British researchers believe that eating lots of broccoli may slow down and even prevent osteoarthritis.
The University of East Anglia team is starting human trials following on from successful lab studies.
Tests on cells and mice showed that a broccoli compound – which humans can also get from Brussels sprouts and cabbage – blocked a key destructive enzyme that damages cartilage.
Researchers are asking 20 patients to eat a daily dose of “super-charged” broccoli.
This special cruciferous vegetable has been bred to be extra rich in nutrients – it is a cross between standard broccoli and a wild relative from Sicily.
Our body takes this glucoraphanin compound and turns it into another, called sulforaphane, which appears to protect the joints.
The volunteers will have two weeks on the diet before going under the knife to have their badly arthritic knees repaired by surgeons.
Dr. Rose Davidson and her team will look at the tissue that has been removed to see what impact, if any, the broccoli has had.
British researchers believe that eating lots of broccoli may slow down and even prevent osteoarthritis
She said: “We’re asking patients to eat 100 g [3.5oz] every day for two weeks. That’s a normal, good-sized serving – about a handful – and it’s an amount that most people should be happy to eat every day.”
While two weeks is highly unlikely to be enough to cause any big change, Dr. Rose Davidson hopes it will be enough to offer some evidence that “super” broccoli could benefit humans.
“I can’t imagine it would repair or reverse arthritis… but it might be a way to prevent it,” she said.
Her team will be looking for proof that sulforaphane has travelled to where it is needed in the joint and that it is causing beneficial changes at the cellular level.
Another 20 knee replacement patients who have not been on the diet will be used as a comparison group.
Prof. Alan Silman, of Arthritis Research UK, which is funding Dr. Rose Davidson’s work, said: “Until now research has failed to show that food or diet can play any part in reducing the progression of osteoarthritis, so if these findings can be replicated in humans, it would be quite a breakthrough.
“We know that exercise and keeping to a healthy weight can improve people’s symptoms and reduce the chances of the disease progressing, but this adds another layer in our understanding of how diet could play its part.”
The results of Dr. Rose Davidson’s animal trials are published in the journal Arthritis & Rheumatism.
The special broccoli, known as Beneforte, was developed from publicly funded research at the UK’s Institute of Food Research and the John Innes Centre.
A group of brain cells called tanycytes, which were identified as having the power to control appetite, could be the major cause of eating disorders such as obesity, a new research suggests.
In experiments in rodents, tanycytes were found to produce neurons which specifically regulate appetite.
The University of East Anglia (UEA) researchers say their find means appetite is not fixed at birth.
The new study is published in the Journal of Neuroscience.
A group of brain cells called tanycytes, which were identified as having the power to control appetite, could be the major cause of eating disorders such as obesity
It was previously thought that nerve cells in the brain associated with appetite regulation were generated entirely during an embryo’s development in the womb and could not be altered.
However, the UEA study’s discovery of these tanycytes, which act like stem cells, in the brains of young and adult rodents shows that appetite can be modified.
Researchers looked in detail at the hypothalamus section of the brain, which is known to regulate sleep, energy expenditure, appetite, thirst and many other critical biological functions.
They studied the nerve cells that regulate appetite using a “genetic fate mapping” technique and found that some cells added neurons to the appetite-regulating circuitry of the mouse brain after birth and into adulthood.
Dr. Mohammad Hajihosseini, from the university’s school of biological sciences, who led the research, said the discovery could eventually offer a permanent solution for tackling obesity – but it would take up to five or 10 years to translate the findings into humans.
“This study has shown that the neural circuitry that controls appetite is not fixed in number and could possibly be manipulated numerically to tackle eating disorders.
“The next step is to define the group of genes and cellular processes that regulate the behaviour and activity of tanycytes.
“This information will further our understanding of brain stem cells and could be exploited to develop drugs that can modulate the number or functioning of appetite-regulating neurons.”
Although there isn’t one single solution to controlling appetite, Dr. Mohammad Hajihosseini says any sustained solution to obesity must focus on the part of the brain that makes decisions on appetite.
“This is adding another piece to the jigsaw.”
The research was funded by the Wellcome Trust.
A US study found that some antipsychotic medication may increase the risk of death in patients with dementia more than others.
The antipsychotics have a powerful sedative effect so are often used when dementia patients become aggressive or distressed.
A study, published on the BMJ website, argued that antipsychotics should not be used “in the absence of clear need”.
Experts said better alternatives were needed to antipsychotics.
A study in 2009, suggested 180,000 people with dementia were taking antipsychotic medication in the UK and said the drugs resulted in 1,800 additional deaths.
Researchers at Harvard Medical School followed 75,445 people in nursing homes who had dementia and were prescribed antipsychotics.
The researchers said some drugs were associated with more than twice the risk of death than risperidone, another antipsychotic which was used as a benchmark to compare the other drugs.
The study concluded: “The data suggest that the risk of mortality with these drugs is generally increased with higher doses and seems to be highest for haloperidol and least for quetiapine.”
However, the way the study was conducted meant it could not say definitively that certain drugs actually caused more deaths, merely that there was a link between the two.
The Department of Health said antipsychotic use was “resulting in as many as 1,800 unnecessary deaths per year. This is simply unacceptable.”
“That’s why reducing the level of antipsychotics prescribing for people with dementia by two-thirds is one the key priorities in the National Dementia Strategy.”
A US study found that some antipsychotic medication may increase the risk of death in patients with dementia more than others
The Dementia Action Alliance – which includes the Alzheimer’s Society, Age UK and the Department of Health – has called for all prescriptions for antipsychotics to be reviewed by the end of March 2012.
Dr. Chris Fox, who researches dementia at the University of East Anglia, said: “This study provides an interesting insight into the differential harm of these medicines.
“More work is needed on alternatives to these medicines in dementia with behavioral problems.
“In addition, there is a need to consider duration of use in more acute situations such as severe distress. Is six or 12-week use safe in people with dementia?”
Alzheimer’s Research UK’s chief executive Rebecca Wood said the risks of antipsychotics were “well-established” yet “progress has been frustratingly slow” in reducing their use.
She said the drugs “should only be used for people with dementia where there is no alternative for dealing with challenging behavior”.
Dr. Anne Corbett, research manager at Alzheimer’s Society, said: “For a minority of people with dementia antipsychotics should be used, but then only for up to 12 weeks, and under the correct circumstances. For the majority, they do far more harm than good.”