levels in humans consuming different types and quantities of fat and wanted to share it here. Essentially all of the rat studies show that PUFA cause endotoxemia, and damage the liver while SAT reduces it, and protects the liver from any LPS. Yet, all the human studies seem to show that SAT (coconut oil in particular) seems to aggravate endotoxemia. The problem with all the studies is that they only look at a single meal, and observe postprandial LPS levels. They all find that SAT increase them while PUFA even lower them compared to control low-fat diets.
Lopez-Moreno et al. finally conducted a long-term intervention study and fed people different diets for 12 weeks. They either provided a high-fat diet rich in SAT, a high-fat diet rich in MUFA, or two control low-fat diets (one enriched with n-3). As all the other studies before they found that the SFA-diet increased postprandial LPS. The interesting thing are the fasting levels for LPS. In accordance with the theory that postprandial LPS levels are higher after consuming SFA because they kill bacteria, but will otherwise lower the potential for LPS production, fasting levels were only half in the SFA group. As I see it, this confirms that SFA do not aggravate endotoxemia, and are likely to lower the total burden from systemic endotoxins in humans.

Sci-Hub | Effect of Dietary Lipids on Endotoxemia Influences Postprandial Inflammatory Response. Journal of Agricultural and Food Chemistry, 65(35), 7756–7763 | 10.1021/acs.jafc.7b01909

View attachment 11931

Very interesting find, thanks! I wonder why there was no group on high-PUFA diet. Isn't that a very realistic diet given the commercial junk most people eat on a daily basis?
Also, did you check the fat composition for the SFA and MUFA? Often then will label a diet high SFA when it is fact a lard-based diet (which has up to 30% MUFA and up to 25% PUFA).

 

[Kartoffel]

Very interesting find, thanks! I wonder why there was no group on high-PUFA diet. Isn't that a very realistic diet given the commercial junk most people eat on a daily basis?
Also, did you check the fat composition for the SFA and MUFA? Often then will label a diet high SFA when it is fact a lard-based diet (which has up to 30% MUFA and up to 25% PUFA).

A high PUFA diet would have been very interesting indeed. I think the significant increase in fasting LPS in the low-fat group supplemented with n-3 is already a good indicator.
They say the HSFA diet focused on butter and whole milk for fat.

 

[lvysaur]

I finally found a paper that looked at long-term endotoxin levels in humans consuming different types and quantities of fat and wanted to share it here. Essentially all of the rat studies show that PUFA cause endotoxemia, and damage the liver while SAT reduces it, and protects the liver from any LPS. Yet, all the human studies seem to show that SAT (coconut oil in particular) seems to aggravate endotoxemia. The problem with all the studies is that they only look at a single meal, and observe postprandial LPS levels. They all find that SAT increase them while PUFA even lower them compared to control low-fat diets.
Lopez-Moreno et al. finally conducted a long-term intervention study and fed people different diets for 12 weeks. They either provided a high-fat diet rich in SAT, a high-fat diet rich in MUFA, or two control low-fat diets (one enriched with n-3). As all the other studies before they found that the SFA-diet increased postprandial LPS. The interesting thing are the fasting levels for LPS. In accordance with the theory that postprandial LPS levels are higher after consuming SFA because they kill bacteria, but will otherwise lower the potential for LPS production, fasting levels were only half in the SFA group. As I see it, this confirms that SFA do not aggravate endotoxemia, and are likely to lower the total burden from systemic endotoxins in humans.

Sci-Hub | Effect of Dietary Lipids on Endotoxemia Influences Postprandial Inflammatory Response. Journal of Agricultural and Food Chemistry, 65(35), 7756–7763 | 10.1021/acs.jafc.7b01909

View attachment 11931

Amazing find.

 

[Kartoffel]

Amazing find.

Thanks. I was always a bit puzzled by the studies seemingly implicating that SFA does the exact opposite of what it does in rat studies.

 

[haidut]

A high PUFA diet would have been very interesting indeed. I think the significant increase in fasting LPS in the low-fat group supplemented with n-3 is already a good indicator.

View attachment 11932

Thanks. As I suspected, there is no true high SFA diet in this study. The ratio of SFA/(MUFA+PUFA) even in the SFA diet is <1. A true SFA diet not only has a ratio of >1 but in animal research it is usually defined as a at least 75% of the fat being SFA. For that reason, some studies won't even consider palm oil suitable as SFA diet, and the truly well-done SFA diet studies use mostly coconut oil or fully hydrogenated peanut/soy oils.
It is hard to explain this in any other way than deliberate manipulation. The lack of a high-PUFA diet is especially telling since the high PUFA diet would mirror much more closely the dietary patterns of most Westerners.

 

[tankasnowgod]

I finally found a paper that looked at long-term endotoxin levels in humans consuming different types and quantities of fat and wanted to share it here. Essentially all of the rat studies show that PUFA cause endotoxemia, and damage the liver while SAT reduces it, and protects the liver from any LPS. Yet, all the human studies seem to show that SAT (coconut oil in particular) seems to aggravate endotoxemia. The problem with all the studies is that they only look at a single meal, and observe postprandial LPS levels. They all find that SAT increase them while PUFA even lower them compared to control low-fat diets.
Lopez-Moreno et al. finally conducted a long-term intervention study and fed people different diets for 12 weeks. They either provided a high-fat diet rich in SAT, a high-fat diet rich in MUFA, or two control low-fat diets (one enriched with n-3). As all the other studies before they found that the SFA-diet increased postprandial LPS. The interesting thing are the fasting levels for LPS. In accordance with the theory that postprandial LPS levels are higher after consuming SFA because they kill bacteria, but will otherwise lower the potential for LPS production, fasting levels were only half in the SFA group. As I see it, this confirms that SFA do not aggravate endotoxemia, and are likely to lower the total burden from systemic endotoxins in humans.

Sci-Hub | Effect of Dietary Lipids on Endotoxemia Influences Postprandial Inflammatory Response. Journal of Agricultural and Food Chemistry, 65(35), 7756–7763 | 10.1021/acs.jafc.7b01909

View attachment 11931

Very cool. Looking at the study, the "challenge meal" relied on white bread as the main carbohydrate, and for the LFHCC they keep saying "high complex carbohydrate," which would mean more fiber and more starch. I would think that if sugar had been the main carb source, the fasting levels might be even lower, especially considering the study that found that Orange Juice could stop the post meal endotoxin effect, even when it had a lot of carbs and a lot of PUFA-

https://www.ncbi.nlm.nih.gov/pubmed/20200256