Anti-Peat Grant Genereux's Theory Of Vitamin A Toxicity

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Normalizing your liver retinol level is one of the most important things you can do for your health. We are pioneers. Serum retinol testing and a low vA diet will become very big in the future.
Hi Tim! I'm planning to do some bloodwork next week. What tests would be useful to do, besides serum retinol, to evaluate my status? I'm planning to check Serum Retinol, copper, zinc, coeruloplasmin and some other things (b6, b12, iron status, vitamin D).
 

tim333

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Hi @Sulcuscentralis,

I got a thyroid panel done since people here were going on so much about Hypervitaminosis A being a thyroid issue, TSH came back as 1.9 and it's taking me years to deplete my liver retinol so that's further evidence against the thyroid function claims.

Liver enzymes and cholesterol have normalized for me so you could always test them if you want to see lab evidence of improvements over time.

My understanding of how calcidiol relates to retinol stores is that elevated levels of retinoic acid will deplete calcidiol faster. I believe this is due to the kidneys producing more calcitriol to counteract the elevated retinoic acid levels.
 

gaze

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Normalizing your liver retinol level is one of the most important things you can do for your health. We are pioneers. Serum retinol testing and a low vA diet will become very big in the future.

I though the consensus here was that serum retinol has nothing to do with liver retinol. seems like the body maintains a certain amount in the blood through sporadic release of vA from the liver, going up and down constantly, so how is serum retinol testing any help?
 

tim333

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In fact, a limited capacity to produce nitric oxide is associated with heart disease, diabetes and erectile dysfunction.

https://www.healthline.com/nutrition/how-to-increase-nitric-oxide

Inhibition of nitric oxide synthesis in vascular smooth muscle by retinoids

Abstract
1
These studies examine the effect of retinoids on interleukin 1β (IL‐1β)‐induced nitric oxide synthase (NOS) activity in cultured rat aortic vascular smooth muscle (VSM) cells and isolated rat aortic rings.

2
All‐trans‐retinoic acid (all‐transM‐RA, 0.1–10 μm) and its active analogues produced concentration‐dependent inhibition of IL‐1β (0.1–10 ng ml−1)‐induced nitrite production in cultured VSM cells. In contrast, the inactive retinoid, Ro 14–6113 (0.1–10 μm), had no effect on IL‐1β‐induced nitrite production.

3
Since some of the actions of retinoids are mediated by induction of transforming growth factor beta (TGF‐β), its effect on inducible NOS activity in VSM cells was examined. TGF‐β produced concentration‐dependent (0.1–10 ng ml−1) inhibition of IL‐1β‐induced nitrite production and the maximum effect (approximately 90% inhibition) was significantly greater than that seen with all‐trans‐RA (approximately 70% with 10 μm). However, an anti‐TGF‐β antibody (50 μg ml−1) which blocked the effect of exogenous TGF‐β (5 ng ml−1) did not significantly reverse the inhibitory action of all‐trans‐RA (10 μm).

4
In addition to inhibiting IL‐1β‐induced nitrite production, all‐trans‐RA (10 μm) reduced substantially inducible NOS mRNA and protein levels in IL‐1β‐induced VSM cells (P < 0.01).

5
Incubation of isolated rat aortic rings with IL‐1 β (10 ng ml−1) caused a progressive resistance of the rings to the vasoconstrictor action of phenylephrine (10 nm to 10 μm). This effect was abolished by the addition of the nitric oxide synthase inhibitor L‐NG‐monomethyl‐L‐arginine (L‐NMMA, 1 μm). All‐trans‐RA (IO μm) also markedly and significantly reversed this IL‐1β‐induced vascular hyporeactivity (P < 0.01).

6
These data show that all‐trans‐RA and other active retinoids are able to block cytokine‐stimulated expression of inducible NOS in cultured VSM cells and isolated aortic rings.

 

tim333

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I though the consensus here was that serum retinol has nothing to do with liver retinol. seems like the body maintains a certain amount in the blood through sporadic release of vA from the liver, going up and down constantly, so how is serum retinol testing any help?
Serum retinol can be low in Hypervitaminosis A, zinc deficiency can cause this. The normal pattern though is for serum retinol to increase with increasing liver retinol stores. Age is highly correlated with serum retinol level because of increased median liver retinol stores with age. The body does maintain serum retinol homeostasis but the regulated level is partly determined by liver retinol stores.
 

gaze

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@tim333 I see. thanks.

Also, for anyone on the low A diet who's not including low fat unfortified dairy or calcium supplements, have a look at nearly every single dog food that exists. All of them have a 1:1 ratio of calcium to phosphate. There may be things you disagree with Ray about, but the importance of balancing calcium and phosphorus has been proven to be important for in a variety of mechanisms. I personally have noticed great success in my overall health with unfortified dairy.
 

Vinero

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@tim333 I see. thanks.

Also, for anyone on the low A diet who's not including low fat unfortified dairy or calcium supplements, have a look at nearly every single dog food that exists. All of them have a 1:1 ratio of calcium to phosphate. There may be things you disagree with Ray about, but the importance of balancing calcium and phosphorus has been proven to be important for in a variety of mechanisms. I personally have noticed great success in my overall health with unfortified dairy.
Most dog food is also high in vitamin A, so ofcourse you need more calcium in that situation. If you don't eat any vitamin A the rules change and your calcium needs decrease. The small amount found in most foods is enough, because you aren't losing your calcium from your bones from the vitamin A. All foods high in calcium that are found in nature such as dairy and leafy greens also contain large amounts of vitamin A or carotenoids. That's not a coincidence.
 
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gaze

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Most dog food is also high in vitamin A, so ofcourse you need more calcium in that situation. If you don't eat any vitamin A the rules change and your calcium needs decrease. The small amount found in most foods is enough, because you aren't losing your calcium from your bones from the vitamin A. All foods high in calcium that are found in nature such as dairy and leafy greens also contain large amounts of vitamin A or carotenoids. That's not a coincidence.
dogs get they're calcium from bones in the wild, which has no vitamin A. many civilizations also relied on calcium rich water, not just greens or dairy. Calcium deficiency and/or phosphate excess can become a big problem on a diet of whole grains, legumes, and beef. at the very least try to find some mineral water with some calcium, just to be on the safer side.
 

Vinero

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dogs get they're calcium from bones in the wild, which has no vitamin A. many civilizations also relied on calcium rich water, not just greens or dairy. Calcium deficiency and/or phosphate excess can become a big problem on a diet of whole grains, legumes, and beef. at the very least try to find some mineral water with some calcium, just to be on the safer side.
But you don't know if those dogs in the wild eat vitamin A too, for example organ meats. Also, how many of those civilizations were eating a low vitamin A diet? Since we don't know the answer to that question you can't say people on the low vitamin A diet also need a calcium source. What kind of "big problems" will people encounter because of calcium deficiency on a low vitamin A diet? Grant has been eating rice, beans and beef for 6 years and is doing fine, so what kind of big problems wil he get from his lack of calcium?

Calcium might be useful, I don't know. Will Grant his health improve if he decides to add 2000 mg a day of calcium to his diet? That would be an interesting experiment. At least we can say that you don't need to worry about calcium to heal from auto-immune disease, as Grant and others following the low vitamin A diet have proven.
 

ursidae

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Oh it looks like grants survey is out. Gastrointestinal/acne issues have pretty underwhelming results but the hair loss stats are impressive

1610191359541.png

Damnn
 

somuch4food

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Hello
I have no time to read this 374 page topic
But u have read a lot of positive experience about people that are following a low vit a diet and i want to give it a shot.
One problem, everybody talk about low vit a intake but nobody talk about exact numbers.
So my question is: when you talk about low, what is the limit intake then?
To get the real benefits, I would think the lower the better. A simple approach to get started is to eat only foods that are pale: apples and cucumbers without skin, rice, etc. Protein intake and zinc are also important.
 

iceclear

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Evidence of pro-vitamin A Carotenoid metabolites having beneficial, regulatory effects on Vitamin A activity?
Lycopene and carotene might provide beneficial functions in these seemingly subclinical hypervitaminosis A situations by regulating overexpressed genes/receptors.
Maybe they're also a safer retinoid substrate if you have functioning BCO1 genes.

- We have previously demonstrated that β-apo-13-carotenone, an eccentric cleavage product of β-carotene, antagonizes the activation of RXRα by 9cRA in mammalian cells overexpressing this receptor.
[Sun J, Narayanasamy S, Curley RW Jr, Harrison EH. β-Apo-13-carotenone regulates retinoid X receptor transcriptional activity through tetramerization of the receptor. J Biol Chem. 2014 Nov 28;289(48):33118-24. doi: 10.1074/jbc.M114.610501. Epub 2014 Oct 16. PMID: 25324544; PMCID: PMC4246072.]

- Cell and animal studies indicate that carotenoids and carotenoids derivatives can reduce adiposity and impact key aspects of adipose tissue biology including adipocyte differentiation, hypertrophy, capacity for fatty acid oxidation and thermogenesis (including browning of white adipose tissue) and secretory function. Epidemiological studies in humans associate higher dietary intakes and serum levels of carotenoids with decreased adiposity. Specifically designed human intervention studies, though still sparse, indicate a beneficial effect of carotenoid supplementation in the accrual of abdominal adiposity.

Besides retinoic acid, other retinoids (such as Rald) as well as apocarotenoids different from retinoids (such as b-apo-14 0 -carotenal, b-apo-13-carotenone and apo-10 0 -lycopenoic acid) interact with nuclear receptor transcription factors to either antagonize or promote their action on target genes in cells.
[Bonet, M. Luisa & Canas, Jose & Ribot, Joan & Palou, Andreu. (2015). Carotenoids and their conversion products in the control of adipocyte function, adiposity and obesity. Archives of biochemistry and biophysics. 55. 10.1016/j.abb.2015.02.022.]

- Acyclo-retinoic acid, a novel acyclic analogue of all-trans-retinoic acid, has been previously isolated as one of the in vitro oxidation products of lycopene. The effect of acyclo-retinoic acid on the growth of human prostate cancer cells was compared with those of the four retinoids: all-trans-retinoic acid, geranylgeranoic acid, 9-cis-retinoic acid and N-(4-hydroxyphenyl)retinamide. When prostate cancer cells, PC-3, DU 145 and LNCaP, were cultured in a retinoid-supplemented medium, acyclo-retinoic acid remarkably reduced the viability of the cells except for LNCaP. This effect was significantly higher than that of geranylgeranoic acid, all-trans-retinoic acid and 9-cis-retinoic acid, but was comparable to that of N-(4-hydroxyphenyl)retinamide. DNA fragmentations of nuclei in PC-3 and DU 145 cells treated with acyclo-retinoic acid were detected by in situ TUNEL assay. Furthermore, an apoptotic DNA ladder was observed in PC-3 cells. These results showed that acyclo-retinoic acid reduced cell viability by inducing apoptosis in human prostate cancer cells.
[Kotake-Nara E, Kim SJ, Kobori M, Miyashita K, Nagao A. Acyclo-retinoic acid induces apoptosis in human prostate cancer cells. Anticancer Res. 2002 Mar-Apr;22(2A):689-95. PMID: 12014638.]

- In the course of this work, we have also begun some chemical explorations of the similar apolycopenoids that could derive from the tomato pigment, lycopene (4) (7). For many years, it has been suggested that lycopene consumption has beneficial effects on human health and disease (8), particularly in the areas of cancer, especially of the prostate gland (9), and cardiovascular disease (10). It has also been proposed that oxidative cleavage products of lycopene may also be bioactive (11). For example, a possible product of central cleavage of lycopene, apo-15-lycopenoic acid (5), has been shown to increase gap junction communication in fibroblasts (12). It has recently been shown that lycopene can be cleaved by BCO1 to yield apo-15-lycopenal (6) (13), which could then be oxidized to 5. The very similar synthetic analog, called acyclo-retinoid (7), has also been extensively studied as an inhibitor of hepatic carcinogenesis and is used clinically in Japan to treat recurrent hepatocellular carcinoma (14). A second mammalian carotenoid cleavage enzyme, β,β-carotene-9’,10’-oxygenase (BCO2), has also been found to cleave cis isomers of lycopene excentrically at the 9’-10’ double bond, and the apo-10’-lycopenoic acid that could result from this cleavage has been found to inhibit lung cancer cell growth in vitro and lung carcinogenesis in vivo (15). Thus, there may be value in the further study of the possible actions of the putative oxidative cleavage products of lycopene, as is being done for the β-apocarotenoids.
[Narayanasamy S, Sun J, Pavlovicz RE, et al. Synthesis of apo-13- and apo-15-lycopenoids, cleavage products of lycopene that are retinoic acid antagonists. J Lipid Res. 2017;58(5):1021-1029. doi:10.1194/jlr.D073148]

- Induction of gap junctional communication (GJC) is discussed as one possible mechanism underlying the cancer-preventive properties of carotenoids. Structurally different carotenoids have different effects on this GJC pathway. Beta-carotene, echinenone, canthaxanthin, cryptoxanthin and 4-hydroxy-beta-carotene efficiently induce GJC in murine fibroblasts. Decomposition products of canthaxanthin (e.g. 4-oxo-retinoic acid) enhance both GJC and expression of connexin 43 mRNA. Thus, the biological activity of canthaxanthin is due at least in part to formation of active decomposition products such as 4-oxo-retinoic acid. A number of other small molecules such as 1,25-dihydroxycholecalciferol or thyroid hormones serve as nuclear receptor ligands. Cholecalciferol, 3,3',5-triiodo-L-thyronine and L-thyroxine induce GJC to a similar extent as carotenoids or retinoic acid. Interactions between these signalling pathways may be involved in GJC regulation.
[Stahl W, Sies H. The role of carotenoids and retinoids in gap junctional communication. International Journal for Vitamin and Nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal International de Vitaminologie et de Nutrition. 1998 ;68(6):354-359.]

- Humans cannot synthesize vitamin A and thus must obtain it from their diet. β-Carotene 15,15′-oxygenase (BCO1) catalyzes the oxidative cleavage of provitamin A carotenoids at the central 15–15′ double bond to yield retinal (vitamin A). In this work, we quantitatively describe the substrate specificity of purified recombinant human BCO1 in terms of catalytic efficiency values (kcat/Km). The full-length open reading frame of human BCO1 was cloned into the pET-28b expression vector with a C-terminal polyhistidine tag, and the protein was expressed in the Escherichia coli strain BL21-Gold(DE3). The enzyme was purified using cobalt ion affinity chromatography. The purified enzyme preparation catalyzed the oxidative cleavage of β-carotene with a Vmax = 197.2 nmol retinal/mg BCO1 × h, Km = 17.2 μm and catalytic efficiency kcat/Km = 6098 m−1 min−1. The enzyme also catalyzed the oxidative cleavage of α-carotene, β-cryptoxanthin, and β-apo-8′-carotenal to yield retinal. The catalytic efficiency values of these substrates are lower than that of β-carotene. Surprisingly, BCO1 catalyzed the oxidative cleavage of lycopene to yield acycloretinal with a catalytic efficiency similar to that of β-carotene. The shorter β-apocarotenals (β-apo-10′-carotenal, β-apo-12′-carotenal, β-apo-14′-carotenal) do not show Michaelis-Menten behavior under the conditions tested. We did not detect any activity with lutein, zeaxanthin, and 9-cis-β-carotene. Our results show that BCO1 favors full-length provitamin A carotenoids as substrates, with the notable exception of lycopene. Lycopene has previously been reported to be unreactive with BCO1, and our findings warrant a fresh look at acycloretinal and its alcohol and acid forms as metabolites of lycopene in future studies.
[dela Seña C, Narayanasamy S, Riedl KM, Curley RW Jr, Schwartz SJ, Harrison EH. Substrate specificity of purified recombinant human β-carotene 15,15'-oxygenase (BCO1). J Biol Chem. 2013;288(52):37094-37103. doi:10.1074/jbc.M113.507160]

- Consumption of the tomato carotenoid, lycopene, has been associated with favorable health benefits. Some of lycopene’s biological activity may be due to metabolites resulting from cleavage of the lycopene molecule. Because of their structural similarity to the retinoic acid receptor (RAR) antagonist, β-apo-13-carotenone, the “first half” putative oxidative cleavage products of the symmetrical lycopene have been synthesized. All transformations proceed in moderate to good yield and some with high stereochemical integrity allowing ready access to these otherwise difficult to obtain terpenoids. In particular, the methods described allow ready access to the trans isomers of citral (geranial) and pseudoionone, important flavor and fragrance compounds that are not readily available isomerically pure and are building blocks for many of the longer apolycopenoids. In addition, all of the apo-11, apo-13, and apo-15 lycopenals/lycopenones/lycopenoic acids have been prepared. These compounds have been evaluated for their effect on RAR-induced genes in cultured hepatoma cells and, much like β-apo-13-carotenone, the comparable apo-13-lycopenone and the apo-15-lycopenal behave as RAR antagonists. Furthermore, molecular modeling studies demonstrate that the apo-13-lycopenone efficiently docked into the ligand binding site of RARα. Finally, isothermal titration calorimetry studies reveal that apo-13-lycopenone acts as an antagonist of RAR by inhibiting coactivator recruitment to the receptor. [Narayanasamy S, Sun J, Pavlovicz RE, et al. Synthesis of apo-13- and apo-15-lycopenoids, cleavage products of lycopene that are retinoic acid antagonists. J Lipid Res. 2017;58(5):1021-1029. doi:10.1194/jlr.D073148]

:):
 

tim333

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@iceclear Lycopene, lutein and other non provitamin A carotenoids may have beneficial health effects for many because of RAR antagonistic effects. Their breakdown products have toxic effects though and I'm not convinced they are helpful for those that have normal levels of liver retinol stores. When people go on a low vitamin A diet, carotenoid avoidance may explain some of the exacerbation of symptoms.
 

iceclear

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@iceclear Lycopene, lutein and other non provitamin A carotenoids may have beneficial health effects for many because of RAR antagonistic effects. Their breakdown products have toxic effects though and I'm not convinced they are helpful for those that have normal levels of liver retinol stores. When people go on a low vitamin A diet, carotenoid avoidance may explain some of the exacerbation of symptoms.
The breakdown products are the retinoid antagonists. By ‘toxic effects’, are you referring to the unsaturated, unstable nature of carotenoids?
 

tim333

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The breakdown products are the retinoid antagonists. By ‘toxic effects’, are you referring to the unsaturated, unstable nature of carotenoids?

Abstract
According to Siems and colleagues, free radical attack on β-carotene results in the formation of high amounts of cleavage products with prooxidant activities towards subcellular organelles such as mitochondria. This finding may be an explanation for the contradictory results obtained with β-carotene in clinical efficacy and cancer prevention trials. Since primary hepatocytes proved to be very sensitive indicators of the genotoxic action of suspect mutagens/carcinogens we therefore investigated a β-carotene cleavage products mixture (CP), apo8′- carotenal (apo8′) and β-carotene utilizing primary cultures of rat hepatocytes. The end-points tested were: the mitotic index, the percentage of necrotic and apoptotic cells, micronucleated cells, chromosomal aberrations and sister chromatid exchanges (SCE). Our results indicate a genotoxic potential of both CP and apo8′ already at the concentrations 100 nM and 1 µM, i.e. at pathophysiologically relevant levels of β-carotene and β-carotene breakdown products. A 3 h treatment with CP induced statistically significant levels of micronuclei at concentrations of 0.1, 1 and 10 µM and chromosomal aberrations at concentrations of 1, 5 and 10 µM. Apo8′ induced statistically significant levels of micronuclei at concentrations of 0.1, 1 and 5 µM and chromosomal aberrations at concentrations of 0.1, 1 and 10 µM. Statistically significant increases in SCE induction were only observed at a concentration of 10 µM CP and apo8′. In contrast, no significant cytotoxic effects of these substances were observed. Since β-carotene induced neither significant cytotoxic nor genotoxic effects at concentrations ranging from 0.01 up to 10 µM, these observations indicate that most likely β-carotene breakdown products are responsible for the occurrence of carcinogenic effects found in the Alpha-Tocopherol Beta-Carotene Cancer Prevention (ATBC) Study and the Beta-CArotene and RETinol Efficacy Trial (CARET).
 
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