A festive blog: Happiness and health

Blog on happiness

This is a season in which we all wish one another happiness for both Christmas and for the New Year. It is a time for happiness. However, research into happiness does not confine itself to seasons or birthdays but looks at overall happiness with life and, in some cases, attempts to relate that sense of happiness to our health. For this blog, I draw on a paper published in the Journal of Happiness Studies and no, this is not a joke, such a journal does exist published by the Springer[1] company and edited by Prof Antonella Dell Fave from Milan. Today’s blog centres on a paper from the Erasmus University of Rotterdam entitled:  “Healthy happiness: effects of happiness on physical health and the consequences for preventative care[2]”.

The author begins by accepting the view that physical health can be influenced by positive and negative mental states although this does not suggest any role for positive mental health in prevention of serious illness such as cancer. In this review the author focuses on longevity as a correlate with happiness and then asks how happiness can be exploited as a concept in the promotion of good health. In this context, happiness is defined as “overall appreciation of one’s own life-as-a-whole” or in other words “how much one likes the life one lives”. Such definitions of happiness allow for an objective and universal measure of how happy people are.

The author starts with the World Database of Happiness,[3] which shows that a positive and statistically significant correlation exists between measures of happiness and physical health. Those for self-reported health are greater than those correlations of happiness and health ratings based on medical opinion. However, correlations cannot tell us anything about cause and effect and so the author surveyed the literature in this area. Four studies were identified where some base line measure of happiness was taken and then health status (medically determined or self-reported) studied many years later. In general, those results were inconclusive, which led the author to look at measures of happiness and longevity, an objective measure of overall health. The author recorded a total of 30 such studies, eleven of which were among people who were in bad health. Happiness and longevity among this group was not at all clear-cut, reinforcing the earlier point that the biological evolution of chronic diseases, such as cancer, cannot be abated by happiness. Some 19 studies focused on health and happiness in healthy individuals. The follow up periods ranged from 1 to 60 years with 5 covering 20 years or more.  In total, some 24 effects of happiness and health were studied of which 16 (67%) were statistically positive while in the remaining 8 cases, a positive effect was observed which failed to reach statistical significance. The authors conclude that the evidence clearly points to the fact that happiness “protects” against falling ill.

This blogger would ask whether there are any overlaps between gene profiles for longevity and gene profiles for happiness. And, “surprise, surprise”, happiness is very highly heritable based on a large study of identical and non-identical twins in Minnesota[4]. A basic question on wellbeing was administered to 1380 twin pairs living together and was then re-administered to the same twins some 10 years later, leading to the conclusion that up to 80% of the stable aspect of wellbeing is heritable. So is it that happiness increases longevity or is it that to have the “happiness” genes is also to have the “longevity” genes. At this point in time we don’t know.

Happiness can influence health in many ways. Thus, it is well known that negative mental states promote poorer immune responses, higher blood pressure and other adverse physiological effects. In contrast, happiness is more likely to cope with threatening information and thus less fearful of preventative activities such as health screening. Happier people are more likely to engage in sports and are also less likely to be fatalistic as regards health.

Epidemiology deals with populations and tells us how our health trajectory is determined by our many lifestyle choices. But which is more important, health alone or happiness? Here in Ireland and I assume elsewhere, there is understandably a huge value put on being healthy. But happiness must over-ride health and so many individuals suffering from life-threatening conditions daily exhibit magnificent happiness. This is beyond the metrics of epidemiology for whom the bottom line is disease orientated. And if we move beneath life- threatening conditions and consider the risk factors for disease, the big paymaster of epidemiology, can we be happy and fat, or a happy smoker or a happy hypercholesterolaemic? Of course it would be best to be happy and healthy beyond imagination – Californian healthy even.

But that’s not life. Happiness must enter the lexicon of those concerned with life, lifestyle and wellbeing. It is the highest level of human achievement. And it can even be topped by also making someone else happy.

Happy Christmas to all my readers

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[1] http://link.springer.com/journal/10902

[2] Veenhoven R, (2008) J Happiness Stud, 9, 449-469

[3] http://www1.eur.nl/fsw/happiness

 [4]Hamer DH (1996)  Nature Genetics 14, 125 - 126 (1996)

Swedish report on diet and physical activity revals very weak science

The Nobel Laureate (immunology) Sir Peter Medawar once said that “If politics is the art of the possible, then science is the art of the soluble” and there is no better way of solving a problem than breaking it down to ever smaller units and then building it up again. In cell biology, this is easy. Isolate an enzyme and study its characteristics in the test tube. Then see what happens when an intact cell is put through its paces. Lucky cell biologists! Studying free-living humans poses an entirely different challenge with the boundaries of investigation set by factors ranging from ethics to practicalities of modern day life. Notwithstanding these challenges, the study of how the human diet influences our health must proceed with the highest possible rigour. In certain areas we can claim tremendous success such as the role of nutrients in neural tube defects, in age-related blindness, in blood lipids, in blood pressure, in bone disease and the like. In obesity, we have let ourselves down badly and nothing highlights this more than a recent systematic review of the data on diet and obesity concluded by The Swedish Council on Health Technology Assessment. Founded in 1987, this Council[1] is an independent national authority, tasked by the government with assessing health care interventions based on ‘systematic literature reviews’ of published research.

Last week (November 27^th, 2013) they launched a report: “Diet among obese individuals”[2]. In this instance, the data refer to those who are clinically obese with a BMI greater than 30kg/m². The systematic review covered all dietary intervention studies and those observational studies that lasted at least 6 months. The review covered all known publications up to the end on May this year. The authors used the internationally accepted GRADE[3] system to rank the scientific quality of the data. Studies with inconsistent results or imprecise findings/objectives or confounded by non-controlled factors were excluded. The accepted studies were used to collectively yield a conclusion as to the strength of the evidence linking diet to the treatment of clinical obesity. The following ranking was used: ++++ for high quality evidence, +++0 for moderate quality, ++00 for low quality and +000 for very low quality evidence. The results are presented for a variety of nutritional comparisons and then for foods.

If the document is searched for all conclusions ranked at the highest level (++++), only three appear.  They are:

·      “There is strong scientific data to indicate a link with increasing coffee intake and a reduced risk of diabetes among obese individuals”

·      “There is strong scientific data available to indicate that initiating dietary intervention with a VLED (very low energy diet) regimen of 8–12 weeks can achieve greatly increased weight loss over up to 12 months for obese individuals, but after two years the effect of the regimen is marginal”

·      “There is strong scientific data available to indicate that physical activity as a supplement to dietary intervention with energy restriction has no significant supplementary value for weight reduction after 6 months for obese individuals”

It is remarkable that only three conclusions reach what would be regarded as strong evidence. The report is however large enough for all “activists”, scientists and non-scientists, to find their own gems in the findings. For example, the Internet is awash with claims that this report slams low fat diets and applauds low carbohydrate diets.  However, the report is quite specific about comparisons between moderate low carbohydrate diets and low-fat diets in the clinically obese: “There is moderately strong scientific data to indicate that advice on moderate low carbohydrate diets compared with advice on low fat diets for obese individuals has a more beneficial effect on weight at 6 months. At 12 months, the effect on weight is the same (+++0). There is inadequate data available to assess whether there is any difference between advice on the two diets with regard to weight at 24 months (+000)”.  Twist it how you like but the facts are we have no long-term evidence on which to base such important food and nutrition policies. The same conclusions ring through most of the fat-carbohydrate comparisons in the report.

It is also worth looking at some of the conclusions on foods. On “Sweet drinks” the following is one key conclusion: “There is limited scientific data available to indicate that reduction of sweet drinks is linked to weight loss and lower blood pressure among obese individuals (++00)”.  For “chips” the report finds: “There is no data available to assess any effect of potatoes or chips on body weight (no studies are available)”.  For “Fruit and Vegetables”, the comments are:

·      “There is limited scientific data to indicate that advice on increased intake of fruit and vegetables, compared with advice on reduced fat intake, leads to slightly less pronounced weight loss at 6 months among obese individuals (++00). There is inadequate data available to determine whether there is any difference in effect on waist size (+000). For a longer period (12 months or more), there is inadequate data available to determine whether advice on increased intake of fruit and vegetables has a beneficial effect on body weight or waist size (+000).

• “There is inadequate scientific data available to determine whether intake of fruit and vegetables demonstrates a link with future weight change among obese individuals”.

One must bear in mind that this study was focused on weight management in the clinically obese and that what is relevant to that sector may not be relevant to the prevention of obesity or the long-term treatment of moderate overweight. Nonetheless, this influential report will serve if nothing else to show that of the 43 conclusions as regards to the role of nutrients in the management of clinical obesity, only one single conclusion (Very Low Energy Diets) met the top ++++ GRADE rating. Of the 51 conclusions on foods and lifestyle, two met this standard (coffee and physical activity). How poor is that.

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[1] http://www.sbu.se/en/

[2] http://www.sbu.se/en/Published/Yellow/Diet-and-Obesity/

[3] Oxman et al (2004) BMJ 328; 1490-1494

B-vitamins, brain shrinkage and Alzheimer's disease

Globally, we are approaching a diagnostic rate for Alzheimer’s disease of about I confirmed case per second. This will quadruple by 2040 and by then 70% of all cases will be living in developing and emerging economies. These are average values and although a 100% increase can be expected on average by 2040, this will be as high as 300% in China and India. At present, the costs of Alzheimer’s disease to society in the EU is €160 billion and that would suggest, by extrapolation, a global cost in 2040, of € 1.6 trillion. This, in today’s terms is equivalent to the combined GDP of Ireland, New Zealand, Israel, Singapore, Sweden and Nigeria. That’s a lot of dosh and suffering by any measure.

For many years, researchers in nutrition have been interested in studying the link between Alzheimer’s disease and dietary patters and the two classes of nutrients of interest have been fats, specifically a protective role for omega-3 fats and B-vitamins, specifically a protective role for folic acid and vitamin B12.  The data in this area are strongly supported by epidemiological studies, which use blood markers of these nutrients and the progression on dementia. However, as I pointed out in a previous blog (“Brain food ~ get it early” 18^th of June, 2012), when dietary intervention studies are used to verify the associations found between diet and dementia, the outcomes have been extremely disappointing and this, I suggested may be due to a strong link between certain genetic factors, diet and Alzheimer’s disease.

A recent paper published in the Proceedings of the National Academy of Sciences[1]examines the link between B-vitamin supplementation and the destruction of grey matter material from those parts of the brain specifically associated with Alzheimer’s disease. An initial study was carried out over two years with 156 subjects (mean age of 77 years) with mild cognitive impairment. Half the group received a placebo while the other got a B-vitamin supplement (folic acid, vitamin B12 and vitamin B6). The initial study showed that whereas brain size shrank in both groups, B-vitamin group had, overall, a reduction in the rate of shrinkage of grey matter. This paper now moves the same research from total brain shrinkage to the loss of grey matter specifically in those regions of the brain associated with Alzheimer’s disease (AD) In fact, the rate of shrinkage of AD-sensitive grey matter was 3.7% in the placebo group compared to just 0.5% in those receiving the B-vitamin supplement.

Homocysteine is a natural part of our blood biochemistry and high levels of homocysteine have been associated with adverse health outcomes and, classically, low levels of plasma folic acid and vitamin B-12 lead to high level of blood homocysteine. In this study, the authors considered the effect of B-vitamin supplementation on individuals with initially high or low levels of plasma homocysteine. They found that if the levels of homocysteine were elevated at the outset, the effects of B-vitamin supplementation was amplified among individuals with elevated homocysteine (5.2% brain loss in the placebo group with only 0.6% loss in the B-vitamin group).

This paper doesn’t use the usual “soft” end points used to measure cognitive decline. Instead it used structural imaging techniques of those regions of the brain sensitive to AD atrophy as an outcome measure. This is a very interesting finding and even a strong indication that habitual high intakes of certain B-vitamins will reduce the rate of neuro-degeneration from mild cognitive impairment to AD, specifically, in those subjects with high plasma homocysteine levels. However, it isn’t definitive proof of such a link. To begin to build of a supporting body of evidence, one would need to prove that accelerated (rate to be defined) shrinkage (extent to be defined) of AD sensitive regions of the brain are indeed associated with the development of Alzheimer’s disease in subject’s with specific biochemical (such as low homocysteine levels on blood) and genetic (gene SNP’s to be determined) attributes. Then we would have a robust biomarker. With that established then all manner of dietary and drug interventions could be used to study their outcome on the biomarker and, by implication Alzheimer’s disease itself.

One thing is sure. Alzheimer’s disease, like other neurodegenerative diseases, is likely to have a significant nutritional dimension.

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[1] Douaud et al (2013) PNAS, 110, 9523-9528

Food allergy ~ a fiscal and factual view

According to a very recent paper published in the Journal of the American Medical Association (Pediatrics)[1], food allergy costs a staggering $25 billion annually. This estimate was based on a survey of 1643 caregivers of children with food allergies. These costs are, by any measure, breath-taking. For example, in the case of obesity, for which we have very accurate data of the true prevalence, it is estimated that by 2030, the annual costs to the US will range somewhere between $ 48 and $66 billion[2].  How on earth can childhood food allergy cost as much as obesity? The authors break the costs down as 17% due to the direct costs of clinical care and 83% due to hidden costs such as time off work by parents in looking after sick children. However, the key figure in calculating the true national cost to the US is the prevalence of food allergy, which the authors cite as 8%. That figure was generated by the authors in an earlier study of US children and is based on a large survey involving the carers of over 38.000 children. Therein lies a huge problem in that the figure of 8% is self- reported. Two recent studies have completed a systematic review and meta analysis of the literature in this area. The first[3] focused on the prevalence of food allergy in Europe and found that the lifetime prevalence was 17.3 % meaning that at some point in their lives, about 1 in 6 people had encountered an allergy to food. However, the point estimate, that is the % at a specific time, was only 5.9 %. Both these values refer to self-reported food allergy. When food allergy diagnosis was made using a blood test (specific IgE) the point estimate was 10.1% falling to 2.7% when the more specific skin-prick test was applied. Importantly, when the gold standard test of food challenge was used, the value plummeted to just 0.9%.  The second study[4] focused on allergies to plant foods and accessed data from 36 studies with over 250,000 children. The majority of studies used self-reported values for the prevalence of food allergy. Taking fruit allergies as an example, some 21 studies using self-reporting methods found the prevalence of fruit allergy to be as high as 6.6 % and with most studies coming in at about 1%. However, with skin prick tests, the prevalence fell to less that 0.1%. A similar pattern was found for vegetable and nut allergies. The authors conclude: “Prevalence estimate of plant food allergy based on self-reported symptoms should be treated with caution”.

A final study explored the extreme event of fatal food allergic reactions[5]. The authors searched the literature from 1946 to 2012 and identified 13 studies involving 165 million food allergic person years which recorded 240 fatal food allergic reactions and 14 studies which explored such fatal events but found none. The estimated fatality rate among allergy sufferers was 1.8 per million person years which is less than that associated with accidental death. Peanut allergy, which is often cited in the popular media as the most dramatic of food allergies, had a mortality rate of 2.3 per million person years. Note that the term “person years” refers specifically to the population who are in fact food allergic and excludes the many who are not.

All of these data show that the popular estimates of food allergy and its consequences are grossly inflated, as are the putative economic costs of food allergy to carers. The true diagnosis of food allergy requires a slow methodical approach, ultimately identified by an exclusion diet and with the re-introduction of foods under clinical supervision. Skin prick tests are a next level and after that the diagnostic tools range from the low reliability ones such as blood IgE to downright quackery. For the few who are truly allergic to foods based on a proper diagnosis, the task of avoiding the offending food is a lifelong struggle. For the vast majority, where the diagnosis is self-made or based on some popular quackology, the allergy is no more than a social accessory.

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[1] Gupta et al (2013) JAMA Pediatrics 167, 1026-1031

[2] Wang YC et al (2011) Lancet; 378: 815–25

[3] Nwaru et al (2013) Allergy, DOI 10 11 11

[4] Zuidmeer et al (2013) J Allergy Clin Immunol, 121, 1210-1219

[5] Umasunthar T et al (2013) Clin Exp Allergy (October 5^th e print)