Archive for May, 2013

New Sunscreen Labels Decoded

If you’re out in the sun playing tennis or golf, jogging or cycling, you need to protect your skin from the damaging ultraviolet rays.

Newly revised sunscreen labels should make it easier for you to make a smart choice on which products to use.

The Food and Drug Administration (FDA) now requires that labels must provide information about whether a sunscreen will protect against skin cancer in addition to sunburn, and will also have to indicate whether a sunscreen is water-resistant, which is what you want if you’re exercising outside.

To reduce your risk of skin cancer and early aging, the American Academy of Dermatology recommends using a sunscreen with the following features listed on the label:

Broad spectrum, which means the sunscreen protects against ultraviolet B (UVB) and ultraviolet A (UVA) rays.

A sun protection factor (SPF) of 30 or higher.

SPF 15 is the FDA’s minimum recommendation for protection, but the academy recommends an SPF of at least 30.

Water-resistant for up to either 40 or 80 minutes.

This means the sunscreen provides protection while swimming or sweating for the length of time listed on the label.

Available sunscreen options include lotions, creams, gels, ointments, wax sticks, and sprays.

Creams are best for dry skin and the face.

Gels are good for hairy areas, such as the scalp or male chest.

Sticks are good to use around the eyes.

Sunscreen should be applied liberally, and should be reapplied every 2 hours and after swimming or excessive sweating, according to the National Council on Skin Cancer Prevention.

Dermatologists recommend the equivalent of a shot glass full of sunscreen per application.

Sunscreens that are not water resistant must include a direction instructing consumers to use a water resistant sunscreen if swimming or sweating.

Karthik Krishnamurthy, DO, chief dermatology consultant with the Melanoma Program at Montefiore Einstein Center for Cancer Care, offers the following tips for the summer season:

Give skin the once-over.

Just one full-body skin check by a physician can be a lifesaver.

Additionally, monthly self-exams from the top of the head to the soles of the feet are highly effective in detecting early warning signs of melanoma, such as a mole that looks different.

“I remind patients of the ‘ABCDE’ rule to detect changes in a mole: A is for asymmetry, B is for border, C is for color, D is for diameter, and E is for evolving,” says Krishnamurthy.

“Any suspicious-looking moles or moles that have changed shape or color should be looked at by a physician as soon as possible.”

Know your risk.

Just one blistering sunburn, even in childhood, is enough to substantially increase your lifelong risk for melanoma.

Other risks include frequent sunbathing or indoor tanning, and a family history of melanoma.

“Fair-skinned individuals with red or blond hair and light-colored eyes are also at higher risk,” says Krishnamurthy.

Don’t assume darker skin makes you immune.

A survey of 1,000 Hispanic adults in New York and Miami conducted by Krishnamurthy showed alarming misconceptions about perceived risk.

Nearly half believed those with darker skin cannot get skin cancer.

“This is very concerning because although melanoma is less common in darker-skinned individuals, there is a higher risk of late diagnosis with advanced melanomas and lower survival rates,” he says.

Another way to prevent skin cancer is to wear protective clothing, such as a broad-brimmed hat to protect the back of the neck and ears, which are highly susceptible areas.

Darker clothes and hats block more dangerous ultraviolet rays than light-colored ones, but you have to balance out heat problems.

A light-colored cotton shirt has an SPF of about 8.

The bottom line: choose the best sunscreen for you and use it early and often to protect your skin before you head out to play your chosen sport.

Taking Alzheimer Research Down New Protein Paths

I have been asked to write Commentaries for ConsultantLive, an online publication that reaches about 70,000 unique visitors every month, most of them primary care physicians, for which I am a regular contributor.

Here’s my first one on what’s happening in Alzheimer research.

Researchers around the world have devoted themselves to devising ways of blocking the production or accumulation of beta-amyloid, the protein that accumulates as plaques in the brains of persons with Alzheimer disease.

Now scientists are studying other protein targets, including tau, which accumulates in Alzheimer brains and disrupts the activity of brain networks, and the regulator protein CD33.

Last month, Dan Skovronsky, MD, PhD, Eli Lilly & Company vice president of tailored therapeutics, announced that the drug company was pursuing several potential treatments targeting the neurofibrillary tangles caused by tau and had just bought the rights to 2 tests for measuring tangles in the brain.

“The whole field has been amyloid-centric, amyloid-driven, but we need more than that.

That’s why we’re investing in tau,” Dr Skovronsky told The Wall Street Journal. “The most meaningful impact in Alzheimer’s might involve targeting multiple pathways and using combinations of drugs.”

Targeting Tau

Targeting a reduction in levels of the tau protein is likely to be a useful therapeutic approach in Alzheimer disease in parallel with efforts to target beta-amyloid levels, according to research that has identified a new set of genetic markers for the disease.

“We identified several genes that modulate tau levels in the cerebrospinal fluid.

These genes may be useful therapeutic targets for Alzheimer disease,” senior investigator Alison M. Goate, DPhil, Professor of Genetics in Psychiatry at Washington University School of Medicine in St Louis, told ConsultantLive.

Higher levels of tau and a phosphorylated version of tau (p-tau) in the cerebrospinal fluid are thought to reflect both tangle formation and neuronal cell death.

Because tau levels are proportional to the cell death, higher tau levels are associated with more severe dementia, Goate noted.

In the April 24 online edition of Neuron, Goate and colleagues reported that they had identified several genes that are associated with tau levels, and “thus targeting these pathways may provide a more specific means of reducing tau or p-tau levels,” she said.

If drugs could be developed to target tau, they might prevent much of the neurodegeneration that characterizes Alzheimer disease and, in that way, help prevent or delay dementia, Goate suggested.

Blocking CD33 Activity

Another potential strategy for developing treatments to stem the disease process is based on unclogging removal of toxic debris that accumulates in patients’ brains by blocking activity of CD33.

“Too much CD33 appears to promote late-onset Alzheimer’s by preventing support cells from clearing out toxic plaques, key risk factors for the disease,” said Rudolph Tanzi, PhD, of Massachusetts General Hospital and Harvard University, in an NIH statement.

“Future medications that impede CD33 activity in the brain might help prevent or treat the disorder.”

Tanzi and colleagues have found overexpression of CD33 in support cells, called microglia, in postmortem brains from patients who had late-onset Alzheimer disease.

What’s more, they found reduced amounts of CD33 on the surface of microglia and less beta-amyloid in the brains of persons who inherited a version of the CD33 gene that protected them from Alzheimer disease.

There also is evidence to suggest that CD33 works along with another Alzheimer risk gene in microglia to regulate inflammation in the brain.

Early detection of Alzheimer disease is critical to give persons at risk a better chance of receiving effective treatment.

Perhaps studies of proteins other than beta-amyloid will lead to useful therapeutic targets.