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How does A leave the body?
Patti,
Sorry to hear that. I did read some research that connected retinoic acid to GABA indirectly. And another that said it hyperactivated the HPA axis and prevented it from regaining homeostasis. If Vitamin A is a hormone, then it makes sense.
So, yesterday after my husband's apparent bad reaction I got to thinking about how I had healed both my hub's and infant son's severe eczema 20 years ago with linoleic acid in safflower oil per Adele Davis. They've both never had a recurrence since then, and it was gone within 3 days of taking several spoonfuls of oil a day. If I healed eczema with linoleic acid and Grant healed his with detoxing retinoic acid, then I figure there must be a connection there.
I realized I've rid our diet of linoleic acid in the past few years so well that we're not getting any at all to speak of. So, I bought a bottle of high quality safflower oil again and the whole family took a tablespoonful last night. He was better this morning. Such a relief. I felt much better too. I took 2 tbsp.
I noticed that Grant added flaxseed meal later on. So maybe it's the missing piece of the puzzle for us. I don't know. He took another tbsp tonight, so we'll see if there's more improvement tomorrow. We're sticking with the low A for now unless things take a turn for the worse.
With all the talk about omega 6 fats being bad and omega 3 good I wonder if others are like us and went too far in eliminating it completely? I'm still staying away from soybean and canola oil, and will not continue large amounts of the safflower long term. We used to use Hain Safflower mayonnaise occasionally, but our stores stopped stocking it in the last year or so. Maybe it took awhile to catch up with us.
Thank you for answering back so quickly! I appreciate your perspective. Good luck to you and daughter also!
Kathy
@guest Look for lutein free diet on the forum. I won't be detailing since the information is behind a paywall. You can get a list of food by searching for Sarah's Diet and paying for the document.
It's basically the same as a low A diet just be careful with beef and poultry to take lean cuts wince their fat contain lutein.
Kathy -that's really interesting about the safflower oil, thanks for sharing
I've been really curious about this since someone else posted a video in a thread about the Doctor who was advocating for more Omega 6. Being on the no PUFA train for a really long time myself I've been looking into it, there are lots of positive studies out there about Omega 6!
Anyway, I found this abstract and it seems like a positive thing to me, but maybe some others could help me understand it better. I 'm reading it that Omega 6 gets in the way of retinoic acid binding, but the Omega 6 does not act like the retinoic acid so they see this as bad because the assumption is that the retinoic stops tumor growth.... I might have it wrong though, because then I wonder if maybe the Omega 6 makes it so the retinoic acid doesn't bind correctly, which could make the retinoic acid more harmful..... Any thoughts? The first way it could be a missing link for some....
Interference of retinoic acid binding to its binding protein by omega-6 fatty acids.
Abstract
Cellular retinoic acid-binding protein (CRABP) is the putative mediator of the biological effects of retinoic acid in the control of epithelial differentiation and tumorigenesis. Omega-6 fatty acids such as linoleic acid and arachidonic acid, precursors of prostaglandin synthesis, caused inhibition of retinoic acid binding to CRABP. These fatty acids, however, possessed lower affinity than retinoic acid for the binding protein. Omega-3 fatty acids, such as eicosapentaenoic acid and docosohexaenoic acid, did not cause such inhibition in the binding of retinoic acid. Whereas retinoic acid was a potent modulator of differentiation of F9 embryonal carcinoma cells, neither omega-3 nor omega-6 fatty acids showed any significant differentiation potential. Competition by omega-6 fatty acids with retinoic acid for CRABP may neutralize the binding protein-mediated biological functions of retinoic acid, and could thereby enhance tumor production.
Here's another spin on it 31 years later. Are they ever going to figure out what's going on? It seems like if one keeps adding variables, and machines to measure those variables, and super-computers to crank the statistical variations in the variables, and so on and so forth, maybe the funding will never end. If retinoic acid is always found at the scene of the crime, but it's wearing a police uniform and has carte blanch to muck-around with the evidence, where's NCIS? Asleep at the Wheel? Or, do we take this stuff at face value?
Nutr Cancer. 2018 Sep
Differential Potentiation of Retinoic Acid Effects against Human Breast Cancer Cells by Unsaturated Fatty Acids.
Retinoic acid (RA) and unsaturated fatty acids (UFA) are proposed as nutritional anticancer agents. Nonetheless, the activity of their combination on human breast cancer needs further study. Our aim was to evaluate this activity on the MCF-7 and ZR-75-1 cell lines treated with 1 µM RA and 50 µM of γ-linoleic (GLA, ω-6), eicosapentaenoic (EPA, ω-3), oleic (OA, ω-9), or eicosatrienoic (ETA, ω-9) acids. The following cellular responses were compared by ANOVA and Fisher test (P < 0.05): fatty acids, E-cadherin, actin (differentiation), conjugated dienes, γ-glutamyltranspeptidase activity (stress), and viability, which were correlated by partial least squares regression. Although both cell lines responded differentially, RA modified unsaturated fatty acids, increased differentiation, reduced γ-glutamyltranspeptidase, and viability. RA differentiating activity on ZR-75-1 was morphologically enhanced by UFA. Stress induction with γ-glutamyltranspeptidase decrease and conjugated dienes was promoted by ETA in MCF-7, and EPA and OA in ZR-75-1. RA-related reduced viability was potentiated by EPA and OA in both lines. GLA was less active.
Therefore, unsaturated fatty acids (ω-3/ω-9) potentiated the multitarget retinoic acid activity against these human breast cancer cells.
Any thoughts on succinic acid? It is part of the the citric acid cycle, and read that it helps to boost alcohol dehydrogenase, so should have remove vitA?
I can't find any info on if retinoids are present in sebum. Anyone?
What I'm trying to understand is how do retinoids exit the body in hypervitaminosis. They must do somehow in addition to what is used and eliminated through regular elimination channels. Otherwise with consumption higher than use hypervitaminosis would quickly reach a lethal point instead of remaining chronic and sub clinical for years. Are things like eczema methods to remove excess? For those that have very oily skin and get seborrhoea maybe retinoids get eliminated in the sebum?
Quote from Guest on February 23, 2019, 2:45 pmI can't find any info on if retinoids are present in sebum. Anyone?
What I'm trying to understand is how do retinoids exit the body in hypervitaminosis. They must do somehow in addition to what is used and eliminated through regular elimination channels. Otherwise with consumption higher than use hypervitaminosis would quickly reach a lethal point instead of remaining chronic and sub clinical for years. Are things like eczema methods to remove excess? For those that have very oily skin and get seborrhoea maybe retinoids get eliminated in the sebum?
Good question, and this is not the definite answer, but I think its sweat, urine and stool, those are the three exit points?
Since its believed to be essential, wonder how much info and study is done on depletion?
https://www.ncbi.nlm.nih.gov/books/NBK222318/
Typically, the majority of vitamin A metabolites are excreted in the urine. Sauberlich et al. (1974) reported that the percentage of a radioactive dose of vitamin A recovered in breath, feces, and urine ranged from 18 to 30 percent, 18 to 37 percent, and 38 to 60 percent, respectively, after 400 days on a vitamin A-deficient diet. Almost all of the excreted metabolites are biologically inactive.
UV light may deplete it as well. Nothing makes me feel as good as an hour of full sun. Which is hard to get in the winter living in the mountains but if it's 30+, clear, and no wind I'm out there.
Vitamin A is an intrinsic modulator of proliferation and differentiation in human epidermis, and may be destroyed by ultraviolet radiation (UVR) impinging on the skin. To identify the deleterious effects of a perturbed cellular vitamin A status, we investigated the endogenous retinoid concentrations and the metabolism of [3H]retinol and all-trans [3H]retinoic acid in cultured human keratinocytes and melanocytes exposed to UVR, using high performance liquid chromatography. Before UVR the retinoid content was similar in keratinocytes and melanocytes, but the uptake of [3H]retinol was three-fold higher and the uptake of [3H]retinoic acid was 10-fold higher in the melanocytes. In both cell types, UVR (UVA 360 mJ/cm2 plus UVB 140 mJ/cm2) instantaneously reduced the concentration of retinol by about 50% and that of 3,4-didehydroretinol by about 20%. The retinoid concentrations returned to normal within 1-2 days post-irradiation, despite there being no overt increase in the uptake of [3H]retinol or the biosynthesis of 3,4-didehydroretinol. However, in both types of irradiated cells, the accumulation of the biologically most active metabolite, all-trans [3H]retinoic acid, was about 60% higher than in control cells. Furthermore, the metabolism of authentically supplied [3H]retinoic acid was reduced, especially in irradiated keratinocytes, which probably contributed to the restoration of retinoid levels after UV exposure.
Since going low A, my scalp/hair has gotten extremely oily. I am 53 and I have a history of oily skin and scalp which subsided some what before going low A. Same story with acne. I had also wondered if oily skin and pimples where a way to get rid of A.