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DiscussionLet's talk about it: Diets and foodsThe Anti-Egg Thread 🚫🥚

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The Anti-Egg Thread 🚫🥚

#31 · June 17, 2023, 6:30 pm

I am not interested to look closer at problems with eggs since I think that looking at the microbiome is more important. But here is for anyone that is interested to look closer on a long series of animal studies on eggs by Szepsenwol, J. from the 1950s-1970s. There are at least five studies on eggs, but probably more since not all study titles, of the 27 listed at PubMed, mention egg in the title: https://pubmed.ncbi.nlm.nih.gov/?term=SZEPSENWOL+J&cauthor_id=13485095

I believe this is the first study on eggs from 1957, which is available at sci-hub:
"Presence of a carcinogenic substance in hens' eggs"
https://pubmed.ncbi.nlm.nih.gov/13485095/

PS. Note that DDT use was huge around the time of these studies and DDT became known to cause weak egg shells in some birds thereby threatening their reproduction capability. DDT is now know to be a fat-soluble forever chemical, part of a group of chemicals called: Persistent Organic Pollutants (POPs).

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#32 · June 20, 2023, 7:44 am

Quote from puddleduck on June 20, 2023, 7:44 am
Oh wow, what a fascinating connection between the gut microbiome and emulsifiers in CA patients. 😮 (The book I’m reading about the microbiome hasn’t touched on that at all.) Incredible!

Thanks for posting about the potential problem of fat-soluble pollutants in eggs, too.

Commercial dairy and oils are heavily contaminated with phthalates:

Critical Review on the Presence of Phthalates in Food and Evidence of Their Biological Impact
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7460375/

Eggs are less likely to contain high amounts:

“All phthalates except for DnOP, DiNP and DiDP were detected in eggs with low concentrations across studies.”

From: Phthalates and diet: a review of the food monitoring and epidemiology data
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4050989/

I am glad you are focusing your attention on the microbiome, @david, and look forward to your future posts. 🙂

The past little while I’ve been wondering if the root of this chronic hypervitaminosis A problem is in the gut.

It’s super interesting about fat-soluble compounds (including lutein) as presenting a problem for the cells, since diffusion can’t necessarily be prevented...I wonder if that’s what is going on in the gut, too...Like, if dietary lipids will enhance the diffusion of all forms of vitamin A in the gut?

It looks like there’s evidence of there being some sorta “failsafe” mechanism to prevent the body from converting beta carotene into excess retinoic acid:

“Carotenoid uptake by the enterocytes has been considered to occur by passive diffusion for four decades, which was inconsistent with the high inter-individual variability in absorption observed in humans, as well as with the isomer selectivity and the competition for absorption between carotenoids and other fat-soluble micronutrients observed at the intestinal level (see [20] for review). Different teams started to re-explore carotenoid absorption mechanisms in the 2000s and several lipid transporters playing a role in carotenoid uptake by the intestinal cell have since been identified.”

“Crucial factors modulating the expression and/or the activity of intestinal proteins involved in carotenoid absorption are provitamin A carotenoids, through a feedback regulation. Indeed, studies have pointed out that SR-BI activity is partly controlled by retinoids. Using both mouse models and human cell lines, it was specifically shown that retinoic acid produced from dietary precursors by BCO1 induced the expression of the intestinal transcription factor ISX that repressed the expression of both BCO1 [71] and SR-B1 [72], thus impacting both carotenoid conversion and uptake [73]. Additionally, many dietary factors other than retinoids were shown to regulate transporter expression in the intestine and may, thus, indirectly impact on carotenoid absorption.”

Mechanisms of Carotenoid Intestinal Absorption: Where Do We Stand?https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520933/#B56-nutrients-11-00838

ETA: image file

Oh wow, what a fascinating connection between the gut microbiome and emulsifiers in CA patients. 😮 (The book I’m reading about the microbiome hasn’t touched on that at all.) Incredible!

Thanks for posting about the potential problem of fat-soluble pollutants in eggs, too.

Commercial dairy and oils are heavily contaminated with phthalates:

Critical Review on the Presence of Phthalates in Food and Evidence of Their Biological Impact
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7460375/

Eggs are less likely to contain high amounts:

“All phthalates except for DnOP, DiNP and DiDP were detected in eggs with low concentrations across studies.”

From: Phthalates and diet: a review of the food monitoring and epidemiology data
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4050989/

I am glad you are focusing your attention on the microbiome, @david, and look forward to your future posts. 🙂

The past little while I’ve been wondering if the root of this chronic hypervitaminosis A problem is in the gut.

It’s super interesting about fat-soluble compounds (including lutein) as presenting a problem for the cells, since diffusion can’t necessarily be prevented...I wonder if that’s what is going on in the gut, too...Like, if dietary lipids will enhance the diffusion of all forms of vitamin A in the gut?

It looks like there’s evidence of there being some sorta “failsafe” mechanism to prevent the body from converting beta carotene into excess retinoic acid:

“Carotenoid uptake by the enterocytes has been considered to occur by passive diffusion for four decades, which was inconsistent with the high inter-individual variability in absorption observed in humans, as well as with the isomer selectivity and the competition for absorption between carotenoids and other fat-soluble micronutrients observed at the intestinal level (see [20] for review). Different teams started to re-explore carotenoid absorption mechanisms in the 2000s and several lipid transporters playing a role in carotenoid uptake by the intestinal cell have since been identified.”

“Crucial factors modulating the expression and/or the activity of intestinal proteins involved in carotenoid absorption are provitamin A carotenoids, through a feedback regulation. Indeed, studies have pointed out that SR-BI activity is partly controlled by retinoids. Using both mouse models and human cell lines, it was specifically shown that retinoic acid produced from dietary precursors by BCO1 induced the expression of the intestinal transcription factor ISX that repressed the expression of both BCO1 [71] and SR-B1 [72], thus impacting both carotenoid conversion and uptake [73]. Additionally, many dietary factors other than retinoids were shown to regulate transporter expression in the intestine and may, thus, indirectly impact on carotenoid absorption.”

Mechanisms of Carotenoid Intestinal Absorption: Where Do We Stand?https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520933/#B56-nutrients-11-00838

ETA: image file

Uploaded files:

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#33 · June 21, 2023, 1:28 am

Quote from David on June 21, 2023, 1:28 am
@puddleduck

Thank you for your thoughtful reply!

Most people here are hopefully trying to eat whole foods and by that alone might dodge most of the bad added emulsifiers like: carrageenan (red algae extract), carboxymethylcellulose, methylcellulose, maltodextran and polysorbate-80 (P80). Avoiding these added emulsifiers are probably quite important for anyone with any gut issues.

In the youtube video by the "Alliance to Cure Cavernous Malformation", called "Let's Tak About Emulsifiers", they mention that it is crazy that the emulsifier carragenan isn't simply banned when it has been shown to be terrible for the gut in animal research.
https://youtu.be/mLueRuDLriY
(It is a 1h 17 min presentation + talk between the one who has done the emulsifiers ranking sheet and the one resposible for communication at Alliance to Cure Cavernous Malformation).

It is quite well-known that fat can enhance absorption of carotenoids. Especially for lutein, I have seen a study in which humans ate a normal diet with some amount of fat but when they increased the fat amount further I think only serum lutein increased. The extra fat may aid in diffusion and I think diffusion might help explain why we under certain circumstances can easily absorb carotenoids and just minimally under other circumstances.

[EDIT: This is the 2000 study I was thinking about "Amount of fat in the diet affects bioavailability of lutein esters but not of α-carotene, β-carotene, and vitamin E in humans"
https://doi.org/10.1093/ajcn/71.5.1187

Unfortunately I think it is a study done by or sponsored by Unilever since the scientists had asked for permission to do the study from a Unilever Ethical Commitee. The study were looking to see how to enhance carotenoid absorption of foods fortified with carotenoids. They tested alpha- and beta-carotene and lutein-ester; as they say in the study using lutein-esters might have affected the results.]

I think diffusion might help to explain the attached log-graph from the 1985 Brubacher and Weiser study on rats/mice with low vitamin A stores. Note that this study uses a strange measuring unit called "retinol molecular equivalents" which means 1.874 µg β-carotene = 1 µg retinol molecular equivalent, which I think means 100% theoretical absorption is about 53.3% absorption.

If there is not a lot of carotenoids (or perhaps retinoids) in the outer intestineal cells then there can be a bigger concentration difference and quick absorption of even small amounts of carotenoids (or perhaps retinoids). The outer cells are quickly filled up until diffusion stops. I think could mayne fit with the data that carotenoid absorption at most is around 50 %.

Diffusion between two equal volume seperated stationary fluids whereas one of the fluids from the start had some particles in it should mix perfectly 50/50 over time when being in contact with eachother. Now the chyme in the intestine is moving and is there only for a shorter amount of time but perhaps diffusion is the main explaination behind free carotenoid absorption in the intestines though other factors are also at play like a natural food matrix.

I think diffusion might work the other way around as well, if one's intestinal cells are already filled with carotenoids then not much carotenoids from one's diet would be able to get absorbed. Assumes that their breakdown of carotenoids in the intestine is quite slow as well. If that is the case I think it might be another explaination for those who wonder how some really low fat vegans, which I don't keep track of, might able to do better than expected even though they eat extreme amounts of carotenoids though they probably also eats lots of natural fibers. Some extreme carotenoid eaters might have a localized jaundiced intestine which then puts a limit on the diffusion from the chyme to the intestines.
Though diffusion from intestinal cells high in crotenoids might perhaps then slowly creep further into the body, explaining a quite low carotenoid absorption percentage like seen in the Brubacher and Weiser figure for high intakes of beta-carotene.

If diffusion is also a part of getting rid of carotenoids then it might be one explaination as to why Grant Genereux has not yet tested undetectable for serum retinol, and I know it was some years since Grant was able to test serum retinol.

The 1985 Brubacher and Weiser study is called:
"The vitamin A activity of beta-carotene"
https://pubmed.ncbi.nlm.nih.gov/3997397/
(Not available at sci-hub)

@puddleduck

Thank you for your thoughtful reply!

Most people here are hopefully trying to eat whole foods and by that alone might dodge most of the bad added emulsifiers like: carrageenan (red algae extract), carboxymethylcellulose, methylcellulose, maltodextran and polysorbate-80 (P80). Avoiding these added emulsifiers are probably quite important for anyone with any gut issues.

In the youtube video by the "Alliance to Cure Cavernous Malformation", called "Let's Tak About Emulsifiers", they mention that it is crazy that the emulsifier carragenan isn't simply banned when it has been shown to be terrible for the gut in animal research.
https://youtu.be/mLueRuDLriY
(It is a 1h 17 min presentation + talk between the one who has done the emulsifiers ranking sheet and the one resposible for communication at Alliance to Cure Cavernous Malformation).

It is quite well-known that fat can enhance absorption of carotenoids. Especially for lutein, I have seen a study in which humans ate a normal diet with some amount of fat but when they increased the fat amount further I think only serum lutein increased. The extra fat may aid in diffusion and I think diffusion might help explain why we under certain circumstances can easily absorb carotenoids and just minimally under other circumstances.

[EDIT: This is the 2000 study I was thinking about "Amount of fat in the diet affects bioavailability of lutein esters but not of α-carotene, β-carotene, and vitamin E in humans"
https://doi.org/10.1093/ajcn/71.5.1187

Unfortunately I think it is a study done by or sponsored by Unilever since the scientists had asked for permission to do the study from a Unilever Ethical Commitee. The study were looking to see how to enhance carotenoid absorption of foods fortified with carotenoids. They tested alpha- and beta-carotene and lutein-ester; as they say in the study using lutein-esters might have affected the results.]

I think diffusion might help to explain the attached log-graph from the 1985 Brubacher and Weiser study on rats/mice with low vitamin A stores. Note that this study uses a strange measuring unit called "retinol molecular equivalents" which means 1.874 µg β-carotene = 1 µg retinol molecular equivalent, which I think means 100% theoretical absorption is about 53.3% absorption.

If there is not a lot of carotenoids (or perhaps retinoids) in the outer intestineal cells then there can be a bigger concentration difference and quick absorption of even small amounts of carotenoids (or perhaps retinoids). The outer cells are quickly filled up until diffusion stops. I think could mayne fit with the data that carotenoid absorption at most is around 50 %.

Diffusion between two equal volume seperated stationary fluids whereas one of the fluids from the start had some particles in it should mix perfectly 50/50 over time when being in contact with eachother. Now the chyme in the intestine is moving and is there only for a shorter amount of time but perhaps diffusion is the main explaination behind free carotenoid absorption in the intestines though other factors are also at play like a natural food matrix.

I think diffusion might work the other way around as well, if one's intestinal cells are already filled with carotenoids then not much carotenoids from one's diet would be able to get absorbed. Assumes that their breakdown of carotenoids in the intestine is quite slow as well. If that is the case I think it might be another explaination for those who wonder how some really low fat vegans, which I don't keep track of, might able to do better than expected even though they eat extreme amounts of carotenoids though they probably also eats lots of natural fibers. Some extreme carotenoid eaters might have a localized jaundiced intestine which then puts a limit on the diffusion from the chyme to the intestines.
Though diffusion from intestinal cells high in crotenoids might perhaps then slowly creep further into the body, explaining a quite low carotenoid absorption percentage like seen in the Brubacher and Weiser figure for high intakes of beta-carotene.

If diffusion is also a part of getting rid of carotenoids then it might be one explaination as to why Grant Genereux has not yet tested undetectable for serum retinol, and I know it was some years since Grant was able to test serum retinol.

The 1985 Brubacher and Weiser study is called:
"The vitamin A activity of beta-carotene"
https://pubmed.ncbi.nlm.nih.gov/3997397/
(Not available at sci-hub)

Uploaded files:

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#34 · June 23, 2023, 11:46 pm

Quote from David on June 23, 2023, 11:46 pm
@puddleduck

Just want to add that emulsifier research seems to be focused on mostly existing food additive emulsifiers.

The emulsifier-score PDF (https://www.alliancetocure.org/wp-content/uploads/2022/10/Emulsifier-Scores.pdf) by the Alliance to Cure Cavernous Malformation, unfortunately doesn't feature a hyperlink to studies but has a text like for example "Sandall et. al (2020)" for a lecithin-free diet. That is probably enough to find most of the referenced studies in that PDF. Sandall et. al (2020) gave me this paper:
"Emulsifiers Impact Colonic Length in Mice and Emulsifier Restriction is Feasible in People with Crohn's Disease"
http://www.ncbi.nlm.nih.gov/pmc/articles/pmc7551245/

From the abstract (they also made a small human feasibility test of restricting emulsifiers in people with Crohn's disease):
"Mice were exposed to different classes of emulsifiers (carboxymethycellose, polysorbate-80, soy lecithin, gum arabic) in drinking water for 12-weeks, after which markers of inflammation and metabolism were measured.
...
All emulsifiers resulted in lower murine colonic length compared with control (mean 9.5 cm (SEM 0.20)), but this only reached significance for polysorbate-80 (8.2 cm (0.34), p = 0.024) and carboxymethylcellulose (8.0 cm (0.35), p = 0.013)."

The field of emulsifiers and their effect on the gut microbiome seems to be emerging research field of importance. Though it is a tragedy that common use of food additives like emulsifiers are even allowed before any independent long-term safety trials. From a quick look at this review study it seems like different food additive emulsifiers affect the microbiome in different ways. The 2021 review study (with the earlier mentioned Sandall as a co-author):
"Food Additive Emulsifiers and Their Impact on Gut Microbiome, Permeability, and Inflammation: Mechanistic Insights in Inflammatory Bowel Disease"
https://doi.org/10.1093/ecco-jcc/jjaa254

Just quickly glancing through this review paper, this quote about the intestinal mucus layer really stood out:
"Emulsifier-induced thinning of mucus did not occur in germ-free mice nor was there a change in mucus penetrability, as assessed by gavage with fluorescent beads that were a similar size to bacteria; therefore, demonstrating that changes in mucus via emulsifiers is driven by changes in microbiota composition and function resulting in bacteria penetrating the normally sterile mucus layer.29 Interestingly, there was no change in expression of the MUC2 gene encoding mucin, the glycoprotein that is the major component of colonic mucus, suggesting that emulsifiers have an indirect action on mucus function rather than a direct impact on mucin production.29,38"

@puddleduck

Just want to add that emulsifier research seems to be focused on mostly existing food additive emulsifiers.

The emulsifier-score PDF (https://www.alliancetocure.org/wp-content/uploads/2022/10/Emulsifier-Scores.pdf) by the Alliance to Cure Cavernous Malformation, unfortunately doesn't feature a hyperlink to studies but has a text like for example "Sandall et. al (2020)" for a lecithin-free diet. That is probably enough to find most of the referenced studies in that PDF. Sandall et. al (2020) gave me this paper:
"Emulsifiers Impact Colonic Length in Mice and Emulsifier Restriction is Feasible in People with Crohn's Disease"
http://www.ncbi.nlm.nih.gov/pmc/articles/pmc7551245/

From the abstract (they also made a small human feasibility test of restricting emulsifiers in people with Crohn's disease):
"Mice were exposed to different classes of emulsifiers (carboxymethycellose, polysorbate-80, soy lecithin, gum arabic) in drinking water for 12-weeks, after which markers of inflammation and metabolism were measured.
...
All emulsifiers resulted in lower murine colonic length compared with control (mean 9.5 cm (SEM 0.20)), but this only reached significance for polysorbate-80 (8.2 cm (0.34), p = 0.024) and carboxymethylcellulose (8.0 cm (0.35), p = 0.013)."

The field of emulsifiers and their effect on the gut microbiome seems to be emerging research field of importance. Though it is a tragedy that common use of food additives like emulsifiers are even allowed before any independent long-term safety trials. From a quick look at this review study it seems like different food additive emulsifiers affect the microbiome in different ways. The 2021 review study (with the earlier mentioned Sandall as a co-author):
"Food Additive Emulsifiers and Their Impact on Gut Microbiome, Permeability, and Inflammation: Mechanistic Insights in Inflammatory Bowel Disease"
https://doi.org/10.1093/ecco-jcc/jjaa254

Just quickly glancing through this review paper, this quote about the intestinal mucus layer really stood out:
"Emulsifier-induced thinning of mucus did not occur in germ-free mice nor was there a change in mucus penetrability, as assessed by gavage with fluorescent beads that were a similar size to bacteria; therefore, demonstrating that changes in mucus via emulsifiers is driven by changes in microbiota composition and function resulting in bacteria penetrating the normally sterile mucus layer.29 Interestingly, there was no change in expression of the MUC2 gene encoding mucin, the glycoprotein that is the major component of colonic mucus, suggesting that emulsifiers have an indirect action on mucus function rather than a direct impact on mucin production.29,38"

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#35 · June 24, 2023, 12:24 am

Did you know that in the laboratory to grow viruses such as the coronavirus. they used egg cheese and milk. and the egg is good

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#36 · June 24, 2023, 12:36 am

The flu vaccine is still made from eggs. A slow and complicated method developed during the 1940s is used. Despite the scientific and economic interest around the flu and its new variants, such as influenza A, this method has not yet been improved.

The basic idea of a vaccine is to inject killed or weakened viruses to trigger an immune system response, but that gets complicated with an illness like the flu. Being so variable, it is necessary to produce tens of millions of new doses each year.

In World War II, Thomas Francis and Jonas Salk developed a solution that is still used today. Influenza virus is injected into fertilized chicken eggs which are then incubated under hygienic conditions. Inside the egg, the virus multiplies at the expense of the embryo trying to grow normally. After a certain time the egg is destroyed in order to extract and purify the virus. The vaccine is safe although there is a slight risk for people with an egg allergy.

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#37 · June 25, 2023, 10:31 pm

Quote from puddleduck on June 10, 2023, 8:11 am

Quote from sand on June 10, 2023, 7:25 am

One should not eat eggs because they are a high-VA food. We are here to get rid of VA.

Yeah, and it is probably one of the most absorbable forms of it, too...

The further distance I put between myself and eggs, the better I feel.

Wish it weren’t so, but that’s how it do be.

To expand on your argument, we don’t even necessarily know how much vitamin A is in factory farmed eggs:

“Feeding high levels of vitamins to laying hens can effectively enrich the vitamin component of conventional chicken eggs. Depending on the base supplementation rate, fat soluble vitamins A and K can be increased four- to sixfold...”

— Nelson E. Ward, Chapter 20 of “Egg Innovations and Strategies for Improvements”

Understatement of the year@puddleduck

we fed our chickens as close to keto as we dared for years. sour cream, whipped cream, yogurt, tallow, butter, fish eggs (they turned down canned fish leftovers), cod liver oil laced yogurt, beef liver, carrots, kale,..... when they were not suffering sciatica (we thought it was marek's disease. we now think it was hypervitamin A causing sciatica similar to what I am recovering from.) and or dying, their egg yolks got darker orange and tastier. like the difference between eating red and pink salmon.

now they eat a more fruit, thiamine and fiber now. and much less retinols. we are seeing much less lameness.

I have not looked at their egg yolks to compare yet. Will have to looks soon. Also, their egg production improved.

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#38 · June 25, 2023, 11:03 pm

Quote from Deleted user on June 25, 2023, 11:03 pm

Quote from puddleduck on June 20, 2023, 7:44 am

Oh wow, what a fascinating connection between the gut microbiome and emulsifiers in CA patients. (The book I’m reading about the microbiome hasn’t touched on that at all.) Incredible!

Thanks for posting about the potential problem of fat-soluble pollutants in eggs, too.

Commercial dairy and oils are heavily contaminated with phthalates:

Critical Review on the Presence of Phthalates in Food and Evidence of Their Biological Impact
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7460375/

Eggs are less likely to contain high amounts:

“All phthalates except for DnOP, DiNP and DiDP were detected in eggs with low concentrations across studies.”

From: Phthalates and diet: a review of the food monitoring and epidemiology data
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4050989/

I am glad you are focusing your attention on the microbiome, @david, and look forward to your future posts.

The past little while I’ve been wondering if the root of this chronic hypervitaminosis A problem is in the gut.

It’s super interesting about fat-soluble compounds (including lutein) as presenting a problem for the cells, since diffusion can’t necessarily be prevented...I wonder if that’s what is going on in the gut, too...Like, if dietary lipids will enhance the diffusion of all forms of vitamin A in the gut?

It looks like there’s evidence of there being some sorta “failsafe” mechanism to prevent the body from converting beta carotene into excess retinoic acid:

“Carotenoid uptake by the enterocytes has been considered to occur by passive diffusion for four decades, which was inconsistent with the high inter-individual variability in absorption observed in humans, as well as with the isomer selectivity and the competition for absorption between carotenoids and other fat-soluble micronutrients observed at the intestinal level (see [20] for review). Different teams started to re-explore carotenoid absorption mechanisms in the 2000s and several lipid transporters playing a role in carotenoid uptake by the intestinal cell have since been identified.”

“Crucial factors modulating the expression and/or the activity of intestinal proteins involved in carotenoid absorption are provitamin A carotenoids, through a feedback regulation. Indeed, studies have pointed out that SR-BI activity is partly controlled by retinoids. Using both mouse models and human cell lines, it was specifically shown that retinoic acid produced from dietary precursors by BCO1 induced the expression of the intestinal transcription factor ISX that repressed the expression of both BCO1 [71] and SR-B1 [72], thus impacting both carotenoid conversion and uptake [73]. Additionally, many dietary factors other than retinoids were shown to regulate transporter expression in the intestine and may, thus, indirectly impact on carotenoid absorption.”

Mechanisms of Carotenoid Intestinal Absorption: Where Do We Stand?https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520933/#B56-nutrients-11-00838

ETA: image file

If memory serves, have seen in last 5 months studies using rats and mice intended to find treatments for celiac disease that scientists running the studies had difficulty inducing gluten intolerance in their subjects. They repeatedly fed high gluten diets with low rates of gluten sensitivies induced. Until they fed high retinol diets. This induced high gut permeability (leaky gut) and when these animals were again fed gluten they induced upwards of 50% gluten sensitivities.

Quote from puddleduck on June 20, 2023, 7:44 am

Oh wow, what a fascinating connection between the gut microbiome and emulsifiers in CA patients. (The book I’m reading about the microbiome hasn’t touched on that at all.) Incredible!

Thanks for posting about the potential problem of fat-soluble pollutants in eggs, too.

Commercial dairy and oils are heavily contaminated with phthalates:

Critical Review on the Presence of Phthalates in Food and Evidence of Their Biological Impact
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7460375/

Eggs are less likely to contain high amounts:

“All phthalates except for DnOP, DiNP and DiDP were detected in eggs with low concentrations across studies.”

From: Phthalates and diet: a review of the food monitoring and epidemiology data
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4050989/

I am glad you are focusing your attention on the microbiome, @david, and look forward to your future posts.

The past little while I’ve been wondering if the root of this chronic hypervitaminosis A problem is in the gut.

It’s super interesting about fat-soluble compounds (including lutein) as presenting a problem for the cells, since diffusion can’t necessarily be prevented...I wonder if that’s what is going on in the gut, too...Like, if dietary lipids will enhance the diffusion of all forms of vitamin A in the gut?

It looks like there’s evidence of there being some sorta “failsafe” mechanism to prevent the body from converting beta carotene into excess retinoic acid:

“Carotenoid uptake by the enterocytes has been considered to occur by passive diffusion for four decades, which was inconsistent with the high inter-individual variability in absorption observed in humans, as well as with the isomer selectivity and the competition for absorption between carotenoids and other fat-soluble micronutrients observed at the intestinal level (see [20] for review). Different teams started to re-explore carotenoid absorption mechanisms in the 2000s and several lipid transporters playing a role in carotenoid uptake by the intestinal cell have since been identified.”

“Crucial factors modulating the expression and/or the activity of intestinal proteins involved in carotenoid absorption are provitamin A carotenoids, through a feedback regulation. Indeed, studies have pointed out that SR-BI activity is partly controlled by retinoids. Using both mouse models and human cell lines, it was specifically shown that retinoic acid produced from dietary precursors by BCO1 induced the expression of the intestinal transcription factor ISX that repressed the expression of both BCO1 [71] and SR-B1 [72], thus impacting both carotenoid conversion and uptake [73]. Additionally, many dietary factors other than retinoids were shown to regulate transporter expression in the intestine and may, thus, indirectly impact on carotenoid absorption.”

Mechanisms of Carotenoid Intestinal Absorption: Where Do We Stand?https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520933/#B56-nutrients-11-00838

ETA: image file

If memory serves, have seen in last 5 months studies using rats and mice intended to find treatments for celiac disease that scientists running the studies had difficulty inducing gluten intolerance in their subjects. They repeatedly fed high gluten diets with low rates of gluten sensitivies induced. Until they fed high retinol diets. This induced high gut permeability (leaky gut) and when these animals were again fed gluten they induced upwards of 50% gluten sensitivities.

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#39 · June 27, 2023, 6:56 am

its so cool these animal studies with high vitamin A / betacarotene... the ones here who has animals, so nice if you share your experiences!

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#40 · June 28, 2023, 9:56 am

Quote from Tommy on June 28, 2023, 9:56 am

Quote from Joe on June 25, 2023, 11:03 pm

Quote from puddleduck on June 20, 2023, 7:44 am

Oh wow, what a fascinating connection between the gut microbiome and emulsifiers in CA patients. (The book I’m reading about the microbiome hasn’t touched on that at all.) Incredible!

Thanks for posting about the potential problem of fat-soluble pollutants in eggs, too.

Commercial dairy and oils are heavily contaminated with phthalates:

Critical Review on the Presence of Phthalates in Food and Evidence of Their Biological Impact
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7460375/

Eggs are less likely to contain high amounts:

“All phthalates except for DnOP, DiNP and DiDP were detected in eggs with low concentrations across studies.”

From: Phthalates and diet: a review of the food monitoring and epidemiology data
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4050989/

I am glad you are focusing your attention on the microbiome, @david, and look forward to your future posts.

The past little while I’ve been wondering if the root of this chronic hypervitaminosis A problem is in the gut.

It’s super interesting about fat-soluble compounds (including lutein) as presenting a problem for the cells, since diffusion can’t necessarily be prevented...I wonder if that’s what is going on in the gut, too...Like, if dietary lipids will enhance the diffusion of all forms of vitamin A in the gut?

It looks like there’s evidence of there being some sorta “failsafe” mechanism to prevent the body from converting beta carotene into excess retinoic acid:

“Carotenoid uptake by the enterocytes has been considered to occur by passive diffusion for four decades, which was inconsistent with the high inter-individual variability in absorption observed in humans, as well as with the isomer selectivity and the competition for absorption between carotenoids and other fat-soluble micronutrients observed at the intestinal level (see [20] for review). Different teams started to re-explore carotenoid absorption mechanisms in the 2000s and several lipid transporters playing a role in carotenoid uptake by the intestinal cell have since been identified.”

“Crucial factors modulating the expression and/or the activity of intestinal proteins involved in carotenoid absorption are provitamin A carotenoids, through a feedback regulation. Indeed, studies have pointed out that SR-BI activity is partly controlled by retinoids. Using both mouse models and human cell lines, it was specifically shown that retinoic acid produced from dietary precursors by BCO1 induced the expression of the intestinal transcription factor ISX that repressed the expression of both BCO1 [71] and SR-B1 [72], thus impacting both carotenoid conversion and uptake [73]. Additionally, many dietary factors other than retinoids were shown to regulate transporter expression in the intestine and may, thus, indirectly impact on carotenoid absorption.”

Mechanisms of Carotenoid Intestinal Absorption: Where Do We Stand?https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520933/#B56-nutrients-11-00838

ETA: image file

If memory serves, have seen in last 5 months studies using rats and mice intended to find treatments for celiac disease that scientists running the studies had difficulty inducing gluten intolerance in their subjects. They repeatedly fed high gluten diets with low rates of gluten sensitivies induced. Until they fed high retinol diets. This induced high gut permeability (leaky gut) and when these animals were again fed gluten they induced upwards of 50% gluten sensitivities.

@joe

This is massive. Can you please link one of these studies?

Quote from Joe on June 25, 2023, 11:03 pm

Quote from puddleduck on June 20, 2023, 7:44 am

Oh wow, what a fascinating connection between the gut microbiome and emulsifiers in CA patients. (The book I’m reading about the microbiome hasn’t touched on that at all.) Incredible!

Thanks for posting about the potential problem of fat-soluble pollutants in eggs, too.

Commercial dairy and oils are heavily contaminated with phthalates:

Critical Review on the Presence of Phthalates in Food and Evidence of Their Biological Impact
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7460375/

Eggs are less likely to contain high amounts:

“All phthalates except for DnOP, DiNP and DiDP were detected in eggs with low concentrations across studies.”

From: Phthalates and diet: a review of the food monitoring and epidemiology data
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4050989/

I am glad you are focusing your attention on the microbiome, @david, and look forward to your future posts.

The past little while I’ve been wondering if the root of this chronic hypervitaminosis A problem is in the gut.

It’s super interesting about fat-soluble compounds (including lutein) as presenting a problem for the cells, since diffusion can’t necessarily be prevented...I wonder if that’s what is going on in the gut, too...Like, if dietary lipids will enhance the diffusion of all forms of vitamin A in the gut?

It looks like there’s evidence of there being some sorta “failsafe” mechanism to prevent the body from converting beta carotene into excess retinoic acid:

“Carotenoid uptake by the enterocytes has been considered to occur by passive diffusion for four decades, which was inconsistent with the high inter-individual variability in absorption observed in humans, as well as with the isomer selectivity and the competition for absorption between carotenoids and other fat-soluble micronutrients observed at the intestinal level (see [20] for review). Different teams started to re-explore carotenoid absorption mechanisms in the 2000s and several lipid transporters playing a role in carotenoid uptake by the intestinal cell have since been identified.”

“Crucial factors modulating the expression and/or the activity of intestinal proteins involved in carotenoid absorption are provitamin A carotenoids, through a feedback regulation. Indeed, studies have pointed out that SR-BI activity is partly controlled by retinoids. Using both mouse models and human cell lines, it was specifically shown that retinoic acid produced from dietary precursors by BCO1 induced the expression of the intestinal transcription factor ISX that repressed the expression of both BCO1 [71] and SR-B1 [72], thus impacting both carotenoid conversion and uptake [73]. Additionally, many dietary factors other than retinoids were shown to regulate transporter expression in the intestine and may, thus, indirectly impact on carotenoid absorption.”

Mechanisms of Carotenoid Intestinal Absorption: Where Do We Stand?https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520933/#B56-nutrients-11-00838

ETA: image file

If memory serves, have seen in last 5 months studies using rats and mice intended to find treatments for celiac disease that scientists running the studies had difficulty inducing gluten intolerance in their subjects. They repeatedly fed high gluten diets with low rates of gluten sensitivies induced. Until they fed high retinol diets. This induced high gut permeability (leaky gut) and when these animals were again fed gluten they induced upwards of 50% gluten sensitivities.

@joe

This is massive. Can you please link one of these studies?

PJ has reacted to this post.

The Anti-Egg Thread 🚫🥚

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