No. It doesn’t. This is probably one of the most persistent myths. Like many of the myths, it probably started with valid observations but with invalid conclusions. Men who are experiencing hair loss wear hats more often to either protect their scalp from the sun or to hide their hair loss. When the hat comes off, observers note the hair loss and falsely attribute the hair loss to the innocent hat. The idea that ‘wearing a hat causes hair loss’ may have also originated in the military. Young men entering the service were required to wear hats and soon showed signs of thinning hair or going bald. But the two events are simply related due to serendipitous timing. The ages that young men enter the military are also the same ages that male pattern hair loss becomes apparent.

The idea that plugged hair follicles cause hair loss is a long held myth perpetuated by the many companies exploiting hair loss myths in order to sell bogus hair products. The hair follicle is deep in the dermis of the scalp. Not even scrub brushes and abrasive cleansers will ‘clean out the hair follicles’. So, if any company is claiming that their product unplugs follicles, you can be assured that the claims for the product are fraudulent. It’s more likely that they’re implying that their product will clear the opening on to the skin through which the hair shaft grows. Which is fine, but what they don’t tell you is that the follicles don’t get obstructed and that ‘plugged pores’, whatever they define that to be, has nothing to do with male or female pattern hair loss (MFPHL).

In regards to the “dirty scalp theory” of pattern hair loss, there is no credible rationale to it at all. If this ‘theory’ had any credibility, you would expect a decreasing incidence of male and female pattern hair loss in today’s population as compared to past centuries, since it has become routine for many people to bathe/shampoo on a daily basis as compared to earlier times, when bathing would be a weekly or even a monthly event. But, there is no evidence to suggest that the incidence of pattern hair loss is declining despite the fact that we are ‘unplugging our pores’.

Poor blood flow can compromise any human tissue so getting good blood flow to all tissues, including hair, is important. However, poor circulation is far from the primary mechanism involved in pattern hair loss. As a general rule, pattern hair loss is not caused by poor or decreased circulation. We have had many patients lose significants amounts of hair by spending months and years focusing on improving blood flow to the scalp instead of on the primary mechanisms of hair loss.

If poor circulation caused pattern hair loss, there would be no explanation for the hair loss to occur in a symmetrical pattern. Instead, balding would occur in accordance to the areas of coverage of the various arteries to the scalp, which just doesn’t happen. Furthermore, hair follicles would never be successfully transplanted, if pattern hair loss were due to decreased blood supply, since the transplants are used to fill in the balding areas affected by male and female patterns hair loss (MFPHL).

All organs and tissues require proper circulation to maintain their health and all portions of the scalp receive large amounts of oxygenated blood. In fact, 20% of the output of the heart goes to the head, so the scalp is highly vascularized. Numerous studies have shown that the vascular supply to the balding scalp is just as good as the vascular supply to the non-balding scalp. 

That’d be nice, but it’s just not generally true. Which is not to say that nutritional deficiencies can’t cause hair loss or poor hair growth. The cells that comprise the hair follicles in the scalp are some of the most active in the entire human body. Those active follicles require a constant supply of nutrients, vitamins and minerals. So, it only stands to reason that there are many causes for poor hair growth or even hair loss due to dietary reasons. For example, patients who have protein deficiencies, either because of malabsorption or because of lack of intake, can present with poor hair growth and even hair loss. Patients with iodine deficiency can have the coarse hair and hair loss of hypothyroidism. Biotin deficiency can cause poor hair growth. Iron deficiencies are often overlooked as a cause of hair loss, especially in women. Etc. However, for patients with a normal western diet and calorie consumption, nutritional intake is not the primary mechanism causing hair loss. Improving nutrition should be pursued at the same time, and in concert with, other treatments for hair loss. We have seen many patients lose significant amounts of hair because they spend months or even years trying to improve their diet and ignore the primary mechanisms of hair loss. Dietary improvements must be pursued simultaneously with medical treatment because with hair loss, time is of the essence.

Not really. Some people just have more active sebaceous glands than others do, so the skin on their faces and on their scalps is more ‘oily’. But there is no relationship between an oily scalp and MPB. Whereas, it is true that DHT will concentrate in the sebaceous secretions, because DHT is fat soluble, the DHT in the sebaceous secretions is not the cause of MPB. The sebaceous glands are superficial to the hair follicles, and the DHT in the sebum does not affect the hair follicles, which are deep in the dermis.

There is a relationship between sebum and DHT, but not between sebum and MFPHL. DHT is found in the sebum in a high concentration because DHT is soluble in fatty substances such as sebum. But the sebaceous glands are superficial to the hair follicles and the DHT in the sebum does not affect the hair follicle. Damage due to DHT occurs at the base of the hair follicles, where testosterone is converted into DHT via types 1 and 2 5 alpha- reductase enzymes. Routine shampooing or otherwise removing sebum will not prevent or reverse PHL.

Wrong. There are a number of reasons why the number of hairs shed in the shower is not an accurate measure of shedding. Normal shedding of scalp hair is 50 to 100 strands per day. You will lose some of these on your pillow at night, some into the air as you perform your daily routine, and, of course, when you shampoo your hair. When the end-telogen hair shaft become wet and soapy, they also become more adhesive to your fingers and are easily extracted from the scalp. Since the hairs accumulate at the drain, the total number of hairs appears exaggeratedly increased. The less frequently you shampoo the greater the total number of telogen hairs that will accumulate and shed when you do shampoo again.

In the normal scalp, approximately 10% of the hair follicles are in various stages of the telogen phase. During the telogen phase, the hairs are easily extracted with a quick tug, of the hair shaft. Only about 1% of the telogen hairs will fall out with no encouragement. That’s because the telogen phase lasts ~100 days and only those at the end of the phase fall out without any assistance. The other 90% of the hairs not in the telogen phase are mostly in the anagen phase and are strongly anchored in the dermis of the scalp. Anagen hairs cannot be pulled out of the scalp with a simple tug.

Actually, there’s no association between dandruff and MFPHL. Dandruff is not a cause of hair loss. Dandruff is a chronic, non-inflammatory scalp condition that results in excessive scaling of the scalp epidermis (the most superficial of the skin layers) and is clinically visible in approximately 20% of the population. The severity of dandruff declines in the summer and, despite popular misconceptions is not proved to be aggravated by emotional stress.

Although it is normal for epidermal cells on the scalp to continually slough off (just as they do elsewhere on the body), in patients with dandruff the turnover rate of epidermal cells on the scalp is about twice that of those on the normal scalp. Dandruff scales often appear around a hair shaft because of the epithelial growth at the base of the hair, but there is no association with hair loss.

Routine washing with a non-prescription shampoo is usually sufficient to control dandruff. The active ingredients in dandruff shampoos include selenium, coal tar, salicylic acid, ketoconazole, pyrithium zinc, etc. Use whichever product works most effectively for you.

True, but you don’t always see the bulb. The collection of dead cells and debris at the scalp end of a hair that has spontaneously shed is extremely friable and is easily abraded off.

No such luck. The length to which the hair on your scalp will grow depends on your hair’s natural cycle, which is unique to you. The longer the hair’s growth phase (anagen), the longer the hair will grow. The length of the anagen phase of terminal scalp hair is generally in the range of 3 to 5 years. If you have a naturally long growth phase, you can grow your hair to well below your waist. Whereas, if you have a naturally shorter growth phase, your hair will shed before it grows to that length. The length of your particular growth phase is strictly based on heredity. The rate at which hair on the scalp will grow is roughly 1/2 inch (1 cm)/month.

Wrong. Shaving the head has no effect on either hair growth or hair loss. The common misperception that shaving enhances growth is probably due to the appearance of all of the hair shafts from anagen follicles re-emerging at the same time. So, it looks optimistically like a synchronized, enhanced period of growth. But it’s an illusion. Hair on the scalp grows approximately one-half inch (1 cm) per month and there’s nothing we can do to change that. Take note that men may shave their beards daily. If shaving enhanced growth, it would become impossible to shave after months of repeated shaving.

Never happens. MFPHL has no cure. Products that are effective in treating MFPHL require “the norm of 4 to 6 months” to see significant results, e.g. either a loss reversal or new hair growth. The reason is simple. What we are trying to do is to replace thin or fine hair shafts by thicker ones. In order for that to happen, the follicle producing the fine hair shaft has to shift into the telogen phase, which lasts ~100 days, shed the fine shaft, and start growing an observable thicker shaft. That requires 4 to 6 months.

Big mistake. Here’s an excerpt from a TIME magazine article in 2001: “Each year a quarter of a million Americans shell out up to $70 a pop for a hair analysis, but reports show that the tests, which is supposed to diagnose nutritional problems, are, at best, unreliable. Six popular labs were asked to test hair samples, all from the same head, for 30 minerals and metals, including selenium, aluminum and lead. Result? Reported concentrations for the same hair differed wildly from lab to lab, often varying 10-fold. If that’s not enough to make your hair curl, most of the labs also sell supplements to remedy the ills they purportedly find.”

Here’s another article: Hair Analysis Debunked by Dr. Isadore Rosenfeld A study reported 15 years ago in the Journal of the American Medical Association found no scientific basis for using hair analysis to determine nutritional needs. Still proponents continue to offer it to patients. A new study, in the same journal, reports similar findings.

Hair samples from the same people were sent to six labs specializing in this technique. Results varied widely, and recommendations often were completely contradictory. For example, one lab said a patient was a ‘fast metabolizer’ and should avoid vitamin A. Another said the same individual was a ‘slow metabolizer’ and suggested vitamin A supplements. So, if advised to have a hair analysis to define your nutritional status, I suggest you use the money to go to dinner or flush it down the toilet or something else cool.

Not so. In medicine there are no absolutes and there are no guarantees. Likewise, legitimate hair growth medicines cannot be guaranteed to reverse hair loss. If a product is guaranteed to reverse hair loss or your money will be refunded, then you should be wary of the product. Any marketing specialist will tell you that less than 1/3 of consumers will ever demand their money back from a product, regardless how egregious the product might have been. In medicine (as in life), there are no guarantees. A surgeon can never guarantee the result of an operation anymore than an internist can guarantee the result of any particular medication. You should feel uneasy when there is a ‘money-back guarantee’ on any ‘medical’ products.

It would be nice, if MFPHL could be so easily treated. There have always been advocates of scalp massages to improve circulation, but there is no proof that doing so is of any benefit in treating MPB.

All organs and tissues require proper circulation to maintain their health and function. 20% of the output of the heart goes to the head, so the scalp is highly vascularized. MFPHL is not caused by poor or decreased circulation. Numerous studies have shown that the vascular supply to the balding scalp is just as good as the non-balding scalp.

Common sense would tell you that if poor circulation were the cause of MFPHL, then hair loss would be in a pattern corresponding to the blood flow and it isn’t. Furthermore, if poor circulation were the cause of MFPHL, then hair transplants would never be successful, since hair is being placed into balding areas supposedly having decreased blood flow.

That being said, all tissues require proper circulation and poor circulation could be a very minor contributor to some cases of hair loss. If you are inclined to pursue scalp massages, then do so in concert with a medical treatment regimen, and not as your sole therapy.

It’s just the opposite. First of all, take careful note of the active ingredients. Have the ingredients been proven to do whatever has been claimed in the advertisement? Are there references to studies in recognized scientific or medical journals? That’s going to be very unlikely. If the manufacturer makes it difficult for you to find the list of ingredients, you have reason to be wary of the product.

Here’s why you should have misgivings in regards to products that have multiple ‘active’ ingredients: each ingredient may be safe and effective, but there could not possibly be sufficient studies to prove that the ingredients are compatible together. Nor can you know whether or not they may have adverse reactions with one another, either while they are in solution or on the scalp. There are many substances that become ineffective when combined, although they may be effective when applied separately. Minoxidil and spironolactone are good examples of this type of incompatibility. Another example of medications used for the same purpose (antibiotics), but shouldn’t be used together because they become ineffective, would be tetracycline and penicillin.

This should really speak for itself. If a clinic does not have a business site other than the internet, where are they compounding medications? Is their compounding facility licensed and meeting national requirements? Where and how do they see patients? The development and production of products to treat MPB require a physical space for such activities. If the manufacturer does not give you a postal address and a telephone number, it should raise suspicions as to the legitimacy of the business. There should also be a way to contact the business by phone or email and a place to visit to see the products being compounded according to national regulations.

No, but shedding is a part of MFPHL. MFPHL and shedding should not be used interchangeably to describe a cause of hair loss. MFPHL, which entails miniaturization of the hair follicles, is the result of one’s genetic predisposition and is the result of very complicated and incompletely understood biochemical reactions in the cells that comprise the hair follicle. This miniaturization results in progressively thinner hair in a symmetrical pattern typical of MFPHL. There is no loss in the number of hairs on the scalp, but there is a loss in the quality of the hair on the scalp. On the other hand, shedding is a part of the normal cycle of hair growth. The hair shafts on the scalp will spontaneously shed at the end of the telogen (resting) phase. If you shampoo, brush, or pull on hairs in the telogen phase, they will dislodge easily. The same is not true for hairs in the anagen (growing) phase. Hairs in the anagen phase are firmly rooted and are difficult to dislodge.

Unfortunately, this is a myth. Hair transplants can nicely disguise MFPHL and medical treatment or the combination of surgical and medical treatments may be excellent temporizing measures. However, none of the treatments for MFPHL currently available offer a permanent cure for MFPHL. They can prevent and/or partially reverse the process, but we’re only buying time. The five-year studies on the effects of finasteride and topical minoxidil on scalp hair show that there is a dramatic difference between patients continuing on these medications and patients who did not treat their PHL at all. Untreated patients almost invariably showed progressive thinning and/or recession of their hair, whereas patients on treatment kept most of their hair. However, as compared to their own results at the end of two years, the patients who remained on treatment had slightly less hair at the end of five years than they did at the two-year mark. These two and five year results were qualitative and represented self-assessments by the patients.

Not true. There is no correlation between a hyperactive sex life or masturbation and hair loss, just as there is no direct correlation between the serum testosterone level and PHL. In the adult human male, there is a very wide ‘normal range’ for serum testosterone (300-1200 ng/dL), but there is no direct relationship between the testosterone level and MPHL.
However, it is a long established fact that there is a correlation between MPHL and DHT (dihydrotestosterone), which is why many of the treatments for MPHL include decreasing the amount of DHT in the scalp that can affect the hair follicles. The rate-limiting factor in the production of DHT is primarily the amount of the enzyme 5 alpha reductase available to convert the testosterone to DHT. So, having more testosterone in the body does not necessarily mean there is also going to be more DHT.

Not true. In reality, pattern hair loss is just as common in women as it is in men, though the degree of loss, the age of onset, and the overall pattern usually differs in women as compared to men. Statistically, after the teenage years, the incidence of MPHL is reflected by the decade in life, i.e. 20% of men in their 20’s are affected by MPHL, 30% of men in their 30’s are affected by MPHL, etc. By the age of 50, over 50 percent of men have significant hair loss. For women, about 25 percent have significant hair loss by the age of 50, though it may be less apparent because women are more conscientious about hiding it than men are.
The areas of pattern baldness are also different in men and women. While men have a tendency to first lose hair in the frontal, temporal and/or vertex of the scalp, pattern baldness produces thinning hair diffusely throughout the scalp with sparing of the frontal hairline.

For most, MFPHL is a gradual process, but it can occur with devastating suddenness as well. The sudden massive shedding will cause the next generation of hair to have considerably less texture and body, sometimes to the point of appearing as vellus hairs. These hairs will have shortened anagen phases. The affected areas are confined to those areas of the scalp where the hair follicles have active and sensitive androgen receptor sites, i.e. the vertex, crown and frontal regions.

If you do not have a genetic predisposition for MPHL, then taking anabolic steroids will not cause hair loss. But, if you do have a genetic predisposition for MPHL, then taking anabolic steroids can accelerate the process. Even though anabolic steroids are not androgens per se, the body can convert them into androgens.

Here’s an excerpt from an article by Dr. David Whiting, a widely acknowledged leading researcher/dermatologist: “Testosterone and dihydrotestosterone can circulate systemically to follicles, or be manufactured locally in the follicle from circulating weak androgens (dehydroepiandro-sterone and androstenediol) via complex enzyme-mediated processes involving specific dehydrogenase and reductase enzyme pathways. All of these enzyme reactions are dependent upon specific pyridine cofactors. It is clear that reductase, dehydrogenase, and probably aromatase enzymes are of major importance in hair growth as they mediate the complex interchange of sex hormones implicated in anagen activity.”

If hair loss occurs primarily on the back of your scalp, above the ears, in patches, or is brittle, then you have hair loss due to causes other than MFPHL. MFPHL is not a matter of losing hair, i.e., shedding. Shedding 50-100 hairs/day is normal. MFPHL is a matter of atrophy or miniaturization of the hair follicle due to a combination of genetic predisposition of the hair follicles and the presence of DHT. Embryologically, skin in the frontal, temporal, crown, and vertex of the scalp derives from a different set of germ cells than does the skin on the sides and back (occiput) of the scalp. The hair follicles in the sides and back of the head do not contain androgen receptors and consequently do not become similarly affected by DHT or involved in the process of MFPHL as the aforementioned areas.

MPHL would never occur before puberty. Why? MPHL is the common name for alopecia androgenetica, a name that emphasizes that the cause is related to androgens and genetics. Androgens are not produced in the body until puberty, so MPHL can become noticeable as early as the onset of adolescence. Our youngest patient is 13 years old. Unfortunately, early onset portends an ultimately severe case of MPHL.

This is a very controversial subject. Women normally have only 1/10 the levels of DHT as do men, yet women also suffer from PHL. The age of onset is later than in men. The pattern of involvement is diffuse as opposed to the typical pattern in men. The frontal hairline is usually preserved. And finasteride is less effective in treating post-menopausal female patients. But, the underlying pathophysiology is probably basically the same. When you consider causes for hair loss, there are more medical conditions causing hair loss in women than there are for men. These reasons include iron deficiency, menopause, post partum telogen effluviums, etc.

This is a difficult myth to refute because neither the age of onset of MFPHL, nor the rate at which the MFPHL will progress nor the final extent can ever be predicted. However, as a general rule, the earlier MFPHL is treated, the better the positive results will be.

A report from Moscow Medical University stated that there is some fibrotic encapsulation (irreversible hair loss) to the hair follicles 30 months from the onset of alopecia androgenetica occurred in some patients. Their conclusion was to prevent loss by treating alopecia androgenetica when the first signs of alopecia androgenetica appear.

Any of the medications for treating MFPHL work best if the hair loss has been within the past few years. For a patient with recent hair loss, the reversal of MFPHL is usually quite successful, if the patient uses a combination of a medication to promote hair growth (minoxidil) along with a medication or medications to inhibit the quantity of action of DHT in the scalp.

This is a qualified true and false statement. If you use a shampoo containing ketoconazole that can affect the biochemical environment around the follicles, then it is possible to reverse hair loss. Any other shampoo will remove DHT from the surface of the scalp, but they are of no benefit in preventing MPHL because it is the DHT around the hair follicle that is causing the damage. These shampoos and conditioners cannot change the biochemical environment around the hair follicles, which is deep in the dermal layers of the scalp. Otherwise, whether you never shampoo or shampoo daily will not affect the age of onset or the rate of progression of MPHL.

Shampoos are designed to clean the hair and leave it manageable and looking good. If they do that for you, it’s as much as you can ask for. Other than shampoos containing ketoconazole, which have been shown to reduce DHT in the scalp, shampoos really have no effect on hair growth or loss. See also Myth: MFPHL is caused by plugged pores.

No, but there is a cause of telogen effluvium associated with scalp pain. The biochemical processes that result in MFPHL are not accompanied with any physical sensation. If you are experiencing scalp pain, it may be a good idea to have a dermatologist examine your scalp.

An article in the March 1998 issue of Archives of Dermatology describes “Scalp Dysesthesia”. Some individuals who develop a telogen effluvium report painful burning sensations in association with excessive shedding of the hair. Until recently this problem was not officially identified by dermatologists. The syndrome has been called “scalp dysesthesia” or “burning scalp syndrome”. The cause of burning scalp syndrome is unknown. It has been successfully treated by some dermatologists with antidepressants such as doxepin or amytryptaline.

It’s an enduring and common misconception among patients that PHL is ‘inherited from the mother’s side’. Well, that statement is neither right nor wrong. Pattern baldness can be inherited from the mother’s side. But it can also be inherited from the father’s side.

Despite the fact that the entire human genome, comprising approximately 30,000 genes in the human DNA, was completely mapped out as of April 2003, the gene or, more likely, genes responsible for MPB, have not been identified. What is known is that the age of onset, the rate of progression, and the pattern of follicular miniaturization are all influenced by heredity. Generally, the earlier the onset of hair loss, the more extensive the degree of hair loss will eventually be.

Considering the high proportion of men affected by PHL, its distribution in the general population, the increased risk of PHL as the number of affected close relatives increases, and the high risk of inheritance from either or both affected parents, one can support a strong argument in favor of an autosomal, polygenic inheritance.

It seems ironic that with all the knowledge that has been accumulated in regards to PHL in the past several decades, we still do not know the exact genetic inheritance. What is known is that the genes are autosomal (not on the X or Y chromosomes), dominant (as opposed to recessive), and have variable penetrance (so it may not affect siblings of the same parents to the same degree).

However, in a recent article on WebMD (http://webcenter.health.webmd.netscape.com/content/article/106/108259.htm) entitled “Blame Male Pattern Baldness on Mom?” the authors have found a gene variation that may explain some cases of MPB. The suspect gene variation sits on the X chromosome, which is handed down to men by their mother. It had been previously presumed that the genes involved in the transmission of MPB were always autosomal.

The genes for hereditary hair loss are carried on both sides of the family. And the tendency to hereditary hair loss can skip generations. If many close members of the family are afflicted with MPB, the greater the likelihood is that you will also have MPB. On the other hand, if they all have full heads of hair, it’s likely you’ll keep yours as well.

Wrong. MFPHL results in a change in the texture and the quality of the hair. It does not change the number of hairs on the scalp. You are born with ~100,000 hair follicles in the scalp, and you keep that same number of hair follicles throughout your lifetime.

The sizes of the hair shafts are directly related to the sizes of the hair follicles from which they are growing. During any single anagen (growing) phase, the size of the hair shaft will remain essentially the same for its entire length. When a hair follicle is affected by PHL, the hair shaft will become thinner in the subsequent growth cycle, because the follicle begins to miniaturize.
It is not unusual for a sudden, dramatic, extensive miniaturization of an area of scalp within a single hair growth cycle. This phenomenon explains the recession of the frontal hairline and/or the temples. The number of hair follicles remains the same, but the vellus-like hairs that they produce make them ‘invisible’.

No. It just doesn’t happen. It is important to make a distinction between pharmacologic versus cosmetic actions of any product or treatment. There are many products, which can make the hair ‘thicker’ or ‘fuller’, but they have nothing to do with stimulating hair growth or preventing and reversing MFPHL.

A cosmetic can be defined as either a preparation, such as powder or a skin cream, designed to beautify the body by direct application or as something superficial that is used to cover a deficiency or defect. There are excellent cosmetic preparations for the hair, but none of them promote hair growth.

Not really. Dyeing, as well as all other cosmetic procedures on the hair, has no effect on the growth or loss of the hair unless the chemical and/or physical agents used are injurious to the hair follicles, which rarely occurs. But cosmetic changes to the hair can definitely damage the hair shafts. Chemical and physical agents (bleaches, dyes, heat, etc.) used by the cosmetologist can cause the hair shafts to be more brittle and more easily broken, when they are combed or brushed.

It is also a myth that hair damaged by cosmetic coloring and other procedures takes longer to grow back. Growth of the hair shaft is regulated by the hair follicle, which is deep in the dermis of the scalp and is not affected by hair dyes and other cosmetic procedures. The hair that does grow back won’t be brittle, because whatever chemical and physical agents previously used on the hair will not have damaged the re-emerging hair shafts.

Questionable. The problem with any herb or natural product for MFPHL is that we have a Catch-22 situation. In fact, there may be some very beneficial herbs and natural products. However, these ‘herbs and natural products’ are never prescribed in Western academic medicine, because they have never been tested or approved by the FDA. It costs in the hundreds of millions of dollars to obtain an FDA approval for a new drug. The FDA will not grant an exclusive patent for ‘herbs and natural products’. The pharmaceutical company cannot recapture the cost of its research and development. As a result, we have no well-designed studies to prove the value of or to establish the optimal doses for “any herb or natural product for MPB”. Herbal products for treating MPB often have multiple ingredients. These ingredients are often mixed together without any studies to determine whether or not they are compatible in the same solution or whether or not there are adverse interactions among them.

DMSO hasn’t been proven safe for human use as a solvent for topical medications. Here is an excerpt from an FDA alert of 1992 (http://www.fda.gov/ora/fiars/ora_import_ia6206.html): DMSO is dimethyl sulfoxide, a solvent derived from wood, which has been the subject of considerable interest for its potential as a drug. Testing of DMSO as a drug began in the early 1960’s but was halted in 1965 after experiments in animals indicated that it had adverse effects on the eyes. Experiments were resumed the following year with restrictions to assure that patients were adequately protected. At present, the only human use for which DMSO has been approved is for interstitial cystitis, an inflammatory urinary bladder condition.

DMSO is an excellent carrier for many topically applied drugs and is widely used in veterinary medicine, because DMSO can carry other drugs with it across membranes. It is more successful ferrying some drugs, such as morphine sulfate, penicillin, steroids, and cortisone, than others, such as insulin or minoxidil. What it will carry depends on the molecular weight, shape, and electrochemistry of the molecules.

Questionable. The purported advantage of using MSM (Methyl Sulfonyl-Methane) is to provide increased amounts of sulfur to the tissues. However, sulfur deficiency is very rarely encountered in medical practice.

There is no evidence of which I am aware, which suggests that increasing the amount of sulfur to the scalp increases hair growth or supports hair transplants. You can access the website (http://www.arthritis.org/) for more information on MSM and DMSO. I agree with the advice given: “Don’t buy DMSO on your own: Ask your doctor to find a medical-grade source. Almost all DMSO available to the public is industrial grade – including most veterinary DMSO and products sold in health food stores and on the Internet and may not be safe for medical use.”

It’s possible that L-arginine promotes hair growth, but there aren’t any credible supportive studies. Unquestionably, L-arginine is essential to good health and it has been demonstrated to open up blood vessels throughout the body, including those of the heart by forming NO (nitric oxide), which dilates blood vessels. There is a popular mistaken idea that it is decreased blood flow that causes MFPHL and that minoxidil promotes hair growth because it dilates blood vessels (See Myth: Poor Blood Flow Causes Pattern Hair Loss), but that is far too simplistic an explanation. Other agents, such as nitric oxide, can also cause vascular dilatation, but they have not been shown to promote hair growth. For detailed information about nitric oxide, access http://www.pasteur.fr/applications/euroconf/nitric-abstracts.html.

There is a popular misconception in regards to the pharmacological effect of saw palmetto. Since it is an effective treatment for men with enlarged prostates, it has been erroneously presumed that saw palmetto acts similarly to finasteride in reducing the amount of DHT in the prostate by inhibiting the enzyme, 5 alpha-reductase. However, 5 alpha reductase levels in prostatic tissue and testosterone, DHT, and PSA are not significantly reduced by saw palmetto (Marks LS, Tyler VE. Saw palmetto extract: newest (and oldest) treatment alternative for men with symptomatic benign prostatic hyperplasia. Urology 1999; 53: 671-678). In fact, saw palmetto does not affect overall prostate size, but shrinks the inner prostatic epithelium (USRF Research. “Clinical Effects of Saw Palmetto Extract in Men with Symptomatic BPH” webpage: http://www.usrf.org/spepapers.html [accessed 26 Jan 00]). It is the shrinkage of the prostatic epithelium that allows for the improved passage of urine from the bladder. Consequently, saw palmetto has proven valuable for treating the symptoms of benign prostatic enlargement, but there is no evidence that taking saw palmetto decreases the DHT levels in the prostate gland or in the scalp.

Yes, but the answer needs to be qualified. Only hairs already in the telogen (resting) phase will be caused to shed by the use of topical minoxidil. With the initial use of topical minoxidil, hair follicles in the telogen phase, normally about 10% of all of the hair follicles on the scalp, can shed their hair shafts. That’s not necessarily bad news. Those hairs were imminently going to shed in any case and continued use of minoxidil may help the thinning hair to be replaced with thicker, healthier hair.

No. Minoxidil doesn’t work for everyone. Approximately 17% of patients will continue to see progression of their PHL while using topical minoxidil. But don’t mistake the progression of PHL as an adverse reaction to topical minoxidil. In almost all cases, the use of minoxidil is slowing the rate of progression of PHL, even if it is not entirely preventing its progression.

How well minoxidil works to treat PHL is not so much dependent on the patient’s age as it is dependent on the genetic propensity of the patient to have PHL. Unfortunately, one’s genetic propensity for PHL is not something we can assess. In any case, there is no evidence that minoxidil will force hair in the anagen phase into the telogen phase and cause it to shed or ‘not to regrow’. Just the opposite reaction occurs. Minoxidil helps to keep the hair follicles in the anagen phase. It may not have visibly positive results for everyone, but it does not hasten PHL, i.e. it does not cause miniaturization of the hair follicles.

Wrong. Minoxidil doesn’t really cause a tolerance, i.e. as long as you apply minoxidil, it will extend the anagen phase of the hair follicles. However, the amount of scalp hair loss reversal is maximized at about two to three years. It’s unlikely that more hair follicles will be recruited to produce a terminal hair shaft again after that time unless you increase the concentration of minoxidil delivered to the follicles and/or take measures to protect the follicles from DHT. There seems to be a threshold level at which hair follicles can be recruited to grow a terminal hair shaft again. Using a high concentration topical minoxidil ensures the best results. Some patients will be able to maintain the hair on the scalp with continued treatment, but most patients will gradually see some thinning again. Patients who stay on treatment with topical minoxidil definitely do much better than untreated patients, but the positive results will decline over time.

This myth requires explanation. The packaging for Rogaine says topical minoxidil is for ‘growing hair at the vertex’. That doesn’t mean it won’t promote hair growth in the frontal areas. Actually, it does, but it is not as effective in promoting hair growth as it is at the vertex. Understandably, Upjohn did not include statistics for frontal hair growth to the FDA, when it applied for an approval. So, the FDA required Upjohn to state that Rogaine is to be used to ‘grow hair at the vertex”. And the myth persists that topical minoxidil “does not grow hair in the front hairline area”.

Hair affected by PHL on the anterior (frontal) parts of the scalp is more resistant to treatment than is hair at the vertex. Using topical minoxidil alone or using an agent to reduce the DHT alone has rather limited success in reversing hair loss in the frontal or temporal areas of the scalp. So, male patients are usually better off using both medications.

Wrong. If you discontinue using minoxidil after a single application, or even after a few days of applications, you will not experience any minoxidil induced shedding. The effects of topical minoxidil are very much dose/time related. You will not have started any significant biochemical changes after a single dose.

It just doesn’t happen. It would be nice, if minoxidil were such a potent promoter of hair growth, but it isn’t. Besides, the palms of the hands do not contain hair follicles and the hair follicles on the face of women do not usually have the potential for growing terminal hair. Even with an alcohol base, the amount of absorption of minoxidil averages only 1.4%. After the solution has dried on the scalp, there is negligible additional absorption.

Unfortunately, no. With the current treatments for PHL, the amount of scalp hair loss reversal is maximized at about two to three years. Many patients will be able to maintain the hair on the scalp with continued treatment, but most patients will gradually see some thinning again. Patients who stay on treatment with topical minoxidil definitely do much better than untreated patients, but the positive results will decline over time. Of course, if a patient discontinues treatment at any time, he will lose all of the gains he has made, and it may not be possible to achieve the same recruitment upon restarting treatment.

All of the current medications for treating MPHL are ‘temporary solutions’. They are not cures. We don’t have a cure for MPHL, but all of the long-term studies show that using topical minoxidil and an agent or agents to reduce the amounts of DHT in the scalp will definitely allow you to keep more of your hair as compared to using a placebo. For now, that’s about the best we can do. If you’re using a medication to stimulate hair growth (minoxidil) and an agent to decrease the DHT in the scalp, you’re doing as much as has been proven beneficial to prevent and/or reverse your MPHL.

It is not normal for finasteride to cause shedding at any time during its use. Binding the type 2 5-alpha reductase does not cause a shift from anagen to telogen, so no shedding would be expected to occur. If shedding does occur, it is not a sign that finasteride is working. There have been rare cases in which patients have reported a telogen effluvium months after initiating treatment with finasteride. Apparently, a drop in the systemic levels of DHT had been the inciting event in causing these cases of telogen effluvium. Although a telogen effluvium usually begins somewhere between 11 and 16 weeks after the inciting event, it can start as soon as 4 weeks thereafter.

There are no specific numbers that we can put on the amount or percentages of hair shed in a telogen effluvium. The amount and degree of hair loss is dependent on the severity of the telogen effluvium. Rarely, will the amount of hair loss exceed 50%. The shedding is generally diffuse (global) and can affect areas of the scalp not usually affected by MPHL. So, it would be common to note shedding from the sides and back of the head in addition to the crown, vertex and frontal areas. The shedding tends to be fairly symmetrical, but will be more noticeable in the areas affected by MPHL, because there is a higher ratio of hairs in the telogen phase than in the other areas of the scalp not involved with MPHL. The shedding lasts about 6 weeks. It usually takes 4 months to a year for the hair to grow back.

The techniques and, consequently, the results of the evolving field of hair restoration have been very impressive over the past few decades. Unfortunately, much the general public still perceives hair transplantation as being comparable to the plugs of hair seen in dolls or the placement of bristles in a toothbrush. The truth is, one does not ‘see’ the results of modern hair restoration surgeries, because they look so natural. The 4mm multiple-punch autographs, each containing 8 to 20 hairs, were first described by Orentreich in 1959. Not until Bradshaw’s description of minigrafts in 1984 and Limmer’s first use of follicular units in 1988, did the results of hair restoration surgeries begin to achieve a more natural appearance.

The two most widely utilized methods of hair restoration surgery are microscopic dissection of follicular unit grafts and the increasingly popular technique of follicular unit extraction (FUE). In the traditional method of microscopic dissection, the follicular units are removed from the donor area in the occiput (back of the head) by single-bladed elliptical excision microscopically dissected beneath the binocular stereoscope. The donor tissue is trimmed into follicular units and implanted into the balding area using a needle tunnel or small slit incision.

In the FUE method, a specially designed surgical punch is used to remove single follicular units from the donor area for transplantation to the recipient site. This surgical technique has the advantages, at least theoretically, of “a more rapid recovery, minimal or undetectable scarring, more rapid graft growth, and the possible expansion of total available donor sites.” The disadvantages include a significantly increased surgical time necessary to transplant any fixed number of follicular units and a steeper learning curve for the surgeon in order to achieve excellent results.

If you would like more information about hair restoration surgery or want a referral to a surgeon, who is a member of the International Society of Hair Restoration Surgery, access http://www.ishrs.org/hair-doctor.htm

No. It doesn’t. Psoriasis is a common scaling skin disease that affects around 1 to 2 percent of the population. Scalp psoriasis occurs in at least half of all patients afflicted with psoriasis. Psoriasis can range from very mild with fine scaling to very severe with thick, crusted plaques and the condition can be both distressing and cosmetically disfiguring. However, psoriasis does not generally cause permanent loss of hair. This is because psoriasis involves the epidermis and not the dermis. The dermis is where the hair follicles develop. Any hair loss that psoriasis may cause would be separate from male pattern baldness.

Psoriasis itself will not cause the hair to fall out. However, very thick scales in the scalp can entrap hair and as you attempt to remove the scales, the hair shafts can be pulled out in the process. Psoriasis can contribute to the hair being ‘brittle, thin, split ended, and difficult to manage’, but the psoriatic process does not harm the hair follicles themselves. Sometimes medicated shampoos and other topical medications can adversely affect the hair. Any alcohol-based solution can irritate areas of psoriasis, so patients would need to be judicious in their use. Unfortunately, there is no cure for psoriasis. But there is good treatment. You can get reliable information at many non-commercial websites such as http://www.nlm.nih.gov/medlineplus/psoriasis.html or http://www.psoriasis.org/home/

Seborrheic dermatitis affects areas with high densities of large oil glands, e.g. the scalp, behind the ears, eyebrows, etc. Despite the name, the composition and flow of sebum are usually normal. As explained below, seborrheic dermatitis does not cause permanent hair loss. Most dermatologists (and all the standard dermatology textbooks) say, “seborrheic dermatitis does not cause hair loss”. The inflammation that may occur with seborrheic dermatitis is thought to be due to the body’s reaction to a yeast in the scalp (Pityrosporum) and to products that break down oil.

Temporary hair loss can occur in the areas of seborrheic dermatitis because the inflammatory changes are unhealthy for the hair follicles. However, when the seborrheic dermatitis improves, the hair grows back again. This is different and unrelated to the type of ‘hair loss’ that occurs with PHL. In PHL, hair also grows back again, but the size of the hair shaft may be significantly reduced. It is not unusual to experience seborrheic dermatitis and PHL at the same time and neither condition exacerbates the other. Sebum does contain concentrated levels of DHT, but since the sebum on the scalp is very superficial to the androgen receptors at the level of the hair follicles, which are deep in the dermis, it plays no role in initiating the chain of events, which results in miniaturizing the hair follicle in the process of PHL.

Wrong. When DHT attaches to the androgen receptor sites at the hair follicle, it triggers a very complicated chain of events that results in the miniaturization of the follicles with a surrounding inflammatory response. When the pathologist refers to microscopic inflammatory changes, he is describing an autoimmune response, not any kind of infection, which is defined as an invasion by and multiplication of pathogenic microorganisms in a body part or tissue. MPHL is not due to any kind of infection.

No. It won’t. Superficial irritations of the scalp will not cause any injury to your hair or to your hair follicles. There are up to 10% of patients who have an adverse effect on the scalp due to the applications of minoxidil solutions containing propylene glycol, which comprises 50% of the base of many 5% minoxidil solutions. The growing hair follicles are embedded deep in the dermis of the scalp and are not affected by any superficial irritation to the scalp.