Quote from tim on July 2, 2019, 5:36 am

I posted this in my log thread, @rachel suggested that I post it here.

During the recent flu/stomach bug illness that I had I had VA detox symptoms. One undeniable symptom was that the dandruff that has gone since starting low VA returned with a vengeance to the sides of my head, red and inflamed skin with massive flakes of dandruff. I used selenium based anti dandruff shampoo (that normally works well) and the next day it had returned with the same degree of severity! And then it was gone like it had never come!

While I was sick I did some research on how the flu relates to VA.

I highly recommend reading this hidden gem of an 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 also talks about how 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].