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Friday, August 14, 2015

Shed fats, not carbs ~ new human study

In recent years, it has become quite fashionable to argue that the real culprit in obesity are carbohydrates and as such fats have gained considerably good marks in the hierarchy of villainous calories. Gary Taubes, a highly influential author on this topic wrote thus: ‘‘Any diet that succeeds does so because the dieter restricts fattening carbohydrates .Those who lose fat on a diet do so because of what they are not eating—the fattening carbohydrates’’. The argument is that carbohydrates cause a surge in insulin release and insulin is what keeps fat within fat cells. When carbohydrates are restricted, this insulin surge falls allowing fats to be released from fatty tissue for burning (oxidation) for energy. All very well in theory but now, the results of an impeccably designed human study will greatly challenge this recent view that fats are good and barbs are bad[1]. So what makes this study so solid.

The volunteers were extremely obese. The males had a BMI of 38 while that of females was 33. The study randomized the subjects into two arms for 11 days of dietary intervention and all of the period of dietary intervention was conducted in a metabolic ward with strict clinical supervision. For the first 5 days in each study arm, the subjects ate what is referred to as a eucaloric diet. That is, they received the exact amount of calories that they needed simply to neither gain nor lose weight. The nutritional composition of each subjects eucaloric diets was identical with 50% energy from carbohydrate, 35% from fat and 15% from protein. For the next 6 days, their caloric intake was reduced by 30% either through a very low fat diet or a very low carbohydrate diet. There were no other changes in the composition of the calorie reduced diets. The only foods available to the subjects were those prepared by the research team and all eating occasions were supervised.

 On days 2 and 5 of the eucaloric diet and on days 1, 4 and 6 of the energy restricted diets, the subjects spent 23 consecutive hours inside a metabolic chamber. This would be a small room with a bed, seat, bathroom and other facilities but which is specially constructed to measure the inflow and outflow of oxygen and carbon dioxide. By measuring the loss of oxygen (used for fuel) and the gain of expired carbon dioxide, it is possible to accurately tell what type of fuel is being burned by the body for energy.  When the six days of dieting ended, the subjects took a 2-4 week break before resuming the same protocol but switching from the low fat arm to the low carbohydrate arm and vice versa.

The main effects were as follows, as outlined by the authors: “Body fat loss was calculated as the difference between daily fat intake and net fat oxidation measured while residing in a metabolic chamber. Whereas carbohydrate restriction led to sustained increases in fat oxidation and loss of 53 g/day of body fat, fat oxidation was unchanged by fat restriction, leading to 89 g/day of fat loss, and was significantly greater than carbohydrate restriction”.

To those of us in experimental nutrition for some time, these results come as no surprise. Very similar results were found in a series of studies carried out at the UK Dunn Nutritional laboratory in the 1990s. The bottom line is this. If you want to lose fat from the body, first lose it from the plate but make sure that the caloric deficit of fat leads to an overall deficit of calories form the diet.  

[1] Hall K et al (2015) Cell Metabolism, 22, 1-10

Tuesday, July 14, 2015

Peanut allergy - a new breakthrough

Between 1997 and 2010, the incidence of peanut allergy quadrupled in the US In 2000, the American Academy of Pediatrics recommended that for children who were inclined toward allergic diseases, peanuts should be avoided until 3 years of age. Moreover, recommendations were made to pregnant and lactating mothers to avoid peanut consumption. Everywhere, from schools to jet aircraft, from restaurants to kiddies’ parties, the terror of peanuts prevailed. A group of UK allergists noted that among Jewish children in London, the risk of developing peanut allergy was 10 times that of Jewish children living in Israel. This was associated with a difference in the age when peanuts were introduced. Among the London Jewish kids, peanuts were generally not introduced until the second year of Life. Among Israeli based Jewish children, it was on average 7 months when peanuts were introduced. Several small and generally inconclusive studies had suggested that in fact early introduction of allergens such a cows’ milk or eggs, tended to reduce the severity of the disease. Thus the UK researchers set out to design a large randomised trial of the early versus late introduction of peanuts to children. The trial was called the LEAP trial: (Learning Early About Peanut Allergy[1])

To enter the study, the infant had to be aged between 4 months and 11 months and to suffer either severe eczema or severe egg allergy. The children then underwent a skin prick test for peanut allergy. Of the 834 infants who were screened for the study (194 did not meet the exact inclusion criteria), 640 underwent randomization. Of these 542 had shown a negative skin prick test to peanut allergy while 98 did show a positive test.  Half of these groups were then allocated to either complete peanut avoidance or controlled peanut consumption. Controlled peanut consumption involved a weekly intake of at least 6 grams of peanut protein from an Israeli peanut snack “Bamba”. The consumption and avoidance of peanuts would continue for 60 months. The prevalence of peanut allergy at 60 months was the chosen end point. In randomised controlled trials, there are two ways to analyse the data. One in called “intention to treat” and this includes all subjects irrespective of how they adhered to the protocol. The second is the “per protocol analysis” which includes only those children that adhered to the study protocol as set out at the beginning. Taking the former approach first, at 60 months, on average 17% had peanut allergy and 3% didn’t. When one looked the those who had a positive skin prick test, a staggering 35% of those who avoided peanuts went on to be peanut allergic while among those exposed to peanuts, the level was just 11%. This was thus a 3-fold higher risk. Now taking the per-protocol analysis and focusing on those who were skin prick positive to peanuts at the outset, 34% of the avoidance group went on to be peanut allergic (in effect the same as the intention-to-treat analysis). But among the children who had a positive skin prick test to peanuts at the outset, and who consumed peanuts, not a single case of peanut allergy was seen at 60 months.
This trial will have profound effects on how we treat infant and childhood food allergy. Avoidance is obviously not the key. Controlled introduction and controlled feeding is the key but more needs to be done to figure out how this best operates for different foods and for infants with different allergy experience. However, one thing is sure. The old default of avoidance is out the window

[1] Du Toit et al (2015). Randomization trial of peanut consumption in infants at risk for peanut allergy. N Eng J Med 372, 803-813

Tuesday, June 9, 2015

Real nutritional science re-affirms advice to lower dietary saturates

In the last few years there has been a flurry of scientific papers published showing no apparent association between deaths from cardiovascular disease and the consumption of dairy products leading to an amazing level of interest in the traditional and the social media in these new revolutionary findings. “Butter is back”, wrote the New York Times while Time Magazine featured a cover story headlining “Eat butter – the scientists labeled fat the enemy. Why they were wrong”. The Wall Street Journal ran a feature entitled “The questionable link between saturated fatty acids and heart disease. The meat, dairy and egg industries had a field day. However, little ol’ me pointed out in a blog entitled “Fats, facts and baloney[1]”, that these scientific assertions were based on a re-analysis of all existing data that examined the association between consumption of dairy foods, saturated fats and heart disease rates. Let me stress the word “association”. Epidemiological studies examine some aspect of lifestyle such as diet and some putative link to that lifestyle and seek to explore whether the link is positive, negative or otherwise on the basis of statistical analyses. No matter what statistically significant effect is seen and no matter how often it is repeated across time and space, it remains an association. A causal effect of the lifestyle factor and the putative end point of that lifestyle has not been proven. In certain areas of epidemiology, it is impossible to follow this association up with a human intervention study to prove the cause-effect association. Thus when epidemiologists studied the link between cancer and tobacco, experiments in humans were out of the question. To that end, a famous English epidemiologist, Sir Austin Bradford-Hill set out a list of criteria that should be considered in perusing epidemiological data to ensure that any conclusion drawn on such data, are, as far as is humanly possible, plausible and actionable. I have never seen or read of any nutritional epidemiologist citing the Bradford Hill criteria.

Now what makes nutritional issues different from the tobacco issue is that we can and do large human intervention studies in which one group has their food intake or nutrient intake manipulated, while another serves as a control. Examples include studies of diet and cancer and cardiovascular disease in women[2], studies of the Mediterranean diet[3] or studies of dietary lipids and the metabolic syndrome[4] to mention just a few.

In recent months, two papers have appeared from UK researchers, in which the level of dietary fat and the type of dietary fat were manipulated[5], [6]. The first in volved195 subjects aged 21 to 60 years with moderate risk of cardiovascular disease. They were randomly allocated to one of three intervention diets for 16 weeks in which the ratio of saturated to monounsaturated to polyunsaturated fats varied: 17, 11, 4 versus 9, 19, 4 versus 9, 13, 10 to provide diets high in saturates, monounsaturates or polyunsaturates. Replacing saturates with monounsaturates or polyunsaturates resulted in statistically significant falls in plasma cholesterol both total and LDL cholesterol (about 9% and 12% respectively). This was calculated to translate into a reduction on cardiovascular disease mortality by up to 20%. The second study involved 165 healthy adults assigned to a standard British diet or to a diet that attempted to meet the UK dietary guidelines.  The group assigned to the dietary guidelines arm of the treatment showed a reduction in the intakes of total, saturated and trans fat intakes with a partial substitution with increased intakes of polyunsaturates but especially, monounsaturated fats. Total and LDL cholesterol fell significantly over the 12 weeks in the group assigned to the dietary guidelines. The estimated overall reduction in heart disease mortality was between 15 and 30%.

Now it matters nothing as to how many epidemiologists dance on a decimal point, the facts remain that adhering to existing dietary guidelines on the composition of dietary fat, which have changed rather little in the last 50 years, will significantly reduce heart disease death rates. These data are experimental proofs of what was already proven many times many years ago. However, in an era where epidemiology and its statistical gymnastics rule, it was necessary once again, to show that the adherence to prevailing dietary guidelines is justified and will save lives. These papers won’t hit the Wall Street Journal, Time Magazine or the New York Times. The general public will never hear about them. I happen to care, hence another rant!

[3] Estruch R et al (2013) N Eng J Med, 368, 1279-1290
[5] Vafeiadou K et al (2015) Am J Clin Nutr, e pub ahead of print
[6] Reidlinger DP et al (2015) Am J Clin Nutr, 101, 922-930

Thursday, May 28, 2015

Obesity, poverty and convenient myths

Policy makers don’t read tabloid newspapers. They read more serious broadsheets from the London Times to Figaro to the Washington Post. And these broadsheets often perpetuate the beliefs that make the upper social echelons happy or indeed smug. And among these beliefs is that which argues that the present epidemic in obesity is primarily a problem of the lower socio-economic groups. One cannot argue against the line that obesity rates are higher among the socially disadvantaged. Neither can one argue against comparably higher rates of suicide, homicide, drug abuse, violent crimes, indebtedness, heart disease, cancer and anything you care to mention but which you’d rather do without, thank you very much.

The fact that obesity, like suicide and homicide, is higher in those who are socially disadvantaged doesn’t mean it is absent in the socially advantaged. The differences in obesity rates are in high fractions such as 0.8 or thereabouts such that for every 5 obese persons who are socially disadvantaged, there are 4 obese persons among the economic elite. Think of the Clintons, Hilary in recent times and Bill, a while back. However, as I’ve already said, obesity is higher among the socially deprived. The question is why so and what to do about it.

A recent paper in the American Journal of Public Health[1] looked at residence mobility in relation to social status and the economic deprivation of the areas of residency in the city of Dallas. The study was part of an on-going study on heart disease and followed subjects (about 1,800) over the period 2000 to 2009. Weight was monitored at baseline, at various intervals and at follow up. Half the subjects moved from one neighbourhood to another and of these, 600 subjects moved to a neighbourhood with a higher ‘Neighbourhood Disadvantage Index’ (NDI: ~ perceived neighbourhood violence, poor physical environment, and low social cohesion). Compared to those who moved to a neighbourhood with a lower NDI or who remained where they originally resided, those moving to a higher ranked NDI suburb gained significantly more weight and the longer the residence in the higher NDI suburb, the greater the weight gain.

Well of course, the answer is simple. These people moved to “food deserts”, the trendy middle class quasi left wing term to describe regions which are so poor, its not worth anyone’s time and money in building them a supermarket. Consequently, the creed goes, they cannot get access to affordable and varied food supplies but are forced to shop in local stores that don’t sell fruit and vegetables at a reasonable price and which prefer to stock their shelves with cheap and, of course, high fat, high sugar and high salt foods (Credo in unum dieta!). Enter a governmental initiative that subsidised the building of a brand new supermarket in the suburb of Morrisania in the New York borough of the Bronx with a ‘control’ suburb of Highbridge where no such investment was made. A research paper just published[2] examined food choice 5 weeks and 52 weeks after the supermarket was opened. The authors concluded as follows: “The introduction of a government-subsidized supermarket into an underserved neighbourhood in the Bronx did not result in significant changes in household food availability or childrens dietary intake. Given the lack of healthful food options in underserved neighbourhoods and need for programmes that promote access, further research is needed to determine whether healthy food retail expansion, alone or with other strategies, can improve food choices of children and their families”. So, access to healthy food options is not the issue. It is most likely lifestyle choice arising from a particular educational stance.

Now enter the ultimate holy grail of the urban middle class food priests, the Farmers Market. What can be more morally upright than buying wholesome food directly from the farmer who toiled the land to produce such heavenly fare? Well, a recent study[3], also in the Bronx, paints a different picture. Following a comprehensive study of farmers markets (FMs) in this region, they conclude as follows:  (1) FMs operate overwhelming fewer months, days, and hours than nearby stores, (2) FMs carry less-varied, less-common, more-expensive produce than nearby stores. (3) FMs offer many items not optimal for good health (e.g., jams, pies, juice drinks) and OMG, (4) FMs might provide little net benefit to food environments in urban communities.

Social inequality lies at the heart of many patterns of chronic disease. Tackling it is outside my expertise but I’ll vote for it

[1] Tiffany M. Powell-Wiley et al (2015) Am J Public Health, in press
[2] Ebel B et al (2015) Public Health Nutrition, Feb 26:1-10.

[3] Lucan SC et al (201)  Appetite 90, 1 July 2015, Pages 2330