What is the disease of having excess body hair called?
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Hirsutism is the excessive growth of hair, particularly on a woman's face, torso and limbs, and is generally caused by increased androgens. It is a common sign of polycystic ovary syndrome in women. It can also be caused by a pituitary tumour or other serious medical conditions. \n\nOne method of evaluating hirsutism is the Ferriman-Gallwey score which gives a score based on the amount and location of hair growth on a woman. \n\nMany people with unwanted hair seek methods of hair removal to control the appearance of hirsutism. \n\nFor men to be diagnosed with hirsutism, the amount of hair has to be exceptionally large. Often, such men (and rarer, also women) are known as "wolf people". Fedor Jeftichew suffered from the condition, as did his father, Adrian. \n\nHypertrichosis, a genetic condition that results in unusually thick body hair.
666792
Nearly all the skin of the human body except palms of hands and soles of feet is covered with hairs. The density of the hairs (in hair follicles per square centimeter) thickness of the hairs, color of the hairs, speed of hair growth, and qualities such as kinkiness, vary from one part of the body to another, and from one person to another. All of these features have strong genetic determinants, as demonstrated by the heritability of these qualities.\n\nDoctors generally distinguish scalp hair, vellus hair, and androgenic (terminal) hair. \n\nVellus hair is the hair on the rest of the body which has not been stimulated and transformed by sex hormones. Androgenic hair is the hair that greatly increases in heaviness and rate of growth with puberty.
486444
Men have more male hormones near the genitals that tend to stimulate hair growth thus we have more hair there
107940
<Folliculitis, is inflammation of one or more hair follicles. The condition may occur anywhere on the skin.\nCauses\nFolliculitis starts when hair follicles are damaged by friction from clothing, blockage of the follicle, or shaving. In most cases of folliculitis, the damaged follicles are then infected with the bacteria Staphylococcus (staph).\nBarber's itch is a staph infection of the hair follicles in the bearded area of the face, usually the upper lip. Shaving aggravates the condition. Tinea barbae is similar to barber's itch, but the infection is caused by a fungus.\n\nPseudofolliculitis barbae is a disorder occurring primarily in men of African extraction. If curly beard hairs are cut too short, they may curve back into the skin and cause inflammation.\n\nSymptoms\nrash (reddened skin area) \npimples or pustules located around a hair follicle \nmay crust over \ntypically occur on neck axilla, or groin area \nmay present as genital lesions \nitching skin \nTreatment\n\n1. Topical antiseptic treatment is adequate for most cases 2. Some patients may benefit from systemic flucloxacillin 3. Topical antibiotics such as mupirocin ointment
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Go laser, espically if you are of certian eastern europian origin which are prone to excessive body hair.  Mediterranian ladies have this problem as well.\n\nIt is nothing to be ashamed of.  Now breast hair.. that's not so fun.  You have to pluck that stuff (knows from experience)
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BooooooYaaaaaaaah\n\nThis is a normal thing... Why do you have flakes after you got a haircut? It is bcoz your hair is adjusting...\n\nIt caused by testosterone. Testosterone is the most biologically active male hormone, produced primarily in the testicles as well as in the adrenal glands. Testosterone is responsible for male secondary sexual characteristics such as voice and beard. Testosterone masculinizes the brain in male fetuses and plays a major role in the sexual desire and drive of both sexes.\n\nFrom menshealth:\nThe Cause of Male Pattern Baldness\nMost men are genetically predisposed to male pattern baldness. It is the effect of hormones on the hair follicle that produces male pattern baldness. Testosterone, a hormone that is present in high levels in males after puberty, is converted to dihydrotestosterone (DHT) by an enzyme called 5-alpha reductase. DHT has an adverse affect on the hair follicles. Acting on a hormone receptor on the hair follicle it slows down hair production and produces weak, shorter hair, sometimes it stops hair growth from the follicle completely. This process gradually depletes your stock of hair and is normal hair loss.\n\nThat article may help you...
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I noticed a drastic increase in pubic hair on my wife after 2 kids.  The spread increased.  I think it was the hormones and body changes form both childbearing and age she is 29 now.
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Actually, your hair keeps growing throughout your life (excluding the upper scalp hair on some men). It's just that the hair folicles each have a programed length to which the hair shaft will grow. When the shaft reaches that length, it falls out and a new one starts to grow. Obviously, for some folicles, this programed length is longer than it is for others. That is why body hair is usually shorter than head hair. This is also why it is silly for a man to start worrying about going bald just because he sees some hairs in his brush. We are all constantly shedding hairs that have reached their maximum length. So, seeing a few hairs come off is normal. You only need to worry about it if you see an actual thinning of the hair.
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Body hair is governed by your genes. There are things you can do to remove it, or to lighten it, but you cannot do anything about its growth rate. There are some products out in the market that is suppose to retard hair growth, but I don't know how effective they are.
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Pubic hair. That technically means anything below the head. My anckle hairs are very curly, and so are my armpit hairs.\n\nA specific country is unlikely. As said, predominance, but thise does not mean *everyone* has curly hair.
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Background\n\nThis is a chronic and relapsing condition occurring within apocrine sweat glands, most commonly in women. Deep seated inflammatory nodules form in the axilla, groin, pubic region, and perineum. It is an androgen-dependent disorder and results from keratinous material occluding the sweat pores. There is an association with lithium therapy and Crohn's disease.\n\nEtiology\n\nHS often occurs in multiple members within families, suggesting a genetic predisposition (5). Various etiological agents have been associated. The increased incidence of HS in obese women with acne led to the theory of HS being associated with an hyperandrogenic endocrine disorder (6,7). One study did not find evidence for biochemical hyperandrogenism in women affected with HS (8). Thus, the role of androgens in HS is still not clear. Smoking (9), lithium (10) and oral contraceptives (11) may also be associated with HS, possibly as triggering factors. Nonetheless, the etiology of the disease is unknown. \n\nFrequency\n\nIn the US: In the United States, the prevalence of HS appears to be 1-2% in the general population. \n\nInternationally: The prevalence of HS appears to be 1% of the general population; it was 4% in a group of young adults who were treated at a clinic for sexually transmitted diseases. HS is probably more common than once thought, but the diagnosis is frequently ignored or missed. HS has a worldwide distribution, though hot, humid environments tend to support its development. \n\nMortality/Morbidity\n\nThe death rate is similar to that in the general adult population. \n\nAlthough rare complications of the disease are described, little is known about the typical effects of HS. HS is a chronic disabling disorder that relentlessly progresses and leads to keloids, contractures, and immobility; patients can become outcasts or at least have difficulty in making social contact. \n\nPathogenesis \n\nHistorically, apocrinitis was believed to be the defining histologic feature and pathogenetic mechanism of HS (12,13). Characteristic lobular abscesses in the apocrine gland, demonstrated histologically, seemed to further implicate apocrine gland involvement in the manifestation of disease (12-14). Recently, histological evidence points to HS being a follicular disease (1,15-19). Histological examination in the majority of specimens reveals follicular involvement, including poral occlusion and folliculitis (1). Apocrinitis as the dominant histological feature is found in only a small number of specimens (1,17). Furthermore, a paucity of apocrine glands was demonstrated in the genitofemoral region, one area commonly affected by HS (1). This finding supports the theory that apocrine gland inflammation is not the etiological and pathogenetic mechanism of HS, but rather a secondary manifestation of follicular involvement (1). \n\nClinical Features \n\nHS may arise singularly or multifocally in the genitofemoral, perianal and axillary areas (1-4). The lesions are painful and have a foul odor attributed to bacterial colonization. Erythematous dermal abscesses form that measure up to 2 cm in diameter. Untreated abscesses will gradually increase in size and may drain to the surface. The course of HS is chronic and remitting, with new abscesses arising in previously unaffected areas or in regions of past involvement. Scarring, fibrosis and sinus tract formations are manifestations of late disease. Strictures can occur secondary to sinus tracts; fistulas may also complicate HS. Squamous cell carcinoma is a rare sequella of longstanding HS (20-24). These cancers may be locally aggressive with distant metastases and a high mortality rate (25). \n\nRace/Sex/Age\n\nRace: Although many authors report no racial predilection, an increased incidence is observed in blacks, possibly because blacks have a greater density of apocrine glands compared with whites. \n\nSex: Although HS is widely considered to occur more frequently in females than in males, with
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Had to look it up at Wikipedia cuz I think I know what you are talking of:  body dysmorphic disorder.   Many people suffer from it.  Famous example is Michael Jackson, he underwent surgery on his nose, facial features, cuz he thought he didn't look good.  \n\nHave you talked about this with anyone?  PLEASE do so, if you have not.  Such thoughts can breed and grow into something even worse like bulimia, aneorexia nervosa, which can lead to death if left untreated.  :-((
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There is a term for that - some people yank all their hair out.  Kinda like a compulsive habit.  It is called trichotillomania.  Hypnosis or therapy should help.\n\nhttp://groups.msn.com/HairpullingSufferers
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Causes of Excessive Hair Loss\n\nThe rate of hair shedding in androgenic alopecia is speeded up by three forces: advancing age, an inherited tendency to bald early, and an over-abundance of the male hormone dihydrotestosterone (DHT) within the hair follicle. DHT is a highly active form of testosterone, which influences many aspects of manly behavior, from sex drive to aggression. \n\nThe conversion from testosterone to DHT is driven by an enzyme called 5-alpha reductase, which is produced in the prostate, various adrenal glands, and the scalp. Over time, the action of DHT causes the hair follicle to degrade and shortens the anagen phase. Thought the follicle is technically still alive and connected to a good blood supply--it can successfully nurture a transplanted follicle which is immune to the effects of DHT--it will grow smaller and smaller (figure 3). Some follicles will gradually die, but most will simply shrink to the size they were when you were born which produce weaker hairs. With a steadily shorter anagen growing cycle, more hairs are shed, the hairs becoming thinner and thinner until they are too fine to survive daily wear and tear. Balding hair gradually changes from long, thick, coarse, pigmented hair into fine, unpigmented vellus sprouts. \n\nHowever, the sebaceous gland attached to it remains the same size. As the hair shafts become smaller, the gland continues to pump out about the same amount of oil. So as your hair thins, you will notice that your hair becomes flatter and oilier. \n\nBut the hormonal link in balding is complex. Eunuchs, who produce no testosterone, never go bald -- even if carrying a baldness gene. However, if castrated men with a family history of baldness are given testosterone, they lose hair in the classic horseshoe-shaped pattern. \n\nStudies show that while balding men don't have higher than average circulating testosterone levels, they do possess above-average amounts of a powerful testosterone derivative, dihydrotestosterone in the scalp follicles. In male balding, genetically primed follicles convert circulating testosterone to dihydrotestosterone, which successively diminishes or miniaturizes follicle size, producing ever weaker hairs. With a steadily shorter anagen growing cycle, more hairs are shed, the hairs becoming thinner and thinner until they are too fine to survive daily wear and tear. Balding hair gradually changes from long, thick, coarse, pigmented hair into fine, depigmented vellus sprouts. \n\nOther physiological factors might cause hair loss. Recently, a group of Japanese researcher reported a correlation between excessive sebum in the scalp and hair loss. Excessive sebum often accompanying thinning hair is attributed to an enlargement of the sebaceous gland. They believed excessive sebum causes an high level of 5-alpha reductase and pore clogging, thus malnutrition of the hair root. \n\nAlthough this condition could be hereditary, they believe diet is a more prominent cause. The researchers note that Japanese hair was thick and healthy, with a small gland and little scalp oil, until the occidental habit of consuming animal fat crept into their diet after World War II. This change has led to a significant height increase in the Japanese population, but it has also resulted in more Japanese men losing hair. To some extent, their observation makes sense since problems with greasy hair have often been noted as much as six months to a year prior to when thinning hair becomes noticeable, but this might be just one of the symptoms, not underlying cause, more research is needed. Most doctors agree that if you have a oily scalp with thinning hair, frequent shampooing is advised. shampooing can reduce surface sebum, which contains high levels of testosterone and DHT that may reenter the skin and affect the hair follicle.
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Trichotillomania is hair loss caused by compulsive pulling and/or twisting of the hair until it breaks off. The hair may be lost in round patches or diffusely across the scalp. The effect is an uneven appearance. \n\nTrichotillomania is a type of compulsive behavior and its causes are not clearly understood. Symptoms usually begin before the age of 17. People with this disorder will often seek the help of a dermatologist initially. Women are 4 times more likely to be affected than men.\n\nThese symptoms are usually seen in children:\n\n1. constant tugging, pulling, or twisting of hair \nincreasing sense of tension is present before \nthe hair pulling. \n2. sense of relief, pleasure, or gratification is reported after the hair pulling. \n3. hair pulling leads to an uneven appearance \nbare patches or diffuse loss of hair.\n4. hair regrowth in the bare spots that feels like stubble \n5. some individuals may develop a bowel obstruction if they eat the hair they pull out. \n6. other self-injury behaviors may be present.\n7. people suffering from this disorder often deny pulling out their hair.\n\nI dont know it this is what he has but it seems possible see #5 above.  Did it appear that he was missing patches of hair?  It may also be a nervous disorder.  Hope this helps.
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I got crap from people in high school (in the locker room before and after P.E.) for not having hairy arms.  With me, it just took time.  I'm almost 30 now and still have hair popping up in new places.  Just relax about it, because you can't control it.
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congenital generalized hypertrichosis. Makes people look like a ware wolf.