Normal Hair Growth Cycles
Undisturbed, each terminal scalp hair usually grows continuously for about approximately three to five years. Then, the hair transitions into a resting state where the visible portion above the skin is shed. No hair grows from the follicle for 90 days. Once this time has passed, a new hair begins growing through the skin and continues for another three to five years at a rate of approximately 1/2 inch per month.
It is thought that as many as 100 genes are involved in regulating the creation, construction and cycling of scalp hair. To date, very few of these genes have been identified.
Common Pattern Hair Loss
Hamilton-Norwood Hair Loss Scale
For those concerned about hair loss, many myths and half-truths abound, but useful information can be difficult to obtain. Therefore, an objective overview of pattern hair loss is presented herein.
In healthy well-nourished individuals of both genders, the most common form of hair loss is androgenetic alopecia (AGA), also known as pattern hair loss. The disorder affects approximately 40 million American men. Perhaps surprisingly, the same disorder affects about 20 million American women. The difference between men and women is that a woman suffering hair loss usually retains her feminine hairline and experiences thinning behind this leading edge. In men, a distinct “pattern” of loss manifests where the frontal edge recedes at the same time that a thinning zone expands from the posterior crown. In more pronounced cases, these zones meet and the person is said to be clinically bald.
Importantly, three things need to occur in order for one to be affected by AGA. First, one must inherit the genetic predisposition. This means that the problem comes from one or both sides of the family. Second, one needs to attain a certain age. Nine year old children do not experience pattern hair loss. And third, one needs to have the circulating hormones that precipitate onset and progression of the disorder.
Typically, the earliest onset of AGA occurs in late puberty or one’s early 20’s. As a general rule, the earlier hair loss begins, the more pronounced it is likely to become.
Hormones, Enzymes & Other Factors
Crystallography of DHT molecule
From a susceptibility standpoint, the principle hormonal trigger linked to pattern hair loss is 5-alpha dihydrotestosterone, commonly referred to as DHT. Intriguingly, it has been shown that in persons genetically insensitive to DHT, pattern hair loss does not occur. DHT is synthesized from the androgen hormone testosterone and is useful early in life and during puberty.
In adults, DHT is thought to cause significant harm, but very little good. Disorders as disparate as benign prostatic hyperplasia and pattern hair loss are both triggered by DHT. The synthesis of DHT occurs via two closely related forms of the enzyme 5-alpha reductase. Hair loss treatment options that efficiently interfere with the interaction between 5-alpha reductase and androgen hormones like testosterone have been shown to offer clinical benefit in treating pattern hair loss.
Because hair growth is regulated by multiple genes and attendant biochemical pathways, the underlying factors are extremely complex. Another challenge to understanding hair loss has been the fact that humans, alone among mammals, suffer from androgenetic alopecia. Thus, no efficient animal model exists that would otherwise tend to shed light upon the key factors at work.
Hair Loss Variations Other Than AGA
In either gender, the differential diagnosis is typically made based on the patient’s history and clinical presentation. The common differentials for AGA include alopecia areata (AA), Trichotillomania, and telogen effluvium. Less often, the cause of hair loss may be associated with disorders such as lupus erythematosis, scabies or other skin manifesting disease processes. Scalp biopsy and lab assay may be useful in ascertaining a definitive diagnosis, but, in such cases, should generally only follow an initial clinical evaluation by a qualified treating physician.
Pattern Hair Loss Treatment Options
It has wryly been observed that the choices for dealing with hair loss are “rugs, plugs, or drugs”. This quip articulates three treatment options that are more kindly referred to as non-surgical hair systems, surgical hair restoration, and pharmacotherapy. A fourth option has recently evolved, which will also be touched on herein. This is non-drug based therapy.
Typical Hair Piece
Hair replacement systems have been in regular use at least since the time of ancient Egypt. These products also go by the term hair integration systems, wigs, weaves, hair pieces, toupees and many other names. All have one thing in common—they are not growing out of one’s scalp. Thus, they must somehow be attached either with the bald skin or the fringe of hair remaining above the ears and in the back of the scalp.
Such attachment to the living scalp is almost never permanent, and for good reason. Aside from the fact that the unit itself wears out, basic hygiene dictates that the wearer regularly remove the unit to clean the underlying hair and scalp. There are almost always three basic elements to a hair replacement system. The first is the hair itself which may be synthetic, natural, or a combination thereof. The second element is the base of the unit. Typically, the hair is woven in to a fabric-like base which is then attached in some fashion to the scalp. This brings up the third element; which is the means of attachment. Methods include sewing the base to the fringe hair, gluing the base to the fringe hair, or gluing the base to the bald scalp.
Potential advantages to hair systems include the immediacy of achieving a full hair “look” that can appear, to the casual observer, to approximate a full head of hair. The potential disadvantages of hair systems are many and varied.
In persons who are actively losing hair, vs. those who are essentially bald, the hair system itself may rapidly accelerate the process of going bald. Another disadvantage is the hard leading edge that can give away the fact that a person is wearing a hair system. In the past, this problem has been addressed by using delicate lace front artificial hairlines that look quite natural but tend to be extremely fragile.
Because they are nonliving, hair systems must be serviced and eventually replaced themselves. The costs of servicing and maintaining a hair replacement system are not insubstantial–and such costs can dramatically exceed the initial price of acquisition.
Surgical Hair Restoration
Surgical hair restoration, commonly known as hair transplantation, exploits a phenomenon first described in the 1950’s. This phenomenon, donor dependence refers to the observation that hair bearing tissue, when relocated to a previously balding area of the same person’s scalp, continues to produce viable, vigorously hair that persists in its new location as it otherwise would, had it not been “relocated”. In appropriately selected patients, surgical hair restoration can constitute a positive solution to pattern hair loss
There are important caveats to hair transplantation. The first concerns supply and demand. At the present time, one may not transplant hair from one person to another without causing a florid and destructive foreign body response in the recipient. Thus, both operator and patient are relegated to whatever permanent hair bearing tissue is in place. Accordingly, it is highly important to conserve and strategically place this precious resource appropriately.
The second major caveat to hair transplantation concerns achieving clinically beneficial endpoint results. A hair line that is spotty or too abrupt may look worse than it did before it was restored. By the same token, hair behind the leading edge that is not restored in a fashion that yields meaningful density (e.g. 1 hair per mm/sq) often fails to approximate a full head of hair. Therefore, in selecting a transplant surgeon, artistic excellence is at least equal in importance to basic surgical skill.
The third caveat to hair transplantation refers to a problem known as chasing a receding hair line. Because hair loss is progressive and relentless, it is possible that donor hair restored integrated into an apparently intact area of scalp hair may end up as an island of hair because the hair behind it continues to erode. In this situation, patients are compelled to augment hair behind the restoration zone in order to retain a full appearance. This works reasonably well until either the hair stops thinning or one eventually runs out of donor hair.
Ideally, for persons undergoing transplant surgery, it would be helpful to incorporate a treatment option that safely and effectively arrested the progression of hair loss, allowing the treating surgeon to fill in the thin areas without the concern of chasing a receding hair line.
Drug-based Hair Loss Treatment Options
From a treatment perspective, the two most widely used therapeutic interventions against pattern hair loss have been topical minoxidil and oral finasteride.
Minoxidil, first sold under the trade-name Rogaine(TM) was initially developed as the oral antihypertensive drug, Loniten(TM). In some patients who used minoxidil to treat blood pressure problems, it was observed that unusual hair growth occurred on the face and scalp. This was somewhat colloquially referred to as the werewolf affect. >From this observation, topical compositions containing minoxidil were successfully tested on balding scalps. Rogaine(TM) (2% minoxidil) was the first hair loss treatment drug approved by the FDA for use in men. Eventually, Rogaine(TM) (2% minoxidil) was approved for use in women. Extra Strength Rogaine(TM) (5% minoxidil) was approved by the FDA for use solely in men.
The advantages of Rogaine(TM) include the ability to arrest, and possibly reverse, pattern hair loss. Based on Pfizer’s own marketing materials, Rogaine(TM) has primarily been shown to be effective in treating hair loss in the vertex and posterior scalp, but not the anterior hairline. Minoxidil is a potent drug with potential side effects that include hypotension and skin irritation.
Finasteride, a selective type II 5-alpha reductase inhibitor was originally developed, in 5 mg oral dosage, under the trade name Proscar(TM) to treat benign prostatic hyperplasia (BPH). Because BPH is linked biochemically to the same metabolic pathways that trigger pattern hair loss, it was hypothesized that finasteride could be clinically useful in both pathologies. From this work, Propecia(TM) (1 mg finasteride) was developed. In placebo-controlled studies on men with mild to moderate hair loss, Propecia(TM) was shown to produce clinically relevant benefit in arresting, and in some cases, reversing the progression of the disorder. Propecia(TM) is not indicated for use in women. Noted side effects include reduced libido, as well as reduced ejaculate volume. Gynecomastia (male breast enlargement) is another potential side effect. Finasteride can also artificially lower the levels of a key protein (PSA) used to screen for prostate cancer. Finasteride is considered a teratogen (may cause feminizing birth defects) and should not be handled by pregnant women or even those persons who may come into contact with pregnant women.
Like finasteride, dutasteride was originally developed to treat BPH. Unlike finasteride however, dutasteride inhibits both isoforms of 5-alpha reductase, while finasteride inhibits only type II 5-alpha reductase. Interestingly, a clinical study undertaken by GlaxoSmithKline, the EPICS trial, did not find dutasteride to be more effective than finasteride in treating BPH.
At the present time, dutasteride is approved to treat BPH. Clinical trials for dutasteride as a hair loss drug were undertaken, but halted in late 2002. Potential side effects noted with the use of dutasteride include gynecomastia, changes to PSA levels, teratogenic effects and others that closely parallel the negative side effect profile described by the makers of finasteride.