Low Toxin Diet Grant Genereux's Theory Of Vitamin A Toxicity

[postman]

Yes im not eating the actual rice. I do know though that purple potatoes are on the “safe” list as far as vitamin A safe fruits and veggies to eat, as are all purple foods. I haven’t eaten it or looked into it but I’m guessing it’s not a major issue if you did. But just to reiterate eating the rice like that won’t do what the MRP is capable of doing.

That's not true. But some can tolerate larger amounts so for you it might be true.

 

[Lynne]

On the subject of tonsils, has anyone noticed any changes to the size of theirs?
For the last approx 30 years, my tonsils on one side (but not the other) have been enlarged and protruding (size etc fairly consistent). At 15 weeks low VA I noticed this tonsil had receded by around 75% to almost flat. It's not just a dairy elimination thing as when I was strictly zero dairy for a number of years and there was no change and, while having almost none now, I do have very small amounts and was eating A LOT prior to low VA.
I've noticed several changes with VA but this is interesting and unexpected. 7 and 15 weeks have been 2 notable markers for change for me so far.

 

[Tarmander]

On the subject of tonsils, has anyone noticed any changes to the size of theirs?
For the last approx 30 years, my tonsils on one side (but not the other) have been enlarged and protruding (size etc fairly consistent). At 15 weeks low VA I noticed this tonsil had receded by around 75% to almost flat. It's not just a dairy elimination thing as when I was strictly zero dairy for a number of years and there was no change and, while having almost none now, I do have very small amounts and was eating A LOT prior to low VA.
I've noticed several changes with VA but this is interesting and unexpected. 7 and 15 weeks have been 2 notable markers for change for me so far.

YES

I totally forgot about this. Both my tonsils shrunk and there seems more room in the back of my throat now.

 

[Lynne]

YES
I totally forgot about this. Both my tonsils shrunk and there seems more room in the back of my throat now.

Wow, it might be a VA thing!

 

[postman]

I found a study that looks at the nutritional content of many fish. It sounds like they took multiple samples of each type of fish so it should be accurate.

It looks like cod, striped catfish, scallops and more should be very safe, these are even lower numbers than in beef. I don't think they measured astaxanthin though so it's probably a good idea to stay away from anything that looks red/orange even if it's listed as not having any retinol in this chart.

https://www.livsmedelsverket.se/glo...ts---analysis-of-nutrients-rapport-1-2012.pdf

 

[Orion]

Same here!

@Tarmander @Blossom I have added an additional 175 pushups per day to workouts 5 days a week, no negatives. This would have been brutal in the past.

 

[Orion]

Yes even consuming extremely small amounts for over 4 months my Vitamin A blood levels (I know not the best marker but wanted to see where they were at) were still in the very high levels of the “range”. But like I said, I ate at least 4 eggs, one or two large sweet potatoes, carrots, and pounds of leafy greens pretty much daily for at least 5 years if not more. Also took Vitamin A pills, at least 2 a day (I believe that’s 20,000 iu alone in just those 2 pills), for over 3 years to “lower my sky high CA levels” on my hair test. When I put all of that into a cronometer it’s several hundreds times over the RDA every single day for about 5 years. I think it’s going to take me quite a while to lower those stores throughout the body and skin.

I am with you on this. Into my fifth month low VA, and at my lowest VA intakes, symptoms seems way worse this month. Two time accutane and high dose retinyl palmitate were my poisonol. I am committed to Dec 1st, to see where I stand moving forward.

 

[Orion]

Wow, it might be a VA thing!

YES

I totally forgot about this. Both my tonsils shrunk and there seems more room in the back of my throat now.

I have a young relative about to get them removed because they are too big at 3yrs old. My mom had this done at a young age as well. Curious if its all related to VA overload.

 

[Amazoniac]

Interestingly, I could not build muscle at all while on the poisonal, but seem to be having some luck building muscle now that the diet is different.

Could it be B12? No. But it's a curious book title.

I don't think it changes anything in case the person has accumulated poison. Increasing muscle mass from consumption to tolerance on should speed up the depletion without having to deal with the negatives.

It might be related to the normal oxidative stress of exercise and excess carotenoids prolonging the effects before they can be resolved.

- Carotenoids and Human Health (978-1-62703-203-2)

 

[Amazoniac]

This is a serious toxin in the environment. We need reform the world and its foods from red-yellow to white, symbolizing a change from inflammation to stillness and peace. Let's exterminate everything that's colored.

- News and Views about Carotenoids: Red-hot and True

"[..]too much dietary poison/"vitamin" A promotes aberrant immune responses and inflammation in the mouse intestine (22-24)."

"Dr. Ribot and colleagues report another intriguing finding about vitamin A and neonatal life [this issue (25)]. Their analyses in rat pubs revealed that even modest vitamin A supplementation during the suckling phase can impact methylation marks in developing white adipose. This genomic imprinting is in keeping with their previous observation that neonatal vitamin A supplementation favors body fat gain later in life (26). Notably, dietary β-carotene does not exert such effects on adipocytes (27), most likely because its absorption and bioconversion is tightly controlled by bodily demands (28, 29)."

"Similar to humans, knockout mice for the carotenoid-oxygenases, BCO1 and BCO2, accumulate β-carotene, lycopene, lutein, and zeaxanthin in blood and many tissues (36-38). Initial studies in these mice focused on the carotenoids’ role in vitamin A metabolism, metabolic control, and reproduction (39-42). By exploiting these mice, Dr. Wang and colleagues here report on an interaction of these enzymes with hepatic lipid and cholesterol homeostasis [this issue (43)]. Disturbances in this metabolism are common in the general population and are associated with fatty liver disease that eventually can progress into liver inflammation and cancer."

"Carotenoids are not only produced in photosynthetic organism but also in many bacteria and fungi. For instance, staphyloxanthin is formed by some strains of Staphylococcus aureus, and is responsible for the golden color of this pathogen. This carotenoid is an important virulence factor and helps the microbe evade death by reactive oxygen species produced by the host immune system (9). Dr. Cueno and colleagues used a computational network approach to identify potential anti-virulence drug targets within the staphyloxanthin biosynthetic pathway [this issue (10)]. Screening for small molecule inhibitors for the identified proteins may support future efforts in the fight against methicillin-resistant Staphyllococcus strains, which are a serious health problem in the clinic."​

- Color me bad: microbial pigments as virulence factors

"Colors are vital to the sensing of the environment and have evolved in higher living organisms to guide their interactions with others. For example, it is well appreciated that many birds exhibit brightly colored plumage to attract members of the opposite sex, that a chameleon’s adaptation to surrounding color is an important means of camouflage, and that the bright coloration of the poison dart frog warn potential predators to stay away. But such explanations cannot be offered to explain why certain microorganisms are pigmented. Since they lack color perception, one must assume evolutionary selective pressures behind the acquisition of pigments that promotes survival independent of their light absorbance, reflection or emission spectral properties (Box 1)."

"Because colors often provide an easy way of identifying certain microbes, they are often coined in names of species. For example, Rosenbach in 1884 named the golden-colored pathogen Staphylococcus aureus (aureus = “golden”, Latin) to distinguish it from nonpigmented staphylococci of the resident skin microflora that he named Staphylococcus alba (alba = “white”, Latin)[1]. Likewise, the blue-green Pseudomonas species not infrequently found in the lungs of cystic fibrosis patients is given the name aeruginosa, which derives from a Latin word denoting the color of copper rust. Chromobacterium violaceum not surprisingly elaborates a blue-violet pigment. These hallmark phenotypes not only provide an easy nomenclature for the microorganisms, but continue to be important diagnostic clues in clinical laboratories today for the identification of microbes. Pigments have also played a role in the discovery of infectious pathogens. In the late 1870’s, while tending to pathology specimens from malaria patients in a military hospital in Algeria, Alphonse Laveron, a student of Pasteur, astutely noted that the only common element found in the blood and organs of these patients was a brown black pigment granule. This major observation was to open the gateway to discovery of the malaria parasite as the infecting agent for which Laveron was awarded a Nobel Prize in 1907[2]."

"With biotechnological advances, contemporary researchers are in position to study the molecular genetic and biochemical basis for microbial coloration. Investigations using purified pigments or isogenic mutants with altered pigmentation have begun to reveal how these molecules can provide a survival advantage for the pathogen in the host environment and/or produce significant alterations in host cells and immune response pathways (Table 1)."​

- ProCarDB: a database of bacterial carotenoids

"Carotenoids are found in all the photosynthetic organisms as well as in a variety of non-photosynthetic organisms [2]. They perform a variety of functions, ranging from harvesting solar-energy [3, 4] to serve as antioxidants [5, 6] to radio-resistance [7] and as virulence factors in several pathogens [8–10]."​

[10] Staphylococcus aureus golden pigment impairs neutrophil killing and promotes virulence through its antioxidant activity​

- Colorful World of Microbes: Carotenoids and Their Applications

"Color of colonies is a hallmark feature of several pathogenic microbes. By interfering with host immune clearance mechanisms or by exhibiting proinflammatory or cytotoxic properties the microbial pigment sometimes contributes to disease pathogenesis. Contribution of pigmentation in virulence by allowing a given microbe to evade host immunity by killing or provoking inflammatory damage to cells and tissues is given in Table 5 [18] [same as Table 1 (↑)]."

Spoiler

"Nature is rich in colors (minerals, plants, microalgae, etc.) and pigment producing microorganisms (fungi, yeast, and bacteria). As stated in introduction among the molecules produced by microorganisms (carotenoids, melanins, flavins, and quinones, and, more specifically, monascins, violacein, and indigo); pyocyanin and pyorubin pigments of Pseudomonas aeruginosa showed distinct antibacterial effect against Citrobacter sp., a member of the family Enterobacteriace, which causes urinary tract infections, wound infections, and sometimes pneumonia in humans especially in immunocompromised persons [11]. Seven carotenoids, namely, (all-E)-luteoxanthin, (all-E)-neoxanthin, (9′Z)-neoxanthin, (all-E)-antheraxanthin, (all-E)-violaxanthin, (9′Z)-violaxanthin, and (all-E)-lutein, were isolated from golden delicious apple and showed potent anti-Helicobacter pylori activity (CMIC50 = 36 μg/mL) [93]. An actinomycete strain, Streptomyces hygroscopicus subsp.ossamyceticus D10, produced a yellow color sugar containing pigment with antimicrobial activity against drug resistant pathogens such as methicillin resistant and vancomycin resistant strains of Staphylococcus aureus, β-lactamase producing culture of E. coli, Pseudomonas aeruginosa, and Klebsiella sp. [94]. Similarly, a yellowish pigment 4-hydroxynitrobenzene from Streptomyces species was isolated which later showed antibiotic activity against Bacillus subtilis and Shigella shiga [95]. Hydrophobic amino acid derivatives (L-Tyr and L-Phe) from monascins exhibited antimicrobial activity against E. coli [96]. Inhibition of human pathogenic bacteria,Staphylococcus aureus, Klebsiella pneumoniae, and Vibrio cholera, was observed by endophytic fungal pigment of Monodictys castaneae [97]."

- Genetic and Virulent Difference Between Pigmented and Non-pigmented Staphylococcus aureus

 

[postman]

This is a serious toxin in the environment. We need reform the world and its foods from red-yellow to white, symbolizing a change from inflammation to stillness and peace. Let's exterminate everything that's colored.

- News and Views about Carotenoids: Red-hot and True

"[..]too much dietary poison/"vitamin" A promotes aberrant immune responses and inflammation in the mouse intestine (22-24)."

"Dr. Ribot and colleagues report another intriguing finding about vitamin A and neonatal life [this issue (25)]. Their analyses in rat pubs revealed that even modest vitamin A supplementation during the suckling phase can impact methylation marks in developing white adipose. This genomic imprinting is in keeping with their previous observation that neonatal vitamin A supplementation favors body fat gain later in life (26). Notably, dietary β-carotene does not exert such effects on adipocytes (27), most likely because its absorption and bioconversion is tightly controlled by bodily demands (28, 29)."

"Similar to humans, knockout mice for the carotenoid-oxygenases, BCO1 and BCO2, accumulate β-carotene, lycopene, lutein, and zeaxanthin in blood and many tissues (36-38). Initial studies in these mice focused on the carotenoids’ role in vitamin A metabolism, metabolic control, and reproduction (39-42). By exploiting these mice, Dr. Wang and colleagues here report on an interaction of these enzymes with hepatic lipid and cholesterol homeostasis [this issue (43)]. Disturbances in this metabolism are common in the general population and are associated with fatty liver disease that eventually can progress into liver inflammation and cancer."

"Carotenoids are not only produced in photosynthetic organism but also in many bacteria and fungi. For instance, staphyloxanthin is formed by some strains of Staphylococcus aureus, and is responsible for the golden color of this pathogen. This carotenoid is an important virulence factor and helps the microbe evade death by reactive oxygen species produced by the host immune system (9). Dr. Cueno and colleagues used a computational network approach to identify potential anti-virulence drug targets within the staphyloxanthin biosynthetic pathway [this issue (10)]. Screening for small molecule inhibitors for the identified proteins may support future efforts in the fight against methicillin-resistant Staphyllococcus strains, which are a serious health problem in the clinic."​

- Color me bad: microbial pigments as virulence factors

"Colors are vital to the sensing of the environment and have evolved in higher living organisms to guide their interactions with others. For example, it is well appreciated that many birds exhibit brightly colored plumage to attract members of the opposite sex, that a chameleon’s adaptation to surrounding color is an important means of camouflage, and that the bright coloration of the poison dart frog warn potential predators to stay away. But such explanations cannot be offered to explain why certain microorganisms are pigmented. Since they lack color perception, one must assume evolutionary selective pressures behind the acquisition of pigments that promotes survival independent of their light absorbance, reflection or emission spectral properties (Box 1)."

"Because colors often provide an easy way of identifying certain microbes, they are often coined in names of species. For example, Rosenbach in 1884 named the golden-colored pathogen Staphylococcus aureus (aureus = “golden”, Latin) to distinguish it from nonpigmented staphylococci of the resident skin microflora that he named Staphylococcus alba (alba = “white”, Latin)[1]. Likewise, the blue-green Pseudomonas species not infrequently found in the lungs of cystic fibrosis patients is given the name aeruginosa, which derives from a Latin word denoting the color of copper rust. Chromobacterium violaceum not surprisingly elaborates a blue-violet pigment. These hallmark phenotypes not only provide an easy nomenclature for the microorganisms, but continue to be important diagnostic clues in clinical laboratories today for the identification of microbes. Pigments have also played a role in the discovery of infectious pathogens. In the late 1870’s, while tending to pathology specimens from malaria patients in a military hospital in Algeria, Alphonse Laveron, a student of Pasteur, astutely noted that the only common element found in the blood and organs of these patients was a brown black pigment granule. This major observation was to open the gateway to discovery of the malaria parasite as the infecting agent for which Laveron was awarded a Nobel Prize in 1907[2]."

"With biotechnological advances, contemporary researchers are in position to study the molecular genetic and biochemical basis for microbial coloration. Investigations using purified pigments or isogenic mutants with altered pigmentation have begun to reveal how these molecules can provide a survival advantage for the pathogen in the host environment and/or produce significant alterations in host cells and immune response pathways (Table 1)."​

- ProCarDB: a database of bacterial carotenoids

"Carotenoids are found in all the photosynthetic organisms as well as in a variety of non-photosynthetic organisms [2]. They perform a variety of functions, ranging from harvesting solar-energy [3, 4] to serve as antioxidants [5, 6] to radio-resistance [7] and as virulence factors in several pathogens [8–10]."​

[10] Staphylococcus aureus golden pigment impairs neutrophil killing and promotes virulence through its antioxidant activity​

- Colorful World of Microbes: Carotenoids and Their Applications

"Color of colonies is a hallmark feature of several pathogenic microbes. By interfering with host immune clearance mechanisms or by exhibiting proinflammatory or cytotoxic properties the microbial pigment sometimes contributes to disease pathogenesis. Contribution of pigmentation in virulence by allowing a given microbe to evade host immunity by killing or provoking inflammatory damage to cells and tissues is given in Table 5 [18] [same as Table 1 (↑)]."

Spoiler

"Nature is rich in colors (minerals, plants, microalgae, etc.) and pigment producing microorganisms (fungi, yeast, and bacteria). As stated in introduction among the molecules produced by microorganisms (carotenoids, melanins, flavins, and quinones, and, more specifically, monascins, violacein, and indigo); pyocyanin and pyorubin pigments of Pseudomonas aeruginosa showed distinct antibacterial effect against Citrobacter sp., a member of the family Enterobacteriace, which causes urinary tract infections, wound infections, and sometimes pneumonia in humans especially in immunocompromised persons [11]. Seven carotenoids, namely, (all-E)-luteoxanthin, (all-E)-neoxanthin, (9′Z)-neoxanthin, (all-E)-antheraxanthin, (all-E)-violaxanthin, (9′Z)-violaxanthin, and (all-E)-lutein, were isolated from golden delicious apple and showed potent anti-Helicobacter pylori activity (CMIC50 = 36 μg/mL) [93]. An actinomycete strain, Streptomyces hygroscopicus subsp.ossamyceticus D10, produced a yellow color sugar containing pigment with antimicrobial activity against drug resistant pathogens such as methicillin resistant and vancomycin resistant strains of Staphylococcus aureus, β-lactamase producing culture of E. coli, Pseudomonas aeruginosa, and Klebsiella sp. [94]. Similarly, a yellowish pigment 4-hydroxynitrobenzene from Streptomyces species was isolated which later showed antibiotic activity against Bacillus subtilis and Shigella shiga [95]. Hydrophobic amino acid derivatives (L-Tyr and L-Phe) from monascins exhibited antimicrobial activity against E. coli [96]. Inhibition of human pathogenic bacteria,Staphylococcus aureus, Klebsiella pneumoniae, and Vibrio cholera, was observed by endophytic fungal pigment of Monodictys castaneae [97]."

- Genetic and Virulent Difference Between Pigmented and Non-pigmented Staphylococcus aureus

Let's ban all colors! And colored TV too.

 

[Amazoniac]

This looks better:

But it can still be improved. The borders are annoying and potentially harmful; there should be no separation, we're all one:

 

[Cirion]

That's racist man. Amazoniac is a white supremacist... the proof is here for all to see... lol...

 

[tankasnowgod]

- Color me bad: microbial pigments as virulence factors

Wow, that is legit the name of the study? Too badd they misspelled badd.

 

[Amazoniac]

- Regulation of Hepatic Retinol Metabolism: Perspectives from Studies on Vitamin A Status

Elevations in poisonoic acid signal esterification for storage:

"From these studies conducted over a wide range of vitamin A status, LRAT mRNA varies progressively: vitamin A deficient < marginal < control ≤ supplemented = RA-treated. A model of the regulation of LRAT expression can be proposed in which RA, the most active end-product of retinol metabolism, functions directly as a signal of the body's vitamin A adequacy (Fig. 4)."

"As long as the concentration of RA is adequate, RA provides a “feed forward” signal to positively regulate LRAT in the “on” position. When RA falls, as in the case of marginal vitamin A deficiency, LRAT expression is no longer fully on, and it continues to fall as vitamin A deficiency becomes overt. Physiologically, the maintenance of liver LRAT expression by RA appears to subserve a useful function by conserving unneeded retinol in a readily retrievable storage form. Coincidentally, retinol may be effectively diverted away from one or more of the other biochemical fates available to it, as indicated in Figure 1, thereby affecting these processes as well."​

On degradation:

"[..]CYP26 expression may be regulated according to the liver's cumulative exposure to poison/"vitamin" A (total poisonol content), rather than the amount of poisonol in the diet (daily influx)."

"Based on studies in models of acute and chronic retinoid exposure, hepatic CYP26 expression is regulated dynamically in the order: vitamin A-deficient < marginal < control < vitamin A-supplemented (45), and in a dose-dependent manner by exogenous all-trans-RA (46). The increase in CYP26 expression above ∼70 nmol retinol /g liver compares well with a previously described increase in the biliary excretion of 3H-RA and its metabolites when liver retinol concentration exceeded 20 μg/g (70 nmol/g) (47)."​

Oh shiτ (?):

"It is interesting that CYP26 did not metabolize 9-cis-RA, an RXR ligand, or 13-cis-RA (40,48), nor was RA metabolism induced by these isomers (48). The selectivity for all-trans-RA as inducing agent and substrate for CYP26 suggests that the metabolism of all-trans-RA is segregated from that of 9-cis-retinoids. If this is the case, the implications for gene expression are likely to be significant. Essentially, the regulation of gene promoters to which ligand-activated RAR/RXR heterodimers bind could be controlled separately from those of promoters that bind the numerous other nuclear receptors for which RXR also is a partner. Specificity for retinoids in the transor cis conformations has also been demonstrated for several enzymes involved in RA biosynthesis (see Blaner et al. in this symposium). Together, these data suggest the possibility of two parallel but independently regulated metabolic systems, one for trans and another for cis retinoids. However, considerable additional research is needed to test this hypothesis."​

Storage and degradation might be more determinant than other factors (which can affect those indirectly):

"The expression of retinol and retinal dehydrogenases may vary somewhat with vitamin A status, but we are unaware of dramatic regulation of these enzymes by vitamin A nutritional status, or RA. The activity of several retinyl ester hydrolases was unchanged in vitamin A deficiency or following administration of RA, while LRAT activity in the same livers was markedly affected in both cases (18). Thus, while the overall regulation of vitamin A's economy would be predicted to involve the interaction of all of these multiple factors, some of them such as LRAT and CYP26 appear to much more strongly regulated than others."​

On making sure that the poison recirculates in the body before excretion:

"Kinetic studies have shown that each molecule of retinol circulates several times between plasma and liver before undergoing irreversible disposal (3). In humans, ∼50 μmol/d (14.3 mg/d) of retinol passes through plasma, compared to an estimated disposal rate of 4 μmol/d (1.14 mg/d) (56). Conceptually, recycling seems to provide an ideal means for the liver to constantly sample and adjust the concentration of retinol available in plasma for peripheral tissues. Although recycling has been less thoroughly studied for RA, the same type of interorgan flux is likely to exist, as RA is readily diffusible across plasma membranes (57). Moreover, kinetic studies indicate that the preponderance of liver RA is obtained by uptake from plasma (57). A model (Fig. 6) illustrates the possible “cross-talk” between the liver and peripheral tissues in the export of retinol, peripheral metabolism of retinol to RA, return of excess RA to the liver, and regulation by RA of liver retinoid metabolism."​

In conclusion..

"From the viewpoint of evolution and adaptation, the hepatic regulation of both LRAT and CYP26 would provide a dual means to adapt to a diversity of diets in which vitamin A may be available only seasonally, or sporadically, or in excess. In this framework, an economic analogy may be appropriate. Long-term vitamin A status, indicated by the body's total of stored retinyl esters may be viewed as “money in the bank”—readily deposited and withdrawn on demand. The liver's role as central bank and banker seems undisputed, as vitamin A in liver may be deposited in long-term storage or withdrawn and “wired” to other accounts (exported to peripheral tissues) as needed. But vitamin A status may also have a short-term component, analogous to cash on hand. It seems plausible and indeed likely that RA functions both physiologically as an indicator of the body's short-term vitamin A status, and biochemically as a direct molecular signal to which genes including LRAT and CYP26 respond. In liver, their dose-responsive expressions appears to be significant mechanisms for adjusting retinoid partitioning and maintaining whole-body retinoid homeostasis."​

--
- Mechanisms controlling vitamin A homeostasis in the gut and periphery - (dissertation by) Mary E. Kelly

 

[charlie]

Hypercarotenemia in children with Down's syndrome. - PubMed - NCBI

 

[Lynne]

I have a young relative about to get them removed because they are too big at 3yrs old. My mom had this done at a young age as well. Curious if its all related to VA overload.

Yes it would be very interesting to know but, unless the parents are very open-minded, etc, I suspect we never will ...

 

[Spondive]

Yes it would be very interesting to know but, unless the parents are very open-minded, etc, I suspect we never will ...

At least not in our lifetimes

 

[Amazoniac]

A few pages ago it was posted that sterilization of dairy occurs after defatting it and that casein might bind nutrients when it's coagulated. Strained yogurts aren't fortified with toxins and there options where they had to use sterilized milk with no fat for fermentation (coagulation), so it meets the criteria above. It should also lose some of its whey lactoglobulin.

If you react just as badly to them, it casts a shadow on the speculation that it's due to hidden toxins and suggests that it's a broader problem involving deranged immunity. It may or may not have been caused by excess "vitamin" A; it's also possible that the person was already susceptible and extra poison A was enough to trigger.

- Milk derived bioactive peptides and their impact on human health – A review​

Cirion, those who tell others to disfavor casein that comes from Holstein cows are black or white supremacists?

I think that thymus has been neglected whereas the gut has not.

--
- Parasite Infections in Multiple Sclerosis Modulate Immune Responses through a Retinoic Acid-Dependent Pathway

"Figure 1. Parasite-infected MS patients showed higher serum levels of RA compared with healthy controls, uninfected MS patients, and treated parasite-infected MS patients (p < 0.001). Each circle represents serum levels of RA from a single individual. Horizontal lines indicate mean group values. In six parasite-infected MS patients, serum samples were obtained before and after antiparasite treatment."

Spoiler: Not a nude

- Hey My Nudes [PUFA, Ketosis, Insulin Resistance]
- Particles March 2019 Excellent

 

[Amazoniac]

- Retinol status and expression of retinol-related proteins in methionine-choline deficient rats

Spoiler: Table 2. Poisonol and biochemical parameters between control and MCD rats

Spoiler: Figure 6. LRAT expression

"[..]in the current study, hepatic poisonol levels in MCD rats were higher than the levels in control rats. This finding may be explained by the markedly enhanced LRAT expression in MCD rats, which may have led to poisonol storage in the liver despite accelerated poisonol catabolism."

--

Spoiler: Figure 5. CPBP and ALDHs expression

--

Spoiler: Figure 4. BCMO expression

"BCMO expression is regulated by several dietary components including lipids, protein, antioxidant agents, and carotenoids in addition to poisonol status (21-25)."

"BCMO-disrupted mice experience dysregulation of lipid metabolism and the development of hepatic steatosis (32)."

"In the current study, BCMO expression in the liver and the intestine of MCD rats was lower than that in control rats. Repressed expression of BCMO in the liver and the intestine may lead to reduced plasma poisonol levels. Furthermore, a mutually influential relationship might exist between BCMO expression in the liver and the intestine and hepatic steatosis."

"In contrast, BCMO expression in the kidneys and the testes was higher than in the controls, which may have been caused by reduced plasma poisonol levels. Due to lower circulating poisonol levels, the retinol metabolism in the testes and kidneys might have been controlled at the level of b-carotoxin conversion to poisonal. Poisonoids play important rôles in the development and function of both testes and the kidneys." "Mild poison/"vitamin" A deficiency in rats results in a reduced number of nephrons (35)."

"The regulation of BCMO expression may differ among tissues that require poisonoic acid and/or metabolize poisonol. The differences in the BCMO gene expression patterns between tissues were reported in type 2 [two] diabetes and obesity (24, 25)."​

[20] Nitrosative stress predicts the presence and severity of nonalcoholic fatty liver at different stages of the development of insulin resistance and metabolic syndrome: possible role of vitamin A intake

- Altered retinol status and expression of retinol-related proteins in streptozotocin-induced type 1 diabetic model rats (same authors)