Exercise May Be an Effective and Nonpharmacologic Treatment Option for Alcohol Dependence

Alcohol abuse is highly disruptive of circadian rhythms, and circadian disruptions can also lead to alcohol abuse as well as relapse in abstinent alcoholics. Circadian timing in mammals is regulated by light as well as other influences such as food, social interactions, and exercise. A new study of the relationship between alcohol intake and wheel-running in hamsters has found that exercise may provide an effective alternative for reducing alcohol intake in humans.

Results will be published in the September 2010 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

“Alcohol abuse, characterized by routine craving for and consumption of alcohol as well as an inability to function normally without it, disrupts both the timing and consolidation of daily circadian rhythms — when to sleep, eat, and mate — driven by the brain circadian clock,” explained J. David Glass, professor of biological sciences at Kent State University and corresponding author for the study. “With continual alcohol use, one may go to bed too early or late, not sleep across the night, and have an unusual eating regime, eating little throughout the day and/or overeating at night. This can lead to a vicious cycle of drinking because these individuals, in response, will consume more alcohol to fall asleep easier only to complain of more disrupted sleep across the night and additionally have a greater craving for alcohol.”

In other words, said Alan M. Rosenwasser, professor of psychology at the University of Maine, chronic alcohol abuse and circadian disruption become reciprocally destructive and result in negative effects on physical and emotional health. “It is therefore very interesting that access to running wheels or other forms of voluntary exercise in animal experiments has emerged as a powerful environmental factor influencing brain health, circadian rhythms, and emotional well-being,” he said.

Glass agreed, noting that exercise is important in the non-photic regulation of circadian timing. “Restricting animals from exercising,” he said, “such as blocking access to a running wheel as we did in this study, had a significant stimulatory effect on alcohol consumption.”

Glass and his colleagues tested for three things: the effects of wheel-running on chronic free-choice consumption of an alcohol (20% v/v) and water solution; the effects of alcohol consumption on wheel-running in alcohol-naïve hamsters; and the influence of constant light (LL) on both alcohol consumption and wheel-running behavior.

“In this study, we found that the more the hamsters ran, the less they consumed alcohol,” said Glass. “The ‘lazier’ hamsters that did not run as much had a greater craving for and consumption of alcohol, suggesting that exercise may be an effective, beneficial, and non-pharmacologic treatment option for alcoholism.”

“It seems that alcohol intake and voluntary exercise represent two forms of inherently rewarding behavior,” added Rosenwasser, “and the rewarding effects of these two behaviors may partially substitute for one another. This finding suggests that the two behaviors are regulated by overlapping systems in the brain.”

Glass agreed, noting that exercise appears able to alter the chemical environment of the brain in a manner similar to alcohol. “Dopamine is the primary chemical released within the brain in response to any type of reward, including exercise, drugs, food, and sex,” he said. “For humans, exercise may be an effective, beneficial, and naturally rewarding substitute for any type of addiction. It may also reduce the risk of addiction in individuals who have a family history of it, in addition to significantly reducing the risk of cardiovascular disease and mood disorders. But like all rewards, exercise should be used in moderation, and not interfere with an individual’s normal daily functioning.”

A second key finding was that hamsters that displayed greater sensitivity to the disruptive effects of constant light on circadian rhythms also craved alcohol less. “Thus, there may be an underlying genetic predisposition for alcohol dependence and abuse that is expressed under challenging circadian conditions,” said Glass, “such as shift work, sleep problems or repeated jet-lag exposure.”

“Several research groups have recently become interested in relationships between circadian clocks, exercise, and alcohol and drug abuse,” said Rosenwasser. “In general, research in this area has shown that alcohol abuse can dramatically disrupt biological rhythms, that these disruptions can promote subsequent alcohol abuse, and that exercise is an important environmental factor influencing both circadian rhythms and alcohol drinking. These studies have opened several new directions for alcohol researchers, and raise the hope that circadian-based and/or exercise-based interventions may be developed for improved management of the serious and debilitating disorders associated with excessive drinking.”

“Many members of the general public, and indeed, many medical professionals, continue to view alcohol abuse and alcohol addiction as character flaws and as failures of ‘willpower,’” said Rosenwasser. “Findings such as these help put alcohol abuse disorders in a broader biological context, and show that both physiological and environmental factors contribute to excessive alcohol intake. Accordingly, these physiological and environmental factors will need to be addressed in order to effectively control alcohol abuse and other forms of excessive behavior.”?

Seaweed could hold the key to tackling obesity after it was found it reduces fat uptake by more than 75 per cent, new research has shown.

Now the team at Newcastle University are adding seaweed fibre to bread to see if they can develop foods that help you lose weight while you eat them.

A team of scientists led by Dr Iain Brownlee and Prof Jeff Pearson have found that dietary fibre in one of the world’s largest commercially-used seaweed could reduce the amount of fat absorbed by the body by around 75 per cent.

The Newcastle University team found that Alginate — a natural fibre found in sea kelp — stops the body from absorbing fat better than most anti-obesity treatments currently available over the counter.

Using an artificial gut, they tested the effectiveness of more than 60 different natural fibres by measuring the amount of fat that was digested and absorbed with each treatment.

Presenting their findings at the American Chemical Society Spring meeting in San Francisco, Dr Brownlee said the next step was to recruit volunteers and study whether the effects they have modelled in the lab can be reproduced in real people, and whether such foods are truly acceptable in a normal diet.

“The aim of this study was to put these products to the test and our initial findings are that alginates significantly reduce fat digestion,” explains Dr Brownlee.

“This suggests that if we can add the natural fibre to products commonly eaten daily — such as bread, biscuits and yoghurts — up to three quarters of the fat contained in that meal could simply pass through the body.

“We have already added the alginate to bread and initial taste tests have been extremely encouraging. Now the next step to to carry out clinical trials to find out how effective they are when eaten as part of a normal diet.”

The research is part of a three year project being funded by the Biotechnology and Biological Sciences Research Council. It addresses the new regulations set out by the European Food Safety Authority that any health claims made on a food label should be substantiated by scientific evidence.

“There are countless claims about miracle cures for weight loss but only a few cases offer any sound scientific evidence to back up these claims,” explains Dr Brownlee.

Alginates are already commonly used at a very low level in many foods as thickeners and stabilisers and when added to bread as part of a blind taste test, Dr Brownlee said the alginate bread actually scored higher for texture and richness than a standard white loaf.

“Obesity is an ever-growing problem and many people find it difficult to stick to diet and exercise plans in order to lose weight,” explained Dr Brownlee.

“Alginates not only have great potential for weight management — adding them to food also has the added advantage of boosting overall fibre content.”

What is a dietary fibre?

Dietary fibre would be scientifically classified as a group of carbohydrates of plant origin that escape digestion by the human gut.

“Actually, there’s still quite a lot of confusion about fibre,” says Dr Brownlee. “I think most people would describe it as roughage — the bit of your food that keeps you regular and is vital for a healthy gut.

“Both of these facts are true but the notion that all fibre is the same and that it simply goes through your system without having an effect is wrong.”

Fibre is made up of a wide range of different molecules called polysaccharides and although it is not digested by the human gut, it both directly and indirectly affects a number of bodily processes.

Dr Brownlee adds: “These initial findings suggest alginates could offer a very real solution in the battle against obesity.”

Scientists have discovered that everyday emotional stress is a trigger for the growth of tumours

They discovered that any sort of trauma, emotional or physical, can act as a “pathway” between cancerous mutations bringing them together in a potentially deadly mix

The findings, published in Nature, seemed to show for the first time that the conditions for developing the disease can be affected by your emotional environment including every day work and family stress.

Professor Tian Xu, a geneticist at Yale University who led the study, said: “A lot of different conditions can trigger stress signaling – physical stress, emotional stress, infections, inflammation – all these things.

“Reducing stress or avoiding stress conditions is always good advice.”

Until now, scientists believed more than one cancer-causing mutation needed to take place in a single cell in order for tumours to grow.

But Prof Xu and colleagues at Yale University, working with fruit flies, showed mutations can promote cancer even when they are located in different cells. This is because stress opens up “pathways” between them.

He said: “The bad news is that it is much easier for a tissue to accumulate mutations in different cells than in the same cell.”

The immune system can also be devastatingly destructive. The body’s tendency to reject organ transplants, attacking them as if they were dangerous foreign invaders, is well known. But more prevalent are autoimmune diseases, in which your immune cells attack your own tissues and organs. Left unchecked, these malfunctions can result in one of more than 80 known conditions, including Type 1 diabetes, rheumatoid arthritis, lupus, multiple sclerosis, inflammatory bowel disease and psoriasis. According to the Autoimmune Related Diseases Association, conditions like these affect more than 50 million Americans.

The perfect immune-modulating drug would target only the part of the system causing the problem. As of now, however, most immunosuppressive drugs work by dampening the entire immune system, which leaves the patient susceptible to short-term problems like infections and long-term afflictions as severe as cancer.

Bluestone, who is now 56, has devoted most of his career to improving on this crude, brute-force approach. In the early days of his “club,” he spent many of those long nights tweaking an organ-transplant drug called OKT3, which he and other researchers thought might also be useful for autoimmune diseases like multiple sclerosis and Type 1 diabetes. The problem was, the drug had severe side effects, including cases in which it sent recipients’ immune systems into a kind of overdrive that could be fatal. Eventually, though, working in mice, Bluestone and his colleagues succeeded in changing the drug’s structure to eliminate these side effects. Then he began investigating what else the drug could do.

In 1987 he joined forces with Kevan Herold, an endocrinologist and researcher who was then a colleague of Bluestone’s at the University of Chicago, and the two began exploring the drug’s effects in mice with Type 1 diabetes, an autoimmune disease caused when a class of white blood cells called T cells mistakenly destroys the cells in the pancreas that produce insulin. As their research progressed, they were thrilled to find that the drug halted the progression of Type 1 diabetes in the mice. Second, the new version appeared to act like a guided missile, targeting problematic cells in the immune system without handicapping the rest of it. Bluestone and Herold began to think it might be possible to use it and other, similar drugs as short-term therapies to “reprogram” the immune system, permanently coaxing it back to its original, balanced state. In the world of immunology, this is referred to as immune tolerance. According to Herold, it is the field’s most sought-after goal. And now, thanks to a number of breakthroughs in targeted immune therapy, that goal seems closer than it has ever been. Jordan Pober, the director of the Human and Translational Immunology program at Yale University, is openly enthusiastic about the state of the science: “We’re in the midst of a revolution in our ability to manipulate the immune system.”

By 1995, Bluestone and Herold were eager to move from mouse to man. They wanted to see if the drug could also have a positive effect on Type 1 diabetes in humans. It wouldn’t be a total cure, but if the drug could stop the normal course of the disease—which usually gets progressively worse over the course of a person’s life as the body finishes killing off the cells that produce insulin—it would be a major breakthrough. So in 2000, they launched a trial of the modified drug.

The advance of targeted immune therapies reaches far beyond the treatment of Type 1 diabetes. After all, anti-CD3 monoclonal antibodies might be more like guided missiles than conventional immunosuppressive drugs, but they can still cause collateral damage. Because they target a receptor that’s found on all T cells—not just the ones that are going after the pancreas—they can have unwanted side effects, such as reducing people’s resistance to opportunistic infections. On the other hand, the fact that anti-CD3 isn’t totally precise means that it can be used for a variety of diseases other than diabetes. Versions of the drug are already being tested for psoriasis, Crohn’s disease and ulcerative colitis, and they’re thought to hold promise for rheumatoid arthritis and multiple sclerosis as well. “The number of diseases potentially affected is huge,” Herold says.

The anti-CD3 monoclonal antibodies have useful relatives, too—different monoclonal antibodies, each of which binds to a different target and therefore can be used to treat a different disorder. Recently, plenty of excitement has focused on rituximab (the “mab” stands for monoclonal antibodies), a drug that affects the surface of a different class of immune cells—known as B cells—and was originally approved in 1997 for non-Hodgkin’s lymphoma. Rituximab was first tested as a cancer drug, but it has since been approved for rheumatoid arthritis and has shown promise in other kinds of autoimmune diseases, including multiple sclerosis. Moreover, in a study on treatments for a type of autoimmune vasculitis (a rare and serious disease in which the body attacks its own blood vessels), rituximab was shown to be just as good as, if not better than, the typical immunosuppressive drugs used to treat the disease. Like many of these precisely targeted treatments, it too had far fewer toxic side effects.

Scientists have discovered immune-programming qualities in other drugs as well. For example, tumor necrosis factor antagonists, which act outside the cells to inhibit inflammation, have not only revolutionized the treatment of rheumatoid arthritis but have also been shown to be effective against a number of other diseases. They’re currently in trials for conditions ranging from eye disease and organ transplantation to osteoarthritis and sepsis.

“The potential that really good drugs which have been developed for one disease might have such efficacy in other diseases is, I think, a very exciting thing,” says Bluestone, who is known for being cautious with his optimism.

Several years after the trial ended, I was asked to share my experience with an audience of people with diabetes at an event sponsored by the University of California at San Francisco. I meant for my story to be inspiring—I’m still making insulin! Look at how great clinical research trials can be!—but instead I ended up feeling like a jerk. Because the drug still hasn’t been approved, I’m one of just a handful of people in the world who have had access to the treatment. And even if the drug were available, it would probably help only people who had been recently diagnosed and still had some insulin-producing cells left, which disqualified most of my audience. It was as if I’d walked into a room full of people who had lost their life savings and bragged about how I’d won the lottery.

But although I’m fortunate to have gotten the drug, my diabetes has not been cured. For that to happen, I’d need replacements for the insulin-producing cells that my immune system knocked off. Since there aren’t enough cadaver-donor pancreases available to cover the millions of Type 1 diabetes patients in America, these replacements would most likely come from stem cells, those malleable creatures that can morph into nearly any cell in the body. The volume of cells I’d need is quite small—a teaspoon’s worth would do—and they could be transplanted via injection in a simple outpatient procedure. Unfortunately, it’s not that easy. First, if you put new insulin-producing cells into my body, whether from a cadaver or stem cells, they would probably be destroyed by the same immune malfunction that caused me to develop diabetes in the first place. And even if you got past that roadblock, there’s another problem, one that arises anytime you try to transplant foreign tissues or cells into the body: rejection. Unless the cells come from your own body or that of an identical twin, the immune system treats the replacement cells as foreign invaders and attacks them just as it would a donor kidney or liver. That means that any treatment derived from stem cells is likely to require some kind of immune-modulating drug to succeed. This, not incidentally, is one of the problems Bluestone is trying to solve at the Immune Tolerance Network.

It’s been nine years since I was diagnosed with Type 1 diabetes. I’ve kept in touch with Herold, who is now director of the Autoimmunity Center of Excellence at Yale University, where he also runs the Yale branch of a network of diabetes researchers called TrialNet. When he received funding last summer to follow up with some of the original study participants to see how long the effects of the anti-CD3 drug might last, I eagerly enlisted. The protocol, known as a mixed-meal tolerance test, was the same thing I’d gone through in the original study. After an overnight fast, I gulped down a glass of Boost nutritional drink, didn’t take any insulin, and then lay in bed for four hours with an IV catheter in my arm so that the nurses could draw multiple blood samples to see how much insulin I was producing. The result? I’m still making a measurable amount, which in the normal course of the disease does not happen.

Unfortunately, my resistance is fading. At nine years out, my insulin levels are roughly half what they were two years after the treatment, and I worry that it’s just a matter of time before my immune system finishes its misguided job of killing off my insulin-producing cells. My hope is that an anti-CD3 drug will gain FDA approval soon so that I can get a second round of treatment, potentially buying me time until researchers like Bluestone and Herold achieve the dream of every person with diabetes: a cure.

Bluestone is just as impatient to see an anti-CD3 monoclonal antibody finally come to market. And although he is reluctant to make assumptions—“Obviously it ain’t over till it’s over”—he’s hopeful that anti-CD3 may soon go into much wider use. “If it does get approved in the next year or two, that would be exciting,” he says. “I would finally feel that what we’ve done would be able to have a real impact on human health.”

LONG-term mobile phone users could face a higher risk of developing cancer in later life, according to a decade-long study.

The report, to be published later this year, has reportedly found that heavy mobile use is linked to brain tumours.

The survey of 12,800 people in 13 countries has been overseen by the World Health Organisation.

Preliminary results of the inquiry, which is looking at whether mobile phone exposure is linked to three types of brain tumour and a tumour of the salivary gland, have been sent to a scientific journal.

The findings are expected to put pressure on the British Government – which has insisted that mobile phones are safe – to issue stronger warnings to users.

Most minor discomfort is a sign of … not much. Maybe you had a heavy meal, a stressful day, a hard workout — and by the next day you feel fine again. But a handful of trivial-sounding symptoms can sometimes be red flags for something more serious. Since it’s often hard to distinguish between the no big deal and the dire, most of us err on the side of ignoring the problem and hoping it goes away. “Women in midlife are often juggling 20 things at once, so they tend to neglect their own health,” says Nieca Goldberg, MD, author of “Dr. Nieca Goldberg’s Complete Guide to Women’s Health.”

“That’s why it’s especially important for them to be informed about what really needs medical attention.” Here, a guide to eight important symptoms: when you should see a doctor and when you can just keep cruising.

Pain and swelling in your calf
Likely cause: Pulled muscle
Worst-case scenario: Blood clot in the leg
Calf pain is the most common symptom of deep vein thrombosis (DVT), a clot in a deep vein, which is a potentially fatal condition that strikes an estimated 350,000 to 600,000 people in the U.S. every year — most of them 40 and over. “The clot blocks blood flow, causing pain and swelling,” says Stephan Moll, MD, of the National Alliance for Thrombosis and Thrombophilia.

Other signs it may be serious: Symptoms of a clot can be pronounced, with significant swelling, redness, and pain, but they can also be mild and easily mistaken for a cramp. The skin may also be warm to the touch. If you’re short of breath, coughing, experiencing chest pain, or having difficulty breathing, a clot may have broken free and traveled to your lungs, clogging a blood vessel there. You’re at increased risk for DVT if you’re on hormone therapy, the pill, patch, or ring; if you smoke or are pregnant; if you’ve just had surgery or have been on a plane flight or car trip longer than three hours; if you’re obese; or if you have a family history of blood clots.

When to act: If the symptoms come on suddenly and don’t go away in a few hours, call your doctor for a same-day appointment. If she can’t see you, go to the ER right away, especially if the swelling and pain are significant, you’re having any breathing or chest symptoms, or you have any other risk factors.

“It’s better to err on the side of caution,” Moll says. “Half of people with DVT develop a blood clot in the lungs, a condition that can be fatal.” Blood clots are usually diagnosed with ultrasound and treated with intravenous blood thinners for a few days, followed by several months of medication. They can be prevented with some lifestyle changes: Maintain a healthy weight; don’t smoke; and on long trips be sure to get up and walk around.

Symptom: Flu-like feelings (fatigue, nausea, sweating, chills)
Likely cause: Virus
Worst-case scenario: Heart attack
“Women tend not to have the Hollywood heart attack with significant chest pain,” Goldberg says. “They sometimes just feel like they’re coming down with an infection.” That could be one reason women having heart attacks take more than 11 minutes longer than men, on average, to go to the ER.

Other signs it may be serious: Shortness of breath; dizziness; pressure, squeezing, or pain in the chest; pain in the back, arm, jaw, or upper abdomen.

When to act: If you have some of the above symptoms, call 911 and say, “I think I’m having a heart attack. I need an ambulance.” At the hospital, the staff should do an electrocardiogram to detect whether your heart is being deprived of oxygen, a blood test to measure cardiac enzymes and proteins, an echocardiogram to see if the heart has been damaged, and possibly cardiac catheterization — inserting dye into the arteries to see them clearly with an x-ray. Getting examined quickly may save your life: It’s estimated that you have a 50 to 70 percent chance of dying if your heart attack takes place outside a hospital. Among women ages 40 to 60, heart disease is as common a killer as breast cancer, but with some precautions, you can decrease your risk. “Keep your blood pressure, cholesterol, and weight under control, and exercise regularly,” Goldberg advises.

Symptom: Burning, tingling, or numbness in your feet
Likely cause: A tight-fitting pair of shoes
Worst-case scenario: Prediabetes (elevated blood sugar levels)
Some 57 million Americans are prediabetic, but because prediabetes is often asymptomatic, most don’t know they’re on the cusp of serious illness. (Without intervention, the condition typically progresses to full-blown diabetes within a decade.) Foot symptoms occur “because the illness damages the nervous and circulatory systems,” says John Giurini, DPM, of the American College of Foot and Ankle Surgeons.

Other signs it may be serious: Some prediabetics may also experience tingling and numbness in the arms or hands, says Giurini. If you have full-blown diabetes, you may also experience frequent urination, excessive hunger or thirst, weight loss, fatigue, or blurry vision. The risk factors for type 2 diabetes include being older than 45, being overweight, being sedentary, having a family history of diabetes, having had gestational diabetes, or having given birth to a baby weighing more than 9 pounds.

When to act: If you have burning or tingling feet for more than a few weeks, call your internist and ask to be seen in the next week for a checkup and a fasting blood sugar test, Giurini suggests. Recent studies have shown that by losing 5 to 7 percent of your body weight through diet and exercise, you can prevent the development of diabetes.

Symptom: Bloating and pelvic pain
Likely cause: Gastrointestinal bug
Worst-case scenario: Ovarian cancer
Several medical groups, including the American Cancer Society, warned in 2007 that bloating and pelvic pain can be early signs of ovarian cancer — big news, since doctors have long believed that this often deadly disease is symptomless until it’s too advanced to treat. “If caught early, ovarian cancer is up to 90 percent curable,” says Barbara Goff, MD, of the University of Washington.

Other signs it may be serious: Additional symptoms of ovarian cancer include feeling full quickly or having difficulty eating, urinating frequently or with great urgency, and changing bowel habits. You’re at increased risk if you have a family history of the illness, have tested positive for mutations in the genes BRCA 1 or BRCA 2, or have been on hormone therapy. (Your risks are lower if you have had at least one child, breastfed a baby, taken birth control pills, and maintained a healthy weight.)

When to act: “If the symptoms are new, occur almost every day, last more than a few weeks, and don’t go away if you eat more fiber, reduce your salt intake, or exercise more frequently, schedule an appointment with your gynecologist,” says Linda R. Duska, MD, of the University of Virginia, in Charlottesville. Ask to be seen within two weeks. Diagnosis is tricky, so don’t be afraid to push your doctor for appropriate testing: a pelvic ultrasound and perhaps a blood test to check your level of CA-125, a substance found in high amounts in the blood of many women with ovarian cancer. Partly because the incidence of ovarian cancer rises with age, the ACS recommends annual pelvic exams for all women over age 40.

Symptom: Persistent cough
Likely cause: A cold
Worst-case scenario: Adult-onset asthma, a condition that can worsen as women enter midlife

Other signs it may be serious: “If you cough only when you’re exercising or sleeping, that can indicate asthma,” says Vincent Tubiolo, MD, of the American Academy of Allergy, Asthma and Immunology. Other symptoms include wheezing, particularly when you exhale; shortness of breath; and tightness in the chest. Risk factors are obesity, allergies, smoking, and a recent respiratory tract infection.

“Women who have taken estrogen for 10 years have a 50 percent higher risk of developing asthma,” Tubiolo says. “And people with acid reflux are at increased risk, possibly because the acid irritates the airways and triggers an asthmatic cough.”

When to act: Asthma isn’t usually an emergency, but it makes sense to consult a doctor since the disease can be progressive (and even life-threatening when breathing problems are severe). Also, the condition can limit your physical activity and interfere with your sleep, both of which can affect your long-term health. Asthma is diagnosed with a pulmonary function test that measures airflow. “People feel a lot better once they receive treatment,” Tubiolo says. Reduce your risk by avoiding smoke, including the secondhand variety, and maintaining a normal weight.

Symptom: No matter how much you sleep, you don’t feel well-rested
Likely cause: The flu
Worst-case scenario: Sleep disorder
Don’t dismiss daily fatigue as an inevitable consequence of aging. Feeling tired is a common symptom of two of the most prevalent sleep interrupters for midlife women: sleep apnea and restless legs syndrome, a neurological disorder that causes an itchy, twitchy sensation in the legs that makes it difficult to stay still and, as a result, fall asleep.

“Many people think sleep apnea only affects overweight men, but it’s nearly as common in women after menopause,” says Lisa Shives, MD, of Northshore Sleep Medicine, in Evanston, Illinois. Like sleep apnea, RLS often worsens as you get older.

Other signs it may be serious: If you’re a snorer and you wake up feeling as if you’ve been hit by a truck, chances are you have sleep apnea. The condition relaxes the muscles of the throat, making it difficult to get sufficient air, and the lack of oxygen triggers mini awakenings — sometimes hundreds of times a night. Other signs of sleep apnea: waking with a headache and sore throat; experiencing memory or concentration problems; feeling irritable or depressed. Fatigue-related symptoms such as irritability are also common with RLS.

When to act: If the symptoms of either disorder persist for more than a month, see your internist, who may be able to diagnose the problem based on your description. If not, she may refer you to a sleep specialist for further evaluation. Sleep apnea is treated with a continuous positive airway pressure device, a mask that fits over your nose and/or mouth during sleep and helps open airways with gentle air pressure. RLS is treated with dopamine-like drugs, but some sufferers can control symptoms by limiting caffeine, walking regularly, and massaging or stretching their legs before bedtime. Practicing yoga or meditation may relieve some symptoms. Likewise, lifestyle changes may ease the effects of sleep apnea: Drop pounds if you’re overweight, avoid alcohol, quit smoking, and try to sleep on your side, a position that sometimes reduces symptoms.

Symptom: Trouble finding the right words
Likely cause: Sleep deprivation
Worst-case scenario: Stroke

It’s easy to laugh off a little brain freeze as a senior moment, but if your word problems amount to more than a minor slipup (for example, saying “runny hosted peanuts” instead of “honey roasted peanuts” is normal; saying “red place mat” when you mean “honey roasted peanuts” is not), it could be a stroke, which occurs when a blood vessel in the brain either bursts or is blocked by a clot, depriving brain cells of oxygen. “Language impairment — when you have trouble speaking, or say nonsense words or words that don’t go together — is common in left hemisphere strokes,” says Argye Hillis, MD, of the Johns Hopkins University School of Medicine.

Other signs it may be serious: Weakness on one side of the body, slurred speech, dizziness, blurred vision, headache, neck stiffness, or lack of coordination are all red flags. A temporary bout of amnesia (not being able to remember what you did for the past few hours) or symptoms that last only a few minutes could signal a transient ischemic attack (TIA), a ministroke that raises your risk of the real deal substantially, especially over the following few days. Certain factors raise your odds of having a stroke: getting migraines with an aura; smoking; being overweight; having heart disease, diabetes, or high blood pressure; and being on the pill or HT.

When to act: “Call 911 if any of these symptoms develop suddenly — for example, if you’re not able to do something that you could do five minutes earlier,” Hillis says. A quick response is critical, because receiving a clot-busting drug within the first three hours improves the odds of recovery by an estimated 30 percent. “Even if symptoms go away on their own, you should get to the emergency room as soon as possible to be evaluated for the cause of the TIA, so a stroke can be prevented,” Hillis recommends.

Symptom: A new mole
Likely cause: Harmless skin growth
Worst-case scenario: Skin cancer
While it’s common to develop new moles before midlife, finding a new one or seeing changes in an existing mole after age 40 could be a sign of melanoma, the deadliest type of skin cancer.

Other signs it may be serious: “If a mole — new or old — turns darker or black, becomes asymmetrical, or causes pain, itching, or bleeding, you should get it checked out right away,” says Robert Brodell, MD, a dermatologist in Warren, Ohio, who is a spokesperson for the American Academy of Dermatology. The more moles you have, the greater your risk for melanoma. Being fair and spending lots of time in the sun (even if you only did so in your youth) raises your risk, as does every single sunburn. “If you have lots of sun damage, like freckles, you have a higher risk too,” Brodell says.

When to act: “Call your dermatologist as soon as you notice something unusual and say, ‘I have a changing mole, and I’m worried about it.’ She should get you in within a week or two,” Brodell says. If you don’t have a dermatologist, ask your doctor for a referral. The dermatologist should check your whole body for signs of skin cancer and biopsy anything that looks suspicious.

“Fortunately, when melanoma is caught early it’s very curable,” Brodell says. To protect your skin, apply a broad-spectrum sunscreen with at least SPF 30 every day, have full-body screenings annually, and check your body for new or changing moles once a month.

WHAT if we could rid the world of AIDS? The notion might sound like fantasy: HIV infection has no cure and no vaccine, after all. Yet there is a way to completely wipe it out – at least in theory. What’s more, it would take only existing medical technology to do the job.

Here’s how it works. If someone who is HIV positive takes antiretroviral-drug therapy they can live a long life and almost never pass on the virus, even through unprotected sex. So if everyone with HIV were on therapy, there would be little or no transmission. Once all these people had died, of whatever cause, the virus would be gone for good.

It’s a simple idea, but the obstacles to implementing it worldwide are enormous. Persuading everyone with HIV to start therapy purely for public health reasons could be ethically dubious. To identify everyone who is HIV positive would require such widespread testing that some may feel it breached their civil liberties. Then there is the question of who would fund such a massive undertaking.

Yet the idea of eliminating HIV is so appealing, and the benefit to humanity so huge, that scientists and policy-makers are seriously considering the concept, albeit on regional scales. In the next few months the World Health Organization (WHO) will meet to discuss how the idea could be tried in developing countries, and something approaching elimination might be attempted in the UK within the next decade. “You could eliminate transmission overnight,” says Marcus Conant, an HIV specialist in San Francisco.

A plan like this can only be countenanced thanks to some sweeping changes over the past decade in the way HIV is managed by doctors and viewed by the public. In 1985, when HIV testing began, no treatment for the virus existed, so a positive result was effectively a death sentence. Fear of the virus and the fact that it spread most easily among gay men and intravenous drug users meant people with HIV were shunned, as well as being barred from taking out health and life insurance. The decision to have the test was generally an agonising one and many decided it was better not to know.

It was not until the mid-1990s and the arrival of cocktails of antiviral drugs that people with HIV could begin to imagine surviving for any significant length of time. Fear of the virus subsided and public attitudes began to soften. The beauty of these cocktails lies in the combination of drugs. If just one drug is taken, HIV can mutate and become resistant to it, but with three drugs the virus would need three simultaneous mutations to become resistant, a highly improbable event. This “triple therapy” stops viral replication in its tracks and seems to hold AIDS at bay indefinitely. People now had every reason to take the test.

If treatment for the virus has changed dramatically, so too has treatment timing. HIV progression is gauged by measuring levels of CD4 cells – immune cells that the virus infects and kills. A typical healthy person has more than 500 of these cells per microlitre of blood, while someone with HIV sees their count gradually fall. Once their CD4 count falls below about 200, the immune system can no longer fight off common pathogens, leading to “opportunistic” infections such as pneumonia and thrush.

In the early days, doctors tended to delay triple therapy until a patient’s CD4 count had dropped to about 200, on the basis that this would catch most people before opportunistic infections struck. There were good reasons not to start treatment sooner: the first antiretrovirals had nasty side effects and involved taking up to 20 tablets a day. What’s more, at a time when only a few antiretrovirals existed, it was a real concern that if drug resistance developed, an individual could run out of medicines to take. Today, these obstacles have largely disappeared: people on the latest regimens take only one or two pills a day with few side effects, if any, and there are two dozen drugs to choose from.

We know now that starting treatment earlier than at a CD4 count of 200 brings health benefits. As well as reducing the risk of opportunistic infections, a large study showed last year that people who began treatment with a CD4 count above 350 are less likely to develop conditions usually seen as unrelated to HIV, such as heart or kidney disease (The Journal of Infectious Diseases, vol 197, p 1133). Researchers now suspect that long-term HIV infection causes a low-level activation of the immune system that can damage the heart, kidneys and liver. For these reasons, the treatment threshold in wealthy nations is now 350.

Of course this can only happen if someone has been diagnosed, something that often happens dangerously late. In the west, about one-quarter of people with HIV only discover their status when they are admitted to hospital with an opportunistic infection or cancer. Some die before triple therapy can take effect – from pneumonia, for example.

It is the benefits of early treatment, combined with the perils of late diagnosis, that have convinced many doctors and patient groups to urge that HIV tests be used more widely. For example, last year the UK government’s Health Protection Agency endorsed guidelines saying that in urban areas of the UK where people with undiagnosed infections are likely to be concentrated, HIV tests should be more widely available. In these places, everyone from 15 to 60 should have the test routinely when they register with a primary care doctor or are admitted to hospital. “We want normalisation of testing,” says Barry Evans, an epidemiologist at the HPA. “They should get tested like they get their blood pressure checked.”

Earlier HIV diagnosis not only helps the infected person, it also benefits everyone else. Once someone knows they are HIV positive, they are less likely to pass the virus to others through unsafe sex or sharing needles. The really important factor, though, is that therapy stops viral replication, so that much less virus reaches an infected person’s bodily fluids.

Just how much this reduces the risk of transmission is a matter of great debate. Most of the evidence comes from studies of monogamous heterosexual couples who are “serodiscordant” – in other words one person is HIV positive and the other is not. Some studies have found a transmission rate of zero, but only in people who scrupulously take their tablets, so that no virus is detectable in their blood, and who are free of other sexually transmitted infections.
No condoms needed

Last year, a group of HIV specialists on the Swiss government’s AIDS commission (EKAF) announced that HIV-positive people who met these conditions were “sexually non-infectious”. For the first time serodiscordant heterosexual couples got official approval to bin their condoms. Other experts disagree with the Swiss decision, pointing out that the virus can sometimes be found in semen and vaginal fluid even if it is undetectable in blood. Also, as the research results come from straight couples, it is unclear how the advice applies to gay men. Despite these doubts, some doctors now see patients with normal CD4 counts asking to start therapy purely to avoid passing on the virus.

While it is debatable just how small the transmission risk really is, it is indisputably much lower for patients taking antiretroviral therapy than for those who are not. That has led researchers to start speculating about expanding testing and treatment to everyone with HIV. In November 2008, a paper published in The Lancet, written by five of the WHO’s leading AIDS specialists, drew the widest attention so far (vol 373, p 48).

The researchers looked at the case for elimination in South Africa, which has the highest number of HIV cases in the world. They modelled what would happen if everyone over 15 were given annual tests, with all those who tested positive offered free antiretroviral treatment immediately, regardless of their CD4 count. They plugged in actual figures from a free treatment programme in Malawi to factor in people who decline therapy, stop because of side effects or switch drugs because of resistance.

The team found that within 10 years, the scheme would slash new HIV infections from the 1 in 50 people at present to less than 1 in 1000. Within 50 years, as people with HIV died (mainly from other causes), prevalence in the general population would fall from about 10 per cent to less than 1 per cent.

That all sounds great, but the cost of the scheme would initially be about $3.5 billion a year. That might sound prohibitive, but the key comparison to make is with the cost of alternative plans. Today, aid programmes can fund antiretroviral treatment for only about one-third of people in the developing world with a CD4 count below 200. All the major HIV organisations, such as UNAIDS and the WHO, and several western governments including the UK’s, are now calling for universal access to therapy, by which they mean getting the drugs to everyone with a count below 200. Some want the threshold to be raised to 350 in the developing world too.

However, the problem with this form of universal access is that it would do little to curb transmission, because everyone with CD4 counts above the threshold would still be spreading the virus. The cost of such a scheme would almost certainly rise over time as more people became infected, unlike the WHO experts’ more ambitious scheme. “The [elimination] strategy becomes cost-saving in the future, despite initially increased costs,” says Kevin De Cock, director of the WHO’s HIV/AIDS department and one of the paper’s authors. By 2030 it would become cheaper than using a 350 threshold (see graph).

The idea is still very much in its early stages, with De Cock stressing they are “not suggesting a change in policy but stimulating a discussion”. In the next few months, the WHO will bring together scientists, policy-makers and funders to discuss employing the strategy in developing countries.

In some ways it might be easier to attempt universal treatment in a developed country. For example, the UK could, if it chose, afford to put every one of its estimated 73,000 HIV-positive residents on antiretroviral therapy. On the other hand with HIV only affecting 0.1 per cent of the UK population, universal testing would be hard to justify. The modelling from The Lancet paper would have to be redone for the UK, where, unlike in South Africa, transmission is primarily among gay men. (Cases among heterosexuals are rising; these are mainly immigrants who have caught the virus abroad.) “We’re trying to focus more on certain population groups or areas,” says Tim Chadborn of the HPA.

Conant, however, argues that testing everyone would help to further reduce the stigma around AIDS. HIV may no longer be an automatic bar for health insurance but there is still an image problem for a disease that in the west is still seen as affecting mainly gay men, immigrants, prostitutes and drug addicts. Conant advocates mass testing in the US at churches and meetings of professional groups such as doctors – as happens today at gay bars. “It has got to be universal,” he says.
Mass HIV testing at churches and meetings of professionals such as doctors would reduce stigma

Perhaps the most medically contentious part of the elimination plan, in any country, is that all those diagnosed positive would begin antiretroviral treatment immediately. At present there is no firm evidence that HIV does any damage to an individual as long as their CD4 count is above 350. “There are great big ethical problems about recommending treatment to someone when it’s not clinically beneficial to that person,” says Chadbourn.
Sex abroad

Still, no one really knows what the effects of starting treatment earlier are. This question should be answered by a large international trial called START, organised by the US National Institutes of Health, to compare the health of people who start therapy at 350 with that of people who start at over 500. The results will not be in for six years, though.

If the people in the over-500 group do best, the main medical objection to elimination disappears. “If we can establish that there’s a benefit, I would imagine that we would try to do exactly what’s being proposed in The Lancet paper,” says Andrew Phillips, an epidemiologist at the Royal Free and University College Medical School in London who is involved in START.

If a western country introduces widespread testing and immediate treatment, new infections should dwindle. “If there are benefits for the individual and benefits for the population, I would very strongly support that,” says Evans. He would contemplate elimination even if the over-500 group in the START trial does no better than the 350 group, as long as it does no worse.

Perhaps the biggest obstacle would be the importation of HIV from abroad. The HPA now recommends that migrants from countries with high HIV rates be offered a test when they access any health service, such as registering with a primary care doctor. The agency frowns on testing at ports of entry in case it encourages discrimination.

Residents also import HIV by having unsafe sex while abroad. People would have to be persuaded to take the test when they returned. For Brian Gazzard, one of the UK’s leading HIV specialists, based at the Chelsea and Westminster Hospital in London, this makes elimination on a country-by-country basis unfeasible. “It’s got to be done worldwide,” he says. “A public debate about that issue would be wonderful.”

Western countries without state-funded healthcare would hit bigger problems. In the US, for example, many people with HIV delay starting therapy because they pay part or all of the cost. “The government would have to pay,” says Conant.

Treatment standards would also have to improve in the US. Some health insurers insist that patients see primary care doctors rather than more expensive specialists. According to Conant, some non-specialists fail to use drug regimens that totally block viral replication, so the virus can still be transmitted. “That’s the most common mistake I see,” he says.

There are many obstacles to be overcome if any form of elimination plan, national or global, is to be attempted. Yet the damage done by AIDS is so huge that the chance to rid just some places of it has to be worth considering.

What is certain is that, however and wherever it is attempted, such a scheme will be controversial. Hard-line religious groups that view AIDS as divine retribution are unlikely to help out. Some liberals, on the other hand, might resist the idea of mass testing. “Should we try a social intervention which infringes on people’s civil liberties?” asks Conant. “AIDS infringes upon people too. If we’re going to stop this epidemic, this is a responsibility that society has to shoulder.”

A 42-year-old HIV patient with leukemia appears to have no detectable HIV in his blood and no symptoms after a stem cell transplant from a donor carrying a gene mutation that confers natural resistance to the virus that causes AIDS, according to a report published Wednesday in the New England Journal of Medicine.

“The patient is fine,” said Dr. Gero Hutter of Charite Universitatsmedizin Berlin in Germany. “Today, two years after his transplantation, he is still without any signs of HIV disease and without antiretroviral medication.”

The case was first reported in November, and the new report is the first official publication of the case in a medical journal. Hutter and a team of medical professionals performed the stem cell transplant on the patient, an American living in Germany, to treat the man’s leukemia, not the HIV itself.

However, the team deliberately chose a compatible donor who has a naturally occurring gene mutation that confers resistance to HIV. The mutation cripples a receptor known as CCR5, which is normally found on the surface of T cells, the type of immune system cells attacked by HIV.

The mutation is known as CCR5 delta32 and is found in 1 percent to 3 percent of white populations of European descent.

HIV uses the CCR5 as a co-receptor (in addition to CD4 receptors) to latch on to and ultimately destroy immune system cells. Since the virus can’t gain a foothold on cells that lack CCR5, people who have the mutation have natural protection. (There are other, less common HIV strains that use different co-receptors.)

People who inherit one copy of CCR5 delta32 take longer to get sick or develop AIDS if infected with HIV. People with two copies (one from each parent) may not become infected at all. The stem cell donor had two copies.

While promising, the treatment is unlikely to help the vast majority of people infected with HIV, said Dr. Jay Levy, a professor at the University of California San Francisco, who wrote an editorial accompanying the study. A stem cell transplant is too extreme and too dangerous to be used as a routine treatment, he said.

“About a third of the people die [during such transplants], so it’s just too much of a risk,” Levy said. To perform a stem cell transplant, doctors intentionally destroy a patient’s immune system, leaving the patient vulnerable to infection, and then reintroduce a donor’s stem cells (which are from either bone marrow or blood) in an effort to establish a new, healthy immune system.

Levy also said it’s unlikely that the transplant truly cured the patient in this study. HIV can infect many other types of cells and may be hiding out in the patient’s body to resurface at a later time, he said.

“This type of virus can infect macrophages (another type of white blood cell that expresses CCR5) and other cells, like the brain cells, and it could live a lifetime. But if it can’t spread, you never see it– but it’s there and it could do some damage,” he said. “It’s not the kind of approach that you could say, ‘I’ve cured you.’ I’ve eliminated the virus from your body.” Health.com: 10 questions to ask a new partner before having sex

Before undergoing the transplant, the patient was also found to be infected with low levels of a type of HIV known as X4, which does not use the CCR5 receptor to infect cells. So it would seem that this virus would still be able to grow and damage immune cells in his body. However, following the transplant, signs of leukemia and HIV were absent.

“There is no really conclusive explanation why we didn’t observe any rebound of HIV,” Hutter said. “This finding is very surprising.”

Hutter noted that one year ago, the patient had a relapse of leukemia and a second transplant from the same donor. The patient experienced complications from the procedure, including temporary liver problems and kidney failure, but they were not unusual and may occur in HIV-negative patients, he said.

Researchers including Hutter agree that the technique should not be used to treat HIV alone. “Some people may say, ‘I want to do it,’” said Levy. A more logical — and potentially safer — approach would be to develop some type of CCR5-disabling gene therapy or treatment that could be directly injected into the body, said Levy.

Less invasive options to alter CCR5 could be on the horizon within the next five years, said Levy. “It’s definitely the wave of the future,” he said. “As we continue to follow this one patient, we will learn a lot.”

One drug that’s currently on the market that blocks CCR5 is called maraviroc (Selzentry). It was first approved in 2007 and is used in combination with other antiretroviral drugs. Health.com: Who’s most at risk for STDs?

In 2007, an estimated 2 million people died from AIDS, and 2.7 million people contracted HIV. More than 15 million women are infected worldwide. HIV/AIDS can be transmitted through sexual intercourse, sharing needles, pregnancy, breast-feeding, and/or blood transfusions with an infected person. Health.com:What should I do if the condom breaks?

“For HIV patients, this report is an important flicker of hope that antiretroviral therapy like HAART [highly active antiretroviral therapy] is not the endpoint of medical research,” Hutter said.

TUESDAY, Nov. 18 (HealthDay News) — Although commonly taken to improve memory, new research suggests that the herb ginkgo biloba won’t help prevent dementia, including Alzheimer’s disease.

“We found that giving a standardized dose of ginkgo biloba over a period of time does not slow down the incidence rate of dementia or Alzheimer’s disease,” said the study’s lead author, Dr. Steven DeKosky, who was chair of the department of neurology at the University of Pittsburgh School of Medicine and Medical Center at the time of the study.

The findings were published in the Nov. 19 issue of the Journal of the American Medical Association.

Dementia, including Alzheimer’s disease, currently affects about 5 million people in the United States, according to background information in the article. Dementia is a significant cause of age-related disability and the need for long-term nursing home care, the study reported.

There are currently no medications that have been approved for the primary prevention of dementia or Alzheimer’s disease. However, previous small, short-term clinical trials have suggested there might be a small benefit from ginkgo for people with dementia. Sales of ginkgo biloba are almost $250 million each year in the United States, according to the study.

The current study included almost 3,100 community-dwelling adults aged 75 or older. Most had normal cognition at the start of the study, while 482 had mild cognitive impairment when the study began.

The study volunteers were randomly assigned to receive either a twice-daily dose of 120 milligrams of ginkgo biloba extract or a twice-daily placebo. The study participants were assessed for signs of dementia every six months, and the average length of study participation was just over six years.

During the study period, 523 people developed dementia, and 92 percent of those cases were classified as possible or probable Alzheimer’s disease.

Overall, the dementia rate for those taking ginkgo was 3.3 per 100 person-years of follow-up versus 2.9 per 100 person-years for the placebo group.

“If you’re in your 70s or 80s, and you’re contemplating taking ginkgo to prevent Alzheimer’s or dementia, the idea that it can prevent these is not true,” said DeKosky, who is vice president and dean of the University of Virginia School of Medicine in Charlottesville.

But, said DeKosky, the good news from this study is that there appear to be “no major problems for safety” where ginkgo is concerned.

However, the author of an accompanying editorial in the same issue of the journal, Dr. Lon Schneider, director of the State of California Alzheimer’s Disease Research and Clinical Center at the University of Southern California in Los Angeles, pointed out that for people with a history of cardiovascular disease, there was an increased risk of hemorrhagic stroke in the group taking ginkgo, though the difference didn’t reach statistical significance. Eight people in the placebo compared to 16 in the ginkgo group had a hemorrhagic stroke, Schneider noted.

He also pointed out that at least one smaller trial found an increased risk of the more common type of stroke, ischemic stroke, and transient ischemic attacks, in people taking ginkgo.

“In the absence of efficacy, people should be fairly careful about taking a drug anyway, and here, we’ve seen no evidence for potential gain, and there’s some reason to be concerned about its use in the long term,” said Schneider.

A popular epilepsy drug can reverse the early stages of Alzheimer’s disease, scientists have discovered.

Treatment with valproic acid stops further damage to the brain and improves memory, tests show.

The experiments in mice have proved so successful that the researchers are now testing the drug on Alzheimer’s patients.

With the disease affecting around 500,000 Britons and the number forecast to double within a generation, there is an urgent need for new treatments.

Current drugs can halt the progression of the disease but do not work for everyone and their effects wear off over time.

In addition, a decision by the drugs rationing body the National Institute for Health and Clinical Excellence means they are not available on the NHS to all who would benefit from them.

Valproic acid, which is used to treat manic depression and schizophrenia as well as epilepsy, blocks production of the patches of sticky protein, or plaques, that clog the brain in Alzheimer’s.

Professor Weihong Song, who led the research at the University of British Columbia in Vancouver, Canada, said: ‘We found that if we used valproic in the early stages of Alzheimer’s disease, in mice, it reduced plaque formation and further prevented brain cell death.

‘The drug also improved performance in memory tests. We are very excited about these results.’

A pilot trial testing the effect of valproic acid on Alzheimer’s patients is under way with results expected next year.

The drug, which is also known as Convulex, had less of an effect as the disease progressed, the Journal of Experimental Medicine reports.

Professor Clive Ballard, director of research at the Alzheimer’s Society, said: ‘Although this is encouraging evidence, valproic acid is a licensed epilepsy drug that has a number of side effects.

‘We wouldn’t currently recommend it as a clinical treatment for Alzheimer’s. We look forward to the results of ongoing human trials.’