I needed to disable self sign-ups because I’ve been getting too many spam-type accounts. Thanks.
Persistent Organic Pollutants and vitamin A status from a 1971 study
Found a 1971 study called:
"A Note on the Concentration of Organochlorine Pesticides in Human Liver in Relation to Vitamin A Status"
DOI: https://doi.org/10.1007/BF01559066 (available at sci-hub)
The study might have missed that probably some humans get cirrhosis of the liver while others get fatty livers which probably effects the liver stores of vitamin A in different directions and cause a wide variation in people.
It is a Canadian study and I don't know if it fits with the thesis in one of Grant Genereux's e-books that those Canadians that ate lots of fat and vitamin A rich fish in Canada had much worse health. In this 1971 study Monteral had more people with less liver vitamin A concentration than those in Vancouver. Though the measuring methods used at 1971 was probably a bit imprecise as they found eight people, out of 100, with no detectable levels of vitamin A in their livers:
"Vitamin A analyses performed on 100 human livers obtained at necropsy from one Canadian city demonstrated that the vitamin was not detected in the liver of eight subjects. Thirty-two percent of the liver vitamin A values in subjects over 10 years of age were in the range of 0 to 40 ug per g (1). A second survey (2) extended the study to four additional locations. Regional differences appeared when the data was arranged according to the range of distribution of liver vitamin A and carotene stores for each city. There were more low values from Montreal (40%) than from any other location, while Vancouver had the least number (15%). The reason for differences between cities is not known and may be the result of a number of factors. A dietary survey (in progress)(3) should reveal to what extent differences in intake are responsible. As well as poor nutritional habits, it was considered that disease conditions and unknown environmental factors may contribute to the cause of the low vitamin A status in a high percentage of the subjects. It has been shown (4,5) that the dietary ingestion of DDT will reduce liver stores of vitamin A in experimental animals. It was considered of interest therefore to determine if a relationship existed between the level of vitamin A and certain organochlorine pesticides in human liver."
I attach Table 1 from this study and it seems to show a trend of higher DDT-metabolite concentration in the liver with higher vitamin A concentration in the liver. Perhaps a chicken or the egg problem but burning one's fat cells too fast is known to release fat-soluble toxins, such as this 2017 review paper called: "Increased blood levels of persistent organic pollutants (POP) in obese individuals after weight loss-A review"
https://pubmed.ncbi.nlm.nih.gov/28051929/
very interesting. Might some of the toxic effects of DDT and the variability in its cancerinducing effects, partly be due to the different levels of A being released into the bloodtstream (depending on stores and diet etc)
Veey interesting study rasing a lot more questions. I would love to see the diet of the individuals (as well as a serum A test and biopsies from other organs) with no detectable A in the liver. I don't think it necessarily has to be an analysis error. I dunno if they ran the analysis again after receiving 0 but if it was my study I would have.
That is similar to my thought: vitamin A, which is fat-soluble, can probably be closely stored with all kinds of other fat-soluble toxins. I think that might be one explation as to why vitamin A excretion seems to slow down over time, for example see the famous 1975 Sauberlich et al. study (available at sci-hub):
"Vitamin A Metabolism and Requirements in the Human Studied with the Use of Labeled Retinol"
https://doi.org/10.1016/s0083-6729(08)60015-1
It might also be a possible explaination for a detox set-back with more fat-soluble toxins getting released at the same time one is getting rid of the more deeper fat deposits of retinoids and carotenoids.
I think all the modern biopsy studies are done on people who have died since it has been deemed to be un-ethical to do any new vitamin A deficiency study on humans. The 1971 study in the original post is also co-written by K. Hoppner, W. E. J. Phillips and T. K. Murray. The same authors were also co-writers to the 1968 study:
"Survey of liver vitamin A stores of Canadians"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1945441/
What I don't know is what the "Not Detectable" level of vitamin A was in their measurements but it seems to go down to at least 6.2 µg of vitamin A per g of liver from Table 1 in the 1968 study. But on the topic of how vitamin A was measured in their studies, here is a short description of Materials and Methods from the 1968 study above if you are interested:
"Approximately 10 g. of liver tissue from the central portion of the right lobe of the liver removed at autopsy was immediately frozen at -20° C. and analyzed within two weeks for vitamin A content. The amount of vitamin A was determined by procedures described by Mervyn and Morton6 and by Phillips.12 Duplicate analyses were performed on 5-g. liver samples by saponification in ethanolic KOH containing pyrogallol. The isolated non-saponifiable material was separated on deactivated alumina and the vitamin A concentration was determined spectrophotometrically at 325 mµ. (E 1%/1 cm. 1750). Most of the adult liver tissue also contained lycopene in varying concentrations. This material appeared as a pronounced pink zone on the alumina column. Separation from vitamin A posed no difficulties, since most of the material was eluted with the 2% diethyl ether in the petroleum ether fraction."
PS. K. Hoppner, W. E. J. Phillips and T. K. Murray were also co-writers of the 1969 study called:
"Vitamin A Reserves of Canadians"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1946442/
Its Table 4 is attached to the post and seems to be associated with a lower risk of mortality for those with Not Detectable (ND) concentration of vitamin A in the liver of diseased.
Uploaded files:
On the relation between the concentration of Persistent Organic Pollutants (POPs) in different tissues. Here is the a 1968 study on that topic called:
"The Organochlorine Insecticide Content of Human Tissues"
https://doi.org/10.1080/00039896.1968.10665317
The highest concentration of these POPs according to this study is adipose tissue by around 10-100x more than liver and brain tissue.
Uploaded files:
Quote from David on August 12, 2023, 10:55 amThat is similar to my thought: vitamin A, which is fat-soluble, can probably be closely stored with all kinds of other fat-soluble toxins. I think that might be one explation as to why vitamin A excretion seems to slow down over time, for example see the famous 1975 Sauberlich et al. study (available at sci-hub):
"Vitamin A Metabolism and Requirements in the Human Studied with the Use of Labeled Retinol"
https://doi.org/10.1016/s0083-6729(08)60015-1It might also be a possible explaination for a detox set-back with more fat-soluble toxins getting released at the same time one is getting rid of the more deeper fat deposits of retinoids and carotenoids.
I think all the modern biopsy studies are done on people who have died since it has been deemed to be un-ethical to do any new vitamin A deficiency study on humans. The 1971 study in the original post is also co-written by K. Hoppner, W. E. J. Phillips and T. K. Murray. The same authors were also co-writers to the 1968 study:
"Survey of liver vitamin A stores of Canadians"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1945441/What I don't know is what the "Not Detectable" level of vitamin A was in their measurements but it seems to go down to at least 6.2 µg of vitamin A per g of liver from Table 1 in the 1968 study. But on the topic of how vitamin A was measured in their studies, here is a short description of Materials and Methods from the 1968 study above if you are interested:
"Approximately 10 g. of liver tissue from the central portion of the right lobe of the liver removed at autopsy was immediately frozen at -20° C. and analyzed within two weeks for vitamin A content. The amount of vitamin A was determined by procedures described by Mervyn and Morton6 and by Phillips.12 Duplicate analyses were performed on 5-g. liver samples by saponification in ethanolic KOH containing pyrogallol. The isolated non-saponifiable material was separated on deactivated alumina and the vitamin A concentration was determined spectrophotometrically at 325 mµ. (E 1%/1 cm. 1750). Most of the adult liver tissue also contained lycopene in varying concentrations. This material appeared as a pronounced pink zone on the alumina column. Separation from vitamin A posed no difficulties, since most of the material was eluted with the 2% diethyl ether in the petroleum ether fraction."
PS. K. Hoppner, W. E. J. Phillips and T. K. Murray were also co-writers of the 1969 study called:
"Vitamin A Reserves of Canadians"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1946442/Its Table 4 is attached to the post and seems to be associated with a lower risk of mortality for those with Not Detectable (ND) concentration of vitamin A in the liver of diseased.
While I dont seem to disagree with you I cannot either directly follow your line of reasoning. First of all that link "Vitamin A Metabolism and Requirements in the Human Studied with the Use of Labeled Retinol" only shows the average conversion rates of carotenoids to retinol in adults, and seemingly doesnt touch on the subject discussed? Also while DDT is stored in fat like many toxins I dont see how that in itself contributes to vitamin A being released. I was referring to its alleged effect to stop the liver from storing it - while Im sure its unhealthy having stored DDT I dont see how that in itself would contribute to heightened A/dumping
I do appreciate you bringing up POP's @david it had me go down that rabbit hole again, and it's been a while. 😅
POP's are well known for their toxicity and "late onset" diseases such as T2D. And they are still in our foods and water all over the world. Yesterday I found a study where milk from all over the world had been analyzed, organic also, and POP's like DDT (yes, still, after all years of being banned in EU DDT is still found in our foods) were in all samples. ALL! Goat milk from Greece as well.
I think of Monsanto's history (and others of course) and I shake my head. So many poisons they have manufactured and contaminated our earth with, wondering when will Glyfosate finally be banned? And PFAS? And will it even matter, our planet and its inhabitants are poisoned already and this is way beyond vA. It's easy to focus on vA, especially as this is a VA forum after all, but there is so much more to the story. If a body is beforehand burdened with toxins, which has to go through the liver (fat soluble ones), it makes sense one would also have issues with too much A (from foods not supplements, supplement toxicity is sort of given). Some more, some less. Sources of retinol (animal products) are also sources of POP's.
So in the 70's, when we suppsedly started fortifying with A, those POP's had been wrecking havoc for decades but some had not been made yet. Is vA really to blame for everything? Or is it just another burden in an already toxic body?
Many have used those same statistics to "prove" oils are to blame, sugars are to blame, glyfosate is to blame and so forth. Around the 70's is when X went up and that's why we're sick, so stop eating X and you'll be fine... USA is a bit extreme though, as literally everything has added vA in it. I was there as an exchange student back in 2000 and remember finding it so odd that there were VA in cookies. Not that I knew how bad it was back then, because I didn't, but I remember thinking, after finishing a handfull of cookies, great now I have gotten 100% rdi of vA 🤦♀️
However, study after study also point out soluble fiber being protective against many diseases, and I came across a study a while ago showing different types of SF from different foods being better at binding different types of pesticides. SF has been scientifically proven in many papers to bind to a lot of shit (ha!) no matter what one's personal belief is. And we desperately need co-factors to make the wheel go roound. So it is probably a wise idea to eat a little of everything, also from plants which can still be done low A. And watch out for the worst offenders.
I have mentioned before, my country Denmark is contaminated with PFAS (pfas binds to protein not fat though). Like all of it. In the soil. In the water. In thr fish, which cannot be eaten anymore. What else lurks underneath the surface? And if little Denmark is this fxxed up, what about the rest of the world?
This country is also big on animal products like herring, liver and everything in between. Foods known to be contaminated with all sorts of sh*t and also carry vA. Animal livers here contain a LOT more A than in the 50's, because they started supplementing animal feed with it (found a study on that too some time back). And they're big on alcohol (mostly beer). Probably not a great combo. There are a lot of overweight and sick people here, and cancers, like everywhere else.
It's quite depressing, really... and it's all like a circke. I guess my point is, vA toxicity is just one part of a lot of fxxked up things.
As in, totally: "It might also be a possible explaination for a detox set-back with more fat-soluble toxins getting released at the same time one is getting rid of the more deeper fat deposits of retinoids and carotenoids."
The 1975 Sauberlich et al. study showed that the absolute amount of vitamin A excreted becomes less and less over time for the young male test subjects which were on some strange diet that contained varying amounts of casein and soy protein among other unknown things (Table 5). For the depletion rate slowing down over time on the study's test diet see Table 11 and Figure 11.
"Vitamin A Metabolism and Requirements in the Human Studied with the Use of Labeled Retinol"
https://doi.org/10.1016/s0083-6729(08)60015-1
I was looking at the authors from the 1971 study in the original post and saw that the co-author W. E. J. Phillips have done an earlier study in 1963 on how DDT affects vitamin A concentration and amount in rat livers. The 1963 study is called:
"DDT AND THE METABOLISM OF VITAMIN A AND CAROTENE IN THE RAT"
https://doi.org/10.1139/o63-203 (available at sci-hub)
In this 1963 study W. E. J. Phillips shows that the DDT makes the liver contain less vitamin A even though the liver grows bigger (more inflammed?) with more DDT. See the attached TABLE_5_1963, though the study seems to have other interesting tables as well.
Where does this vitamin A not stored in the liver go?
-Perhaps some of the vitamin A is stored in adipose tissue right along with DDT and its metabolites. Perhaps some of it just causes damage and is another way DDT damages people by releasing excess amounts of vitamin A from the liver.
Regarding the effect of already accumulated DDT and vitamin A I think it is important to keep track that of where these compounds are stored in the body.
DDT is mostly stored in adipose tissue, as per the 1968 study and the figure in a previous post.
"The Organochlorine Insecticide Content of Human Tissues"
https://doi.org/10.1080/00039896.1968.10665317 seen in while most of the retinoids are store
While vitamin A, in the form of retinoids, is mostly stored in the liver.
One thought I had on how this could cause problems is that several people have reported a much higher need for calories initially when reducing vitamin A. I think that might be a defense mechanism by the body to avoid using up adipose tissue and/or to quickly try and rebuild adipose tissue as to avoid releasing more fat-soluble toxins like DDT which are stored there. Since if DDT is released from adipose tissue and enter the blood stream and then the liver, that DDT would probably release even more vitamin A from the liver causing acute problems. Perhaps even making someone eat less and less calories would mean more fat-burning and more potential release of stored fat-soluble toxins.
Uploaded files:
Yes, the amount of Persistent Organic Pollutants can easily make one depressed but I think trying to focus on solutions can help reduce that a bit.
Regarding glyphosate you, and others in the EU, can easily send a pre-written email from this site to all of your country's EU representative to put pressure on the to stop the glyphosate renewal that could happen later this year. Bayer et al. are really pushing hard for at least a 5 year renewal.
https://www.savebeesandfarmers.eu/eng
Hopefully banning glyphosate will become the biggest issue in all of the EU countries this fall!
Personally I always feel more hopeful after watching Allan Savory and seeing desertification being reversed by simple means.
Here is his most famous presentation from 2013 called:
"How to green the world's deserts and reverse climate change"
https://www.youtube.com/watch?v=vpTHi7O66pI
PS. Another EU organisation working towards a poison free future:
"Pesticide Action Network Europe"
https://www.pan-europe.info/
There are several chapters of the Pesticide Action Network.
Quote from David on August 13, 2023, 12:56 pmThe 1975 Sauberlich et al. study showed that the absolute amount of vitamin A excreted becomes less and less over time for the young male test subjects which were on some strange diet that contained varying amounts of casein and soy protein among other unknown things (Table 5). For the depletion rate slowing down over time on the study's test diet see Table 11 and Figure 11.
"Vitamin A Metabolism and Requirements in the Human Studied with the Use of Labeled Retinol"
https://doi.org/10.1016/s0083-6729(08)60015-1I was looking at the authors from the 1971 study in the original post and saw that the co-author W. E. J. Phillips have done an earlier study in 1963 on how DDT affects vitamin A concentration and amount in rat livers. The 1963 study is called:
"DDT AND THE METABOLISM OF VITAMIN A AND CAROTENE IN THE RAT"
https://doi.org/10.1139/o63-203 (available at sci-hub)In this 1963 study W. E. J. Phillips shows that the DDT makes the liver contain less vitamin A even though the liver grows bigger (more inflammed?) with more DDT. See the attached TABLE_5_1963, though the study seems to have other interesting tables as well.
Where does this vitamin A not stored in the liver go?
-Perhaps some of the vitamin A is stored in adipose tissue right along with DDT and its metabolites. Perhaps some of it just causes damage and is another way DDT damages people by releasing excess amounts of vitamin A from the liver.Regarding the effect of already accumulated DDT and vitamin A I think it is important to keep track that of where these compounds are stored in the body.
DDT is mostly stored in adipose tissue, as per the 1968 study and the figure in a previous post.
"The Organochlorine Insecticide Content of Human Tissues"
https://doi.org/10.1080/00039896.1968.10665317 seen in while most of the retinoids are storeWhile vitamin A, in the form of retinoids, is mostly stored in the liver.
One thought I had on how this could cause problems is that several people have reported a much higher need for calories initially when reducing vitamin A. I think that might be a defense mechanism by the body to avoid using up adipose tissue and/or to quickly try and rebuild adipose tissue as to avoid releasing more fat-soluble toxins like DDT which are stored there. Since if DDT is released from adipose tissue and enter the blood stream and then the liver, that DDT would probably release even more vitamin A from the liver causing acute problems. Perhaps even making someone eat less and less calories would mean more fat-burning and more potential release of stored fat-soluble toxins.
Im not sure if that has any ramification for my previous question about your line of reasoning but be that as it may. I still - though this is written in the spirit of investigation as I am onboard with the larger picture as previously stated - find some gaps in the reasoning here. First of all - I still dont see why stored DDT would make it worse. I assume the DDT -to directly affect vitamin A levels - would have to be somewhat recently taken in? Im sure it is damaging where it sits but how would it work while sitting in the adipose tissue?? Also while I belive pesticides and other chemicals to definetly be bad for us (and most life), including some of them blocking the enzymes (f.ex(like glyphosate)) helping clearing vitamin A from the body. My thought was that maybe most of /a significant part of DDTs damaging effects (and it's individual variability in doing so) might be due to its effect on releasing vitamin A (f.ex from the liver ) like the papers you show observe. I doubt though that DDT is a major problem for most people these days as it has been banned for 50years or so at least in most of europe (at least scandinavia). Theres traces left but I think most newer things - again glyphosate - is much more of a contributor. I tend to thin its important to seperate agitators and enzyme-blockers etc from the actual poison. Many parts of glyphosate reserach (like dr.zeneff(is that her name)) points to it being much more harmful then officially stated precisely because it blocks enzymes making us store and circulate poisons like retinol. I find no specific fault with the papers as such but I dont think the higher calorie need would be caused by that but just by either a higher amount of circulating retinol (i always had vvvvveeery high calorie needs before starting low A, that has decreased somewhat during my years of detox.) causing us to have inefficient metabolism, or by increased metabolism due to the thyroid functioning better OR yet again because we need more protein and micronutrients and the body signals this by making us hungry so we get enough of these substances by eating more. On a less speculative note, I am at least quite sure its not because of the bodys resistence to use the fat as the process that raises triglycerides in the blood and the process that burns adipose tissue are not the same. You do not need to get liberation of free fatty acids to loose weight . not at all actually. So it doesnt seem to make sense the body would try to avoid that by eating? THe difference here being between putting fat cells into circulation and to use them for fuel (muscles for example naturally use fat-oxidation instead of glucose in their resting state and only utilize glucose to a significant degree during exertion (think while even keto-dieteres needs carbs when doing triathlon), while most of the other human body tissues work the opposite way - using glucose during rest and going to fat-oxidation during stress (i.e. exertion of some kind).