HAIR-AN syndrome as discussed earlier is caused by both gentic and environmental factors. It is found out that women affected by this syndrome or PCOS (polycystic ovary syndrome) are generally accompanied by obesity. Weight loss is most suggested way to combat this syndrome and is helpful for reducing insulin resistance of the body. It is also a good way to have a control on diet. This might help the body to refunction properly and show some resistance to HAIR-AN syndrome. "Suppression of gonadotropin with estrogen-progesterone oral contraceptives" or can say as reducing hyperandrogenism by the use of estoprogestatif can reduce production of androgen by ovaries by cutting down the LH (leutinizing hormone) level in body. Even their sex hormone binding to globulin increase is also responsible for decreasing body's bio-availability of testosterone. There are also few pills of new progestins, such as desogestrel and norgestimate. This pills appear to have fewer androgenic side effects and may be safer to use in persons with abnormal lipid levels or hirsutism. Some antiandrogenic agents can be also used alone or combining it with other oral pills.

"Spironolactone inhibit the actions of testosterone by binding to its receptors." The standard dose for its use is considered to be 50 to 100 mg twice a day. This might lead to irregular menstrual bleeding, which can be improved by oral contraceptives. Flutamide, an another antiandorgen that is used to treat HAIR-AN syndrome, but it has risk of hepatotoxicity. Finasteride is a 5α-reductase inhibitor which can reduces the conversion of testosterone to dihydrotestosterone. It is useful in the treatment of hirsutism with a dosages as low as 5 mg per day.

Insulin-resistant patients can also be treated with metformin which has shown promising results to reduce the insulin resistivity. Metformin improves peripheral tissue sensitivity to insulin but inhibits hepatic glucose formation. The drug reduces the levels of circulating insulin and androgens. Women have shown improved reproductive functioning after the use of metformin.

A 2017 review concluded that while both myo-inositol and D-chiro-inositols may regulate menstrual cycles and improve ovulation, there is a lack of evidence regarding effects on the probability of pregnancy. A 2012 and 2017 review have found myo-inositol supplementation appears to be effective in improving several of the hormonal disturbances of PCOS. A 2011 review found not enough evidence to conclude any beneficial effect from D-chiro-inositol. There is insufficient evidence to support the use of acupuncture.

When appropriate (e.g., in women of child-bearing age who require contraception), a standard contraceptive pill is frequently effective in reducing hirsutism. Progestogens such as norgestrel and levonorgestrel should be avoided due to their androgenic effects.

Other drugs with anti-androgen effects include flutamide, and spironolactone, which can give some improvement in hirsutism. Metformin can reduce hirsutism, perhaps by reducing insulin resistance, and is often used if there are other features such as insulin resistance, diabetes, or obesity that should also benefit from metformin. Eflornithine (Vaniqa) is a drug that is applied to the skin in cream form, and acts directly on the hair follicles to inhibit hair growth. It is usually applied to the face. 5-alpha reductase inhibitors (such as finasteride and dutasteride) may also be used; they work by blocking the conversion of testosterone to dihydrotestosterone (the latter of which responsible for most hair growth alterations and androgenic acne).

Although these agents have shown significant efficacy in clinical trials (for oral contraceptives, in 60–100% of individuals), the reduction in hair growth may not be enough to eliminate the social embarrassment of hirsutism, or the inconvenience of plucking or shaving. Individuals vary in their response to different therapies. It is usually worth trying other drug treatments if one does not work, but drug treatments do not work well for all individuals.

Treatment of hyperandrogenism varies with the underlying condition that causes it. As a hormonal symptom of polycystic ovary syndrome, menopause, and other endocrine disorders, it is primarily treated as a symptom of these disorders. Systemically, it is treated with antiandrogens such as cyproterone acetate, flutamide and spironolactone to control the androgen levels in the patient's body. For Hyperandrogenism caused by Late-Onset Congenital Adrenal Hyperplasia (CAH), treatment is primarily focused on providing the patient with Glucocorticoids to combat the low cortisol production and the corresponding increase in androgens caused by the swelling of the Adrenal Glands. Oestrogen-based oral contraceptives are used to treat both CAH and PCOS caused hyperandrogenism. These hormonal treatments have been found to reduce the androgen excess and suppress adrenal androgen production and cause a significant decrease in hirsutism.

Hyperandrogenism is often managed symptomatically. Hirsutism and acne both respond well to the hormonal treatments described above, with 60-100% reporting an improvement in hirsutism. Androgenic alopecia however, does not show a significant improvement with hormonal treatments and requires other treatments, such as hair transplantation.

Medications consist mostly of antiandrogens, drugs that block the effects of androgens like testosterone and dihydrotestosterone (DHT) in the body, and include:

- Spironolactone: An antimineralocorticoid with additional antiandrogenic activity at high dosages

- Cyproterone acetate: A dual antiandrogen and progestogen. In addition to single form, it is also available in some formulations of combined oral contraceptives at a low dosage (see below). It has a risk of liver damage.

- Flutamide: A pure antiandrogen. It has been found to possess equivalent or greater effectiveness than spironolactone, cyproterone acetate, and finasteride in the treatment of hirsutism. However, it has a high risk of liver damage and hence is no longer recommended as a first- or second-line treatment.

- Bicalutamide: A pure antiandrogen. It is effective similarly to flutamide but is much safer as well as better-tolerated.

- Birth control pills: Consist of an estrogen, usually ethinylestradiol, and a progestin. They are thought to work by 1) stimulating production of sex hormone-binding globulin in the liver, which decreases free concentrations of testosterone in the blood; and by 2) suppressing luteinizing hormone (LH) secretion from the pituitary gland, which decreases production of testosterone by the gonads. Hence, they are functional antiandrogens. In addition, certain birth control pills contain a progestin that also has antiandrogenic activity. Examples include birth control pills containing cyproterone acetate, chlormadinone acetate, drospirenone, and dienogest.

- Finasteride and dutasteride: 5α-Reductase inhibitors. They inhibit the production of the potent androgen DHT.

- GnRH analogues: Suppress androgen production by the gonads and reduce androgen concentrations to castrate levels.

- Metformin: Antihyperglycemic drug used for diabetes mellitus. However, it is also effective in treatment of hirsutism associated with insulin resistance (e.g. polycystic ovary syndrome)

- Eflornithine: Blocks putrescine that is necessary for the growth of hair follicles

In cases of hyperandrogenism specifically due to congenital adrenal hyperplasia, administration of glucocorticoids will return androgen levels to normal.

One possible treatment is with anastrozole. Histrelin acetate (Supprelin LA), triptorelin or leuprolide, any GnRH agonists, may be used. Non-continuous usage of GnRH agonists stimulates the pituitary gland to release follicle stimulating hormone (FSH) and luteinizing hormone (LH). However, when used regularly, GnRH agonists cause a decreased release of FSH and LH. Prolonged use has a risk of causing osteoporosis. After stopping GnRH agonists, pubertal changes resume within 3 to 12 months.

Treatment may consist of hormone replacement therapy with androgens in either sex. Alternatively, gonadotropin-releasing hormone (GnRH)/GnRH agonists or gonadotropins may be given (in the case of "hypogonadotropic" hypoandrogenism). The Food and Drug Administration (FDA) stated in 2015 that neither the benefits nor the safety of testosterone have been established for low testosterone levels due to aging. The FDA has required that testosterone pharmaceutical labels include warning information about the possibility of an increased risk of heart attacks and stroke.

Since risk factors are not known and vary among individuals with hyperandrogegism, there is no sure method to prevent this medical condition. Therefore, more longterm studies are needed first to find a cause for the condition before being able to find a sufficient method of prevention.

However, there are a few things that can help avoid long-term medical issues related to hyperandrogenism like PCOS. Getting checked by a medical professional for hyperandrogenism; especially if one has a family history of the condition, irregular periods, or diabetes; can be beneficial. Watching your weight and diet is also important in decreasing your chances, especially in obese females, since continued exercise and maintaining a healthy diet leads to an improved menstrual cycle as well as to decreased insulin levels and androgen concentrations.

Many women with unwanted hair seek methods of hair removal. However, the causes of the hair growth should be evaluated by a physician, who can conduct blood tests, pinpoint the specific origin of the abnormal hair growth, and advise on the treatment.

There is no cure for any congenital forms of hypertrichosis. The treatment for acquired hypertrichosis is based on attempting to address the underlying cause. Acquired forms of hypertrichosis have a variety of sources, and are usually treated by removing the factor causing hypertrichosis, e.g. a medication with undesired side-effects. All hypertrichosis, congenital or acquired, can be reduced through hair removal. Hair removal treatments are categorized into two principal subdivisions: temporary removal and permanent removal. Treatment may have adverse effects by causing scarring, dermatitis, or hypersensitivity.

Temporary hair removal may last from several hours to several weeks, depending on the method used. These procedures are purely cosmetic. Depilation methods, such as trimming, shaving, and depilatories, remove hair to the level of the skin and produce results that last several hours to several days. Epilation methods, such as plucking, electrology, waxing, sugaring, threading remove the entire hair from the root, the results lasting several days to several weeks.

Permanent hair removal uses chemicals, energy of various types, or a combination to target the cells that cause hair growth. Laser hair removal is an effective method of hair removal on hairs that have color. Laser cannot treat white hair. The laser targets the melanin color in the lower 1/3 of the hair follicle, which is the target zone. Electrolysis (electrology) uses electrical current, and/or localized heating. The U.S. Food and Drug Administration (FDA) allows only electrology to use the term "permanent hair removal" because it has been shown to be able treat all colors of hair.

Medication to reduce production of hair is currently under testing. One medicinal option suppresses testosterone by increasing the sex hormone-binding globulin. Another controls the overproduction of hair through the regulation of a luteinizing hormone.

HAIR-AN syndrome consists of hyperandrogenism (HA), insulin resistance (IR), and acanthosis nigricans (AN). It is a rare disease which is a subset of poly-cystic ovary syndrome [PCOS]. Polycystic ovary syndrome is basically a condition in females which is arise by an increase in the production of androgen (male hormone), leading to an expression of male-like characters in the female body. The name HAIR-AN syndrome is made up of the three conditions of which it consists. The commonly used term "HAIR-AN" is a generic description of the features of SIR (severe insulin resistance)." In particular, although HAIR-AN results from two very different types of abnormalities - blocking antibodies against the insulin receptor OR genetically absent/reduced insulin receptor number/function - patients with "both" types have high levels of androgens (male hormones).

Research on the two types of HAIR-AN demonstrated that patients with both forms of HAIR-AN had very high levels of insulin and, critically, that it was the high insulin that caused the elevation in androgen. The patient affected by HAIR-AN syndrome has insulin resistance inside his or her body. Insulin resistance is a condition in which the body produces insulin but does not use it properly. This causes the pancreas to produce more insulin in the body. High levels of insulin stimulate the ovaries to make excess of androgen, leading to excessive hair growth, acne, and irregular periods in females body. Insulin resistance can also lead to diabetes, heart disease, and excessive growth and darkening of the skin (acanthosis nigricans)

Several medications can cause generalized or localized acquired hypertrichosis including:

Anticonvulsants: phenytoin

Immunosuppressants: cyclosporine

Vasodilators: diazoxide and minoxidil

Antibiotics: streptomycin

Diuretics: acetazolamide

Photosensitizes: Psoralen.

The acquired hypertrichosis is usually reversible once these medications are discontinued.

Treatments for the various forms of hair loss have limited success. Three medications have evidence to support their use in male pattern hair loss: minoxidil, finasteride, and dutasteride. They typically work better to prevent further hair loss, than to regrow lost hair.

- Minoxidil (Rogaine) is a nonprescription medication approved for male pattern baldness and alopecia areata. In a liquid or foam, it is rubbed into the scalp twice a day. Some people have an allergic reaction to the propylene glycol in the minoxidil solution and a minoxidil foam was developed without propylene glycol. Not all users will regrow hair. The longer the hair has stopped growing, the less likely minoxidil will regrow hair. Minoxidil is not effective for other causes of hair loss. Hair regrowth can take 1 to 6 months to begin. Treatment must be continued indefinitely. If the treatment is stopped, hair loss resumes. Any regrown hair and any hair susceptible to being lost, while Minoxidil was used, will be lost. Most frequent side effects are mild scalp irritation, allergic contact dermatitis, and unwanted hair in other parts of the body.

- Finasteride (Propecia) is used in male-pattern hair loss in a pill form, taken 1 milligram per day. It is not indicated for women and is not recommended in pregnant women. Treatment is effective starting within 6 weeks of treatment. Finasteride causes an increase in hair retention, the weight of hair, and some increase in regrowth. Side effects in about 2% of males, include decreased sex drive, erectile dysfunction, and ejaculatory dysfunction. Treatment should be continued as long as positive results occur. Once treatment is stopped, hair loss resumes.

- Corticosteroids injections into the scalp can be used to treat alopecia areata. This type of treatment is repeated on a monthly basis. Oral pills for extensive hair loss may be used for alopecia areata. Results may take up to a month to be seen.

- Immunosuppressants applied to the scalp have been shown to temporarily reverse alopecia areata, though the side effects of some of these drugs make such therapy questionable.

- There is some tentative evidence that anthralin may be useful for treating alopecia areata.

- Hormonal modulators (oral contraceptives or antiandrogens such as spironolactone and flutamide) can be used for female-pattern hair loss associated with hyperandrogenemia.

There is currently no cure for GAPO syndrome, but some options are available to reduce the symptoms. Nearsightedness, which affects some sufferers of the disease, can be treated by corrective lenses. Unfortunately, optic atrophy as a result of degradation of the optic nerve (common with GAPO syndrome) cannot be corrected. Corticosteroids have been proposed as a treatment for optic nerve atrophy, but their effectiveness is disputed, and no steroid based treatments are currently available.

Dietary supplements are not typically recommended. There is only one small trial of saw palmetto which shows tentative benefit in those with mild to moderate androgenetic alopecia. There is no evidence for biotin. Evidence for most other produces is also insufficient. There was no good evidence for gingko, aloe vera, ginseng, bergamot, hibiscus, or sorphora as of 2011.

Many people use unproven treatments. Egg oil, in Indian, Japanese, Unani (Roghan Baiza Murgh) and Chinese traditional medicine, was traditionally used as a treatment for hair loss.

Androgen deficiency is not usually checked for diagnosis in healthy women.

Treatments for CCCA remain investigational. Altering hair care practices has not been proven to assist in hair rejuvenation. High-dose topical steroids, antibiotics, immunomodulators such as tacrolimus (Protopic) and pimecrolimus (Elidel), and anti-androgen/5alpha Reductase inhibitors have been used with unknown efficacy.

There is no known cure at the moment but there are several things that can be done to relieve the symptoms. Moisturising products are very helpful to minimize the scaling/cracking, and anti-infective treatments are useful when appropriate because the skin is very susceptible to infection. Extra protein in the diet during childhood is also beneficial, to replace that which is lost through the previously mentioned "leaky" skin.

Steroid and retinoid products have been proven ineffective against Netherton syndrome, and may in fact make things worse for the affected individual.

Intravenous immunoglobulin has become established as the treatment of choice in Netherton's syndrome. This therapy reduces infection; enables improvement and even resolution of the skin and hair abnormalities, and dramatically improves quality of life of the patients; although exactly how it achieves this is not known. Given this; it is possible that the reason Netherton's usually is not very severe at or shortly after birth is due to a protective effect of maternal antibodies; which cross the placenta but wane by four to six months.

Improving environmental factors will reduce damage to the hair. Gentle brushing with a soft brush should replace more aggressive brushing, ratting, or other procedures. Harsh chemicals such as hair straightening compounds and permanents should be avoided. The hair should not be ironed. Excessively harsh shampoo should be avoided. Hair conditioners should be used.

Early puberty is believed to put girls at higher risk of sexual abuse, unrelated to pedophilia because the child has developed secondary sex characteristics; however, a causal relationship is, as yet, inconclusive. Early puberty also puts girls at a higher risk for teasing or bullying, mental health disorders and short stature as adults. Helping children control their weight is suggested to help delay puberty. Early puberty additionally puts girls at a "far greater" risk for breast cancer later in life. Girls as young as 8 are increasingly starting to menstruate, develop breasts and grow pubic and underarm hair; these "biological milestones" typically occurred only at 13 or older in the past. African-American girls are especially prone to early puberty. There are theories debating the trend of early puberty, but the exact causes are not known.

Though boys face fewer problems upon early puberty than girls, early puberty is not always positive for boys; early sexual maturation in boys can be accompanied by increased aggressiveness due to the surge of hormones that affect them. Because they appear older than their peers, pubescent boys may face increased social pressure to conform to adult norms; society may view them as more emotionally advanced, although their cognitive and social development may lag behind their appearance. Studies have shown that early maturing boys are more likely to be sexually active and are more likely to participate in risky behaviours.

No specific treatment or cure exists. Affected children usually need total parenteral nutrition through a central venous catheter. Further worsening of liver damage should however be avoided if possible. Diarrhea will likely continue even though food stops passing through the gastrointestinal system. They can subsequently be managed with tube feeding, and some may be weaned from nutritional support during adolescence.

Avoid aggressive brushing and grooming, strong chemicals, permanents, straightening, and similar hair-damaging habits.

Crandall syndrome is a very rare congenital disorder characterised by progressive sensorineural hearing loss, hair loss associated with pili torti, and hypogonadism demonstrated through low levels of luteinising hormone and growth hormone. It is thought to be an autosomal recessive disorder closely related to Björnstad syndrome which presents similarly but without hypogonadism.

The condition was first reported by B. F. Crandall in 1973.

A cure for Werner syndrome has not yet been discovered. It is often treated by managing the associated diseases and relieving symptoms to improve quality of life. The skin ulcers that accompany WS can be treated in several ways, depending on the severity. Topical treatments can be used for minor ulcers, but are not effective in preventing new ulcers from occurring. In the most severe cases, surgery may be required to implant a skin graft or amputate a limb if necessary. Diseases commonly associated with Werner Syndrome such as diabetes and cancer are treated in generally the same ways as they would be for a non-Werner Syndrome individual. A change in diet & exercise can help prevent and control arteriosclerosis, and regular cancer screenings can allow for early detection of cancer.

There is recent evidence that suggests that the cytokine-suppressive anti-inflammatory drug, SB203580, may be a possible therapeutic option for patients with Werner's Syndrome. This drug targets the p38 signaling pathway, which may become activated as a result of genomic instability and stalled replication forks that are characteristic mutations in WS. This activation of p38 may play a role in the onset of premature cell aging, skin aging, cataracts, and graying of the hair. The p38 pathway has also been implicated in the anti-inflammatory response that causes atherosclerosis, diabetes, and osteoporosis, all of which are associated with Werner's Syndrome. This drug has shown to revert the aged characteristics of young WS cells to those seen in normal, young cells and improve the lifespan of WS cells "in vitro". SB203580 is still in the clinical trial stages, and the same results have not yet been seen "in vivo".

In 2010, vitamin C supplementation was found to reverse the premature aging and several tissue dysfunctions in a genetically modified mouse model of the disease. Vitamin C supplementation also appeared to normalize several age-related molecular markers such as the increased levels of the transcription factor NF-κB. In addition, it decreases activity of genes activated in human Werner syndrome and increases gene activity involved in tissue repair. Supplementation of vitamin C is suspected to be beneficial in the treatment of human Werner syndrome, although there was no evidence of anti-aging activity in nonmutant mice. In general, treatments are available for only the symptoms or complications and not for the disease itself.

The United States Food and Drug Administration (FDA) has not approved any medications for trichotillomania treatment.

Medications can be used to treat trichotillomania. Treatment with clomipramine, a tricyclic antidepressant, was shown in a small double-blind study to improve symptoms, but results of other studies on clomipramine for treating trichotillomania have been inconsistent. Naltrexone may be a viable treatment. Fluoxetine and other selective serotonin reuptake inhibitors (SSRIs) have limited usefulness in treating trichotillomania, and can often have significant side effects. Behavioral therapy has proven more effective when compared to fluoxetine or control groups. There is little research on the effectiveness of both behavioral therapy together with medication, and robust evidence from high-quality studies is lacking. Acetylcysteine treatment stemmed from an understanding of glutamate's role in regulation of impulse control.

Many medications, depending on individuality, may increase hair pulling.