Anxiety and uncertainty can cause us to become more idealistic and more radical in our religious beliefs, according to new findings by York University researchers, published in this month’s issue of the Journal of Personality and Social Psychology.

In a series of studies, more than 600 participants were placed in anxiety-provoking or neutral situations and then asked to describe their personal goals and rate their degree of conviction for their religious ideals. This included asking participants whether they would give their lives for their faith or support a war in its defence.

Across all studies, anxious conditions caused participants to become more eagerly engaged in their ideals and extreme in their religious convictions. In one study, mulling over a personal dilemma caused a general surge toward more idealistic personal goals. In another, struggling with a confusing mathematical passage caused a spike in radical religious extremes. In yet another, reflecting on relationship uncertainties caused the same religious zeal reaction.

Researchers found that religious zeal reactions were most pronounced among participants with bold personalities (defined as having high self-esteem and being action-oriented, eager and tenacious), who were already vulnerable to anxiety, and felt most hopeless about their daily goals in life.

A basic motivational process called Reactive Approach Motivation (RAM) is responsible, according to lead researcher Ian McGregor, Associate Professor in York’s Department of Psychology, Faculty of Health. “Approach motivation is a tenacious state in which people become ‘locked and loaded’ on whatever goal or ideal they are promoting. They feel powerful, and thoughts and feelings related to other issues recede,” he says.

“RAM is usually an adaptive goal regulation process that can re-orient people toward alternative avenues for effective goal pursuit when they hit a snag. Our research shows that humans can sometimes co-opt RAM for short term relief from anxiety, however. By simply promoting ideals and convictions in their own minds, people can activate approach motivation, narrow their motivational focus away from anxious problems, and feel serene as a result,” says McGregor.

Researchers also measured participants’ superstitious beliefs and deference toward a controlling God in order to distinguish religious zeal from meeker forms of devotion. “Anxiety-provoking threats sometimes also cause people to become paranoid and more submissive to externally-controlling forces, so we wanted to rule out that interpretation for our results,” he says. Anxious uncertainty had no effect on either superstition or religious submission.

Findings published last year in the journal Psychological Science by the same authors and collaborators at the University of Toronto found that strong religious beliefs are associated with low activity in the anterior cingulate cortex, the part of the brain that becomes active in anxious predicaments.

“Taken together, the results of this research program suggest that bold but vulnerable people gravitate to idealistic and religious extremes for relief from anxiety,” McGregor says.

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.”

A Princeton University research team has demonstrated that all sweeteners are not equal when it comes to weight gain: Rats with access to high-fructose corn syrup gained significantly more weight than those with access to table sugar, even when their overall caloric intake was the same.

In addition to causing significant weight gain in lab animals, long-term consumption of high-fructose corn syrup also led to abnormal increases in body fat, especially in the abdomen, and a rise in circulating blood fats called triglycerides. The researchers say the work sheds light on the factors contributing to obesity trends in the United States.

“Some people have claimed that high-fructose corn syrup is no different than other sweeteners when it comes to weight gain and obesity, but our results make it clear that this just isn’t true, at least under the conditions of our tests,” said psychology professor Bart Hoebel, who specializes in the neuroscience of appetite, weight and sugar addiction. “When rats are drinking high-fructose corn syrup at levels well below those in soda pop, they’re becoming obese — every single one, across the board. Even when rats are fed a high-fat diet, you don’t see this; they don’t all gain extra weight.”

In results published online Feb. 26 by the journal Pharmacology, Biochemistry and Behavior, the researchers from the Department of Psychology and the Princeton Neuroscience Institute reported on two experiments investigating the link between the consumption of high-fructose corn syrup and obesity.

The first study showed that male rats given water sweetened with high-fructose corn syrup in addition to a standard diet of rat chow gained much more weight than male rats that received water sweetened with table sugar, or sucrose, in conjunction with the standard diet. The concentration of sugar in the sucrose solution was the same as is found in some commercial soft drinks, while the high-fructose corn syrup solution was half as concentrated as most sodas.

The second experiment — the first long-term study of the effects of high-fructose corn syrup consumption on obesity in lab animals — monitored weight gain, body fat and triglyceride levels in rats with access to high-fructose corn syrup over a period of six months. Compared to animals eating only rat chow, rats on a diet rich in high-fructose corn syrup showed characteristic signs of a dangerous condition known in humans as the metabolic syndrome, including abnormal weight gain, significant increases in circulating triglycerides and augmented fat deposition, especially visceral fat around the belly. Male rats in particular ballooned in size: Animals with access to high-fructose corn syrup gained 48 percent more weight than those eating a normal diet.

“These rats aren’t just getting fat; they’re demonstrating characteristics of obesity, including substantial increases in abdominal fat and circulating triglycerides,” said Princeton graduate student Miriam Bocarsly. “In humans, these same characteristics are known risk factors for high blood pressure, coronary artery disease, cancer and diabetes.” In addition to Hoebel and Bocarsly, the research team included Princeton undergraduate Elyse Powell and visiting research associate Nicole Avena, who was affiliated with Rockefeller University during the study and is now on the faculty at the University of Florida. The Princeton researchers note that they do not know yet why high-fructose corn syrup fed to rats in their study generated more triglycerides, and more body fat that resulted in obesity.

High-fructose corn syrup and sucrose are both compounds that contain the simple sugars fructose and glucose, but there at least two clear differences between them. First, sucrose is composed of equal amounts of the two simple sugars — it is 50 percent fructose and 50 percent glucose — but the typical high-fructose corn syrup used in this study features a slightly imbalanced ratio, containing 55 percent fructose and 42 percent glucose. Larger sugar molecules called higher saccharides make up the remaining 3 percent of the sweetener. Second, as a result of the manufacturing process for high-fructose corn syrup, the fructose molecules in the sweetener are free and unbound, ready for absorption and utilization. In contrast, every fructose molecule in sucrose that comes from cane sugar or beet sugar is bound to a corresponding glucose molecule and must go through an extra metabolic step before it can be utilized.

This creates a fascinating puzzle. The rats in the Princeton study became obese by drinking high-fructose corn syrup, but not by drinking sucrose. The critical differences in appetite, metabolism and gene expression that underlie this phenomenon are yet to be discovered, but may relate to the fact that excess fructose is being metabolized to produce fat, while glucose is largely being processed for energy or stored as a carbohydrate, called glycogen, in the liver and muscles.

In the 40 years since the introduction of high-fructose corn syrup as a cost-effective sweetener in the American diet, rates of obesity in the U.S. have skyrocketed, according to the Centers for Disease Control and Prevention. In 1970, around 15 percent of the U.S. population met the definition for obesity; today, roughly one-third of the American adults are considered obese, the CDC reported. High-fructose corn syrup is found in a wide range of foods and beverages, including fruit juice, soda, cereal, bread, yogurt, ketchup and mayonnaise. On average, Americans consume 60 pounds of the sweetener per person every year.

“Our findings lend support to the theory that the excessive consumption of high-fructose corn syrup found in many beverages may be an important factor in the obesity epidemic,” Avena said.

The new research complements previous work led by Hoebel and Avena demonstrating that sucrose can be addictive, having effects on the brain similar to some drugs of abuse.

In the future, the team intends to explore how the animals respond to the consumption of high-fructose corn syrup in conjunction with a high-fat diet — the equivalent of a typical fast-food meal containing a hamburger, fries and soda — and whether excessive high-fructose corn syrup consumption contributes to the diseases associated with obesity. Another step will be to study how fructose affects brain function in the control of appetite.

The research was supported by the U.S. Public Health Service.

Real sugar, from cane or beets, is expensive to import.  That’s why countries without real sugar, make it from other stuff.

The United States, Canada and the UK consume a lot of sugar and don’t have enough real sugar to meet their needs. A complicated series of transformations involving enzymes and fungi can process corn into a sugar substitute called high fructose corn syrup (known as “glucose/fructose” in Canada and “glucose fructose syrup” in the UK).

It is almost exactly like real sugar. Almost.

The safety of high fructose corn syrup (HFCS) is a hot debate in health circles. Food manufacturers say that it is almost exactly like real sugar and there is no proof that it is any worse for you than real sugar. Other experts point to a key difference between natural sugar (sucrose) and high fructose corn syrup. It’s very technical, but I’ll try to simplify it.

Sucrose and HFCS are both made up of glucose and fructose, which is why the food manufacturers say they’re almost the same. The key difference is that sucrose contains a bond between glucose and fructose, while HFCS does not. Because of this bond, your body must break it down before it can be utilized. In high fructose corn syrup, there is no bond — allowing it to be utilized more easily.

When you have more energy than you can burn, it gets stored as fat. A high absorption of sugar can also lead to insulin resistance and then diabetes.

Pay attention to the type of sugar in your food, it’s important. You might be surprised how many things contain high fructose corn syrup. Some examples include: yogurt, breakfast cereals, granola bars, crackers and of course things like soda/pop and cookies. But, for all of these products, there are brands with natural sugar. Even manufacturers are starting to pay attention, Pepsi is currently offering Pepsi and Mountain “Throwback.” They’re just like their normal drinks, but made with real sugar — a throwback to the good ol’ days.

Remember that if you’re not in the USA, high fructose corn syrup is called glucose/fructose or glucose-fructose syrup.

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.”

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.

However, the United States continues to lag behind about 30 other countries in estimated life span, according to World Health Organization data.

Japan is No. 1 on the list, with a life expectancy of 83 for children born in 2006. Switzerland and Australia were also near the top of the list.

”The international comparisons are not that appealing, but we may be in the process of catching up,” said Samuel Preston, a University of Pennsylvania demographer. He is co-chair of a National Research Council panel looking at why America’s life expectancy is lower than other nations’.

The new U.S. data, released Wednesday, come from the National Center for Health Statistics. It’s a preliminary report of 2006 numbers, based on data from more than 95 percent of the death certificates collected that year.

Life expectancy is the period a child born in 2006 is expected to live, assuming the mortality trends observed in that year stay constant.

The 2006 increase is due mainly to falling mortality rates for nine of the 15 leading causes of death, including heart disease, cancer, accidents and diabetes.

”I think the most surprising thing is that we had declines in just about every major cause of death,” said Robert Anderson, who oversaw work on the report for the health statistics center.

Health statisticians noted declines of more than 6 percent in stroke and chronic lower respiratory disease (including bronchitis and emphysema), and a drop of more than 5 percent in heart disease and diabetes deaths. Indeed, the drop in diabetes deaths was steep enough to allow Alzheimer’s disease — which held about steady — to pass diabetes to become the nation’s sixth leading cause of death.

The U.S. infant mortality rate dropped more than 2 percent, to 6.7 infant deaths per 1,000 births, from 6.9.

Perhaps the most influential factor in the 2006 success story, however, was the flu. Flu and pneumonia deaths dropped by 13 percent from 2005, reflecting a mild flu season in 2006, Anderson said. That also meant a diminished threat to people with heart disease and other conditions. Taken together, it’s a primary explanation for the 22,000 fewer deaths in 2006 from 2005, experts said.

U.S. life expectancy has been steadily rising, usually by about two to three months from year to year. This year’s jump of fourth months is ”an unusually rapid improvement,” Preston said.

Life expectancy was up for both men and women, and whites and blacks. Although the gaps are closing, white women continue to have the highest life expectancy (81 years), followed by black women (about 77 years), white men (76) and black men (70). Health statisticians said they don’t have reliable data to calculate Hispanic life expectancy, but they hope to by next year.

Increases in female smoking are a major reason that men’s life expectancy is catching up with the women’s, Preston said. Improvements in the care of heart disease — a major health problem for black Americans — helps explain an improving racial gap, he said.

About 2.4 million Americans died in 2006, according to the report.

I was surprised to see such a high estimate in the rise. I mean it seems more things are coming up that will shorten life then extend it. For example more cars and more people making it harder to get somewhere and more polluted air. Also drugs are being used more commonly and sports are becoming less looked up to. My guess is about a 20% rise in the next 40 years.