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Fat-soluble Vitamin

The table below shows the recommended daily allowance (RDA) for vitamin A. The RDA is the estimated amount of vitamin A that the vast majority (about 97.5%) of people need to meet their daily requirements.

fat-soluble vitamin

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Although provitamin A is abundant in many fruits and vegetables, it is not always efficiently converted into retinol, the active form of vitamin A. The efficiency of this conversion depends on your genetics (12, 13).

Once absorbed into the bloodstream, your liver and kidneys change calciferol into calcitriol, which is the biologically active form of vitamin D. It can also be stored for later use in the form of calcidiol.

However, many people spend little time in the sun or do so fully clothed. Justifiably, others cover their skin with sunscreen to prevent sunburns. While sunscreen use is highly recommended, it reduces the amount of vitamin D your skin produces.

Your body can produce the vitamin D it needs if you regularly expose large parts of your skin to sunlight. However, most people need to get it from their diet or supplements, such as fatty fish or fish oil.

The most well-known consequences of vitamin D deficiency include soft bones, weak muscles, and an increased risk of bone fractures. This condition is called osteomalacia in adults and rickets in children (28).

The richest dietary sources of vitamin E include certain vegetable oils, seeds, and nuts. The chart below shows some of the best sources of vitamin E and the amount found in 3.5 ounces (100 grams) of these foods (8):

It may have blood-thinning effects, counteracting the effects of vitamin K and causing excessive bleeding. Thus, people who take blood-thinning medications should avoid taking large doses of vitamin E (38, 42, 43).

Additionally, at high doses of more than 1,000 mg per day, vitamin E may have pro-oxidant effects. That is, it can become the opposite of an antioxidant, potentially leading to oxidative stress (44).

Given the potentially adverse effects of vitamin E supplements, they cannot be recommended at this point. High quality studies are needed before solid conclusions can be reached about the long-term safety of these supplements.

Unlike vitamins A and D, vitamin K is not stored in the body in significant amounts. For this reason, consuming a diet lacking in vitamin K may lead you to become deficient in as little as a week (54).

People who do not efficiently digest and absorb fat are at the greatest risk of developing vitamin K deficiency. This includes those who have celiac disease, inflammatory bowel disease, and cystic fibrosis.

Without vitamin K, your blood will not clot, which increases the risk that even a small wound could cause unstoppable bleeding. Fortunately, vitamin K deficiency is rare, since the body only needs small amounts to maintain blood clotting.

Finally, vitamin K1 supplements taken at 0.5 mg every day for 3 years slowed the development of insulin resistance in older men, compared to a placebo. No significant differences were detected in women (63).

For this reason, vitamin D deficiency can occur in people who do not eat a diet filled with a variety of nutrient-rich foods and regularly spend time indoors, which may be due to a variety of factors, including medical reasons or personal choice.

After bariatric surgery, it is not possible to absorb all the vitamins your body needs. It is important when you commit to bariatric surgery, that you also make a life-long commitment to take vitamins. There are a few things to consider to make sure you are not only staying safe, but also financially aware of your vitamin consumption. It starts with understanding the difference between water-soluble and fat-soluble vitamins.

Before taking vitamins or minerals, discuss first with your health care provider. Some medical conditions and allergies may interfere with some vitamins and minerals. If prescribed or allowed by your health care provider, never take more than the recommended dose and take with a full glass of water. If you suspect you are having an allergic reaction or have taken too much, contact your health care provider immediately.

Background: Infants with cholestasis are at risk of fat-soluble vitamin deficiency. The present study amied to review practice relating to the assessment, deficiency and supplementation of fat-soluble vitamins in infants with cholestasis.

Methods: The medical records of all newly diagnosed infants with cholestasis (conjugated bilirubin >17 mmol L-1 />20% total bilirubin) at King's College Hospital between 2017 and 2019 were reviewed. Data extracted included bilirubin, serum vitamin concentrations (A, D, E), international normalised ratio and evidence of supplementation at initial assessment, as well as at 3 and 6 months. Rates of vitamin assessment, deficiency and supplementation were compared using chi-squared or Fisher's exact test.

Conclusions: Supplementation was generally high and continued in many despite cholestasis resolving. Deficiency of vitamin D and vitamin E was high at initial assessment, although lower at follow-up. Actual prevalence of deficiency of all vitamins is unknown because monitoring was not consistently performed.

The fat-soluble vitamins are vitamins A, D, E, and K. Each vitamin has unique characteristics and contributes to the overall health of an individual. These vitamins have complex absorption, metabolism, and distribution elements that provide protection to the cells in the body as well as many organs. Fat-soluble vitamins, once ingested and processed, are stored in the body for use. Most fat-soluble vitamins are obtained from fruits, vegetables, nuts, and animals.

Activated vitamin D,1,25(OH)2D, a steroid hormone, is an immune system modulator that reduces the expression of inflammatory cytokines and increases macrophage function. Vitamin D also stimulates the expression of potent antimicrobial peptides (AMPs), which exist in neutrophils, monocytes, natural killer cells, and epithelial cells of the respiratory tract [37]. Other observations explained by the vitamin D hypothesis are that (i)volunteers inoculated with live influenza virus in winter were more likely to develop fever and serologic evidence of an immune response than in summer months; (ii)vitamin D deficiency predisposes children to respiratory infection; (iii)ultraviolet (UV) radiation reduces the incidence of viral respiratory infections; (iv)vitamin D supplementation reduces the incidence of respiratory infections in children [33].

The vitamin D deficiency hypothesis accounts for many hitherto unexplained facts about the epidemiology of influenza [38, 39]. Influenza is an allegedly highly infectious viral illness that shows marked seasonal fluctuations, peaking in the winter months and then ending abruptly; it has an obscure serial interval, with a very low secondary attack rate that occurs simultaneously in countries of similar latitude; it spreads very rapidly despite the absence of modern transportation; a high percentage of seronegative volunteers escape illness or experience only a mild illness after being inoculated with novel influenza virus; and vaccine effectiveness is questionable [40, 41].

Recognition of microbial particles by toll-like receptors (TLRs) induces expression of antimicrobial peptides such as defensins and cathelicidins, which act broadly against microorganisms, including bacteria, fungi, and viruses. Stimulation of TLRs engages a vitamin D-dependent intracellular circuit that results in the expression of cathelicidin, enhancing the microbicidal capability of the monocyte [56]. Sera from African Americans, who have substantially lower serum vitamin D levels than whites, were inefficient in inducing genetic expression of cathelicidin, but supplementation with vitamin D increased cathelicidin levels to those seen in monocytes from whites. 1,25-OH2D induces expression of cathelicidin and defensin β2 genes [37], and defensin β2 has inhibitory effects on adenovirus and HIV-1 [57, 58]. Defensins block viral infection by directly acting on the virion or by affecting the target cell and indirectly interfering with viral infection [58]. One of the defensins (retrocyclin-2) inhibits influenza virus infection by blocking membrane fusion mediated by viral hemagglutinin [53]. These findings have suggested that vitamin D supplementation could prevent colds and influenza.

There is presently little direct or experimental evidence to support the hypothesis that vitamin D might protect against influenza infection. Experiments have not yet been done in cells or mice to evaluate the effect of vitamin D on influenza virus [59].

Plasma levels of 25(OH)D are lower in African than in white Americans and are insufficient to stimulate the vitamin D-dependent AMPs, although supplementary 25(OH)D can enhance AMP expression [56]. High melanin concentrations in dark-skinned individuals shield keratinocytes from the UV radiation that generates vitamin D in the skin [61]. Production of vitamin D in skin also diminishes with aging [54]. Hence dark-skinned and aged individuals are at risk of innate immune deficiency, especially in winter. Since vitamin D is mostly obtained from sunlight, vitamin D deficiency is generally higher in winter in aged, dark-skinned, and obese individuals as well as in high northern and southern latitudes [48].

Several observations reviewed in this paper suggest that vitamins A and D have interactive roles in influenza and that retinoids (the collective term for vitamin A and its natural and synthetic congeners) have an independent role in influenza infection and pathogenesis. For instance, solar radiation has opposite effects on vitamins A and D, catabolizing vitamin A but increasing the concentration of vitamin D; the effects of the two vitamins are mutually inhibitory; retinoids regulate airway epithelial cell growth, differentiation, and gene expression; the symptoms of influenza are similar to those of retinoid toxicity; supplementary and/or pharmacological concentrations of retinoids induce influenza-like symptoms; viral activity is regulated in part by retinoids; and retinoids influence the mechanisms that both inhibit and contribute to influenza pathogenesis. 041b061a72


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