Question

[meritflyer]

This may be not aviation related so I am sorry if it comes off as quirky..

But, what can a guy do to prevent (not restore) baldness from a doc's perspective?

I've heard multi-vitamins and other stuff so I thought I'd ask a RD..

 

[My Flight Surgeon]

There is NO prevention

Here is a link to an article on baldness http://www.medscape.com/viewarticle/410576
I hope it works since it came from a secure website,

 

[My Flight Surgeon]

Sorry, the link dodn't work Here is the article.



www.medscape.com

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http://www.medscape.com/viewarticle/410576
Male Pattern Baldness

Daniel J. Hogan, MD, Matthew Chamberlain, MD, Section of Dermatology, Louisiana State University School of Medicine, Shreveport. South Med J 93(7):657-662, 2000. © 2000 Southern Medical Association

Abstract and Introduction

Abstract

Background. Male pattern baldness, or androgenetic alopecia (AGA) in men, occurs with varying severity and age of onset. Two new treatments widely available as alternatives to 2% minoxidil are 1 mg finasteride and topical 5% minoxidil. Finasteride is a 5 alpha-reductase inhibitor available by prescription only; 5% minoxidil is available over the counter.
Methods. We searched MEDLINE to identify all articles on AGA and its pharmacologic therapies.
Results. We found limited information on AGA in peer review medical journals. Associated diseases include psychologic disorders and coronary heart disease. Hair growth is unpredictable and limited for all pharmacologic therapies, with the vast majority of treatment studies being industry sponsored.
Conclusion. AGA is not easy to treat. Finasteride and 5% minoxidil offer new therapeutic options to the balding man. Treatment options may improve as new drugs are further investigated.Introduction

Men with male pattern baldness (MPB) or androgenetic alopecia (AGA) seek treatment from a range of physicians -- particularly family physicians and dermatologists.[1] The incidence of MPB is estimated to be from 23% to 87%.[2] It may develop any time after puberty. The mode of inheritance remains unclear, but is more likely to be polygenic than autosomal dominant.[3,4] The relatively strong concordance for baldness between fathers and sons is not consistent with a simple mendelian autosomal dominant inheritance.[4] The high prevalence of AGA, its distribution in the general population, the higher risk of AGA as the number of affected relatives increases, and the high risk of inheritance from an affected parent argue in favor of polygenic inheritance.[3,4]MPB does not occur in men with a genetic deficiency of type II 5 alpha-reductase, which converts testosterone to dihydrotestosterone (DHT).[5] Type I 5 alpha-reductase isoenzyme is present in the skin.[6] The type II isoenzyme is present in hair follicles and the prostate.[6,7] The genes encoding type I and type II 5 alpha-reductase isoenzymes are not associated with male pattern baldness.[4] The clinical pattern of hair loss is apparently the result of genetically determined distribution of androgen-sensitive hair follicles transformed from terminal to miniaturized follicles.
Androgens, especially DHT, play a crucial role in the pathogenesis of MPB. DHT is the most potent of the circulating androgens in human plasma and is a major testosterone metabolite in human skin as well.[8] One of the early findings in MPB is an increased percentage of hairs in the telogen, or quiescent, phase of the hair cycle due to shortening of the anagen, or growing phase.[2] Diagnostic histopathologic features of MPB include a near normal number of hairs but reduced terminal and increased vellus hairs with a terminal:vellus hair ratio of 2:1 rather than the normal terminal: vellus hair ratio of 7:1.[9] The anagen/telogen ratio is reduced in AGA from 14:1 to 5:1.[9] In MPB the follicular growth cycle is altered, with shortened anagen growth and a reduced diameter or miniaturization of the follicle with patchy perivascular and perifollicular inflammation.[9] The average decrease in hair diameter in Japanese men is 1.1 microns per year.[10] Inflammatory infiltrates center around the infundibular hair follicle epithelium in the vicinity of the sebaceous duct orifice, the putative site of hair follicular stem cells.[11] Inflammation of this site is associated with permanent alopecia with fibrosis.[11] Left untreated, androgen-dependent alopecia progressively deteriorates.[12] Black men have less severe male pattern baldness than white men.[13] In both groups, increasingly severe male pattern baldness is associated with increased chest hair.[13]
Other less common causes of hair loss must be ruled out when diagnosing AGA in men. These disorders include alopecia areata, telogen effluvium, hair loss due to thyroid disease, adverse drug effects, nutritional deficiency states, scalp or hair trauma, discoid lupus erythematosus, lichen planus, and structural hair shaft abnormalities.[14] This can be done with a thorough history and physical examination, as well as laboratory tests to support relevant findings and scalp biopsies for transverse as well as vertical sections for histopathologic examination and direct immunofluorescence staining of predominantly lesional skin.[15]
Men with AGA are classified into different stages based on the severity of disease by the Hamilton-Norwood scale (Figs 1 and 2).[16,17] Women are classified by a separate scale (Ludwig scale) and usually have less severe disease with sparing of the anterior hairline.[18,19] This article will focus on AGA in men.

Figure 1. Standards for classification of most common types of male pattern baldness. (Reprinted with permission from Norwood.[17])​

Figure 2. Standards for classification for type A variant male pattern baldness. (Reprinted with permission from Norwood.[17])​

Psychologic Consequences

Our culture emphasizes physical appearance. Patients often feel loss of self esteem because of hair loss, and most men find the balding process moderately stressful.[20] The most distressed balding men are those with early onset of balding and more extensive AGA.[20] Wells et al[21] studied 182 men with a wide range of ages and hair loss. Increasing degrees of hair loss were associated with loss of self-esteem, depression, introversion, neuroticism, and feeling unattractive. These effects on self-esteem, introversion, and feeling unattractive were more marked for young men. In a study using computer-morphing photographs, 96 undergraduates rated a full-hair 30-year-old man significantly more dominant, dynamic, and masculine than the same bald man.[22] One man felt strongly enough about his AGA to do self-castration.[23] Psychiatric assessment may be necessary for a patient obsessive about his condition or fixated on bizarre ideas of treatment. However, balding does not necessarily impair psychologic functioning. Only body image satisfaction appears to be globally affected.[21]
Associated Diseases

There is a strong association of benign prostatic hyperplasia (BPH) with MPB with more severe MPB in those with BPH.[24] Also, several major studies reveal an association between AGA and cardiovascular disease. Lesko et al[25] studied the association between self-assessed baldness and myocardial infarction (MI) among 665 cases of MI and 772 controls.[25] The age-adjusted relative risk (RR) estimates were approximately 1.3 for mild or moderate vertex baldness and 3.4 for extreme baldness. Ford et al[26] found that severe baldness was associated with ischemic heart disease mortality (rate ratio = 2.51; incidence rate ratio = 1.72) in 2,019 men (< 55 years of age at baseline) during an average follow-up period of 14 years. Herrera et al[27] assessed the relation between the extent and progression of baldness and coronary heart disease in a cohort of 2,017 men from Framingham, Mass. Rapid progression of baldness was associated with coronary heart disease occurrence (RR = 2.4), coronary heart disease mortality (RR = 3.8), and all-cause mortality (RR = 2.4).[27] Schnohr et al[28] found a correlation between frontoparietal baldness and crown-top baldness with first time MI during a 12-year follow-up of 750 men. In the 12-year follow-up data of 872 male factory workers from the Olivetti Heart Study, men with hair loss centered over the vertex with M-shaped frontal-temporal recession had higher serum cholesterol and blood pressure compared with those with no baldness and/or those with frontal baldness only.[29] The association between frontooccipital baldness and elevated levels of serum cholesterol became weaker with age.
Management

Treatment options include reassurance, hair prostheses, surgery, and topical and/or oral medications.[13,14] This section will concentrate on pharmacologic management. In general, the earlier treatment is begun, the better the results.[9]Minoxidil

Two-percent minoxidil solution was approved by the Food and Drug Administration (FDA) for use as a topical prescription treatment of MPB in 1988, and this medication became available over-the-counter (OTC) in February 1996. Five-percent minoxidil was released directly OTC in January 1998. Minoxidil is believed to work by direct stimulation of the hair follicle or less likely by vasodilatation of scalp blood vessels.[30] It may do this by upregulating the expression of vascular endothelial growth factor in hair dermal papilla cells.[31] Increased vascularization of the dermal papilla occurs during the anagen phase. Minoxidil, not cyclosporin, another potent cause of hypertrichosis, induces DNA synthesis in all hair follicle cells in a dose-dependent manner. Other epidermal and dermal cells show either suppression or no growth response to minoxidil.[32]When applied topically to the scalp, minoxidil does not reach sufficient blood levels to produce any adverse effects on blood pressure and appears to be very safe in clinical practice with only dermatologic reactions significantly different from controls.[30] These reactions include dryness, itching, and allergic contact dermatitis, but rarely cause discontinuing the drug. These side effects occur in 6% of men using 5% minoxidil solution and in 2% using the 2% minoxidil strength.[33,34] The former contains a higher concentration of propylene glycol, a common cutaneous irritant and potential allergen that enhances penetration of minoxidil through the stratum corneum (Table 1).[35,36]
Allergy to minoxidil may be established by patch testing to both the commercial minoxidil solution and diluted propylene glycol.[36] A 2+ reaction to the commercial minoxidil solution and a negative reaction to propylene glycol indicate allergy to minoxidil and will preclude further use of minoxidil. If both patch tests are 2+ positive, propylene glycol is the most likely cause of the patient's allergic contact dermatitis. A compounding pharmacist may formulate a minoxidil solution free of propylene glycol but the effectiveness of extemporaneous formulations is not as well established as the FDA-approved formulations.
The main problem with topical minoxidil therapy is patient compliance. The drug must be applied twice a day for at least 2 months before an increase in hair amount may be noted. When the drug is discontinued, hair regrowth is lost within 6 months. The most common subjective assessment of those on 2% minoxidil is that of decreased hair loss with moderate or minimal regrowth occurring in about one third of the patients, with 8% or less reporting dense hair regrowth.[30] Results may be seen as early as 2 months after initiating therapy with 5% minoxidil. Five-percent minoxidil produces 45% more hair based on hair counts than 2% minoxidil after 48 weeks.[33,34] The one long-term study published found less difference between 5% and 2% minoxidil hair growth by hair weight and number beyond 20 weeks of therapy in a small number of men.[37] Unlike 2% minoxidil solution, there is no generic version of the 5% minoxidil preparation.
Finasteride

Finasteride is a 5 alpha-reductase inhibitor initially approved for the treatment of benign prostatic hypertrophy (BPH) at a daily dosage of 5 mg. The drug prevents the conversion of testosterone to DHT in the androgen pathway (Fig 3). DHT concentrations are significantly higher in the scalp of men with AGA. At least two isoforms of the enzyme 5 alpha-reductase have been discovered. Type I is the predominant form in scalp skin and sebaceous glands, whereas type II is the predominant form in genital tissues and hair follicles. Finasteride inhibits the type II isoform and is also a slow, time-dependent inhibitor of the type I isozyme.[38] The therapeutic dose is 1 mg daily for treatment of male pattern baldness. Decreased libido, impotence, and ejaculation disorders were the most commonly reported side effects for men with BPH on 5 mg finasteride.[38,39] Impotence was not reported as a significant side effect of the 1 mg dose in men 18 to 41 years of age (Table 2). Only 1.4% of the patients taking 1 mg finasteride and 1.6% on placebo quit therapy due to adverse reactions, and all side effects were reversed upon stopping therapy.[39] The drug also has no noted drug interactions, and no change in dose appears necessary in patients with renal insufficiency. The drug is metabolized extensively in the liver and should be used cautiously if its use is necessary in those with liver disease. Finasteride has no effect on serum lipids. Finasteride is not recommended for the treatment of AGA in fertile women because of potential effects on male fetal development during pregnancy or in postmenopausal women due to lack of efficacy.[40]

Figure 3. Metabolic pathway of androgens in skin. (Reprinted with permission from Sawaya.[48])​

One potential drawback of finasteride therapy is masking the detection of prostate cancer due to lowering of prostate-specific antigen (PSA) levels in men, particularly in men over 40 years of age. However, a recent review of patients diagnosed with prostate cancer while on 5 mg finasteride showed no difference in clinical interpretation of PSA values if the laboratory result is doubled during the first 6 months of therapy.[41] At the 1 mg strength, finasteride lowers the PSA value by about 30%.[40,42] It is unknown if finasteride therapy may prevent the development of prostate cancer.[42]Clinical studies of 1 mg finasteride were done with men ages 18 to 41 with mild or moderate baldness, but not complete male pattern hair loss in the vertex (modified Hamilton-Norwood Scale -- stages 2 vertex, 3 vertex, 4 vertex, and 5 vertex).[39,42] The results revealed a statistically significant increase in scalp hair count versus placebo, and also demonstrated slowing of hair loss by patient self-assessment. Although improvement was seen as early as 3 months, the best results were seen in patients taking 1 mg finasteride for 12 or more months. At 24 months, using standardized photographs, 66% of men treated with 1 mg finasteride showed an increase in hair growth versus 7% on placebo.[39,42] There was no further increase in vertex hair count from 12 to 24 months but clinical appearance may improve as these hairs grow longer or become thicker or more pigmented. Forty-two percent of treated men showed visible anterior mid-scalp (not including the area of bitemporal recession or the anterior hairline) hair regrowth after 24 months.[39,42]
Fourteen men taking finasteride (1 mg) had 4 mm punch biopsies of their balding scalp. The starting ratio of 1 terminal hair to 1.7 vellus hairs improved to 1 terminal hair to 1.1 vellus hairs, suggesting a reversal of the hair miniaturization process in patients treated with finasteride for at least a year. Terminal hairs increased 35% in the finasteride group and 6% in the 12 men in the placebo group. Forty-four postmenopausal women on finasteride and 50 using placebo also had 4 mm biopsies done before and after 12 months of treatment. The study of the biopsies confirmed that postmenopausal women using finasteride did not gain hair.[43]
Balding stump-tail macaque monkeys have a similar balding pattern to humans. Diani et al[44] found that serum testosterone was unchanged while DHT was significantly depressed in monkeys on finasteride alone or in combination with topical 2% minoxidil solution. Monkeys on combination therapy also had a significant increase in hair weight compared with those on either drug alone. Finasteride as monotherapy increased hair weight in four of five monkeys.[44] Combination therapy has been reported in one man; he was treated with 5 mg finasteride orally in combination with topical 2% minoxidil and topical tretinoin. The MPB went from Hamilton stage V to stage III in 12 months.[45] However, further studies are needed to define the role of such combination therapy in AGA.

Monitoring Therapy

Patients may report hair growth subjectively, or the prescribing doctor can use the Hamilton-Norwood scale to give an objective view. Hair counts or weight analysis can also document therapeutic results.[37] Statistically significant increases in hair counts may not be clinically significant if the hairs regrown remain tiny, short, and vellus. The newest method involves computer-generated models and a density scale developed by Savin.[46] Hair density is determined by centrally parting the hair and classifying men into one of eight densities. This system also includes hair loss patterns of frontal, mid, and vertex areas of the scalp. With over 100,000 possible combinations, it allows the physician to categorize the patient very specifically, and follow any therapeutic improvements from a baseline. A similar scale is given as a package insert with Rogaine Extra Strength for Men to help men monitor their hair regrowth.
Conclusion

Both topical and oral therapy offer hope for the balding man, but therapeutic response is not consistent. Any positive results of treatment are not evident for months, so regardless of the choice of therapy, the patient must have realistic expectations for hair regrowth. If pharmacologic methods show insufficient improvement, the patient may consider surgical options. New drugs are being investigated that specifically inhibit the type I 5 alpha-reductase enzyme, or that inhibit type I and type II equally.[47-50] The cytochrome P-450 aromatase is another important enzyme located in the outer root sheath of hair follicles.[51] It converts androgens to estrogens and is found in higher levels in the scalp of women than men and may explain the less severe AGA seen in women. Other potential therapeutic targets include androgen receptors in the hair follicles. It is probable that some new agents will become more effective therapeutic options in the new millenium.
Tables

Table 1. Formulations of Topical Minoxidil Solutions

RogaineRogaine Extra Strength for MenMinoxidil2%5%Vehicle60% ethanol10%030% ethanol025%Propylene glycol10%25%Water80%50%​

Table 2. Percentage of Side Effects in Patients on Finasteride

Side Effects5 mg Finasteride (Proscar)1 mg Finasteride (Propecia)Decreased libido3.3% (1.6%)*1.8% (1.3%)*Decreased volume of ejaculate2.8% (0.9%)*0.8% (0.4%)*Erectile dysfunction3.7% (1.1%)*1.3% (0.7%)**Placebo controls.​

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