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Tim's Log
You getting any beans in your diet? I think they can potentially be a huge aid in excreting VA and preventing their reabsorption from bile. Just gotta balance it with adequate fat, salt and protein too to make sure new bile gets flowing.
Quote from collden on June 25, 2019, 6:45 amYou getting any beans in your diet? I think they can potentially be a huge aid in excreting VA and preventing their reabsorption from bile. Just gotta balance it with adequate fat, salt and protein too to make sure new bile gets flowing.
I was eating beans but slowed down in the last few months. I believe I may have IBS as I'm very sensitive to foods that contain fiber such as beans, whole grains, fruit juice (haven't had any since going low VA) and almond milk. I have had much more normal bowel movements recently and have greatly reduced gas by basically avoiding these foods with the exception of a small amount of almond milk in my tea. Potato and beer don't seem to cause an issue despite containing soluble fiber, maybe I'm within a threshold that my body can tolerate with these foods.
I am eating plenty of fat, salt and protein and will just have to make do with the fiber that my diet does contain in facilitating the disruption of enterohepatic circulation of VA.
Quote from collden on June 25, 2019, 6:45 amYou getting any beans in your diet? I think they can potentially be a huge aid in excreting VA and preventing their reabsorption from bile. Just gotta balance it with adequate fat, salt and protein too to make sure new bile gets flowing.
I wonder if it's worthwhile to rotate them in for just one meal, say monthly? I get the urge now and then. I take MANY "Bean-O's (TM)" with the chili.
It's a must to have a Clear Schedule the next day hahaha. I have better luck with canned than home-soaked.
Give the leftovers away.
During the recent flu/stomach bug illness I had I had VA detox symptoms. One undeniable symptom was that the dandruff that has gone since starting low VA returned with a vengence to the sides of my head, red and inflamed skin with massive flakes of dandruff. I used selenium based anti dandruff shampoo and the next day it was back in the same degree! And then it was gone like it had never come!
I highly recommend reading this article which discusses the idea that the main symptoms of the flu virus are caused by transient hypervitaminosis A:
https://www.hindawi.com/journals/isrn/2013/246737/
In an unusual case report, the symptoms of influenza A infection were described as being perfectly mimicked by the retinoic acid syndrome [116]. A 47-year-old man was hospitalized for typical APL and treated with ATRA and chemotherapy. On day 3 the patient developed fever and acute respiratory distress and was admitted to the critical care unit. ATRA was stopped since the diagnosis of retinoic acid syndrome was suspected. Bronchoalveolar lavage and immunofluorescence examination showed the presence of influenza A virus, which was confirmed by the rise of specific antibody levels in sera obtained during the acute illness and 3 weeks later. This case report shows that an infectious disease—influenza A infection—can perfectly mimic the retinoic acid syndrome and suggests that endogenous sources of retinoic acid could contribute to influenza and its sequelae.
Headache, a common symptom of influenza [117], is also a major feature of retinoid toxicity [118]. Conjunctivitis and photophobia are also common during acute seasonal influenza infection, especially in avian influenza A infections in humans [119]. An oculorespiratory syndrome (ORS) consisting of red eyes, photophobia, blurred vision, palpebral edema, ocular pain and itching, and conjunctival secretions is reported after influenza vaccination [120]. A similar pattern of ocular side effects has been described in diet-induced hypervitaminosis A and secondary to isotretinoin use. In a review of 1,741 spontaneous case reports, as well as data from the Drug Safety Section of Roche Pharmaceuticals and the world literature, adverse ocular reactions classified as “certain” to have been associated with isotretinoin use included photophobia, abnormal meibomian gland secretion, blepharoconjunctivitis, corneal opacities, decreased dark adaptation, decreased tolerance to contact lens, decreased vision, increased tear osmolarity, keratitis, meibomian gland atrophy, myopia, ocular discomfort, and ocular sicca [121]. Similarities between the features of hypervitaminosis A and influenza infection are shown in Table 1.
It's also saying that each time someone eats a meal rich in Vitamin A they also enter a transient state of hypervitaminosis A. So even for people that haven't reached liver capacity they are still causing damage to their body by consuming A rich foods:
Retinyl esters in serum, normally <0.2 μmol/L in the fasting state, increase significantly after a large vitamin A-containing meal, after which they are converted to retinol and stored in the liver. Retinol binds to RBP and is transported to the target tissues. Vitamin A toxicity is generally associated with increased levels of retinyl esters circulating with plasma lipoproteins unbound to RBP. Retinyl esters react more randomly with cell membranes than the physiologically sequestered RBP and hence are a major form of vitamin A toxicity. Fasting retinyl ester concentrations >10% of total circulating vitamin A (retinol plus esters) are considered a biomarker for toxicity [76]. An acute increase in the concentration of other retinoids, for example, retinoic acid, a 40-fold more potent teratogen than retinol [77] occurs after ingesting a large amount of vitamin A.
More discussion implicating VA when it comes to flu symptoms:
It has been recognized for decades that vitamin A deficiency is associated with increased susceptibility to most infections and with defects in the innate and adaptive immune systems [67]. The traditional view of vitamin A as an “anti-infective” vitamin was based partly on earlier studies in which vitamin A—in cod liver oil (CLO)—was successful in preventing infection [122]. Since earlier preparations of CLO contained higher amounts of vitamin D in proportion to vitamin A than do currently available preparations, possibly due to modern deodorization procedures, which remove vitamin D, it has been suggested by Cannell et al. [34, 35] that the anti-infective properties of CLO were partly or wholly due to vitamin A.
Consistent with Cannell’s hypothesis, vitamin A supplementation has not been shown to improve recovery during acute pneumonia in most human clinical trials. In a double-blind, placebo-controlled trial of vitamin A supplementation on childhood morbidity in Haiti, 11,124 children ages 6–83 months were sequentially assigned by household units to receive either a capsule containing 200,000 IU of vitamin A and 40.6 mg vitamin E or a capsule containing only 40.6 mg vitamin E (placebo) every 4 months. Indicators of childhood morbidity were studied 2–8 weeks after each administration of vitamin A and placebo capsules. At 2 weeks after supplementation the vitamin A group had an increased prevalence of all symptoms and signs of childhood morbidity, including diarrhea, rhinitis, cold/flu symptoms, cough, and rapid breathing. The risk of morbidity was highest 8–17 weeks after receiving the megadose of vitamin A. The study showed an increased 2-week prevalence of diarrhoea and the symptoms of respiratory infections after vitamin A supplementation, although mortality rates of the 2 groups were similar [123]. A meta-analysis of vitamin A supplementation trials concluded that when given alone, vitamin A slightly increased the incidence of respiratory tract infections [124].
The model proposed here aims to explain the mechanism of influenza A-associated liver dysfunction and its role in increasing the severity of infection. It is consistent with the overall low vitamin D : A ratio hypothesis of severe influenza and involves alterations in retinoid metabolism. It is suggested that influenza-induced liver involvement worsens the outcome of infection via the hepatic release of unbound retinyl esters and retinoic acids which are transported to and damage the lung as well as other organs, thereby contributing to the development of pneumonia, heart and kidney failure, and sepsis.
In summary, it is proposed that lack of solar radiation and/or vitamin D deficiency increase the availability and potential toxicity of retinoids, and the latter interact with and induce viral activation at the genome level to trigger influenza. On this hypothesis, influenza viral pathogenesis involves both vitamin D deficiency and endogenous retinoid overexpression. In seasonal influenza, ever-present influenza viruses may be activated and disease symptoms triggered by declining vitamin D concentrations and worsened by retinoid accumulation and overexpression. In pandemic influenza, while the virulence of the strain of virus may account for disease epidemicity, the likelihood of particular individuals being infected may depend on the background nutritional status of vitamin A and D, whereby infectivity may be reduced by vitamin D supplementation but enhanced by vitamin A supplementation or excess. Retinoid receptor overexpression may thus contribute to the pathogenesis of influenza and related viral infections, causing an endogenous form of hypervitaminosis A that manifests itself in the symptoms of the disease.
Interesting fact:
Research on vitamin A toxicity has been carried out mostly in animals, but observational studies suggest that >75% of people in developed countries routinely consume more than the recommended dietary allowance (RDA) for vitamin A [80].
That's really interesting Tim. Might be useful to post it also in "The Science of It".
This might explain why young children and older people have more trouble with the flu. In the first case, small livers and low capacity to deal with a flood of retinoic acid, and in the second case, a lifetime of A absorption and overfill.
moved this reply to "the science of it" thread.
I reached month 5 yesterday. Still having symptoms. I have noticed another issue has disappeared though, my voice which has always been hoarse is no longer so. I can get up in the morning and speak immediately with no hoarseness which was not possible before. I speak loudly and continuously with customers all day and never lose my voice whereas before I often did. I even had someone say that I should do professional voice overs the other day which amazed me as friends used to actually mock me for being so croaky.
Quote from tim on July 8, 2019, 5:30 amI reached month 5 yesterday. Still having symptoms. I have noticed another issue has disappeared though, my voice which has always been hoarse is no longer so. I can get up in the morning and speak immediately with no hoarseness which was not possible before. I speak loudly and continuously with customers all day and never lose my voice whereas before I often did. I even had someone say that I should do professional voice overs the other day which amazed me as friends used to actually mock me for being so croaky.
Thanks for the update, very encouraging sign of improvement. I've had a weak/hoarse voice for a very long time and since I've started VA restriction it has on occasion cleared up completely, usually associated with when my bloating is down. Its often attributed to swelling of the thyroid but I'm guessing an inflamed swollen liver pressing on the diaphragm can also cause this.
I just want to say that I have always had this symptom, a very delicate voice which is apt to laryngitis. We'll see if I make progress on this!