Synopsis
Book by Kobren Spencer David Eisman Diane B Eisman Eugene
Extrait
Chapter One: THE ROAD TO PROPECIA
Discovering the Cause and Treatment of Baldness
Innovation is not a random process. When it works, it works because someone has identified a real need and found a way to bring new ideas or new technologies to bear on that need.
LEWIS W. LEHR
Ask any balding man when he first noticed his hair thinning, and odds are he'll remember. Like any other milestone in his life, he isn't likely to forget the event or its accompanying details, like where he was, what he was doing, and, most important, how he felt.
I was in bed, stretching and getting comfortable on the pillow, just like any other night. What made this one different, though, was that when I ran my fingers through my hair, out came, not one or two, but at least ten strands of hair. I couldn't miss it because my hair was worn well below my collar, so these were long strands; a man with shorter hair might not as easily notice the earliest stages of hair loss. I was "lucky."
My heart sank because when this happened, in February 1987, 1 was only twenty-two. Not that I wouldn't have still been upset had the balding process begun in my thirties or forties, but at twenty-two, with my adult life just beginning, the last thing I wanted to worry about was losing my hair.
The next morning, while in the shower, I noticed that the drain was completely clogged -- with my hair. I had a thick head of finely textured hair, and now I was faced with the possibility of losing it to male pattern baldness.
First I tried the then widely advertised Helsinki Formula, then KeraKare, a lotion that's applied to the scalp every night. Neither worked. In fact, some of the over-the-counter topical treatments that used to be marketed as baldness cures disappeared in the wake of the FDA ruling that a product couldn't advertise itself as a hair-loss treatment unless it had specific FDA approval as a hair drug. Yet many of these useless concoctions are still advertised and flood the market because of ineffective enforcement of the law.
For seven years I unsuccessfully experimented with every treatment on the market. I found that I really had two "careers." While running my video-production company, Spence-Comm, Inc., I was on an equally time-consuming quest to save my hair. Not only did I spend hours rubbing my head with lotions, I also had "top" New York dermatologists inject hormones into my scalp at $175 per very painful injection. I researched the biological effects of pulsed electrostatic-field treatment for hair, which turned out to be one of the biggest disappointments in the industry. Then, like so many other hopeful men, I ended up using minoxidil, which was then available by prescription only but would eventually be marketed over-the counter as Rogaine.
A so-called "prominent hair specialist" in New York City was providing me with his own concoction of minoxidil and Retin-A, and he told me to spray this on my scalp four times a day in order to grow hair. According to him, I was the perfect candidate for his potion: I was in my midtwenties then and my hair loss was not that extensive. My crown was beginning to thin, and my hairline had receded by about half an inch. But I was losing a tremendous amount of hair every day; the balding process was progressing very quickly.
The First Approved Hair Loss Drug
Minoxidil (Ioniten) was the first drug approved by the FDA for treatment of baldness. For many years, minoxidil, in pill form, was widely used to treat high blood pressure. It had one strange side effect, though: It grew hair in an unexpected manner. People grew hair on the backs of their hands, or on their cheeks, and some even grew hair on their foreheads.
Some enterprising researchers had the notion that applying minoxidil topically, directly on the head, might grow hair on balding areas. It did, in varying degrees depending upon the extent of hair loss, and at the time it was revolutionary.
Like all legitimate hair loss treatments, minoxidil works in varying degrees, depending on many hair loss factors. Now marketed over-the-counter under the brand name Rogaine, at the standard 2‰ solution or the extra strength 5‰ solution, the drug's side effects include dry, itching or flaking scalp (which is the most common, but easily reduced or eliminated by using common overthe-counter dandruff shampoos like Neutragena T-Gel, Head and Shoulders or Nizoral), and low blood pressure (which is rare and reversible once you stop using the drug). Minoxidil is not advised, however, for anyone who has heart disease because of the potential for cardiac side effects in those people at risk.
The most recent studies show that Rogaine Extra Strength for men (5‰ solution) regrew 45‰ more hair than regular strength Rogaine (2‰ solution). In the same group of studies, hair regrowth that was shown in month four while using regular strength was visible by month two while using extra strength. This indicates that Rogaine Extra Strength actually speeds up the hair growth process, making treatment that much more effective.
Rogaine is thought to work by stimulating and enlarging miniaturized hair follicles and reversing the miniaturization process. According to Pharmacia & Upjohn, which manufactures and markets Rogaine, regrowth is more likely to occur if you have a large number of only partially miniaturized hair follicles. These kinds of follicles still produce hair, but this hair will be thinner than unaffected strands, and must be at least 3/8 of an inch or more in length for it to favorably respond to Rogaine.
Unfortunately, according to Pharmacia & Upjohn, any area of your scalp with no hair or where only vellus (peach fuzz) hair remains is less likely to respond to treatment. Rogaine is the most effective for the earliest stages of hair loss. The manufacturer also cautions that Rogaine should not be used by those under 18 years of age; those using a topical prescription product on the scalp; those experiencing sunburned, inflamed, infected, irritated or painful scalp; or those whose hair loss was sudden, indicating that it is not male pattern baldness, but some other form of hair loss.
Rogaine's effectiveness can be enhanced by simultaneously using other treatments, including Propecia, herbal, and nutritional approaches. Some men with sensitive scalps do not make good candidates for treatment with Rogaine, and once those men stop using the drug, their scalp irritation will go away.
The DHT Connection and Finastefide
By late 1994, 1 had amassed quite an amount of information on baldness, so when I read in the New York Times that a number of drug companies had committed to putting the next baldness breakthrough on pharmacy shelves, I was intrigued that among the drugs that were being studied was finasteride, the prescription prostate drug that Merck & Co., the pharmaceutical company, manufactured and marketed in a 5 mg. dose under the brand name Proscar. Finasteride prevents testosterone from converting into DHT (dihydrotestosterone), the androgen that can cause not only prostate problems but the demise of hair follicles. I knew from my reading about testosterone that Merck was on to something. Only a product that changes the body's chemistry, introduced internally (with a pill, for instance), could combat the hormonal assault on hair follicles.
Doctors and patients discovered that Proscar, originally prescribed to treat benign prostate enlargement, had an exciting, positive side effect: It grew hair on bald men's heads -- "regular" (called terminal) hair, not peach fuzz. The stage was finally set for a truly effective balding treatment.
To understand why this is the case, here's a crash course on how testosterone causes hair loss: For many years, the scientific community and the rest of us were under the impression that androgenetic alopecia (male pattern baldness) was caused by the predominance of the male sex hormone, testosterone. While testosterone does play a role in the balding process, the accumulation of scientific study over the course of decades has revealed that dihydrotestosterone (DHT), a derivative of testosterone, is actually the main culprit.
Testosterone converts to DHT with the aid of the enzyme Type II 5-alpha-reductase, which is held in a hair follicle's oil glands. Scientists now believe that it is not the amount of circulating testosterone but the level of DHT binding to receptors in scalp follicles that determines hair loss. DHT shrinks hair follicles, making it impossible for healthy hair to survive.
The first evidence of the relationship between male pattern baldness and testosterone was discovered by a psychiatrist early in the twentieth century. At the time, castration was commonly performed on some of the more uncontrollable psychiatric patients in sanatoriums. Castrating these patients not only eliminated their sex drive, it also produced a calming effect, much like a sedative.
This particular doctor noted that one of his castrated patients had a full head of hair, while the patient's uninstitutionalized twin brother who came to visit was very bald. The doctor then noted that the mentally ill twin had been castrated before the onset of puberty. The doctor was curious: If a pure form of testosterone was injected into the castrated twin, would it affect his full head of hair? Within weeks of the injection, the twin began to lose his hair.
In 1942 James B. Hamilton of Yale published a report in the American Journal of Anatomy detailing his studies of men whose testes had been removed before puberty for medical reasons and noting the fact that these men never went bald, even if they had bald relatives. When these castrated men were given testosterone injections, however, their hair began to fall out, and they were soon almost as bald as some of their relatives. If the testosterone injections stopped, their hair loss stopped progressing. Interestingly, if the men came from families with few bald men, the testosterone injections didn't cause much baldness. This was the first time science had noted that baldness was linked to both hormones and genes.
These studies revealed that if testosterone has never been introduced into the hormonal pool, then hair loss will not occur. But once testosterone is activated (at puberty, for those who have not had the misfortune of being castrated), it creates a biochemical reaction in people who have a genetic predisposition to androgenetic alopecia, male pattern baldness.
In the case of the twin at the sanatorium who grew bald once testosterone was introduced into his body, it's important to note that when the doctor stopped giving him testosterone, the twin did regrow some of his hair, but not all of it, since many of his hair follicles had died.
Only decades later would scientists discover that follicles die not from the testosterone itself but from its follicle-killing derivative, DHT, and that hair will not grow from dead follicles.
The drug finasteride was the result of a long term research project at Merck that began initially in the mid-1950s, according to the company. At that time, Merck scientists were conducting research into the role of androgens (like DHT) in benign prostate enlargement and male pattern baldness. By the 1960s, Merck researchers had learned that Type II 5-alpha-reductase (an enzyme) was necessary to complete the conversion of testosterone to DHT, and this was the basis for the development of finasteride, which inhibits this particular enzyme.
Merck decided to focus first on prostate enlargement, the company says, because the medical need for a treatment of the condition was greater.
The 1970s brought more confirmation of the DHT and Type II 5-alpha-reductase connection to male pattern baldness. Scientists in the Dominican Republic were looking at the cases of male children who, though born with XY chromosomes, grew up looking like females. Only when they went through puberty was it apparent that they were male. Their genitalia were almost nonexistent as children, but they then grew to normal size once the body manufactured testosterone at the onset of puberty.
The researchers noted that these boys never lost their hair as they grew older. Although all of these boys had normal -- and in some cases raised -- levels of male hormones, they all had no trace of Type II 5- alpha- reductase, the enzyme that converts testosterone to DHT, which then kills hair follicles in the male pattern baldness areas of the scalp.
In the mid-1980s, Merck scientists working with their prostate drug finasteride, marketed as Proscar, knew that cases of male pattern baldness were rare in men with low levels of Type II 5alpha-reductase. The company then turned its attention to using finasteride to treat male pattern baldness. They would need separate FDA approval to market finasteride as a hair-loss drug treatment, though, so in 1992 Merck began testing the drug (which they would eventually market under the brand name Propecia) specifically to treat male pattern baldness so they could head down the road to FDA approval.
Remember that it's actually in the hair follicles that testosterone converts to the more powerful DHT, which behaves differently depending upon where on the body those follicles are located. The male pattern baldness areas of the head -- the front, temples, and crown -- are more sensitive to testosterone and therefore quicker to convert it to DHT. As DHT shrinks a hair follicle, shortening a hair's growth cycle, a normal hair's diameter lessens and lessens over time until the hair is tiny and fine. Ultimately, no hair can grow when the follicle dies.
Elsewhere on the body, DHT behaves differently. It actually stimulates hair growth in follicles located on the chest, back, shoulders, eyebrows, and ears, even though it kills hair follicles on the scalp.
Geographical and cultural influences also affect hormones. Compared to Asian men, Americans have more of the enzyme that converts testosterone to DHT and thus have more body hair and more baldness. The role that a culture's food choices may play in the action of our hormones is the subject of ongoing study by scientists (and is discussed in Chapter Two).
Women naturally have far less testosterone than men -- actually just a trace of the hormone. But when a woman has more than the usual amount in her system -- because of medication, a hormoneproducing growth, or another problem -- she can also develop male pattern baldness. Because finasteride can cause birth defects in a male fetus, women of childbearing age who are not sterile should not take finasteride. Although it is not intended for use by women, in certain circumstances a doctor may prescribe it for a woman with androgenetic alopecia.
Apparently baldness leads to more baldness. In balding areas, the oil glands in the hair follicle become larger. Since it's these glands that hold the enzyme that converts testosterone to the follicle killing DHT, there's always a lot of the enzyme in these enlarged glands in balding areas, ready to further weaken the follicles. Oil gland activity is also increased by higher amounts of circulating hormones.
Hormones are not static. Testosterone levels in some men drop by 10 percent each decade after age thirty. Testosterone levels peak in the fall and are lowest in the spring. During the spring low, hair grows the most. As testosterone levels rise, heading toward fall, so does hair loss. By fall, twice as much hair is lost than was lost in the spring. Both men and women have a similar hair growth seasonal cycle. The cyclic nature of both our hair and hormones is one reason...
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