What vitamin should i take for hair loss

Khetarpal says. Khetarpal says that success depends more on the duration of hair loss than anything else. People who have been losing hair for only two or three years are more likely to see noticeable results than those losing it for 10 or 20 years, she explains.

You have to be reasonable with your expectations. Try these six hair vitamins, hair growth supplements and topicals to heal damaged hair.

Learn more about vaccine availability. Advertising Policy. This vitamin serves many roles in the body: it is critical for vision, involved in immune function, and is necessary for cellular growth and differentiation [ 13 ]. Vitamin A exists in the diet as preformed vitamin A from animal sources and as provitamin A carotenoids sourced from plants. Both sources of vitamin A must be metabolized intracellularly to their active forms retinal and retinoic acid.

The majority of vitamin A is stored in the liver as retinyl esters. When measuring retinol and carotenoid levels, plasma levels are typically sufficient for determining adequacy. In most cases, a balanced diet will supply a healthy amount of vitamin A [ 14 ]. While there is no upper intake level for provitamin A carotenoids, ingestion of very high levels of preformed vitamin A can be toxic.

It is therefore important to consider what form of vitamin A is contained in supplements provitamin A carotenoids or preformed vitamin A and in what proportion. As a general rule, consuming too much or over-supplementing vitamin A can cause hair loss [ 15 , 16 ].

Typically, fat-soluble vitamin A is stored in the liver where its dispersal is tightly regulated by anabolic and catabolic reactions between the inactive and active metabolite. When levels of vitamin A are too high, the capacity of the transport system is exceeded and vitamin A spills over into the circulation [ 17 ]. Maintaining homeostasis—and by extension the proper concentration of active metabolite—is important for healthy hair [ 18 ].

In one study with the aim to determine the effects of isotretinoin on acne vulgaris in the skin, special care was taken to evaluate changes in the hair and hair growth. Thirty patients were evaluated over a 4- to 7-month treatment period, with examinations carried out using a FotoFinder dermoscope FotoFinder Systems, Inc.

Consistent with other findings, the authors reported a decrease in hair count, density, and percentage of anagen hairs [ 19 ].

In a case documented in , a year-old woman undergoing renal dialysis noticed sudden hair loss. Gentle traction yielded four to five hairs, all of which were in the telogen phase. One month after termination of vitamin A supplementation, hair loss was no longer a problem. The authors concluded that signs of hypervitaminosis A were misinterpreted as symptoms of chronic renal failure.

Consumption of vitamin A exceeding the recommended daily limit of approximately 10, IU a day can lead to vitamin A toxicity. In a case report, a year-old male who had been taking excess vitamin A supplements experienced non-scarring fronto-central alopecia as well as decreased pubic and axillary hair.

The patient also reported dystrophic nail changes and an erythematous rash. The vitamin B complex includes eight water-soluble vitamin substances—thiamine B1 , riboflavin B2 , niacin B3 , pantothenic acid B5 , vitamin B6, biotin B7 , folate, and vitamin B12—that aid in cell metabolism. The recommended daily allowances of these vitamins can be reached by eating a balanced diet, with the exception of biotin, which is the only B vitamin produced by the body.

In healthy individuals biotin does not need to be supplemented [ 14 ]. Only riboflavin, biotin, folate, and vitamin B12 deficiencies have been associated with hair loss. The body stores only small amounts of riboflavin, in the liver, heart, and kidneys. Riboflavin deficiency—while extremely rare in the USA—can cause hair loss [ 24 ]. Vitamin B7 biotin or vitamin H is a cofactor for five carboxylases that catalyze steps in fatty acid, glucose, and amino acid metabolism.

Biotin also plays roles in histone modification, cell signaling, and gene regulation [ 25 ]. Most dietary biotin is found in protein. Dietary protein must be broken down into free biotin, which is then stored in the small intestine and liver. The average dietary intake of biotin in Western countries is adequate, and biotin deficiency is rare. Severe biotin deficiency in healthy individuals eating a normal diet has never been reported [ 26 , 27 ].

While there is no upper limit for biotin intake—as there is no evidence for biotin toxicity—high biotin intake can cause falsely high or falsely low laboratory test results [ 28 ].

Many supplements for hair, skin, and nails far exceed the recommended daily intake of biotin [ 28 ]. The presence of biotin can in fact interfere with tests that use biotin—streptavidin technology.

The interaction between biotin and streptavidin is used as the basis for many biotin-based immunoassays, and these immunoassays are vulnerable to interference when they are used to analyze a sample that contains biotin. Exogenous biotin in the sample competes with biotinylated reagents for the binding sites on streptavidin reagents, creating false positive or false negative results [ 29 ].

Biotin interference in biotin—streptavidin immunoassays have been described in patient samples for thyroid-stimulating hormone, free tri-iodothyronine FT3 , free thyroxine FT4 , parathyroid hormone, estradiol, testosterone, progesterone, dehydroepiandrosterone sulfate, vitamin B12, prostate-specific antigen, luteinizing hormone, and follicle-stimulating hormone. Other non-hormonal tests include cardiac and tumor markers, infectious disease serologies, biomarkers of anemia and autoimmune diseases, and concentrations of immunosuppressive drugs [ 29 — 32 ].

Furthermore, according to the U. In addition, a recent study showed that some human chorionic gonadotropin hCG devices are subject to biotin interference in individuals taking dietary biotin supplements. Therefore, clinicians and laboratory technicians need to be aware of this potential interference with qualitative urine hCG tests and should suggest quantitative serum hCG measurement.

The latter is not subject to biotin interference [ 33 ]. Biotin deficiency can be genetic or acquired. Genetic causes of biotin deficiency can be either neonatal or infantile. The neonatal type is a life-threatening condition manifested during the first 6 weeks of life, and it is due to a holocarboxylase enzyme deficiency. It is usually manifested with severe dermatitis and alopecia, where there is loss of vellus and terminal hair on the scalp; eyebrows, eyelashes, and lanugo hair can also be absent.

The infantile form of biotin deficiency occurs after 3 months of delivery and is due to a lack of the enzyme called biotinidase. In this form, hair of the scalp, eyebrows, and eyelashes is sparse or totally absent [ 34 ]. Acquired biotin deficiency can be due to increased raw egg consumption, where avidin particles attach to biotin and inhibit its absorption into the intestinal gut.

In cooked eggs the avidin particles are destroyed [ 35 ]. Other causes of acquired biotin deficiency include states of malabsorption, alcoholism, pregnancy, prolonged use of antibiotics that interrupt normal flora, medications such as valproic acid, and isotretinoin intake. The aforementioned medications interfere with biotinidase activity [ 34 ]. While signs of biotin deficiency include hair loss, skin rashes, and brittle nails, the efficacy of biotin in supplements for hair, skin, and nails as a means to remedy these conditions is not supported in large-scale studies [ 25 , 26 ].

In fact, only case reports have been used to justify the use of biotin supplements for hair growth. These case reports were in children and found that 3—5 mg biotin daily could improve hair health after 3—4 months in children with uncombable hair syndrome [ 37 , 38 ].

A recent review article evaluating biotin and its effect on human hair found 18 reported cases of biotin use on hair and nail. In ten of these 18 cases there was a genetic cause of biotin deficiency; the remaining eight patients had alopecia that was improved after they had taken biotin supplementation. There were three cases of uncombable hair syndrome, three cases of brittle nail syndrome, one case of alopecia due to valproic acid intake, and one case of an infant on a biotin-free dietary supplement.

All of these 18 patients had underlying causes of biotin deficiency and, once treated with biotin supplement, showed clinical improvement in a variable time period [ 35 ]. Researchers in another study investigated the serum biotin level in women participants complaining of hair shedding age range 9—92 years.

These results suggest a multifactorial cause of hair loss [ 39 ]. The authors assessed and compared biotin, folic acid and vitamin B12 levels in both groups. The results showed a deficiency of vitamin B12 and folic acid in the patients evaluated and lower levels of biotin without any obvious biotin deficiency in the cases [ 40 ].

Folate is another water-soluble B vitamin and includes naturally occurring food folate and folic acid fully oxidized monoglutamate. Folate is a coenzyme in the synthesis of nucleic acids and in amino acid metabolism. It exists in the plasma as 5-methyl-tetrahydrofolate, while about half of the total body content exists in the liver [ 22 , 41 ].

The recommended dietary allowance of food folate is mcg daily for adults, which is supported by required fortification of some foods in the USA [ 22 ]. The tolerable upper intake level of folate is mcg [ 42 ]. While most people in the USA ingest adequate amounts of folate, certain groups are at risk for deficiency usually in association with poor diet, alcoholism, or a malabsorptive disorder.

Folate deficiency can cause hair, skin, and nail changes [ 22 ]. Vitamin B12 is necessary for DNA synthesis, neurological function, and red blood cell formation [ 22 ]. The active forms of B12 are called methylcobalamin and 5-deoxyadenosylcobalamin. Vitamin B12 is a cofactor for methionine synthase and thereby affects the synthesis of nearly substrates including DNA, RNA, and proteins [ 22 ].

The recommended dietary allowance of vitamin B12 is 2. There is no established upper limit for vitamin B12 intake, as it has a low potential for toxicity [ 22 ]. The role of folate and vitamin B12 in nucleic acid production suggest that they might play a role in the highly proliferative hair follicle [ 43 ].

However, few studies to date have addressed the relationship between B vitamins and hair loss. Turkish authors investigated folate level in 43 patients with AA and 36 healthy controls and found no significant differences in serum folate and vitamin B12 levels between the AA subjects and the healthy controls [ 44 ].

Also, the authors found that serum levels did not vary with duration or activity of the disease [ 44 ]. In another study conducted in Turkey 75 subjects with AA and 54 controls were enrolled. Blood samples were taken to investigate the serum folic acid and vitamin B12 levels. The results were similar to those reported by the authors of the previous Turkish study [ 44 ], with the authors finding no significant differences in vitamin B12 and folate levels between affected and healthy patients [ 45 ].

Of interest, a genetic study including Turkish patients with AA and healthy controls found that the affected patients had a higher prevalence of mutations in the methylene-tetrahydrofolate reductase MTHFR gene [ 47 ]. This gene regulates folate metabolism, influences nucleic acid synthesis and DNA methylation, and is associated with other autoimmune disorders.

However, there was no difference between serum levels of folate or vitamin B12 in affected patients and controls [ 47 ]. A retrospective cross-sectional study evaluated folate and vitamin B12 levels in patients with TE acute and chronic.

The results showed that 2. The authors of a case—control study attempted to determine the prevalence of trichodynia in 91 patients with diffuse hair loss, including those with AGA and TE. These researchers found no significant difference in folate and vitamin B12 levels between patients with hair loss and control patients [ 35 ].

Ramsay et al. This reduced vitamin B12 level resulted in vitamin Brelated anxiety, causing some patient to stop treatment. Interestingly, the reduction in vitamin B12 levels had no adverse effects on hair shedding or hair growth [ 49 ].

Vitamin C, or ascorbic acid, is a water-soluble vitamin derived from glucose metabolism. It is a potent antioxidant preventing the oxidation of low-density lipoproteins and free radicals damage. It also acts as a reducing mediator necessary for collagen fiber synthesis through hydroxylation of lysine and proline. Vitamin C plays an essential role in the intestinal absorption of iron due to its chelating and reducing effect, assisting iron mobilization and intestinal absorption [ 50 ].

Therefore, vitamin C intake is important in patients with hair loss associated with iron deficiency. Humans are naturally deficient in an enzyme called l -gulonolactone oxidase that is required for vitamin C synthesis, and should therefore take vitamin C through their diet.

Citrus fruits, potatoes, tomatoes, green peppers, and cabbages have particularly high concentrations of vitamin C [ 51 ]. Although vitamin C deficiency is typically associated to body hair abnormalities [ 52 ], there are no data correlating vitamin C levels and hair loss.

Vitamin D is a fat-soluble vitamin synthesized in epidermal keratinocytes [ 53 ]. Vitamin D obtained from the diet or synthesis in skin is inactive and needs to be activated enzymatically.

Serum levels are primarily maintained through the UVB-mediated conversion of 7-dehydrocholesterol in the skin to cholecalciferol, which is hydroxylated in the liver and kidney to the active form of 1,dihydroxyvitamin D [1,25 OH 2D] [ 54 , 55 ]. There is strong evidence that vitamin D exerts an anti-inflammatory and immunoregulatory effect, in addition to its important role in maintaining adequate serum levels of calcium and phosphorus [ 54 , 56 ].

The mechanisms underlying the role of vitamin D in autoimmunity are not fully understood [ 54 , 55 ]. Low vitamin D levels have been reported in several autoimmune diseases [ 54 , 55 , 57 — 60 ]. Vitamin D modulates growth and differentiation of keratinocytes through binding to the nuclear vitamin D receptor VDR. Murine hair follicle keratinocytes are immunoreactive for VDR, showing their highest activity in the anagen stage [ 61 ].

The role of vitamin D in the hair follicle is evidenced by hair loss in patients with vitamin D-dependent rickets type II. These patients have mutations in the VDR gene, resulting in vitamin D resistance and sparse body hair, frequently involving the total scalp and body alopecia [ 62 — 64 ].

In addition, Forghani et al. Published data on AA suggest that vitamin D, due to its immunomodulatory effect, may be involved in AA [ 66 , 67 ]. Lee et al. These authors analyzed a total of 14 studies that involved patients with AA and control patients without AA.

Vitamin D deficiency was also highly prevalent in patients with AA, leading the authors to suggest that the vitamin D level has to be measured in patients with AA. These results also suggest that vitamin D supplements or topical vitamin D analogues should be considered for patients with AA and vitamin D deficiency. However, the meta-analysis did not find any clear correlations between extent of hair loss and serum hydroxyvitamin D level [ 68 ].

Thompson et al. The authors found that there was no significant association between dietary, supplemental, or total vitamin D intake and risk of developing AA [ 69 ]. More recently, a cross-sectional study conducted by Gade et al. The study included 45 adult patients with AA and 45 control subjects. The mean vitamin D level was found to be significantly lower in patients with AA Dorach et al.

These authors evaluated 30 subjects with AA and 30 healthy controls with a mean age of Of the 30 patients, Serum vitamin D levels negatively correlated with the severity of the disease and duration of disease; however, vitamin D did not correlate with the pattern of AA and VDR expression in tissue samples. VDR expression was reduced in all patients and was normal in controls.

Data on vitamin D in female pattern hair loss FPHL and TE contradict data derived from studies indicating that women with FPHL or TE have lower levels of vitamin D than controls, and studies showing no correlation or even opposite results [ 72 — 76 ]. Immune cells are extremely sensitive to oxidative damage. They also produce reactive oxygen species as part of the immune defense mechanism, which can induce a lipid peroxidation reaction.

Antioxidant supplementation fundamentally reverses several age-associated immune deficiencies, leading to increased numbers of total lymphocytes and T-cell subsets, elevated levels of interleukin-2, increased natural killer cell activity, enhanced antibody response to antigen stimulation, improved mitogen responsiveness, decreased prostaglandin synthesis, and decreased lipid peroxidation [ 78 ].

These studies have been reviewed, with most reviewers reporting increased levels of oxidative stress biomarkers and decreased levels of protective antioxidant enzymes in patients with AA [ 79 ].

These results were not confirmed by Naziroglu and Kokcam who found no statistical difference in plasma vitamin E levels between patients with AA and healthy controls [ 80 ]. The most common nutritional deficiency in the world is iron deficiency, which contributes to TE [ 82 , 83 ]. The serum ferritin iron-binding protein level is considered to be a good indicator of total body iron stores and is relied upon as an indicator in hair loss studies [ 84 ]. However, serum ferritin levels may be raised in patients with inflammatory, infectious, and neoplastic conditions, and in those with liver disorders.

Iron deficiency is common in women with hair loss [ 85 ]. Nevertheless, the association of hair loss and low serum ferritin level has been debated for many years. There is an ongoing discussion of whether low serum ferritin levels ought to be designated as a nutritional deficiency triggering hair loss mainly TE [ 86 ].

There is insufficient evidence on the efficacy of the replacement of iron on the outcome of TE, although some benefits have been achieved in a few controlled studies [ 95 ].

Menstruation is the biggest cause of iron deficiency in otherwise healthy premenopausal women. The lower female serum ferritin reference ranges have been questioned due to confounding by widespread iron deficiency in premenopausal females sampled when determining population reference levels [ 96 , 97 ].

The role of essential amino acids in anemia is well known, but just how amino acids affect iron uptake is the subject of ongoing research. Also, the possible impact of amino acids on hair growth has yet to be elucidated. The bioavailability of l -lysine is restricted primarily to fish, meat, and eggs. Little is known about the influence of l -lysine on iron uptake and utilization.

In one study, some of the participating women achieved a modest increase in serum ferritin level after iron supplementation, i. Trost et al.

Pierre et al. Almost all of these studies had focused on non-scarring alopecia and addressed women [ 82 , 93 ]. The authors of most studies suggested that iron deficiency may be related to TE [ 85 , 94 , 98 — ], AA [ 94 , ], and AGA [ 88 , 94 ]—but a few did not [ 86 , — ].

According to Rushton et al. Their results showed that iron deficiency is common in females, but not increased in patients with FPHL or CTE as compared with their control participants [ ]. This paper was also a source of discussion as Rushton et al.

According to Rushton and colleagues, the results of the Olsen et al. Consequently, Olsen and colleagues published a reply letter stating that the serum ferritin was performed in two different laboratories with same normal reference range. Gowda et al. Their results indicate that a relatively higher proportion of participants with TE Furthermore, transferrin saturation and ferritin levels were lower in patients with FPHL Iron deficiencies were found to be related to gender rather than to type of hair loss.

In contrast to the study of Gowda et al. This observational study involved subjects, the majority In , Thompson et al. None of these studies supported an association between AA and iron deficiency [ 27 , 44 , — ].

The subjects were investigated for hemoglobin level, total iron binding capacity, and levels of ferritin, calcium, and iron, and vitamin B12 and D3 levels. The authors of the study reported that serum calcium, serum ferritin, and vitamin D3 levels may play a role in premature graying of the hair [ ]. In , Du et al. Hepcidin is a liver-derived protein that restricts enteric iron absorption; this protein is considered the iron-regulating hormone found in all mammals and to be responsible for iron uptake.

Several proteins stimulate the expression of the gene encoding hepcidin HAMP in response to high levels of iron or infection. However, the mechanism of HAMP suppression during iron depletion is not well understood. Du et al. In mice, a mutation in TMPRSS6 was associated with failure to downregulate the expression of HAMP and was associated with increased levels of the hepcidin, reduced absorption of dietary iron, and, consequently, iron deficiency. Interestingly, iron supplementation in these mice reversed the iron deficiency and induced hair growth [ ].

The role of iron during the hair cycle has not been well studied. In , an investigative study described gene expression specific to the bulge region of the hair follicle [ ].

The genes Decorin and DCT are downregulated in the bulge region and can also be regulated by iron. The authors hypothesized that iron deficiency might change the normal progression of the hair cycle. However, whether these six genes play a role in iron-dependent processes in the hair follicle remains to be elucidated. Although not yet proven, there is a prevailing view that hepcidin upregulation diverts iron from the hair follicle to support the essential iron requirements.

Selenium is an essential trace element required for the synthesis of more than 35 proteins. Glutathione peroxidase antioxidant enzyme depends on selenium as a co-factor.

Selenium deficiency occurs in low-birth-weight infants and in patients requiring total parenteral nutrition TPN. It can also occur among people living in a location where the soil lacks selenium [ 34 ]. Venton et al. Hair started to re-pigment after 6—12 months of therapy with intravenous selenium [ ]. Similar findings, including alopecia with pseudoalbinism, were found in 6 infants receiving nutritional support.

A clinical trial in patients with ovarian cancer undergoing chemotherapy showed a significant decrease in hair loss and other gastrointestinal symptoms in patients receiving selenium supplementation, as compared with controls.

The authors concluded that ingesting selenium is a supportive element in chemotherapy [ ]. The availability of selenium in a variety of foods, such as meat, vegetables, and nuts, are sufficient to meet the daily requirement [ ]. Symptoms of acute or chronic selenium toxicity include nausea, vomiting, nail brittleness and discolorations, hair loss, fatigability, irritability, and foul breath odor [ ].

An outbreak of selenium toxicity from a liquid dietary supplement that contained fold the labeled concentration of selenium resulted in severe hair loss in most patients [ ]. Zinc is an essential trace element, which means that the body cannot generate it on its own; it must be supplied through the diet.

The main dietary sources of zinc are fish and meat. Zinc deficiency can occur in patients consuming large amounts of cereal grain which contains a phytate considered to be chelating agent of zinc , in those with poor meat consumption or TPN, and in infants on milk formula. Other causes of zinc deficiency include anorexia nervosa secondary to inadequate intake, increased zinc excretion, and malabsorption due to laxative abuse , inflammatory bowel disease, jejunal bypass surgery, and cystic fibrosis.

Alcoholism, malignancy, burns, infection, and pregnancy may all cause increased metabolism and excretion of zinc. Alopecia is a well-known sign of established zinc deficiency with hair regrowth occurring with zinc supplementation [ ], [ ]. A retrospective cross-sectional study of subjects diagnosed with TE acute and chronic found that 9.

However, this finding was not confirmed by a recent study of 40 patients with CTE, with 30 healthy subjects as controls, with the authors finding no difference in zinc levels between the affected and control patients. A review article on zinc in patients with AA showed that four of the six case—control studies found low zinc levels in patients with AA as compared to healthy control groups [ 55 ].

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