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Monday, June 25, 2012

Obesity and social disadvantage

Frequently, when chatting with my middle class friends on nutrition and health, I have to argue long and hard against some preconceived notion of the truth behind the topic of discussion. Of all of these issues, the one I encounter most frequently and the one that meets most resistance to change is the view that the problem of obesity is really a problem of the lower socio-economic groups.  A frequent argument put forward is that  “if you look at their shopping trolleys in supermarkets, they are laden with all sorts of junk foods”.  So let me give you the facts. Taking the Irish population as a whole and using the IUNA database, body mass index (BMI kg/m2) is 26.8 among the professional workers, 27.4 among non-manual workers, 28.4 among skilled workers and 26.0 among the unskilled workforce. An acceptable level of BMI is 25 and I should add that the variance (standard deviations) of these figures is broadly similar. Now you can look at this and say: ”See I told you so. There is a graded rise in BMI from professional to skilled workers” and this goes nicely with the social class stereotype. The socio-economically disadvantaged are seen as lacking money to buy healthy food, and so poorly health aware as to not know good food choices from bad food choices and, in some cases, they are deemed to lack the literary skills to read labels correctly. This leads the debate on public health nutrition to shift into policy decisions in which actions toward social issues begin to dominate. In case you think that this Irish data is unique, please consult the Report of the Health and Social Care Information Centre’s report: Statistics on obesity, physical activity and diet: England, 2011.  To directly quote the report: “Table 7.3 on page 128 of the HSE 2009 report shows that there are very little differences in mean BMI by equivalised household income for men with the exception of those in the lowest income quintile who had slightly lower BMI; in contrast for women, those in the lower income quintiles had a higher mean BMI than women in the highest quintile. Among women, the proportions who were obese were higher in the lowest three income quintiles (ranging from 27%-33%) than women in the highest two quintiles (ranging from 17%-21%). The relationships between BMI and income for men were less clear”. Canadian data is quite similar but US data[1] does show quite a different pattern with obesity rising more rapidly among the socially disadvantaged. However, these data when carefully examined reveal some intriguing facts.  Among white men and women, the rate of rise in the % obese has grown equally across socio-economic status (SES) over the 30 years from 1970 to 2000. The lowest SES in 2000 had an obesity rate of 28.3% in men compared with 23.9% among those in the highest SES. For women, the figures were 36.3% and 26.6% respectively. However, when we look at black males, the % obese jumped from 4% to 33% in that 30-year period among the highest SES. The middle and lowest SES groups started off with a figure of 15%, which grew to 24%. For black women, the total reverse was seen. How does on e begin to make sense of that?

I should add that if you look at dietary patterns across socio-economic status in the Irish IUNA data, you see no biologically meaningful change in the % energy from fat or sugar and this is borne out by data from the Household Budget Survey which tracks expenditure on foods. That data shows no difference in food purchasing patterns across socio-economic status.

There is a bottom line here and that is that obesity is everywhere. To argue over one unit of BMI between the haves and the have-nots is to quite simply miss the point. Statisticians can construct models, which show that controlling for age, gender, smoking and so on, the relative risk of obesity rises with lower socio-economic status. They are welcome to that but if it begins to drive public health nutrition policies toward some social solutions, then they are being unhelpful. Of course, social disadvantage needs to be a factor we consider in all aspects of public health. But what is driving the increased adiposity of judges, teachers, doctors and so forth. It is not a lack of knowledge, not due to literacy or lack of income. The do-gooders of public health nutrition need to read the real population statistics and make appropriate recommendations.

[1] The Obesity Epidemic in the United States—Gender, Age, Socioeconomic, Racial/Ethnic, and Geographic Characteristics: A Systematic Review and Meta-Regression Analysis Youfa Wang and May A. Beydoun Epidemiologic Rev 2007;29:6–28

Monday, June 18, 2012

Brain food ~ get it early

The human brain is, pro rata bigger and is far more complex in structure than in any other species. It tends to be a very busy organ and consumes about 25% of the daily caloric intake of an average person. This increases to about 50% of caloric intake in the children aged 1 to 6 years and reaches 55% in 4-6 month olds and a staggering 75% in newborn babies.  Around about the age of 30, the human brain begins to shrink at the rate of 1 milligram per year and if that seems a small rate of decline (a lifetime reduction of 8% volume), the evolution of the human brain to its present size was also 1 milligram per year.  Without question, the biggest fear people have in entering old age is a loss of cognitive function with Alzheimer’s disease the worst-case scenario.  The issue is so important that it attracts all forms of snake-oil merchants promising this or that diet to stave off any decline in cognitive function.

The best place to start the task of ensuring a healthy brain throughout adult life is during pregnancy. During the third trimester of pregnancy, there is a growth spurt in brain development, which continues for 24 months. The human brain is about 60% fat and so when it comes to any discussion of nutrition and brain function, fat is bound to dominate. Specifically, the brain is rich in long chain highly polyunsaturated fatty acids that are abbreviated to EPA (Eicospentaenoic acid) and DHA (Docosahexaenoic acid). These fats cannot be synthesised by the human body and therefore have to be obtained from our diet. Fatty fish are by far the best source of these fatty acids and this raises an interesting question: Why, if the human brain was so important in our evolution, did we not develop the capacity to synthesise these fatty acids ourselves? Stephen Cunnane, author of “Survival of the Fattest” makes the case that man migrated from the Savannah to the shoreline of lakes, rivers and deltas where an abundance of fish, shellfish, eggs, bird and wild life existed. Such a food chain is rich in the brain type fatty acids, EPA and DHA, and there would have been no evolutionary advantage in having the energy demanding metabolic pathways to manufacture these fatty acids ourselves.

The growing foetus is totally dependent on a maternal supply of these fatty acids for brain development and when these enter the mother’s blood supply after a meal, they are preferentially transferred to the foetus. Other types of fats might be shared with the mother’s own fat reserves but not these precious fats. After birth, breast milk should contain adequate levels of these fatty acids and so too should infant formula. The problem begins to arise when post-natal nutrition is inadequate. The first 24 months of life sees a tremendous growth in brain complexity, especially in the frontal cortex through which the new baby acquires the social norms and language of its environment. Inadequate nutrition in this period will greatly diminish intellectual capital for the rest of such an individual’s life.

It goes without saying that an adequate intake of these fatty acids is required throughout adulthood and there are ample studies showing that inadequate intakes of fish oil type fatty acids are associated with a higher risk of loss of cognition in later adulthood.  However, when the putative link between these fatty acids and cognitive decline are tested in dietary intervention studies, the evidence just evaporates. One possible reason for this is in the genetic predisposition to Alzheimer’s disease. There is a protein that is strongly involved in fat transport and distribution, abbreviated to Apo E and it can exist in three different forms of (Apo E2, E3 and E4) and we can inherit any two varieties from either parent. Thus 60% of the population has E3/E3 and they account for 65% of all Alzheimer’s cases. A smaller number (23%) of the population has the E4 variety either alone (E4/E4) or in combination (E4/E3) and this quarter of the population account for nearly half of all cases of Alzheimer’s disease. Thus with such a strong genetic dimension, intervention studies will eventually have to be conducted in which the individuals genetic make-up is taken into account. Moreover, the duration of the studies will have to become much longer if we are to identify a truly protective effect should such an effect actually exist. In addition to fish oil type fatty acids, there has been similar data for some of the B vitamins, most notably, folic acid and vitamin B12. Again, the association data seems very strong but again, when dietary intervention studies are conducted, little supporting evidence emerges. A higher body mass index in middle age is also a risk factor for Alzheimer’s disease and my guess is that this may arise because the more adipose tissue you have the more you will move EPA and DHA to that tissue away from blood which would normally be the route to the brain.

In Celtic mythology, the salmon was referred to as the fish of knowledge and maybe, even as these mythologies evolved, there was anecdotal evidence that fish was good for the brain. In modern Celtic Ireland we have a low intake of EPA and DHA and remarkably, 75% of our intakes of these vital nutrients come from fish oil capsules rather than fish. Some achievement for an island race!

Monday, June 11, 2012

Sugar taxes re-visited: An economic and nutritional analysis

Following an extremely successful Policy Workshop of the UCD Institute of Food and Health last Friday, I return to the issue of fat and sugar taxes. We had two economists and two nutritionists from UCD.  The main focus was a tax on sugar-sweetened beverages, which interests the Irish government, such that they have created a Health Impact Assessment exercise to explore this option.  Just under half or Irish adult males are overweight while the comparable figure for females in just under one third. The respective figures for obesity levels are one quarter and one fifth. So, we have a problem as has most developed countries. Anne Nugent presented data from the National Adult Nutrition Survey and used these data to examine various parameters across quartiles of calories from sugars (non-milk sugars). From the lowest to the highest quartiles, there were no differences in any measure of obesity or of fat distribution.  It could be argued that total non-milk sugars is a poor tracker of the intake of sugar-sweetened beverages so Anne made a comparison of obesity indicators cross thirds of intakes in sugary beverages and only among consumers of these products. Going from the lowest third to the highest third of intakes of sugar-sweetened beverages, there were absolutely no differences in any measure of obesity or fat distribution. One very important statistic is that only 40% of Irish individuals actually consume sugar-sweetened beverages on a regular basis. It is this 40% alone who would pay a tax on sugary beverages.  Moreover, a tax on sugar-sweetened beverages would ignore the obesity issues in the 60% of the population that doesn’t consume these products. The total contribution of sugar-sweetened beverages to caloric intake is 1.2% for the populations as a whole (consumers plus non-consumers) and this rises to 3.6% among consumers only. Even if a tax were to reduce intakes of these products by 50%, it would have reduced their contribution to caloric intake by 1.8%. It’s hard to see how that would have an effect since quite some of that would be compensated by the intake of other foods. Moreover, there is 60% of the population who are mere spectators in this charade since they don’t consume sugar-sweetened beverages.
The question also arises of alternatives to sugar-sweetened carbonated beverages – what could or should people consume instead?  Fruit juices represent the most commonly consumed beverage in Ireland after teas, coffees and waters and could be suggested as a ‘healthier’ alternative. If the 40% of Irish consumers of carbonated beverages were to switch to drinking fruit juice at the same volumes which they currently consume sugar sweetened carbonated beverages, the difference in calorie intakes between the two beverage types works out at a mere 10 kcal/d!
My own contribution ranged across the epidemiology of obesity, physical activity and the genetics of obesity but the most important points relevant to this blog are the policy issues presented. . Most of the studies linking sugar-sweetened beverages and obesity are based on observational studies, an example of which are the data presented by Anne Nugent. These data do not prove cause and effect. To do so, we need to construct very large multi-centre studies of sufficient duration to see any true effect. The Women’s Health Initiative on dietary fat, The DASH study on diet and hypertension, The DART and GISSI studies on fish oil, the MRC trial on folic acid are all examples of these large internationally approved intervention studies specifically design to test the true cause and effect hypothesis. As regards reducing or increasing intakes of sugar-sweetened beverages, no such study exists. In the EU, we demand multiple human intervention trials to sustain health claims on foods and clearly that bar is too high for public health nutrition policy.
Dr Kevin Denny of the UCD Geary Institute gave on over-view of some of the wider issues that economists would take into account with regard to taxes on foods or nutrients. Kevin pointed out that economists start with the view that the individual knows what is best for them personally. However, for some groups and in certain instances, this may not be the case. The information upon which a decision is to be made may be poorly available, too complex or because time and emotion defer an informed decision. Policy decisions in such instances therefore start with education and then move to regulation of some form, which might include taxes. Taxes that are designed to introduce enhanced social behaviour are referred to as Pigouvian taxes and it could be argued that food taxes fall into this category if we think that people’s consumption of food is not socially optimal for some reason.  But one needs to be clear about why people’s food consumption imposes a burden on society. The standard argument is that eating too much (& hence causing obesity) imposes a burden as the tax-payer will pick up most of the additional health costs (estimated at about €400 million p.a. in Ireland). In that context however, taxing nutrients such as calories should only apply to those calories that are consumed in “excess . If for example, people don’t consume many calories or they burn-off what they consume through exercise, there is no reason to tax such calories. Taxing calories for individuals in energy balance would be unfair. The taxing of nutrients is made more complex by the fact that foods contain multiple nutrients. Taxing the fat in cheese ignores the important contribution cheese makes to calcium intake among consumers of cheese. A key point made by Kevin is the sequence of steps the economist would look at always assuming the nutritionists really did have genuine target for taxation in the first instance: How much to tax? How does that affect price given that taxes are often not passed on in full to consumers? In turn, how does that influence consumption of the foods concerned? How the does that influence BMI and, of course eventually health costs? He went on to cite the work of Powell & Chaloupka who conclude that: “The limited existing evidence suggests that small taxes or subsidies are not likely to produce significant changes in BMI or obesity prevalence but that nontrivial pricing interventions may have some measurable effects on Americans' weight outcomes, particularly for children and adolescents, low-SES populations, and those most at risk for overweight. Additional research is needed to be able to draw strong policy conclusions regarding the effectiveness of fiscal-pricing interventions aimed at reducing obesity”. In other words minor taxes will have little effect and that effect would only be seen with quite considerable taxes.
This leads nicely into the paper by Professor David Madden of the School of Economics.  He used data from the nationally representative Household Budget Survey to examine the impact of possible fat taxes on poor households.  His results showed that pretty much any food-based fat-tax will have a disproportionate effect on poor households, reflecting the general tendency across all countries for poor households to devote a higher fraction of their budget to food.  However, a revenue neutral tax/subsidy package, with higher taxes on some foods combined with lower taxes on other foods would be neutral in its poverty impact, and could even be mildly beneficial to poor households.  In terms of a tax on sugar-sweetened beverages, the impact of a 10% tax on poor households would be relatively modest, given that sugar-sweetened beverages are a relatively small fraction of the budgets of poor households.  Depending upon the ability of government to accurately target poor households to compensate them for such a tax, the cost of compensation in 2005 prices would most likely be less than €10m.  However, this takes no account of the loss in welfare borne by non-poor households from such a tax.

So, in summary we have a proposal to tax sugar-sweetened beverages, which contribute 0% of daily calories among the 60% of the population who don’t consume them and which contribute a mere 3.6% to the caloric intake among consumers of these products. In doing so, we ignore the obesity issues of the 60% of non-consumers and, among consumers, we tax those who are lean and those with excess body fat. And we do all this with zero data from internationally acceptable randomised controlled intervention studies on the effects of sugar-sweetened beverages on medium term body weight regulation.  Whereas we insist that such studies govern health claims as regulated by the European Food Safety Authority, that doesn’t seem to apply to public health nutrition policy. Moreover, we do so knowing that food taxes that are small will be ineffective and to be successful they must be significant. And of course we do this knowing that it will hit the poorest in society with the greatest financial burden  unless we find some way to subsidize a healthy food eaten in significant quantities by poorer households. Simple, isn’t it?