Saturday, August 15, 2009

Cannabis ‘can help to prevent osteoporosis in the elderly’ -- but harms the young

Psychotic oldsters with healthy bones coming up? Very strange results. Maybe the researchers themselves were high when they did the study. It's only a mouse study anyway and lots of effects observed in mice turn out differently in humans

Cannabis can help to prevent osteoporosis in the elderly, according to research. The findings could lead to new treatments being developed to treat the crippling condition. Researchers at University Edinburgh also found, though, that the drug can weaken the bones of younger people.

The discovery was described as “exciting” by charities, but they cautioned that it was important to understand the negative consequences of cannabis use on young bones. It was previously recognised that bone development was affected when a molecule in the body, known as the cannabinoid receptor type 1, came into contact with cannabis. It was not clear, though, whether the impact was good or bad. Now the Edinburgh team has established that this depends on the age of the user.

They exposed mice to compounds similar to those found in cannabis. They found that, in the young mice with the receptor, the compounds increased the rate at which bone tissue was destroyed. When the older mice with the receptor were exposed to the same compounds, though, their bone loss decreased and the accumulation of fat in the bones was prevented. Among older people bone regeneration normally slows down and fat builds up, causing osteoporosis.

Stuart Ralston, Professor of Rheumatology at the university, who led the study, said: “This is an exciting step forward, but we must recognise that these are early results. We plan to conduct further trials soon and hope the results will help to deliver new treatments that will be of value in the fight against osteoporosis.”

Professor Ralston said that the ideal way forward would be to develop a drug which was similar to cannabis but which did not have the same psychotropic effects. He added that smoking cannabis with tobacco was bad for bones at any age.

It is estimated that three million people have osteoporosis in Britain. One in two women and one in five men over the age of 50 will suffer broken bones because of the condition.

Claire Bowring, medical policy officer for the National Osteoporosis Society, said: “This is an exciting study ... but it is important to understand the potential negative effects on peak bone mass [in the young] as well as the positive protection from age-related bone loss. We look forward to further research to see if these effects are mirrored in [people].”


Flapjacks to be banned in Britain?

Supermarkets should stop selling high-calorie snacks and treats to help to fight the country’s obesity problem, the outgoing chairman of the Food Standards Agency says. Dame Deirdre Hutton has spoken out as the watchdog prepares new targets for food manufacturers to reduce the calories and saturated-fat content in cakes, pastries, biscuits, chocolate bars and fizzy soft drinks.

A drive against supersize portions and bargain multipack offers on junk food is also part of the effort. “It is my personal view that supermarkets should stop marketing food that is small in size and high in calories. For example, flapjacks should not be on sale,” Dame Deirdre said.

Her remarks were made in an interview with The Times to mark the end of her four-year tenure as head of the agency. “I don’t think that supermarkets should be selling this very energy-driven food,” she said. “We should be making low-calorie food the norm and anything that is high in fat should be niche. We should reverse the norm and stores should sell 90 per cent healthy food and 10 per cent unhealthy.”

Research [i.e. brainless straight-line projections] has found that, without action, about 90 per cent of today’s children will be overweight or obese by 2050, with the bill to the taxpayer estimated at £50 billion. At present 22 per cent of children in England are overweight or obese by the time they start school, and by the age of 10 or 11 the proportion is almost 31 per cent.

Labels on the front of packs to identify unhealthy food items are seen as vital to help to change buying patterns. However, Dame Deirdre’s enthusiasm for them has triggered numerous clashes with food industry chiefs who are vehemently opposed to “traffic light” labels, with some food packaging carrying red alerts, plus guidance on the maximum recommended daily consumption of salt, sugar and fats. Leading companies including Tesco, Nestlé and Danone are against these labels, although the guidance is already used on food sold at Asda and Waitrose. Widespread take-up depends on a decision by the European Commission, which could take at least another year, though it is possible that ministers will introduce new laws in Britain.

Dame Deirdre made clear, however, that the food industry had already shifted its position on labels and the need to improve the nation’s diet. “When I started here they kept saying that food was an individual choice as part of a balanced diet,” she said. “Now they have recognised that they are part of the solution and they need to play ball, and they are. But that’s not to say we won’t be pushing them harder — we will.”

Fraudsters and firms that flout food safety laws should face tougher penalties, Dame Deirdre added. Most cases are heard by magistrates, and many offenders get only light fines.“I would like to see courts hand out much higher fines and penalties, especially as the agency is being more pro-active on enforcement”.

She warned that all food outlets faced more spot checks by enforcement officers. The recent spate of sheep rustling across the country had raised her concerns that illegal slaughter of animals was rife and could pose a threat to human health.

She said that she frowned on the use of “tertiary” labelling by supermarkets, whereby they invent a location brand for products. Marks & Spencer uses the LochMuir name for some of its fish packs, which has a picture of a loch, but no such loch exists. Tesco sells a chicken range under the Willow Farm label, also a fictitious location.


How to cure diseases before they have even evolved

WILL swine flu virus turn nasty as the northern hemisphere winter gets under way? All previous pandemic flu strains started off mild before becoming deadlier, so health authorities are taking the threat seriously. They know that if 2009 H1N1 flu does become more lethal over the next few months, we will be nearly defenceless: there are already signs of resistance to Tamiflu, and any vaccines will be in very short supply.

H1N1 flu is far from the only threat. A new pathogen could emerge at any time, as the SARS virus did in 2002, or a known virus such as that behind Lassa fever could become much better at passing from person to person and spread beyond Africa. Or a rogue scientist, or just a careless one, could release a deadly virus such as smallpox.

We have been relatively lucky so far. The nature of SARS allowed it to be contained, while H1N1 flu remains mild for now. But our luck could run out tomorrow. "Mother Nature is among the worst terrorists," says Michael Goldblatt, who once led the biodefence programme for the Pentagon's research arm, DARPA, and now heads Functional Genetics, a biotech company in Gaithersburg, Maryland.

"If you look at the viruses that are the biggest threats of modern times, most of them were unknown through human history: HIV, SARS, Ebola. You don't know where the next one is coming from. How do you develop therapeutics for the unknown and unknowable, given that you won't have time to develop a vaccine for a new agent after it appears?" he asks.

Goldblatt and a few other researchers think they have the answer. They are working on an entirely new class of antiviral drugs that should do something seemingly impossible: work against a wide range of existing viruses and also be effective against viruses that have not even evolved yet. What's more, it should be extremely difficult for any virus to become resistant to these drugs.

This might sound too good to be true, but the first trials of these drugs are already producing encouraging early results. If just a few of them live up to their promise in full-scale human trials - no sure thing - they will be a medical breakthrough on a par with the discovery of penicillin. At last, doctors will be able to treat viral diseases as ably as they do bacterial ones.

The conventional strategy for developing antivirals is "one bug, one drug" - finding a drug that blocks viral replication by binding to part of a viral protein. The trouble is, any minor mutation that slightly changes the shape of the protein can render these drugs useless, as is happening with Tamiflu. The hundreds of millions of dollars governments worldwide have spent stockpiling this drug could well turn out to be futile.

A few existing antiviral drugs, such as interferons, do work against a wide range of viruses. However, these drugs merely rev up the body's immune system, which makes them less effective than doctors would like.

Back in the late 1990s, when Goldblatt was at DARPA, he began to wonder whether there was another strategy, one that exploits the key weakness of all viruses: their utter dependence on their hosts. By themselves, viruses are more helpless than newborn babies. They can replicate only by tricking their host cells into making more copies of them, a process that can involve hundreds of host proteins.

What if, Goldblatt wondered, some host proteins are essential for viral replication but not for the survival of the host? If so, disabling these proteins should block viral replication without killing healthy cells.

After moving to Functional Genetics, Goldblatt began putting his idea to the test. He and his colleagues disabled one gene at a time in human cells before exposing them to viruses such as flu. This fishing expedition worked beautifully: they identified more than 100 different human proteins that flu viruses need to replicate but which cells can survive without. Only four were previously known to be involved in viral replication.

One especially promising target is TSG101, a protein involved in the transport of materials within cells that many viruses co-opt to break out of cells. Functional Genetics has developed a small-molecule drug that appears to block the interaction between viruses and TSG101. Dubbed FGI-104, the drug inhibits a wide range of viruses in cell culture, including hepatitis C and HIV, and has also been shown to protect mice against Ebola (American Journal of Translational Research, vol 1, p 87).

FGI-104 appears not to be too toxic. Yet it might not even be necessary to inhibit TSG101 to fight infections. When a virus uses TSG101 to escape a cell, some of the normally internal protein ends up exposed on the outside of the cell - a very distinct footprint of viral infection that Goldblatt's team decided to target. They have designed an antibody, called FGI-101, that will bind to any exposed TSG101. As soon as viruses start to bud off from a cell, FGI-101 binds to the TSG101 and triggers the cell's destruction. It might not completely prevent viral replication but it should greatly reduce it.


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