Monday, 31 January 2011

Statins—should we adjust the risk:benefit ratio?

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The prevailing opinion that statins are an elixir for long life was challenged with the recent publication of the Cochrane reviewStatins for the primary prevention of cardiovascular disease. After analysing 16 trial arms with 34 272 participants, the authors found no evidence of harm, and mortality, composite cardiovascular endpoints, and revascularisations were reduced. But they concluded: “caution should be taken in prescribing statins for primary prevention among people at low cardiovascular risk.”
The conclusion seems at odds with the findings. However, the authors found the evidence of insufficient quality to allow them to conclude differently; many trials included patients with a previous cardiovascular event, and the authors state that poor reporting of adverse events and selective reporting of outcomes contributed to their failure to draw a positive conclusion. They state that the evidence is “impossible to disentangle without individual patient data”.
The authors' conclusion is also at odds with the recent Cholesterol Treatment Trialists' (CTT) Collaboration meta-analysis, published in The Lancet. Individual patient data from around 70 000 patients with no previous cardiovascular disease were analysed, and showed that statins significantly reduced the relative risk of a cardiovascular event by 0·75 per 1 mmol fall in LDL cholesterol.
Unfortunately, the media are quick to forget, and have reported the Cochrane's headline-grabbing details with scant regard for the preceding evidence. This approach will have left many patients at best bewildered. The media have also largely ignored the Cochrane authors' conclusion that the results support guidelines from the UK's National Institute of Health and Clinical Excellence, which recommends statins are considered for primary prevention in patients with an annual incidence of cardiovascular events of over 2%.
So what should general practitioners (GPs), who are faced with increasing numbers of low-risk patients worried about mildly raised cholesterol, do? The Cochrane review has muddied the water, but the available evidence shows that statins are safe, and evidence from the CTT Collaboration also shows that reductions in cholesterol per se can produce benefits. So, the simple answer is that GPs should do what they always have done—clearly explain the risks and benefits to patients so that the patient is able to choose the strategy that is best for them.

Thursday, 27 January 2011

Faulty gene involved in cancer spread

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Wednesday 26 January 2011

Scientists at the University of East Anglia have identified a rogue gene that appears to hamper the body's efforts to prevent the spread of cancer.
The WWP2 gene makes a protein that occurs inside cancer cells. It causes the break-down of another molecule in the body that normally prevents cancer cells from spreading, called Smad7.
But, the researchers found that when they blocked WWP2, levels of this natural protector protein, Smad7, increased and the cancer cells remained dormant - they didn't spread.
According to the research team, it may be possible to develop new drugs that deactivate WWP2 and restore the body's natural ability to fight the spread of cancer and prevent it from becoming advanced.
Lead author Dr Andrew Chantry, from the University of East Anglia's School of Biological Sciences, said that such a drug might be able to stop the spread of several forms of the disease, including breast, brain, bowel and skin cancer.
He explained: "The late stages of cancer involve a process known as metastasis - a critical phase in the progression of the disease that cannot currently be treated or prevented.
"The challenge now is to identify a potent drug that will get inside cancer cells and destroy the activity of the rogue gene. This is a difficult but not impossible task, made easier by the deeper understanding of the biological processes revealed in this study."
The study, which is published in the journal Oncogene, was predominantly funded by the Association of International Cancer Research.
Dr Mark Matfield, the association's scientific co-ordinator, added: "This is a perfect example of the way that basic research into cancer can open up ways to develop new ways to treat cancer."
Dr Kat Arney, science information manager at Cancer Research UK, said: "Over recent decades researchers all over the world have discovered genes that drive the growth and spread of cancer, and this research adds one more to this ever-growing list. But, while these new results aid our understanding of the complexities of cancer and could point towards potential leads for future anti-cancer drugs, the work is still at the laboratory stage."

NICE issues new guidance on preventing skin cancer

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Thursday 27 January 2011

The National Institute for Health and Clinical Excellence (NICE) has published new guidelines to help the NHS, local authorities and other organisations in their work to prevent skin cancer.
The guidelines say that some sun exposure is important, as it allows people to make vitamin D as well as providing an opportunity to be physically active.
But too much exposure to UV light is known to increase the risk of skin cancer.
Professor Mike Kelly, director of the institute's Centre for Public Health Excellence, revealed that about 100,000 people each year are diagnosed with non-melanoma skin cancer and over 10,000 with malignant melanoma, the most serious type of skin cancer.
He explained: "Through this guidance we hope to raise awareness of the risks of UV exposure and help people to protect themselves and others.
"Simple actions can greatly reduce the risk of developing skin cancer - opting to stay in the shade, wearing protective clothing in the sun, avoiding too much sun during the middle of the day and using sunscreen can all have an effect."
The guidance contains simple and practical recommendations for preventing over-exposure to the sun.
For instance, developers should attempt to create shaded areas around buildings, while schools should encourage children to use sunscreen and stay in the shade during breaks.

Sara Hiom, director of health information at Cancer Research UK, said that avoiding sunburn is one of the best ways to reduce the risk of skin cancer.
"Many of us like to make the most of the UK's rare sunny days and should be able to enjoy the sun safely.
"If we all make sure that our skin doesn't redden or burn in the sun, it could help to reduce the rocketing number of people who develop skin cancer every year. And that's the aim of Cancer Research UK's annual SunSmart campaign."

Stop, rewind: the scientists slowing the ageing process

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Stop, rewind: the scientists slowing the ageing process

woman and childThe ageing process has been linked with many biological mechanisms

Related stories

Scientists are slowly unlocking the secrets of ageing, and some suggest treatments may soon be at hand to slow or even reverse the ageing process.
But what can science really achieve, and what are the dangers of meddling with our biological clocks?
Could such treatments induce cancers in humans, for example, and what about the world's burgeoning population and the West's "pension time bomb"?
Chromosome tips
The ageing process is a complex one, and for long remained an impenetrable mystery, but progress is now being made.
Late last year, a team at the Dana-Farber Cancer Institute in Boston published a Nature paper in which they detailed the reversing of the ageing process in mice.
They targeted the chromosomes that reside within the nuclei of all cells, and specifically telomeres, caps at the tips of chromosomes. The telomeres protect the chromosomes from damage, but also shorten with age, until the cells are no longer able to replicate.

Start Quote

By understanding the ageing process, we can help combat arthritis, diabetes and heart disease”
Professor Tim SpectorKing's College London
Professor Ronald DePinho and colleagues manipulated the enzyme that regulates these tips - known as telomerase - and witnessed dramatic results. Boost the enzyme, and the mice appeared to rewind the clock.
Click to play
The BBC's Neil Bowdler reports on the science of ageing
"What we were expecting was a slowing or stabilisation of the ageing process," he told the BBC. "Instead we witnessed a dramatic reversal in the signs and symptoms of ageing."
"These animals had their brains increase in size, they improved their cognition, their coat-hair was restored to a healthy sheen and their fertility was also restored."
Of course, this was a story of mice, not men, and applying such principles to humans could be an altogether bigger challenge. Telomerase has been linked with cancer, and there are likely to be many other mechanisms involved in ageing.
Many believe mitochondria may play a bigger role - genetic material contained within the cell but outside the nucleus. Mitochondria are the "power houses" of cells, but have also been seen to generate harmful chemicals linked with aging.
Then there is the role played by free radicals, highly reactive atoms or molecules that attack our bodies. Stem cells, primitive cells which play a key role in renewing the human body, are also likely to be involved.
Anti-ageing drug
But even though a comprehensive picture of how we age is still to be constructed, there are scientists who are already testing anti-ageing treatments on humans.
Chromosome with telomeres at tipsTelomeres (in red) are found at the ends of each chromosome, and shorten with age
Professor David Sinclair also works in Boston at an ageing laboratory at Harvard Medical School. He and his colleagues have been working on synthetic drugs called "Sirtuin activating compounds" or STACs.
Animal studies have indicated STACs can restore the health and life prospects of obese mice and early-stage trials in humans are now underway.
The research follows earlier work on resveratrol, a naturally-occurring ingredient of red wine. Both resveratrol and STACs appear to mimic the effects of restricting calorie intake, which has been seen to slow ageing in animals.
"This isn't going to be an excuse to eat French fries all day and watch TV but is a way to augment your healthy lifestyle and give you the ultimate benefits of perfect health which your body is capable of," Professor Sinclair told the BBC.
"It doesn't change food intake - the mice eat just normally or they get fatter, but their body doesn't seem to know they're fat and their organs and even their longevity is as good as a really healthy mouse."
But should we be experimenting with something so fundamental as ageing in the first place? And what of the ethical issues?
Professor Tim Spector of King's College London, who also works on the ageing process, says the focus is not on extending life, but on extending good health.
"If it means by living a long time you're crippled by arthritis and can't get out of the house that's not much use to anyone."
"But by understanding the ageing process, we can help combat arthritis, diabetes, heart disease, all these things which are age-related."
Professor James Goodwin, head of research at Age UK, believes access will quickly emerge as a key issue, should effective anti-ageing medical treatments be developed.
"Will everybody be able to get this technology which will give them a longer healthier life, or will it be restricted to the rich and wealthy?" he asks.
"Or how will the poorer countries regard the richer countries of the world where everyone is living well and living longer?"


Can Aspirin Reduce Cancer Risk and Mortality? - National Cancer Institute

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A Special Report of Peter Rothwell Lancet study for the National Cancer Institute, USA reproduced here in full with my comments. The new piece of news to me is:-

The trials included in The Lancet meta-analysis, Dr. Rothwell noted, had more fatal bleeding events among participants who took a placebo than among those who took aspirin (60 versus 40). 

The figures are starting to look too rosy! What is causing the all-cause 8% mortality if not fatal bleeds? Confused.

Can Aspirin Reduce Cancer Risk and Mortality?

Aspirin pillsAs optimism for aspirin’s apparent anti-cancer effects grows, unanswered questions remain.
The prospect is too enticing to dismiss: a single pill—a cheap one, too—that, when taken regularly, can reduce the risk not only of heart attack or stroke, but also of developing or dying from some types of cancer.

The pill is aspirin, and a host of studies have suggested that it can prevent and possibly reduce the risk of dying from some cancers. The data in support of aspirin’s anticancer effects recently received another boost, with one of the largest analyses to date—a meta-analysis of eight clinical trials involving regular aspirin use, published online December 6 in The Lancet—showing a substantial reduction in mortality for a number of different cancers.

As is often the case, though, the story is not that simple. None of the trials included in the meta-analysis, for example, was designed specifically to assess whether aspirin reduces cancer incidence or mortality. And although many studies, including a few clinical trials, support the notion that aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs) can reduce the risk of developing or dying from some cancers, other studies, including clinical trials, have reached a different conclusion.

This study used aspirin every other day, not daily.

It would certainly be welcome news to say this century-old pill may be the next great clinical cancer advance. But at this point, the sentiments among researchers in the field are mixed, and no medical organization has issued guidelines or recommendations on aspirin’s use as an anticancer therapy. For the moment, at least, the emergence of aspirin into a cancer prevention role seems to be on hold.

Lots of Data, but Still Unknowns
The meta-analysis, led by Dr. Peter Rothwell from the University of Oxford, found that after 5 years of follow-up, trial participants who took aspirin daily—regardless of dose—for a mean of 4 years had a 44 percent reduced risk of dying from cancer compared with participants who took a placebo. The largest decrease in risk was for gastrointestinal cancers.
One of the strong points of the meta-analysis, noted Dr. Rothwell, is that it included 20 years of follow-up data for individual participants in three of the eight trials, rather than relying solely on combined data from the original studies. In this subset of patients, there was a 20 percent lower risk of dying from cancer after 20 years, with the largest benefit seen again for gastrointestinal cancers. Overall in the meta-analysis, trial participants who took aspirin had a decreased risk of dying from relatively rarer but highly deadly cancers such as pancreatic and esophageal, as well as from common cancers such as lung and prostate. The longer the duration of aspirin use in the trials, the greater the benefit.

Recently, a similar meta-analysis from the same research team, this one focused specifically on the effect of aspirin use on colorectal cancer, showed large and statistically significant reductions in both incidence and death from the disease. The finding, the study team pointed out, is consistent with results from numerous studies that have shown regular NSAID use reduces or prevents the growth of precancerous growths in the colon.

The mounting evidence of aspirin’s strong anticancer effect is hard to ignore, argued Dr. Rothwell. “At a minimum, in combination with the appropriate screening, the data indicate that aspirin would be highly effective in preventing colon cancer,” he said.

Dr. Rothwell is not alone in his opinion. “I do believe there is a role for using [NSAIDs] at a subtherapeutic level for various types of tumors,” said Dr. Randall Harris from Ohio State University. Dr. Harris led a prospective observational study of participants in the Women’s Health Initiative (WHI), which found that women who took aspirin or ibuprofen at least twice a week for 5 years or more had a reduced risk of breast cancer. “The data are strong for colon cancer and reasonably strong for breast cancer,” he said.

That sentiment, though, is not universal.

“It would be premature to recommend that people start taking aspirin specifically to prevent cancer,” said Dr. Eric Jacobs, strategic director of pharmacoepidemiology for the American Cancer Society, in an e-mail. Potential side effects have to be taken into consideration, he continued, noting that even low dosages of aspirin “can substantially increase the risk of serious gastrointestinal bleeding.”

The side effects are assessed in the Rothwell paper. 

Reasons for Caution
Targeting Colorectal Precancers
The strongest data supporting the use of NSAIDs to reduce cancer risk is in colorectal cancer. One phase III trial on the horizon will assess whether an NSAID called sulindac, in combination with an investigational drug called DFMO, prevents the recurrence of colon polyps (which can eventually progress to become colorectal tumors) in patients who have previously had polyps removed.
The upcoming trial, according to Dr. Umar, follows from the very strong results seen in an earlier phase III trial in which participants who received the sulindac/DFMO combination had marked reductions in the return of colorectal polyps compared with patients who received a placebo. For advanced adenomas, which are most lik Cely to progress to malignant colorectal tumors, the reduction was 95 percent.
This new trial will be larger than the previous trial and will examine the effects of sulindac and DFMO separately as well as in combination, Dr. Umar explained, with a primary endpoint of reduction in advanced adenomas. If the results are similar to the earlier trial, he added, they would form the basis for a submission to the FDA for approval of the drug combination to prevent advanced adenomas.
Much of the hesitation, explained Dr. Asad Umar of NCI’s Division of Cancer Prevention, stems from the lack of data from appropriately designed randomized clinical trials focused specifically on a cancer outcome. “Only when you do a randomized clinical trial do you get the complete picture of what’s going on,” he said, including potential benefits and harms.

How long would these trials focused on a cancer outcome take? Another 20 years?

Dr. Umar cited the experience with a different NSAID, the COX-2 inhibitor celecoxib (Celebrex). Celecoxib is approved by the FDA as an adjunct to surgery to prevent polyp formation in people with a disorder called familial adenomatous polyposis (FAP) that puts them at an increased risk for colorectal cancer. Early, smaller clinical trials to test whether daily use of celecoxib could prevent the return of colon polyps in people without FAP didn’t reveal any meaningful side effects from the drug, and did show significant reductions in polyp formation and growth. It was only in much larger trials, including the NCI-funded Adenoma Prevention with Celecoxib trial—which assessed effects of using the drug daily for 3 years—that evidence emerged for potential adverse cardiovascular effects of regular, long-term treatment with celecoxib.

The trials included in The Lancet meta-analysis, Dr. Rothwell noted, had more fatal bleeding events among participants who took a placebo than among those who took aspirin (60 versus 40). 

Where in the Rothwell paper is this info? Maybe a verbal comment? I would have thought that aspirin would have caused more fatal bleeds than the placebo. Compare the fatal bleeding events: 60 placebo versus 40 aspirin figures above with the deaths from cancer (fig 1 below) 327/11535 placebo versus 347/14035 control. 

The analysis also showed a more than 8 percent reduction in all-cause mortality among aspirin users by the end of the trials included in the analysis, “nearly all of which was due to the reduction in cancer deaths,” he said.

If fatal bleeds and cancer are both reduced with aspirin what fatal illness is causing the 8% all-cause mortality?  The figures don't make sense to me now.

Despite the promising data from these studies, Dr. John Baron of the University of North Carolina said he is not yet ready to endorse aspirin’s widespread use for cancer prevention. “We need to consider all of the benefits and harms that can accrue from aspirin use in various population groups,” he said. “We don’t quite have that yet.”

How many more years research needed to compare various population groups?

Filling in the Blanks
In a consensus statement published last year, an international group of researchers reviewed the published data on aspirin’s effects on cancer incidence and mortality and laid out what they determined to be the most important clinical questions that still need to be answered. These questions included how long people should take aspirin for the optimum effect, the age when they should start taking it, and the best dose, among others.
Dr. Baron, a statement co-author, admitted that it will be difficult to answer these questions. “The most important issue that needs to be dealt with immediately is the dose issue,” he said.

This paper is cited by Rothwell, his reference number 7. 

Opinions on dose vary. A daily low-dose aspirin (such as 81 mg) is likely to be the proper choice, Dr. Rothwell said. But Dr. Harris suggested that a higher dose, up to 325 mg at least twice a week, would also be effective.

In The Lancet meta-analysis, the risk of dying from cancer decreased regardless of the aspirin dose. But observational data from a recent Harvard study showed that, at least in people already treated for colorectal cancer, the extent of the risk reduction seemed to increase with dose. “That certainly needs to be considered,” Dr. Baron said, “because side effects from aspirin also increase with dose, although not strikingly.”

Typically, clinical trials could help to provide more definitive information on dose. But large cancer prevention trials of aspirin are very difficult to conduct, Dr. Umar acknowledged. A trial using cancer mortality as an endpoint would require a very long study with a large number of participants to demonstrate any effect. And many people are already taking aspirin for cardiac prevention and pain relief, Dr. Harris said, so gathering enough participants who don’t take aspirin for the sake of comparison would also pose a difficulty. 

So should we wait for more trials taking maybe 20 years or go with the evidence that Rothwell has provided?

As far as clinical trials are concerned, Dr. Umar said, “We need to develop carefully designed studies, identify high-risk groups and surrogate endpoints, and get a genomic signature of response in addition to clinical endpoints.”

Several trials focused on high-risk groups are planned or ongoing. (See the sidebar.) In the United Kingdom, for example, participants are being enrolled in the phase III AspECT trial, which will test whether aspirin in combination with a drug that prevents and treats acid reflux (and may prevent or limit gastrointestinal bleeding) can reduce the risk of esophageal cancer in people with Barrett esophagus, which can be a precursor to the cancer.

Dr. Rothwell predicts that the findings from these trials and other studies will “firm up the evidence” in support of aspirin for cancer prevention.

In the meantime, Dr. Jacobs advised, the average person needs to proceed with an abundance of caution. “Decisions about aspirin use should be made by balancing the risks against the benefits,” he said, “so any decision about daily aspirin use should be made only in consultation with your health care professional.”

Wednesday, 26 January 2011

New approach to weight loss debated

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The Daily Mail says that “staying fat may be better for your health”. The newspaper reports that there is evidence that “overweight people live longer than normal” and that they “are also more likely to survive certain health conditions, such as type 2 diabetes, heart disease and kidney failure”.
The news is based on a research article that discusses the merits of promoting “health at every size”. It puts forward the idea that overweight people would receive greater health benefits from learning to rely on internal cues to direct their eating and building activity into their day than they would from focussing specifically on losing weight. It quoted six relevant studies that found that the new approach improved various health behaviours, as well as psychosocial and physiological outcomes. However, the trials mentioned were small, short-term (most lasted a year or less) and in women only. The studies also did not appear to assess long-term outcomes such as mortality or risk of cardiovascular disease.
Suggesting that individuals should be encouraged to have healthy behaviours at any weight does seem to make sense, but there needs to be more research to determine the long-term health benefits of this approach before it can be recommended over conventional appraoches.

Where did the story come from?

The review in question was written by two researchers from the University of California and Coventry University. They did not report any sources of funding for this specific article, although the authors reportedly speak and write on the concepts discussed in the article and sometimes receive payments for these activities. One author receives funding from the West Midlands Nursing, Midwifery and Allied Health Professions Research Training Award. The review was published in the open access, peer-reviewed Nutrition Journal.
The Daily Mail reported on this article, saying that it “includes analysis of 350,000 people in the US”. It did not make clear that the current study was summarising previous research, and that this “large study” was not in fact a single study but an analysis of 26 pooled studies in a previous systematic review. This systematic review, which was mentioned in the more discursive part of the current review, examined the association between weight and longevity rather than specifically looking at the “health at every size” approach, which was the focus of the currentnarrative review.

What kind of research was this?

This was a narrative review debating whether there should be a shift in focus from promoting weight loss in overweight and obese individuals to promoting “health at every size”, an approach that concentrates on body acceptance, using internal processes (such as hunger and fullness) to regulate eating, and finding enjoyable ways to build more activity into daily routines.
The authors say that although interventions involving diet, exercise and other behavioural changes can reliably lead to weight loss in the short-term, most people are not able to maintain this weight loss in the longer-term and therefore do not achieve the potential benefits of reduced weight. They also suggest that these weight-focused interventions may have unintended side effects, such as contributing to cycles of weight loss and regain, preoccupation with food and body image, lower self-esteem and eating disorders.
The authors say that concentrating on weight loss takes focus away from other health goals and issues that also affect health. They say that there is a growing movement towards focusing on “health at every size” rather than weight loss and dieting.
A narrative review is typically used as a way of discussing new or emerging theories.

What did the research involve?

The authors discuss the evidence and rationale behind “health at every size” (HAES) in several sections.
First, they carried out a search of one major literature database to identify randomised controlled trials (RCTs), comparing the effects of interventions focusing on HAES and size acceptance with traditional interventions focusing on weight loss or weight maintenance. They summarise the findings of the RCTs they identified. Our report focuses on this aspect of the review.
The researchers then go on to list the assumptions underlying the conventional weight-focused approach, and discuss the evidence regarding these assumptions. They detail and discuss the ways in which HAES differs from weight-focused approaches. Finally they discuss the clinical and public health ethics surrounding these different approaches.

What were the basic results?

The researchers identified six fully published RCTs based on HAES principles. These RCTs included between 60 and 185 people each, with 620 people included in total. They all included overweight or obese women, some of whom were chronic dieters or binge eaters. The studies compared HAES approaches with various alternatives including social support, dieting, cognitive behavioural treatment, education and weight loss approaches. They lasted for between 26 and 78 weeks post-treatment.
They found that:
  • Of five RCTs assessing health behaviours, four found statistically significant improvements in the HAES group compared with the control in at least one measure (e.g. activity or eating behaviours).
  • Four RCTs assessed psychosocial outcomes, and three of these found statistically significant improvements in the HAES group compared with the control in at least one area (e.g. self-esteem, body image, depression).
  • Three out of four RCTs assessing metabolic outcomes showed significant improvements in at least one of these measures, such as blood pressure and blood lipids.
  • The actual figures for individual measures were not shown in the review, but the improvements seen were reported to be “statistically and clinically relevant”.
  • None of the measures showed any adverse change with HAES approaches.
Another RCT published only as a conference abstract, a non-randomised controlled study and five uncontrolled studies was also described as having positive results, but no further details were provided.

How did the researchers interpret the results?

The researchers concluded that: “From the perspective of efficacy as well as ethics, body weight is a poor target for public health intervention.” They say that there is “sufficient evidence to recommend a paradigm shift from conventional weight management to HAES”. They also call for further research into the unintended consequences of weight-focused approaches, and into the best “health at every size” interventions.


This narrative review has summarised the evidence and rationale behind the “heath at every size” (HAES) approach, which focused on following a healthy lifestyle rather than weight loss.
  • The RCTs identified were all small, had relatively short follow-up periods and only appeared to include women.
  • To determine whether HAES approaches do produce greater health benefits in the long run there must be much larger, longer studies comparing standardised HAES approaches with accepted weight-loss focused approaches in both men and women.
  • The review did not provide information about the methods of the RCTs (e.g. how they assessed the outcomes), or quantitative results of these RCTs. Therefore it was not possible to judge the quality of this research or the magnitude of benefits seen with HAES.
  • Although a search was performed for RCTs looking at HAES approaches, other sections of the article are more descriptive in nature and may not have included all relevant research.
While suggesting that individuals should be encouraged to have healthy behaviours at any weight does seem to make sense, it is not possible to say yet whether HAES approaches are more effective than other approaches. In order to evaluate the health benefits of HAES there must be further research looking at it as a long-term approach in larger populations and directly comparing it with weight-loss measures.

Links to the headlines

Links to the science

Bacon L and Aphramor Lucy. Weight Science: Evaluating the Evidence for a Paradigm shift Nutrition Journal, January 24 2011