α-Lipoic acid (ALA) has been shown to be protective against acute mercury poisoning in several mammalian species when it is given soon after exposure; correct dosage is required, as inappropriate dosages increase toxicity. Although it has been hypothesized that frequent low dosages of ALA may have potential as a mercury chelator, studies in rats have been contradictory. Glutathione and N-acetylcysteine (NAC) are recommended by some physicians, but have been shown to increase mercury concentrations in the kidneys and the brain.Chelation therapy can be hazardous if administered incorrectly. In August 2005, an incorrect form of EDTA (edetate disodium) used for chelation therapy resulted in hypocalcemia, causing cardiac arrest that killed a five-year-old autistic boy. Other
Experimental animal and epidemiological study findings have confirmed the interaction between selenium and methylmercury. Instead of causing a decline in neurodevelopmental outcomes, epidemiological studies have found that improved nutrient (i.e., omega-3 fatty acids, selenium, iodine, vitamin D) intakes as a result of ocean fish consumption during pregnancy improves maternal and fetal outcomes. For example, increased ocean fish consumption during pregnancy was associated with 4-6 point increases in child IQs. Prognosis
Some of the toxic effects of mercury are partially or wholly reversible provided specific therapy is able to restore selenium availability to normal before tissue damage from oxidation becomes too extensive. Autopsy findings point to a half-life of inorganic mercury in human brains of 27.4 years. Heavy or prolonged exposure can do irreversible damage, in particular in fetuses, infants, and young children.
Hair loss may be present in the family, highlighting genetic causes. Causes
Causes of noncicatricial alopecia can be separated based on focal or diffuse hair loss:Diffuse:

Androgenetic alopecia: androgenic DHT leads to catagenic miniaturization of hair follicles. Diffuse alopecia areata: diffuse autoimmune destruction of hair follicles
Alopecia totalis: unknown but thought to be autoimmune
Telogen effluvium: emotional or physiologic stress
Anagen effluvium: cancer treatments such as radiation and alkylating agents
Dermatopathia pigmentosa reticularis: genetic autosomal dominant conditionFocal:

Alopecia areata: autoimmune destruction of hair follicles
Tinea capitis: fungal infection
Traction alopecia: pulling force applied to hair
Trichotillomania (Trichotillosis)

Diagnosis
There are a number of conditions that may cause non scarring hair loss and the first step is to determine the pattern: focal or diffuse. The next step is to identify if the hair loss is scarring or non scarring. A history and physical examination is necessary as this will provide clues to the ultimate diagnosis. It is essential to ask about the onset, observed pattern, hairstyles, family history, diet, and social history.Diffuse:

Androgenetic alopecia: history of gradual thinning of hair and characteristic pattern. Males start to lose hair in the front and temples while females lose hair at the top of the head
Diffuse alopecia areata: exclamation point hairs
Alopecia totalis: concomitant loss of facial and skull hair
Telogen effluvium: history of emotional or physiologic stress
Anagen effluvium: history cancer treatments such as radiation and alkylating agents
Dermatopathia pigmentosa reticularis: genetic autosomal dominant conditionFocal:

Alopecia areata: smooth and round lesions
Tinea capitis: black dots with broken hair strands, may see red, scaly lesions and swollen lymph nodes on the back of head.