Dr Jebb was first to comment, and the presenter Jane Garvey was quick to point out that her recommendations were essentially to do what Sue had tried (and failed at) before. For my part, I attempted to explain why ‘eating less and exercising more’ generally destines would-be slimmers to failure. This is a personal view, but my overwhelming impression from Dr Jebb was that she could only trot out the tired conventional wisdom about weight loss and the need to find a plan Sue could stick to, without ever considering why individuals can’t stick to ‘diets’ or make them work.

Is this the best the British Government can do in terms of weight loss advice? I suspect many will feel somewhat let down.

I am quite-often asked why someone like Dr Jebb would continue to persist to spout the usual rhetoric regarding weight loss despite the fact it clearly does not work, and that plenty of evidence exists to show this too. That is not really a question for me to answer, but for her.

However, it occurs to me that one reason why Dr Jebb would take the line that she does is because, to be frank, it pays her to do so. Here, for example, is an excerpt from a declaration of Dr Jebb’s conflicts on interest from a paper she published in 2010 in the American Journal of Clinical Nutrition:

SAJ [Susan Jebb] is a member of Scientific Advisory Boards for Coca-Cola, Heinz, PepsiCo, Nestlé and Kellogg’s.

This does not mean that Dr Jebb is corrupt. But it also should not stop us asking questions about the independence of someone who hold considerable sway in terms of health policy.

It should also perhaps be noted that another ‘acknowledgement’ in the paper referred to above tells us that Dr Jebb:

[sits] on government advisory boards that also include food industry members.

 

How does look to you? To me it looks like our Government and its chief advisor on obesity have a unhealthily cosy relationship. Some may know that the British health minister Andrew Lansley has been criticised for partnering with food companies in an effort to crack our obesity. Talk about getting the fox to guard the hen coup.

The Government set up an expert advisory group on obesity, chaired by Dr Jebb. Many members of which were publicly critical of the Government’s alliance with the food industry. What did the UK Government do? It disbanded the group near the end of last year.

Though we’re informed that one member of the group would be retained to advise the Government. Guess who?

We get more insight in this regard from clinical studies in which individuals are, say, treated with vitamin D and their outcomes compared to a group treated with placebo. Recently a study was published on-line which did just this, and it turned up at least some interesting results, I think [1].

The study in question involved treating overweight and obese Iranian women with 1000 IU of vitamin D3 (cholecalciferol) for a period of 12 weeks. A number of different parameters were measured, including:

• HDL-cholesterol levels – higher HDL levels are associated with reduced risk of heart disease
• Apolipoprotein A-1 (ApoA-1) levels – ApoA1 is a component of HDL-cholesterol, and is associated with a reduced risk of heart disease
• LDL-cholesterol:Apoliprotein B100 (ApoB-100) ratio – this ratio is a marker for the size and density of LDL-cholesterol particles. Lower ratios correspond with larger, less dense LDL-cholesterol, which appear to be harmless in comparison to so-called ‘small, dense’ LDL-cholesterol
• Fat mass

Compared to the group taking a placebo, those taking vitamin D saw:

• Significant increase in HDL levels
• Significant increase in ApoA-1 levels
• Significant decrease in LDL-cholesterol: ApoB-100 ratio

All of which point to a reduced risk of cardiovascular disease over time. In addition though, the vitamin D-treated group saw a reduction in their fat mass of 2.7 kg on average (compared to the placebo group’s average loss of less than ½ kg).

This study provides at least some evidence which supports the idea that vitamin D has a ‘causal’ link with cardiovascular disease and other chronic conditions.

My personal aim is to keep my vitamin D levels at around 50-60 ng/ml (125-160 nmol/l). I get as much summer sun-exposure as I possibly can (without burning), but also supplement with vitamin D3. One thing I’ve realised is that to optimise my vitamin D levels I’m needing to take much higher doses of vitamin D than the usually recommend daily intake of 400 IU. Typically, I require several thousand IUs per day to do this.

How do you know if you’ve got enough vitamin D on board? The only sure way to know is to test.

References:

1. Vafa M, et al. Vitamin D₃ and the risk of CVD in overweight and obese women: a randomised controlled trial. British Journal of Nutrition Published online: 09 February 2012

Dr John Briffa – How to Escape the Diet Trap Interview from Matt Edmundson on Vimeo.

© New England Journal of Medicine 2012

This picture, I think, serves also as a useful reminder of the potential roles that insulin has in the body. Insulin is essential to life, because without it glucose cannot be transported into the cells for fuel, and dangerously high levels of glucose can build up in the bloodstream.

However, insulin has other effects too. It is integral to fat storage, for instance. Here are three pertinent effects here:

Insulin stimulates the uptake of fat into the fat cells

Insulin activates the enzyme ‘lipoprotein lipase’ that catalyses the conversion of fat in the form of triglcyerides into smaller molecules known as fatty acids. These fatty acids, unlikely triglyceride, can make their way into the fat cells.

Insulin increases the supply of glycerol for the ‘fixing’ of fat in the fat cell

Insulin also facilitates the uptake of sugar into cells where it can be converted into glycerol In combination with fatty acids, glycerol forms triglyceride again, effectively ‘fixing’ fat in the fat cells.

Insulin inhibits breakdown and release from the fat cells

Triglyceride in the fat cells is disassembled through the action of an enzyme known as ‘hormone-sensitive lipase’. Insulin inhibits this enzyme, and therefore slows fat release from the fat cells (lipolysis).

These inherently fattening effects of insulin make it a likely key player in individuals who are struggling with their weight. More importantly, eating and living in a way which helps lower insulin levels provides the opportunity to reverse the processes listed above an facilitate fat loss.

In essence, what this means is eating a diet based on natural, unprocessed, ‘primal’ foods such as meat, fish, eggs, nuts, seeds, non-starchy vegetables and some fruit. What is notably missing from this diet are the starchy carbohydrates we’re sometimes urged to eat for their ‘essential and nutritious’ nature. The thing is, though, starchy carbs are neither essential nor especially nutritious. And the surges of insulin they tend to induce can lead us down a path to excess weight, and other health issues including cardiovascular disease, and type 2 diabetes.

Much more about all this can be found in my latest book Escape the Diet Trap.

However, in recent years there has been some interest in the idea that light delivered via the eye is not the only way to combat problems associated with lack of light. It is possible that the brain can responds to light that is bright enough to make its way through the skull. One practical approach here might be to shine light into the ears, because the skull is relatively thin in this region.

Recently, a pilot study was published in which 13 individuals with seasonal affective disorder were treated with light therapy into their ear canals for 8 or 12 minutes a day, five days a week for 4 weeks.

The results were dramatic. Scores of depression according to what is know as the Hamilton Depression Rating Scale were about 23 at the start of the study. Scores fell by at least half in 12 of the 13 subjects. 10 out of the 13 subjects had complete remission of their depression. Similar improvements were seen in anxiety scores too.

One major deficiency of this study is that it failed to include a placebo group (e.g. a group using earplugs and a device that delivered no light or a non-therapeutic light). The authors of this study recognise that a placebo group would be easy to incorporate, and they rightly call for further study.

While this study is flawed, I still think it is interesting. As the authors of the study point out, the results achieved are unlikely to be due solely to the placebo response. Let’s hope that a placebo-controlled study is done soon.

However, in the meantime, some might be interested to know that a Finnish company called Valkee is manufacturing and selling a device which provides light therapy via ear plugs (see picture below). The company website also contains other pieces of research some may find interesting. I’m not averse to a bit of self-experimentation, and would almost certainly have invested in this device if I didn’t already have a traditionally light therapy box.
The price of this device might be prohibitive for some, but other may reason that if it provides significant relief from low mood and seasonal affective disorder, it would have been money well spent.

References:

1. Timonen M, et al. Can transcranial brain-targeted bright light treatment via ear canals be effective in relieving symptoms in seasonal affective disorder? – A pilot study. Med Hypotheses 2012 Jan 30. [Epub ahead of print]

However, what we eat (and how much) is not the only lifestyle factor that can affect appetite. It’s been know for a long time that sleep has a role to play here. Studies have found that sleep deprivation can induce changes in hormones that regulate appetite. For example, sleep deprivation has been found to boost levels of the hormone ghrelin – a hormone that stimulates appetite. Sleep deprivation can also lower levels of the hormone leptin. This is not good, seeing as leptin not only suppresses appetite, but also speeds the metabolism.

I was interested to read of a study recently which tested the effect of sleep deprivation on appetite ratings in response to images of food [1]. In this study, individuals were tested on separate occasions after either a night or normal sleep, or total sleep deprivation the previous evening. Overall, subjective feelings of hunger were significantly greater after the night of sleep deprivation. The study subjects underwent brain scanning too (functional magnetic resonance imaging). After a night of sleep deprivation, there was enhanced activity in a part of the brain known as the anterior cingulate cortex. This structure, among other things, influences our sense of appetite and hunger. The increased appetite ratings and activity in the anterior cingulate cortex were seen after a night of sleep deprivation, despite the fact that blood sugar levels were the same as after a good night’s sleep.

What this study provides is further objective evidence that a lack of sleep might drive a tendency to overeat. For some people, therefore, it may make sense to ensure adequate sleep if the goal is to attain and maintain a healthy weight.

References:

1. Benedict C, et al. Acute Sleep Deprivation Enhances the Brain’s Response to Hedonic Food Stimuli: An fMRI Study. J Clin Endocrinol Metab 2012 Jan 18. [Epub ahead of print]

Yesterday, based on its normal calculations, NICE took the decision for a prostate cancer drug to be banned from provision by the NHS. Basically, the drug does not provide good value for money. This morning, a piece appears in the paper The Independent which highlights the fact that as is often the case, a charity is rails against NICE’s decision. The author of the piece, Jeremy Laurence, specifically mentions objections raised by the Prostate Cancer Charity regarding yesterday’s decision. He also cites objections raised by the charity Beating Bowel Cancer regarding a similar situation with a bowel cancer drug.

Jeremy Laurance makes the point that not all treatments can be made available to all patients irrespective of cost. And he also asks why the ire of charities always seems to be directed at NICE, and not the drug companies. After all, we know that pharmaceutical drugs have a generally spectacular mark-up, and there might be some room for some reduction in price while still preserving a healthy profit for the drug companies.

Jeremy Laurance asks if we should know if there is some conflict of interest within patients groups and charities, in the form of pharmaceutical funding. Back in 2008, Jeremy’s own publication conducted an investigation into such matters which it reported here. This article claims that Beating Bowel Cancer received 10 per cent of its income from drug companies.

I personally have looked into the funding of health charities before. My overwhelming experience is that it’s generally hard to find information about this and true transparency. This morning, I went looking for information about the funding of the Prostate Cancer Charity. I found this document which outlines the charity’s policy regarding funding from pharmaceutical companies. It was published in July 2008, and states is due for revision in July 2010, but it does not appear to have been reviewed.

Here’s a quote from the opening page of the document:

Whilst we acknowledge that support from pharmaceutical companies is an important resource, we recognise that partnerships with these companies should be approached with caution. The Prostate Cancer Charity seeks to make clear that it will not permit any company with a direct commercial interest in prostate cancer to influence its activities.

Would it be unduly cynical for some of us to have a ‘they would say that’ attitude to this statement? Here’s another quote, this one from the 2008 piece in the Independent. It comes from Tim Kendall, director of research at the Royal College of Psychiatrists:

Drug companies will try to do anything to align their interest with those of patients. They do things at every level of the health service and we know they do it with patient groups.

It is a multi-pronged approach to persuade patients that their drug is the one.

I’m of the mind that healthy choices need to be enjoyable and easy. I’ve noticed over the years that one thing that can have a corrosive effect here is just plain hunger. When individuals seek to improve their diet, particularly if the goal is to lose weight, then hunger often comes into it. Some people believe (consciously or unconsciously) that hunger means they must be in caloric deficit and therefore they must be losing weight. But even if weight loss is not the goal, many individuals will find themselves hungry because they have shifted towards a diet rich in fruits and vegetables, which have some nutritional merit, but generally fail to satisfy the appetite properly.

Just this week I saw a classic example of this. An overweight man told me how 3-4 months ago he’d decided, with the assistance of his girlfriend, to improve his diet. Out went a lot of rubbishy processed, grain-based foods. In came lots of fruit and vegetables in its place. Breakfast was now a grapefruit. Mid-morning snack was more fruit. Lunch was often a vegetable soup, followed by more fruit in the afternoon. His evening meal was decent (meat or fish with vegetables).

Anyway, what was the result of all this ‘healthy eating’. Two main things: almost perpetual hunger and zero weight loss. I admired this man’s ability to persist with this regime in the absence of any tangible benefit, but also how long it would be before he gets fed up with the hunger and stagnant weight and just defaults back to his original crappy (by his own admission) diet.

Of course, he won’t be the first person to lapse from some healthy eating regime. Many individuals have the experience of ‘toughing it out’ on a ‘diet’ for a limited period of time before ‘caving’ and feeling unable to resist foods such as bread, pasta, pizza, confectionary and patisserie. And while hunger appears to sap at the resolve, I’ve noticed consistently how keeping hunger at bay makes not having these foods so, so much easier.

When an individual does not let their appetite get out of hand, they usually find it relatively easy to eschew sandwiches at lunch and opt for a better option such as a salad or soup. I read a interesting piece in the New Scientist magazine yesterday that got me thinking about this phenomenon in a whole new way.

The piece was written by psychologist Dr Roy Baumeister, co-author of the book Willpower. In the piece he makes the point that willpower is a bit like a muscle. Once it’s ‘exercised’, it is weaker for some time after. In other words, once someone has to be exert some willpower and self-discipline, their ability to do that again is diminished until the willpower has been rested for awhile. Could this help explain why dietary restraint over time almost always comes back to bite people in the bum?

But perhaps even more interesting is this scientific observation: if individuals are given sugar between two tests of self-control, they do better on the second one if they are given a sugary drink compared to an artificially sweetened one. Could it be that somehow sugar feeds the willpower ‘muscle’ and strengthen the resolve? It wouldn’t surprise me at all, given just how often people find keeping blood sugar levels stable and rampant hunger at bay makes healthy eating a relative breeze. I’ve also witnessed just how not being very hungry can lead to people automatically drinking less alcohol too.

There’s a killer paragraph in the New Scientist piece that I’m reproducing here in full:

This glucose research also suggests why dieting is so fiendishly difficult. In order to resist tempting foods, we need willpower but to have willpower, we must eat. The essence of dieting (restricting food intake) robs us of the psychological strength needed to succeed. Perhaps dieters should concentrate on filling up with healthy food so they have the willpower to resist fattening stuff.

Yes, yes and yes, Dr Baumeister! Psychology may be his thing, but I feel he may have missed another potential vocation as a weight loss and healthy eating expert.

References:

1. Baumeister RF. Weak will comes from tired mental muscles. New Scientist. 1 February 2012.

One specific form of honey that is renowned in natural medicine for its curative properties is manuka honey. I was interested to see that a recent study supports its use in chronic wounds [1]. The research involved assessing the impact of manuka honey on an organism known as Streptococcus pyogenese (S. pyogenes). This bacterium is commonly found in wounds that are chronically infected.

One characteristic of S. pyogenes is that it has the ability to clump together and cause what is called a ‘biofilm’. Biofilms can form when proteins on the bacterium attached to another protein (called fibronectin) on the surface of damaged tissue cells. The biofilm that can for as a result can protect the bacterium by making it inaccessible to antibiotics.

In this recent research, manuka honey was found to reduce the expression of the proteins it uses to attach to fibronectin, thereby disrupting the formation and maintenance of the biofilm. This research provides some insight in the mechanism through which manuka honey may prevent or treat wound infections. It is perhaps also worth bearing in mind that manuka honey has been found to inhibit literally dozens of bacterial species.

This piece of research reminded me of a conversation I had with a friend. His mother-in-law was in hospital and had been diagnosed with a chronic infection in an ulcer. My friend has some interest in natural medicine, did some on-line research, through which he learned about manuka honey and its potential for assisting wound healing. He took the idea to his mother-in-law’s doctors here in the UK. The response? They flatly refused to use it, though it was not clear quite what the objection was.

Research like this recent study should help mainstream acceptance of a nature substance which appears to have genuine value in the treatment of chronically infected wounds. This will be a good thing, as more widespread use is likely to save a lot of money and a lot of suffering.

References:

1. Maddocks SE, et al. Manuka honey inhibits the development of Streptococcus pyogenes biofilms and causes reduced expression of two fibronectin binding proteins. Microbiology. Published online ahead of print January 31, 2012

Here is a link to an item which aired yesterday on BBC Radio 4’s Today programme. There are comments from individuals within this item that leave one with the distinct impression that many health professionals are unaware of the issue of vitamin D deficiency in children. A lawyer who represented parents who were wrongly accused killing their child (who after death was diagnosed with rickets) tells of how a senior radiologist at Great Ormond Street Hospital (generally regarding as the UK’s ‘best’ children’s hospital) failed to recognise rickets or the importance of vitamin D.

The item features Dr Marta Cohen (from Sheffield Children’s Hospital) who has discovered vitamin D deficiency in 75 per cent of children who had died of sudden infant death syndrome. This does not mean that the vitamin D deficiency caused any or all of these deaths. Nevertheless, there are ways in which vitamin D deficiency might cause death, and it’s clearly valid for vitamin D deficiency to be considered in children who appear to have suffered abuse or have died suddenly.

Recently, the BBC featured paediatrician Dr Benjamin Jacobs who is seeing increasing numbers of children with rickets where he works at the Royal National Orthopaedic Hospital here in the UK (video below).

Dr Jacobs makes the point that doctors are often failing to recognise and treat rickets appropriately. Dr Jacobs is quoted here as saying:

There are many other children who have less severe problems – muscle weakness, delay in walking, bone pains – and research indicates that in many parts of the country the majority of children have a low level of vitamin D.

It’s obviously not a good thing that so many children may be suffering from compromised health and possibly lose their lives as a result of vitamin D deficiency. What is good, though, is that this issue is getting mainstream attention, and that some dedicated individuals are doing what they can to raise awareness of this issue.

I came across this very interesting article today published on-line in the Scientific American. It features the ideas of Susan Cain, author of Quiet: The Power of Introverts. In the article, Susan makes the point that our society is set up to reward bold, extrovert individuals. As a result, introverts can sometimes feel the need to make themselves seem more extrovert than they are, and Susan claims that ‘… whenever you try to pass as something that you’re not, you lose part of yourself along the way.’

There’s much information in this article that really resonates with me. For example, I am the sort of person who much prefers a one-on-one dinner and the conversation that goes with it than a full-on party. It’s not so much that I don’t like groups, it’s more that I prefer more intimate environments. I also, like Susan and other introverts, really enjoy time on my own. For example, I can quite happily spend two or more days on my own writing without ever growing bored or lonely.

Another part of the interview I found really interesting concerned group-work. Here’s an extract from the piece:

When you’re working in a group, it’s hard to know what you truly think. We’re such social animals that we instinctively mimic others’ opinions, often without realizing we’re doing it. And when we do disagree consciously, we pay a psychic price. The Emory University neuroscientist Gregory Berns found that people who dissent from group wisdom show heightened activation in the amygdala, a small organ in the brain associated with the sting of social rejection. Berns calls this the “pain of independence.”

This would at least partly explain why I have a dislike of meetings. And the ones I go to rarely have more than two other people present.

It turns out that about one third to a half of us are introverts. And the article lists a few notable human introverts too, including Gandhi, Rosa Parks and Larry Page (co-founder and CEO of Google). Maybe it’s true that ‘Blessed are the meek, for they shall inherit the earth’.

Many men can find their excess fat to be stubbornly tenacious: after shifting a few or more pounds, they’ll go on to witness their weight quickly rebounding to where it was before. Scientific evidence suggests that this phenomenon is not necessarily the result of personal failings, but down to the body’s efforts to maintain fat levels as a certain ‘set point’. Understanding what determines this set point and how to lower it is critical to ensuring lasting weight loss success.

The central player in ‘set point theory’ is the hormone leptin. Leptin is secreted by fat cells and acts on a part of the brain known as the hypothalamus to speed the metabolism and suppress appetite. As we gain weight leptin levels rise to stop the rot. However, if for any reason leptin fails to do its job properly – a state known as ‘leptin resistance’ – the body will naturally gravitate to a weight that is often undesirable from a health and aesthetic standpoint.

One potential cause of leptin resistance is inflammation in the hypothalamus, and a known provoking factor here is spikes in blood sugar levels. The foods most likely to induce surges in sugar are those with added sugar, as well as many starchy carbohydrates including bread, potato, rice, pasta and breakfast cereals. Other inflammatory foods include so-called ‘omega-6 fats’ found in vegetable oils and margarine.

By inducing leptin resistance, a supposedly ‘healthy’ diet can actually lead to a sluggish metabolism and heightened hunger – not an ideal state of affairs for someone seeking to lose weight and keep it off. Critically, a diet more restricted in carbohydrate and replete with natural, unprocessed foods can put all this in reverse, allowing the body to settle at a lower and altogether more desirable weight.

But there’s another reason why curbing carbs can help men lose their guts for good: carbohydrate is the major stimulus for the secretion of insulin – the hormone chiefly responsible for the deposition of fat in the fat cells. So, a diet lower in carbohydrate facilitates fat loss by lowering insulin levels. Fat liberated in this way can fuel the body is essentially food. This way of eating can therefore turn men into ‘hibernating bears’ – able to subsist off their fat stores with their appetites naturally quelled – now we’re talking.

What to eat

Breakfasts based on cereal and perhaps wholemeal toast might have healthy reputations, but the ability of such foods to cause gluts in insulin and disrupt leptin make them nutritional disaster areas. A better option would be, say, some Greek yoghurt with nuts (e.g. almonds and walnuts) and some fruit (berries are best on account of their low-sugar and highly nutritious nature). Eggs are another good breakfast option, particularly if coupled with some smoked salmon (see below) and tomato or wilted spinach for their nutrient value.

Sandwiches are off the menu at lunch, and are ideally replaced with meat, fish or an omelette with salad and/or cooked vegetables. Oily-fish such as salmon, trout, sardines or mackerel are particularly beneficial, as the ‘omega-3’ fats these contain are anti-inflammatory, and have been linked with enhanced health and weight loss. Olive oil-based salad dressing and butter on your vegetables are fine. This same format should be used for dinner. Other options include hearty soups, stews and casseroles, accompanied with some more salad or vegetables.

For some, it can be a long time between lunch and dinner, and this can cause our appetite to run out of control and weaken the resolve. A snack of a handful or two of nuts can do wonders in terms of tiding us nicely over until our evening meal and making healthy choices there a relative breeze even when eating out.

How to exercise

Those wanting to couple this dietary approach with exercise might hold back on churning through the miles on a treadmill, the pavement or bike: ‘aerobic’ exercises such as these has been found to be generally ineffective for the purposes of weight loss. The truth is, aerobic exercise doesn’t generally burn masses of calories, and can make us hungrier to boot. Short bursts of intense exercise interspersed with periods of relative rest (high intensity intermittent exercise) is a more time-efficient and effective way of getting fit and losing weight, and can boost leptin levels too.

Lack of sleep can make you fat

One other lifestyle factor that might be added into the mix is sleep. Sleep deprivation has the capacity to lower leptin levels and therefore predispose to the body keeping itself at a higher fat set point. No surprise then that short sleep is associated with heightened risk of obesity. Those feeling they should perhaps get more shut-eye might consider hitting the sack a bit earlier when opportunity allows.

I say that because back in the year 2000, many Israeli doctors went out on strike for about three months. This coincided with a very real drop in mortality rates. The situation was reported in the British Medical Journal [1], and I remember reading the article at the time. Here are some quotes from it:

Industrial action by doctors in Israel seems to be good for their patients’ health. Death rates have dropped considerably in most of the country since physicians in public hospitals implemented a programme of sanctions three months ago, according to a survey of burial societies.

The Israel Medical Association began the action on 9 March [2000]… Since then, hundreds of thousands of visits to outpatient clinics have been cancelled or postponed along with tens of thousands of elective operations.

In the absence of official figures, the Jerusalem Post surveyed non-profit making Jewish burial societies, which perform funerals for the vast majority of Israelis, to find out whether the industrial action was affecting deaths in the country.

“The number of funerals we have performed has fallen drastically,” said Hananya Shahor, the veteran director of Jerusalem’s Kehilat Yerushalayim burial society. “This month, there were only 93 funerals compared with 153 in May 1999, 133 in the same month in 1998, and 139 in May 1997,” he said.

Meir Adler, manager of the Shamgar Funeral Parlour, which buries most other residents of Jerusalem, declared with much more certainty: “There definitely is a connection between the doctors’ sanctions and fewer deaths. We saw the same thing in 1983 [when the Israel Medical Association applied sanctions for four and a half months].”

Motti Yeshuvayov of Tel Aviv’s only burial society said that he had noticed the same trend in the Tel Aviv metropolitan area in the past two months.

There are reports of similar drops in death rates when doctors have gone on strike in Canada and Los Angeles (though I’ve not been able to confirm the veracity of these reports) .

I don’t want to denigrate the whole of conventional medicine. Actually, some aspects of it (high-tech diagnostics, surgery and emergency medicine, for example) I think are broadly genuinely worthwhile. However, a lot of what we do in medicine I think is not as effective as we’ve perhaps been led to believe. It can also be very hazardous (and take lives) of course.

There’s a kinda cloak of respectability that still surrounds modern medicine. But the fact that death rates appear to fall when doctors go out on strike suggests that when we peel back that cloak, we find plenty of things we won’t like the look of.

References:

1. Doctors’ strike in Israel may be good for health. BMJ 2000;320:1561.1

It would be comforting to think of these events as isolated incidences in the scientific community. However, according to a recent piece in the British Medical Journal, scientific misconduct is ‘worryingly prevalent’, at least in the UK [1].

The BMJ sent out a questionnaire to more than 9,000 researchers and reviewers asking if they has knowledge of colleagues “inappropriately adjusting, excluding, altering, or fabricating data” for the purpose of publication. Of those who responded, 13 per cent admitted they had such knowledge. 6 per cent admitted they were aware of misconduct within their own institutions which remained insufficiently investigated.

On January 12, the Committee on Publication Ethics (COPE) held a summit to address the problem of research misconduct in the UK. Referring to the BMJ survey, the Chair of COPE Dr Elizabeth Wagner is quoted as saying “This survey chimes with our experience from COPE where we see many cases of institutions not cooperating with journals and failing to investigate research misconduct properly.”

In a recent editorial in the BMJ [2], Dr Wagner and the BMJ’s editor Fiona Godlee wrote: “There are enough known or emerging cases to suggest that the UK’s apparent shortage of publicly investigated examples has more to do with a closed, competitive, and fearful academic culture than with Britain’s researchers being uniquely honest.”

My feeling is if the culture wasn’t so ‘closed, competitive, and fearful’ we’d probably see that misconduct is even more prevalent than the recent BMJ survey suggests. And that’s a problem because we really do need to rely on the integrity of research findings in making truly informed decisions about health and the management of disease.

Personally, I’m delighted that institutions such as the BMJ and COPE are shining a light onto this issue and thinking about how we might curb research misconduct.

References:

1. Tavare A. Scientific misconduct is worryingly prevalent in the UK, shows BMJ survey. BMJ 2012;344:e377

2. Godlee F, et al. Research misconduct in the UK. BMJ 2012;344:d8357

But it’s not all sweetness and light with aspirin because this drug also has the potential for adverse effects too, and in particular the ability to induce bleeding in the lining of the gut.

A recent review in the Archives of Internal Medicine set about assessing the impact of aspirin on not just cardiovascular events, but risk of bleeding too [1]. The review took data from 9 studies in which aspirin was used in dosages ranging from 75 mg to 500 mg per day. In total, the studies involved over 100,000 people, and the average duration of the studies was 6 years.

The populations studied in the individual studies were free from known cardiovascular disease at the start (so-called ‘primary prevention’).

This review revealed that compared to placebo, aspirin:

• Reduced the risk of cardiovascular events (e.g. heart attacks and stroke, fatal and non-fatal) by 10 per cent.
• Did not reduce the risk of death from cardiovascular disease.
• Increased the risk of bleeding by 70 per cent.
• Increased the risk of ‘nontrivial’ bleeding by 31 per cent.
• Did not clearly reduce the overall risk of death.

The authors of this study conclude that ‘… routine use of aspirin for primary prevention is not warranted and treatment decisions need to be considered on a case-by-case basis.’

It’s likely that aspirin has some value for some people in terms of overall disease prevention and perhaps life extension. What this latest review suggests, however, that our faith in aspirin as a preventive medication is largely misplaced.

References:

1. Seshasai SRK, et al. Effect of aspirin on vascular and nonvascular outcomes. Arch Intern Med 9 Jan 2012 [epub ahead of print]