SUN PROTECTION: Myths and truths

                                                                   

            Summer is here, and despite growing familiarity with the concept of sun protection over recent years, misconceptions abound concerning sun safety and how best to protect yourself from the damaging effects of the sun. The causative role of the sun is indisputable in skin cancer and premature aging of the skin. Even melanoma, the most rapidly increasing cancer in white populations, is strongly associated with intermittent sun exposure.

            Here are six of the most commonly held myths surrounding sun protection.

            Myth #1: All skin types require sunscreens.

            The truth: Individuals with very fair skin (red hair, freckles, sunburn always) and fair skin (blue to hazel eyes, light skin, sunburn easily) benefit most from regular use of sunscreens. Natural pigment (i.e. melanin in the skin) is by far the most effective sunscreen. The darker a person’s skin, the greater the innate protection. Individuals with olive-colored (tan easily, rarely burn) or darker skin (never burn) have very little risk of developing the types of skin cancer that arise on sun-damaged skin. Sunscreens can help prevent further darkening after exposure to the sun, but skin cancer prevention and photo-aging is much less of an issue for individuals of color.

            Myth #2: If you use appropriate sunscreens, sun exposure is safe.

            The truth: Sunscreens mostly protect against burning rays (ultraviolet B, or UVB). Deep penetrating tanning rays (UVA) still get through to the dermis where they contribute to aging and skin cancer. The absence of sunburn with sunscreen gives a false sense of security and often translates to spending more time in direct sun. This is a potentially harmful practice, one that explains, in part, the increased incidence of melanoma that has been reported in sunscreen users.

            The correct approach, then, for preventing skin cancer and photo-damage is to use sunscreens regularly as one part of a lifestyle of sun avoidance behavior (hats, long sleeves, long pants, shade). Daily sunscreens are especially important on the face, ears, neck and hands where coverage with clothing is difficult. If your goal is getting a tan or a dose of Vitamin D, it is safer to spend short amounts of time in the sun without sunscreen, then cover up or seek an umbrella.

            Myth #3: If SPF-30 is good, SPF-60 must be twice as good.

            False. Two points are crucial here. First, SPF-4 or SPF-8 sunscreens deliver inadequate protection, but once you get to SPF-15, you achieve more than ninety-two percent protection. Increasing to SPF-30 or SPF-60 merely takes it to ninety-four or ninety-five percent. The amount and frequency of application become the important issues, as long as you are using SPF-15 or higher.

            Second, SPF grades only UVB protection (the burning rays). There is no equivalent grading system for UVA protection. One must rely on the ‘broad spectrum’ labeling to indicate UVA protection, and it is often inaccurate. The best UVA blockers are zinc oxide and titanium dioxide.

            Myth #4: You don’t need sunscreens on a cloudy day.

            The truth: Ultraviolet light intensity is not reduced on cloudy days. The rays get jumbled in the clouds, but the intensity hitting a person’s skin at ground level is the same as on a clear day. Cooler temperatures with clouds give a false sense of security which often means that people spend more time exposed without protection. Also, with ultraviolet intensity being greatest on June 21^st every year in the Northern hemisphere, UV intensity in May can be the same as July, April can be the same as August, and March the same as September. Sunscreens should be used at least from March through September.

            Myth #5: Sunscreens must be applied thirty minutes before going in the sun.

            The truth: This is totally false. The chemicals and blocking agents in sunscreens are fully effective right out of the tube. In fact, the sun-blocking effects of sunscreens have been shown to be the strongest immediately after applying to the skin, and gradually fall off in strength over several hours.

            Myth #6: Only specialty clothing provides good sun protection.

            The truth: All types of clothing, when dry, protect from the skin from both UVB and UVA radiation. Of course, the tighter the weave, the better the protection. Specialty clothing manufacturers have designed excellent sun-protective clothing and have confirmed high SPF equivalency values, but the real benefits lie more in the comfort and lightness of their fabrics, not the sun protection per se.

            The exception to this rule happens when fabrics get wet. Most standard clothes, t-shirts for instance, become worthless as sun barriers when they get wet. Specialty sun-protective garments maintain their SPF when wet, and highly protective swimwear is available for children and others spending hours in the water.

            

Vitamin E and THE SKIN, PART II: ANTI-OXIDANT EFFECTS

In the last posting, I laid out the uncertainties of using Vitamin E directly on skin to reduce or prevent scars. In this post, I discuss the antioxidant effects of Vitamin E.

OXIDATIVE STRESS is the issue. Oxidative stress occurs when chemicals called ‘free radicals’ form naturally or following injury (surgery, smoking, sun damage). Free radicals damage DNA, destroy cell membranes, and trigger inflammation. They have been implicated in the development of skin cancer. Vitamin E neutralizes free radicals, thus protecting cells from oxidative stress.

True Vitamin E deficiency occurs only in rare diseases where dietary absorption is poor. However, a study of almost 10,000 individuals suggested that the majority of men and women in the U.S. don’t meet current recommended dietary intake of Vitamin E. In addition, studies have shown that outer layers of skin have a relative shortage of natural antioxidant protection.

THEREFORE, THE QUESTION: Does supplemental Vitamin E (orally or topically on the skin) deliver real health benefits?

THE ANSWER: Possibly.

THE EVIDENCE: Hundreds of well-designed trials have been published in which oral Vitamin E alone or in a cocktail of multiple antioxidants was used as treatment in a wide range of diseases. Some were successful, some failed.

A partial list of successes with oral Vitamin E: Eczema (atopic dermatitis); tinnitus; mucositis after chemo in kids; glaucoma; early macular degeneration; kidney damage after lithotripsy; skin barrier function; post-radiation saliva flow; recurrent embryo loss; cholesterol levels in kidney patients; vitiligo; melasma; kidney damage after contrast exposure; cardiovascular disease; mastalgia; non-alcohol fatty liver.

A partial list of failures: Sjogren’s syndrome; exercise-induced oxidative stress; drug-induced neurological side effects (tardive dyskinesia); sexual dysfunction in men; acute mountain sickness; glaucoma surgical complications; prostate cancer; fatty liver in adolescents; Down’s syndrome; throat cancer; and SKIN CANCER.

Re: failure of Vitamin E in SKIN CANCER: A huge study in France showed that dietary supplementation with a cocktail of oral Vitamin E, C, Zinc, selenium and carotene was associated with an increase in skin cancers in women but not in men. The authors speculated that the sun damage may have occurred long before the antioxidant treatment was started. They also reported prior studies showing increased melanoma risk in women who had supplemented with selenium.

The largest body of evidence with topical Vitamin E supports its use as a photo-protective agent. Many studies demonstrate that Vitamin E protects against the damaging oxidative effects of sunlight (ultraviolet light exposure). Studies have also proved that the addition of topical Vitamin C enhances the antioxidant effect of Vitamin E. Unfortunately, concentrations of Vitamin E in cosmetic products vary widely and an optimal concentration has never been established.

In summary, topical Vitamin E can help protect against sunburn and the long-term aging effects of UV. Whether it protects against skin cancer is not known. A bigger question remains, though: Is Vitamin E more effective than sunscreens and sun avoidance behavior? More studies are needed. At the present time, no dermatologist would recommend Vitamin E-containing products as substitutes for sunscreens.

TAKE-AWAY POINTS:

1. Vitamin E can help in the management of several medical conditions.
2. Most of the known benefits of Vitamin E come from antioxidant properties that prevent or reduce tissue damage from inflammation.
3. Since dietary intake of Vitamin E is often inadequate, daily supplementation in the range of 400 to 800 I.U. may be beneficial and appears to be safe.
4. Topical Vitamin E can help prevent oxidative stress in the skin, and may be helpful in treating vitiligo (pigment loss) and melasma (increased pigment).
5. Vitamin C enhances the antioxidant effect of Vitamin E.
6. Although skin reactions can occur with topical Vitamin E, they are not common.

Disclaimer: Dr. Shaw has no financial conflicts of interest pertaining to the products discussed in this blog post.

NEXT: Sun protection: myths and truths.

VITAMIN E AND THE SKIN: part one

        or

Does Vitamin E prevent or treat SCARS?

                               by James Channing Shaw, MD

Vitamin E is an immensely popular treatment for minor wounds and scars. Belief in this treatment, however, is not entirely based on scientific evidence.

What is the evidence that Vitamin E prevents scars?

The answer: The evidence, so far, is mixed.

Scar, thickened dermis

Normal skin, low-power

Evidence does exist to support the concept of scar treatment with Vitamin E. Scars are made by cells called fibroblasts in the dermis layer of the skin. Vitamin E applied to the skin does penetrate into the dermis where collagen is made and in laboratory settings, Vitamin E can prevent the production of collagen by fibroblasts.

Despite the laboratory evidence, studies of Vitamin E and scars in human patients are small and have shown mixed outcomes.

In a study of 159 scar revisions in burn patients (1986)¹, researchers showed no benefit with Vitamin E cream over plain cream or steroid cream, and almost twenty percent of patients developed rashes from the Vitamin E product.

In a small study (1999) ², fifteen patients applied a plain cream to one half of their healing scar, and a Vitamin E cream to the other half. There was no long-term benefit with the Vitamin E cream, and one third of those using Vitamin E developed skin reactions. The authors discouraged the use of Vitamin E.

A more promising study involved 428 children in Italy (2010) ³  under the age of ten. Half of the children undergoing a small inguinal (hernia) surgery were given a Vitamin E gel to use twice daily for fifteen days before the surgery and thirty days after the surgery. After six months, parents reported ‘keloids’ in 6.5% of the non-Vitamin E group, but no parents reported ‘keloids’ in the treatment group. While this study had design flaws, and no pictures of the keloids (which are highly unusual in children anyway), the authors proposed a possible benefit with Vitamin E.

One study⁴  suggested that it is likely the moisturizing barrier protection of Vitamin E oil and silicon gels that had benefit in wound healing and scar prevention. To add to that theory, two well-designed studies ^{5 ,6}  of wound healing showed that a non-medicated ointment (Aquaphor in this case) was superior to antibiotic ointments after laser surgery, supporting the thinking that moisturizing barrier protection may be more important that the Vitamin E itself.

TAKEAWAY POINTS:

1. Topical Vitamin E has properties that have the potential to be beneficial to the cosmetic appearance of certain scars.
2. Large, well-designed studies are needed to prove it.
3. The risk of using Vitamin E on wounds following minor surgeries is small.
4. Up to one third of patients using topical Vitamin E can develop rashes.
5. It may be the oil base, not the Vitamin E itself, that helps with healing.

Next blogpost: Vitamin E as antioxidant

References:

1. Jenkins M et al. JCBR, July/August 1986
2. Baumann L et al.  Dermatol Surg 1999;25:311–315
3. Zampieri N et al. Journal of Plastic, Reconstructive & Aesthetic Surgery (2010) 63, 1474-1478.
4. Panin G et al. Ann. N.Y. Acad. Sci. 1031: 443–447 (2004).
5. Draelos Z et al. J Am Acad Dermatol 2011, VOL 64, N0 3; S23-S29.
6. Trookman N et al. J Am Acad Dermatol 2011 VOL 64, No 3; S8-S15.

SHINGLES (Herpes Zoster): Progress has been made!

Shingles is a household term these days. The medical term is Herpes Zoster. Everyone over age sixty likely knows someone who has had a case of Shingles. An estimated 500,000 Americans per year get Herpes Zoster, and up to one per hundred adults per year if you are older than 65. Worldwide, it's a huge problem that, while usually non-fatal, can cause terrible suffering.

The amazing development is that advances have been made in the vaccine arena that could almost make Herpes Zoster a thing of the past. See end of this posting.

In my 25-plus years in dermatology, I’ve frequently observed Herpes Zoster (Shingles) misdiagnosed, even by dermatologists, which delays treatment and leads to protracted and debilitating pain. The pain and suffering that comes from Herpes Zoster is underappreciated by doctors and patients alike. Furthermore, patients with suppressed immune systems (AIDS, organ transplant patients, certain malignancies) can develop life-threatening illness from Herpes Zoster when it spreads throughout the body.

Fortunately, if caught early enough, there are excellent treatments for Herpes Zoster. Diagnosing it early is not always easy. In addition to treating the ‘rash’ after it starts, there is a new vaccine that promises to prevent cases of Herpes Zoster. For us aging baby boomers, that is a real advance. Ads for Shingrix are plastered all over television because doctors haven't recognized that the vaccine has huge benefit.

So, what is Herpes Zoster and how can it be recognized, treated, and prevented?

Herpes Zoster comes from the reactivation of the chickenpox virus, called Varicella-Zoster Virus (VZV). After childhood chickenpox, the Varicella viruses (probably millions of them) become dormant and retreat to nerves in the spinal cord where they remain for the rest of our lives. With aging, or in the setting of certain diseases, immunity against VZV weakens, and the virus can become reactivated. When it does, instead of reactivating throughout the entire body, it reactivates in one nerve ‘root’ only. This single nerve root reactivation is what causes Herpes Zoster.

Herpes Zoster blisters on the right arm

small cluster of blister on the neck

DIAGNOSIS: Because only one nerve root is involved, the rash of Herpes Zoster happens on one side of the body along the path of a nerve, hence, one side of the face, across one side of the trunk, down one side of the arm, etc. In dermatology, we learn that with any new rash on one side of the body, we MUST consider Herpes Zoster as a possible diagnosis. Even with new-onset of pain without a rash along the path of one nerve, we have to think about early Herpes Zoster. The reverse is also true: any new skin rash involving both sides of the body or multiple limbs is probably NOT Herpes Zoster. Typically in Herpes Zoster, pain/burning/tingling usually comes first, followed in 24 to 48 hours by small red bumps and fluid-filled blisters where the nerve branches up to the skin.

TREATMENT: Early treatment limits the severity of Herpes Zoster in most cases. Once the rash of blisters and pain are established, it is too late, and treatment can only be directed toward reducing pain, not preventing it.

Three anti-viral drugs exist to treat Herpes Zoster: acyclovir, valacyclovir, and famciclovir. The latter two achieve much higher blood levels orally and are the treatments of choice. The first drug, acyclovir, has excellent anti-viral activity against the other Herpes virus called Herpes Simplex, but is less effective as an oral drug against Herpes Zoster. Patients with poor kidney function require lower doses.

The key to successful treatment is to treat early. This means patients need to seek help early and doctors need to have a high index of suspicion and institute treatment based on probability, not proof of the diagnosis. There is little to no risk to patients in treating in this manner, but delaying treatment can lead to months or even years of misery, pain, and disability. Doctors who see emergency or walk-in patients are the ones best able to help patients with evolving Herpes Zoster.

In severe or untreated cases, patients are often left with protracted pain called ‘postherpetic neuralgia’. Although it usually improves slowly over time, it can be excruciatingly painful for weeks to months, sometimes years. Treatments can be helpful, but often require sophisticated combinations of pain killers, gabapentin-like drugs, anti-depression drugs, and occasional use of nerve blocks.



disseminated VZV

In patients with suppressed immune systems for any reason, Herpes Zoster can trigger a more wide-spread illness throughout the body that can be life-threatening. Again, early diagnosis and treatment with anti-viral drugs is life-saving.

PREVENTION: Back in 2006, a live vaccine against Herpes Zoster was approved in the U.S. The vaccine, called Zostavax®, is basically a larger-than-normal dose of the Chickenpox vaccine used routinely in children. Zostavax® has been shown to reduce by 50% the risk of getting Herpes Zoster. It also reduces the risk of the protracted postherpetic neuralgia by two-thirds. Every individual age 60 or older who qualifies should request and receive Zostavax®.

The recent development: Shingrix® is a vaccine made from molecular subunits of the chickenpox virus plus an immune enhancer.  It has been shown to be safe (no accidental infection) and highly effective for up to three years (so far) of protection. Two doses are given a few months apart, and the injection into the deltoid can produce significant pain. The cost is around $300 but because it is so effective, it is likely that insurers will cover the cost, and many countries already provide the vaccine as a public health initiative.

If you are over 60, get Shingrix vaccine against shingles!

jameschanningshaw.com 

INGROWN TOENAILS: ANY WAY YOU CUT IT

by James Channing Shaw, MD

Twenty-five years of practice in dermatology has taught me that ingrown toenails have little or nothing to do with whether nails are cut straight across or with a curve. What you mostly read is 'cut toenails straight or you'll get ingrown nails'. The message comes from supposed experts such as podiatrists and doctors. Every child on the face of the earth grows up thinking this. And why not? They hear it from grown-ups who must know everything. Grown-ups, after all, are supposed to know stuff.

Once again, I am here to dispel another myth: the myth of the straight-cut toenail. There is no evidence to support the notion that cutting nails with a curve causes ingrown nails, or that cutting straight prevents them. Those who preach straight-cut are merely perpetuating unsubtantiated traditional beliefs. Studies have not been done and closer examination of the rationale exposes its faults.

In every case I've seen, and there have been many, patients have always done exactly as they were told: they cut their toenails straight across and still developed ingrown toenails. Ingrown nails are more about an individual's own anatomy, plus, in some cases, trauma from shoes.

The photograph below shows a typical ingrown toenail. The nail is straight-cut, but the ingrown nail goes nearly to the cuticle. The manner in which the nail was cut couldn’t have influenced the ingrown nail close to the cuticle.



What, then, is an ingrown nail? Most importantly, it appears NOT to be an infection in the true sense, i.e. caused by bacteria. Most cases of ingrown nail don't respond at all to antibiotics. Instead, an ingrown nail results when the tissues at the side of the nail get irritated, inflamed, and swollen, leading to redness, pain, and tissue breakdown with oozing and pus. There is one exception: if you cut too close and injure the skin, you can introduce real infection, but it behaves differently: more rapid in onset, more painful, and responds to antibiotics.

It is thought that the sides of the nail must play a role in ingrown nails, that the edge 'digs' into surrounding tissue, either naturally or from shoe pressure. We know this because the problem goes away when the lateral sides of the nail or excess nail fold skin are permanently removed by surgery. Whether from the nail itself, or excessive surrounding skin, the individual's reaction to microscopic trauma is probably a key factor.

What makes NO sense is the belief that cutting the nail influences how a nail grows. If that were the case, we might expect to see it happen with finger nails, but we don’t: fingernails and toenails grow out regardless of how they are cut. Nails grow by sliding horizontally outward from the cuticle area. Whether you cut straight or curved, the nail still slides toward the tip in the way it is genetically programmed to do. The white part that gets clipped away has already separated from its base (the nail bed), and even if you cut too close, it cannot influence how the nail grows.

The big question is whether we have ANY control over preventing ingrown toenails. My suspicion is that we do not. Reasonable hygiene (but not too aggressive) is as much as we can recommend. Plenty of toe space in shoes also seems wise (but not proven). All definitive treatments, however, involve surgery, although many devices and practices to flatten out the nail have been tried with mixed results.

It would be good if someone did a scientific study of curved cut versus straight cut, but since this is a non life-threatening condition, it’s not likely to happen. In the meantime, if you would like some contour with your pedicure, give it a try. If you have never had ingrown nails, the odds are in your favor. Go easy at first. A little rounding of the edges of the big toenail won't hurt you.

WINTER ITCH AND WINTER DRY SKIN

                                                                         James Channing Shaw, MD

If you look with a magnifying lens at very dry skin, it looks like a dry lakebed, with multiple shallow cracks. The medical name for this dryness is xerosis. How does xerosis happen, who gets it, and what can be done to treat it?

Normally the skin acts as a barrier to evaporation; water is prevented from escaping by the top most layer of the skin called the stratum corneum. In this layer skin cells are stacked on top of each other, each one overlapping the ones below. Each stratum corneum cell contains material called keratin that is nearly impermeable to water. Between the cells is a mixture of lipids (fats), called the lipid layer.



This multlayered sandwich of cells and lipids creates an armor that protects against water loss. However, since we are all different, some individuals have better functioning stratum corneum than others and are better protected from drying out. Those of us who are genetically unlucky in this regard are susceptible to dry skin, primarily from two environmental causes. One is decreased humidity in the air and the other is a damaged lipid layer. Low humidity pulls water from the cells of the stratum corneum, making them brittle, curled at the edges, and separated. Add wind to the dry air and the problem gets worse.


Damaged lipid layer comes from chemicals on the skin that wash away the lipids. Our hands are the most susceptible to this kind of damage because they have the least amount of lipid in the stratum corneum layer. Ironically it is our hands that get most exposed to chemicals such as soap and detergents. Solvents like alcohol, cleansers, and ammonia are even worse. With the amount of hand washing we have all been taught to do, it is no surprise that dry cracked hands are a common problem in the winter.

Severe xerosis: this case has become erythema craquelé

 
Why is winter air such a problem? Two reasons: 1) cold air holds less moisture than warm air, and 2) artificial heat in our homes dries the air to extremes. Indoor humidity of less than 10% is common during a cold winter. Only the heartiest of stratum corneum can withstand this desert-like effect without becoming dry and cracked.

When skin dries out, most people start itching. The shins and the lower back are the most common places for ‘winter itch’. Faces and lips can also become dry, flaky and cracked. The hands are different: finger tips can split and are very painful. While this can be annoying and uncomfortable, the good news is that very little serious illness comes from skin dryness.

So….what to do? There are basically two ways to minimize the problem: 1) increase humidity in the air, and 2) provide skin barrier protection against water loss. A vacation in the tropics returns skin to normal within a week or two. The increased humidity in the warm air of the tropics stops water loss from skin. A humidifier, while not as good as a tropical environment, can be helpful in your home. For dry cracked hands, a lesson from feet is instructive. Feet don’t dry out as commonly as hands because they are protected all day in warm humid shoes and socks. Gloves provide the same protection for hands that sox do to for feet. Soft comfortable gloves, not rubber gloves, are best. The goal is to increase humidity, not cause perspiration and soaking.

For more skin barrier protection, additional ‘lipid layer’ needs to be applied. There is an important lesson here concerning lotions, creams, and ointments. Lotions are mostly water with some oil (lipid) and when applied to the skin, the water evaporates leaving a small amount of oil remaining. This gives the false impression of 'absorption', but lotions help only in the mildest cases of dryness. Severe dryness calls for thick creams (less water, more lipid), or ointments like petroleum jelly (all lipid, no water). The greasy ointments give the best protection but take some getting used to.

The worst cases of dryness may require professional help and prescription treatments. For splits in the hands, cover with tape or a bandage which helps the pain and speeds healing. Soaking hands in warm water for 10 minutes puts some moisture back if a thick cream or ointment is applied immediately, followed by gloves. The same is true for the whole body: a plain water soak for 10 minutes followed immediately by greasy creams or ointments can help the driest skin. The secret is to not let the water evaporate before applying moisturizers. Apply the cream or ointment within 60 seconds. It takes a while to get used to the greasy feel but the improved moisture in the skin should be apparent within a few days.

Finally, two common misconceptions deserve mentioning:
1. Applying moisturizers does not shut down your skin’s ability to make its own oil. It is safe to use moisturizers as much as needed; the skin will not become dependent on them.
2. Moisturizers per se will not prevent aging of the skin unless they contain sunscreens.

HORMONAL ACNE IN WOMEN

by James Channing Shaw, MD

It is common for women to get acne in their 20s or 30s for the first time. The cause usually centers around hormonal issues.

A common scenario is the woman who gets acne within a year of stopping birth control pills. Women often take birth control pills for years in their teens or early 20s, and their acne is controlled. When they stop taking birth control pills, hormones return to having fluctuations that lead to acne.

Another cause comes from irregular ovarian activity that causes hormone fluctuations. These women often have irregular periods or acne that gets worse a week before each period. Any woman can have this problem, and at its worst, it is part of polycystic ovarian syndrome. There are other diseases that lead to hormonal acne, but fortunately they are rare.

The hormone that causes acne is the male hormone testosterone and its metabolites. Women produce testosterone in small quantities, but several conditions lead to increased testosterone effect. An increase in body weight, for example, shifts hormones toward more testosterone effect. Ovaries or adrenal glands can spontaneously overproduce male type hormones. Stress causes acne mainly through overproduction of hormones by adrenal glands.

This photograph shows a typical woman with moderately severe hormonal acne. Women with adult hormonal acne commonly have pre-menstrual worsening, and involvement of the lower face and jaw-line. Their acne is usually larger red pimples instead of blackheads on the forehead. Increased oiliness on the face is common. Some women have unwanted hair growth on the face. Irregular menstrual periods are common as well.

Standard topical acne treatments can be effective in women with adult acne, but most need hormonal treatments for optimal control. Even Accutane® is less effective in women with hormonal acne. The best treatments for adult women are birth control pills and spironolactone.

Birth control pills not only provide a steady state of hormones, they reduce overall testosterone effect through a protein called SHBG (sex hormone binding globulin). The net effect (in addition to not ovulating, i.e. prevention of pregnancy) is less stimulation of the oil glands and facial hair follicles. Many women can achieve complete control of their acne with birth control pills alone. Health risks from birth control pills are fortunately very low, but certain women have higher risks of blood clots, and full discussion with the prescribing doctor is essential. Brands of birth control pills differ by country, and some are marketed for acne.

Spironolactone is an oral drug that blocks the receptor for testosterone and prevents hormonal stimulation of acne. This drug is mainly used as a diuretic in older patients. The acne benefit was discovered as a side effect years ago. Spironolactone is well tolerated by itself, with a 40 year track record of safety in young women, but works best when given together with birth control pills. Side effects include menstrual irregularities when it is given alone.

This photograph is the patient above after a year of combination hormonal treatment. Her acne is much improved and the hair on her lip has reduced. Many women achieve excellent control within a few months with hormonal treatments, but ongoing treatment is necessary in most cases. It is important to find a doctor who is familiar with the use of these drugs for purposes of monitoring.

Finally, two recent developments in acne: 1) Cosmetics have been shown not to aggravate or cause acne in most cases. 2) Dietary influences of a western diet high in carbohydrates and dairy products may worsen acne through complex hormonal mechanisms, so a reduction in carbs and milk products may be beneficial.

HAIR LOSS (ALOPECIA)

                                      James Channing Shaw, MD

 Some of the most worried patients in a dermatologist’s practice are those who are losing their hair. The medical term for hair loss is ALOPECIA. The most common type of alopecia is male balding, but there are many conditions that lead to hair loss, some temporary, some permanent. In this post, I discuss only the most common causes.

Hair growth cycles. To understand hair loss, you have to understand hair growth cycles. 80% of hairs on the scalp are in active growth-phase (called Anagen phase), which lasts for years. When growth-phase is completed, the hair stops growing, the root becomes small and round, and the hair goes into a resting-phase (called Telogen phase). After about ninety days in resting-phase, the hair falls out, and a new hair root begins making a new hair. Only 20% of human hairs are in resting-phase at any one time. By comparison, some animals ‘shed’ seasonally because all hairs go into resting-phase at the same time.

Growth-phase (anagen) roots are the ones most vulnerable to illnesses or medications. The prime example is cancer chemotherapy. Chemotherapy destroys rapidly growing cancer cells and growth-phase hair roots get damaged as innocent bystanders.

Androgenetic alopecia. The most common form of hair loss is male pattern balding (medical term: ‘androgenetic alopecia’). It is a genetic response to the male hormone testosterone which men have in abundance and women have in small amounts. Androgenetic alopecia usually happens gradually with no noticeable shedding of hair, just a relentless thinning and shortening of existing hair until (in worst cases) there is complete balding of the top of a man’s scalp. Women with androgenetic alopecia usually do NOT go bald, just thin. The growth-phase hair roots become smaller and smaller over years until they are too small to make visible hair.




Androgenetic alopecia





Treatments for androgenetic alopecia. It is now known that the naturally modified form of testosterone called dihydrotestosterone (DHT) is the culprit of androgenetic balding. Without DHT, there is no balding whatsoever in men. (We know this from studying families that cannot make the DHT). Therefore, the drug finasteride (Propecia®) was designed as the first effective drug for male balding because it blocks the conversion of testosterone to DHT. Unfortunately, Propecia does not grow new hair, it merely slows the balding process. In post-menopausal women, sadly, it has very little positive effect.


Minoxidil (a blood pressure drug) was discovered to have the side effect of hair growth, so a topical product Rogaine® was developed which can be a helpful adjunct to treatment but rarely produces a full head of hair. Statistically, about one third of men see benefit after a year, slightly higher in women.


For women with androgenetic alopecia, hormonal treatments are the most effective, though limited. In young women, birth control pills plus antiandrogen drugs (spironolactone) are used together, along with Rogaine® topically. Occasionally Propecia® is added but no large studies have proven its effectiveness in women. In older women, hormone replacement therapy (HRT) plus spironolactone are most commonly used.

Telogen effluvium

Telogen effluvium. Shocks to the system cause hair to fall out by converting growth-phase hair to telogen (resting) hairs. A high fever or general anesthesia during surgery can trigger many hairs to stop growing. They don’t fall out right away but go into the resting phase for 60 to 90 days and then fall out. Pregnancy is another example. Many of us know women who delivered a baby, and three months later started losing their hair. Fortunately the hair usually grows back. This kind of resting-phase hair shedding is called ‘telogen effluvium’. Other stresses that cause telogen hair loss are surgery, blood loss, or any severe illness.

Chronic telogen effluvium. This is the diagnosis when increased shedding lasts for months. Thinning of total hair mass occurs in worst cases. In young adult women, low iron has long been thought to contribute by triggering growth-phase hairs to convert to resting-phase hairs, and if thirty or forty percent of hairs are constantly in resting-phase, shedding increases, in the shower drain, on brushes, on clothes. Since women lose blood every month with menstruation, and if iron intake is inadequate, healthy growth of hair may be impaired. The diagnosis requires a specific iron test called ferritin which indicates the total body iron stores. The ferritin level should be above 40 for adequate hair growth. Eating more red meat or taking iron supplements can reverse the problem. The iron theory has recently been challenged in new studies, and further investigations are needed.


Many drugs can trigger ongoing hair loss of the ‘chronic telogen’ type. Fortunately it is not permanent, but it is often difficult to identify the medication causing the problem when multiple medications are being given. Stopping or changing medications requires careful monitoring by a physician.

Other diagnoses:

Alopecia Areata

Alopecia Areata. AA, though not as common as the types described above, is a huge topic that goes beyond the scope of this posting. Briefly, it is immune-mediated (autoimmune) hair loss. It can be mild, occurring in localized areas of the scalp, or in the worst cases, it can affect every hair follicle on the body. Patients with AA should be screened for other autoimmune conditions such as diabetes, thyroid disease, and anemia. All treatments for AA are designed to turn off the immune destruction of growth-phase hair follicles. Treatments range from local injections of steroids all the way to internal immune-suppressing drugs. Results are frequently unpredictable.

Tinea Capitis (ringworm)

   Ringworm (medical term: tinea capitis). This is a fungal infection of the scalp, common in children. It is contagious through direct contact, combs and brushes. Any child with patches of hair loss should be seen by a skilled nurse or doctor to make the diagnosis and treat with anti-fungal drugs.



Lupus. A more severe and different autoimmune disease, Lupus erythematosus can affect hair, leading sometimes to permanent scarring hair loss. Treatments also range from injections to serious immune suppressants.

Natural approaches, vitamins, nutrients. Iron and protein are probably most important. Iron is discussed above. Modern western diets frequently do not have enough protein for healthy hair. While not studied scientifically, individuals should eat three portions of protein per day for optimal hair growth.

Too much vitamin A (greater than 25,000 IU/day) can cause hair loss. Biotin deficiency causes hair loss, and supplementation with Biotin can be beneficial in telogen type hair loss. Research has shown that ingredients in Chinese green tea block 5- reductase and could lessen androgenetic alopecia, although no large scale clinical studies have been done.

Finally, a word on commercial hair care products. There is no hair care product that penetrates deep enough to influence hair growth at the level of the roots. Most products are washed off and even those that remain on the scalp cannot penetrate deep enough to influence the roots. No matter what they claim about roots, hair care products can only affect the shape and texture of existing hair and the top layer of scalp skin. If too harsh, they cause breakage over time.