Monday, February 12, 2007

Hope for asthma sufferers

Scientists appear to have found the cold-fighting protein that asthmatics lack - thus potentially saving many lives

About one child in eight in the UK has asthma, and one adult in twelve. For most of them the cold season is misery. Common cold viruses trigger about 85 per cent of asthma attacks in children, and 60 per cent of those in adults, so picking up a winter bug isn't just annoying, it can be life-threatening. "A cold is never just a cold," says Jackie Fielding, the mother of Michael, who has had a 16-year struggle with acute asthma brought on by viruses. "It's his worst enemy."

What if you could stop people with asthma reacting so badly to cold and flu viruses? It could transform millions of lives at a stroke. A London researcher believes that he may have found the key to doing just that. On February 19, at a Body&Soul-sponsored event, Professor Sebastian Johnson, one of the UK's leading asthma specialists, will describe new research that, for the first time, explains exactly why people with asthma are so susceptible to bad, attack-inducing colds. It paves the way for new drugs that could prevent cold-induced acute attacks within five years, and bring relief to families such as the Fieldings.

It's all to do with a virus-fighting protein. Johnson has discovered that this protein is singularly lacking in people with asthma. For his research, at Imperial College London, he examined cells from the lungs of volunteers with and without asthma after they had been deliberately infected with the same cold virus. He found that the lung cells of the people with asthma produced half the usual levels of a type of interferon, a protein generated by the immune system to neutralise viruses. This means that when they get a cold, they simply can't fight it off and it gets worse and worse, making their airways more inflamed, and causing a full-blown asthma attack.

Having identified the missing protein, Johnson is working with drug companies to find a way of replacing it in asthmatics and making them as good at fighting off infection as the rest of the population. "These are exciting findings and have opened up new avenues of asthma treatment that haven't been thought of before," says Johnson, who is a professor of respiratory medicine, and investigator with the Medical Research Council's Centre in Allergic Mechanisms of Asthma at Imperial College London.

His discovery follows 18 years of research, prompted by the simple question: why do people with asthma react so badly when they get a cold? His earlier studies - looking at spouses of asthmatics infected with exactly the same germs - demonstrated that viruses persisted in the system of people with asthma longer, replicating more, going deeper into the respiratory tract and causing more damage than in the rest of the population.

His latest experiments used new techniques of molecular analysis to test cells from the lungs of volunteers with and without asthma, and found in the asthma group low levels of infection-fighting lambda interferon proteins. Exactly why people with asthma have such low levels is still a mystery. According to Johnson, one explanation could be that the process of allergic inflammation in asthma itself suppresses the protein. Another is that people with asthma have a defect in the signalling pathway that leads to the release of the protein, a defect that could be linked to the reasons people develop asthma in the first place. "We know that those who have very low exposure to infections in childhood seem to be more likely to develop asthma," says Johnson. "And it could be that because of this low exposure they never develop the immune responses they should." This would fit with the so-called "hygiene hypothesis", a theory that allergies arise because we do not condition our immune system by exposing it to germs early in life.

What he's hoping is that simply replacing the deficient protein will provide the answer for asthma sufferers. A similar protein called interferon beta is already used to treat multiple sclerosis and some types of leukaemia, but in large doses by injection. Asthma sufferers would need much lower doses fed into the respiratory tract by inhaler. "I'm working with one drug company on this," says Johnson. "If the results look good, and we're really lucky, it could be available in four years." Asthma UK, which supported the research, says Johnson's research is a "break-through in understanding" and the British Lung Foundation says it will be "invaluable in improving the treatment of people with asthma".

So how does Johnson feel about being behind such a significant medical step forward? "It's been a gradual process of discovery since 1989, and I got excited at each stage. The problem is that each discovery leads to new questions, and you just want to answer those." Having provided some answers about virus infections, there's another puzzling question to be worked on, this time concerning bacteria. Johnson's analysis of samples from 114 schoolchildren suggested that the bacterium chlamydia (a different type from the one involved in sexual infections) is also involved in acute asthma attacks.

The bacteria sit in most of our lungs causing low-level mischief but, in people with asthma, it seems to burst into activity once a cold virus takes hold. Perfecting antibiotic drugs that could target this bacteria could substantially reduce the severity of asthma attacks, and Johnson believes that he's found a drug that could help people to recover three days faster. The results of early trials were published in the New England Journal of Medicine last year. "I will feel I've made a major contribution when I see the treatments on the shelf," he says.



You can get it at any health-food shop. Journal abstract below:

Suppression of Human Immunodeficiency Virus Type 1 Viral Load With Selenium Supplementation: A Randomized Controlled Trial

By: Barry E. Hurwitz et al.

Background: Despite findings that selenium supplementation may improve immune functioning, definitive evidence of its impact on human immunodeficiency virus (HIV) disease severity is lacking.

Methods: High selenium yeast supplementation (200 mu-g/d) was evaluated in a double-blind, randomized, placebo-controlled trial. Intention-to-treat analyses assessed the effect on HIV-1 viral load and CD4 count after 9 months of treatment. Unless otherwise indicated, values are presented as mean ~ SD.

Results: Of the 450 HIV-1-seropositive men and women who underwent screening, 262 initiated treatment and 174 completed the 9-month follow-up assessment. Mean adherence to study treatment was good (73.0% ~ 24.7%) with no related adverse events. The intention-to-treat analyses indicated that the mean change (delta = 32.2 ~ 24.5 vs 0.5 ~ 8.8 mu-g/L; P<.001), and greater levels predicted decreased HIV-1 viral load (P<.02), which predicted increased CD4 count (P<.04). Findings remained significant after covarying age, sex, ethnicity, income, education, current and past cocaine and other drug use, HIV symptom classification, antiretroviral medication regimen and adherence, time since HIV diagnosis, and hepatitis C virus coinfection. Follow-up analyses evaluating treatment effectiveness indicated that the nonresponding selenium-treated subjects whose serum selenium change was less than or equal to 26.1 mu-g/L displayed poor treatment adherence (56.8% ~ 29.8%), HIV-1 viral load elevation (delta = -25.8 ~ 147.4 cells/mu-L). In contrast, selenium-treated subjects whose serum selenium increase was greater than 26.1 mu-g/L evidenced excellent treatment adherence (86.2% ~ 13.0%), no change in HIV-1 viral load (delta = +27.9 ~ 150.2 cells/mu-L).

Conclusions: Daily selenium supplementation can suppress the progression of HIV-1 viral burden and provide indirect improvement of CD4 count. The results support the use of selenium as a simple, inexpensive, and safe adjunct therapy in HIV spectrum disease.



But brain-exercise may help

This week the Australian Institute of Health and Welfare released a report highlighting the social and economic burdens that dementia creates - and predicting the number of people living with dementia will skyrocket from 175,000 at last count in 2003 to 465,000 by 2031 as the population continues to age....

Alzheimer's disease is the most common form of dementia, accounting for about 60 per cent of all cases. The average healthy person loses about 1 per cent of their brain cells every year, but that number climbs to 5 per cent in people with dementia. As brain cells shrink or disappear, abnormal material builds up as "tangles" in the centre of the brain cells, and "plaques" outside the brain cells. They disrupt messages within the brain, damaging connections between brain cells, which eventually die. The result is that information cannot be recalled. As Alzheimer's disease runs its course on each area of the brain, certain abilities are lost and personalities can change dramatically, says David Ames, professor of psychiatry and old age at the University of Melbourne....

As yet dementia has no cure, though more than 100 trials for drugs are in progress in Australia, including some that could have a preventative function.... Increasing evidence shows that keeping your mind active and staying socially engaged could go some way toward achieving that. A metanalysis of 29,000 people across 22 research studies found that people with a history of complex mental activity were 46 per cent less likely to develop dementia than those who had less active minds. The research was published in the journal Psychological Medicine (2005;35:1-14).

Playing games or just keeping your mind exercised through hobbies or continuing education can all have a protective effect, says professor Michael Woodward, who heads the Memory Centre at the Austin Hospital in Melbourne and developed the content for Mind Your Mind. "It doesn't have to be specifically crosswords or sudoku, but certain mental activities are better than others," Woodward says. Sitting in front of the TV is not as effective as engaging in social events, card games or board games, or physical activity such as walking, dancing or even knitting.

The more mentally demanding the activities are, the better. The reason is that the more your brain is stimulated, the greater connections form between the neurons in your brain. "What that does is it creates more reserve, so you have more protection from the damage that amyloid (a plaque deposited in your brain that is found in patients with Alzheimer's disease) does - there's a greater buffer," Woodward says.

Surveys by Alzheimer's Australia have found most people know that their genes and getting older increase their chance of getting the disease, but much of the public is unaware that lifestyle factors are associated with increased risk, says Lynette Moore, executive director of Alzheimer's Australia Victoria, which is managing the Mind Your Mind campaign.

Having cardiovascular disease increases your risk of dementia, and not surprisingly the risk factors for both seem to overlap. "High cholesterol and high blood pressure in mid-age does increase people's risk of dementia in their 70s and 80s," Moore says. "If you're carrying a particular gene you're more likely to get it, but even adjusting for that, lifestyle factors do make a contribution. There are no guarantees but it's worth a go to adopt a healthy lifestyle - that way you have the best chance possible."

To do that, experts recommend many of the same things that help prevent cardiovascular disease: get at least 30 minutes' of physical activity a day, eat a balanced diet that's low in saturated fat and rich in fruits and vegetables, don't smoke, limit the amount of alcohol you drink.

Research is still in progress, but there is also some evidence that diets that are high in antioxidants, as well as some vitamins and minerals such as folate and vitamin B12, may also provide some protection, Woodward says. A healthy diet and exercise also reduces your chances of developing high blood pressure, type 2 diabetes and obesity, which are all other risk factors for dementia. Injury to your head also increases your risk so taking precautions such as protective gear when you play sport is also important.

Still, there are no hard and fast rules. The evidence shows that at a population level people with certain risk factors are more likely to have dementia, but at an individual level you could have several of the risk factors but never develop dementia. And the opposite is also true. "Unfortunately the biggest risk factor for dementia is something we can't address: getting older," Ames says.



Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.


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