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Monday, November 23, 2015

Physical activity and the politics of healthy eating

When the food industry or its trade associations are questioned about the global problem of obesity, they tend to draw heavily on the modern rise in the physical inactivity side of the coin rather than the energy intake side. Since they have a significant vested interest in the latter, that is understandable. But it does lay them open to the criticism that they have precious little interest in the caloric intake side of obesity and simply argue that energy imbalance is largely due to the decline in physical activity in the last half century. Much of this criticism comes from those who brand the food industry in the worst possible light right down to the direct comparison with the tobacco industry and scientists who receive money from the food industry in the study of physical activity are drawn into this scenario. I have previously blogged on this issue so I will just highlight here some of the arguments. Those that belittle or reduce the role of physical activity point out that in the last 50 years, there has in fact been a rise in leisure time physical activity. Now this is true for a proportion of the population but it is be no means universally true and endless national reports document the continued domination of a sedentary lifestyle. They are also likely to cite published papers, which argue that the rise in caloric intake exactly parallels the rise in obesity. They are more likely than not to ignore the compelling data that whereas leisure time physical activity has increased, work related physical activity has plummeted. They are also likely to ignore data on daily physical activity among the traditional Amish community who continue to live a life of high work and leisure-related physical activity, a lifestyle now utterly demolished at work due to the advent of multiple labour-saving devices, from automation to the silicon era. They are also likely to downplay the importance of papers that argue that the rise in obesity does not match the rise in caloric intake when correct adjustments are made for rising food wastage. So lets look again at the issue of physical activity in the management of bodyweight.

Question 1: Is physical inactivity really a serious contributor to ill health? The WHO certainly thinks it is. They write thus: “Physical inactivity (lack of physical activity) has been identified as the fourth leading risk factor for global mortality (6% of deaths globally). Moreover, physical inactivity is estimated to be the main cause for approximately 21–25% of breast and colon cancers, 27% of diabetes and approximately 30% of ischaemic heart disease burden.” Rightly they point out the “exercise” is not the same as “physical activity”: The term "physical activity" should not be mistaken with "exercise". They write: “Exercise, is a subcategory of physical activity that is planned, structured, repetitive, and purposeful in the sense that the improvement or maintenance of one or more components of physical fitness is the objective. Physical activity includes exercise as well as other activities which involve bodily movement and are done as part of playing, working, active transportation, house chores and recreational activities”. In short, exercise implies changing into sports gear. Physical activity you can do in your work clothes.

 Question 2: Is body weight the correct end point to use when considering physical inactivity and health? Physical inactivity is ranked 4th by the WHO as a major contributor the global burden of disease while obesity is ranked just below that as the 5th biggest cause of global mortality. Two of the major adverse effects of obesity are poor cardio-respiratory function and poor blood glucose control and physical activity can greatly reduce these two adverse effects.  So obesity is visible but you can’t eyeball someone to ascertain his or her cardio-respiratory or blood glucose function. Thus, it is far more important to regard the role of physical activity as maintaining optimal heart and blood glucose function than it is to regard enhanced physical activity as a solution to obesity. Nonetheless, the absence of modest levels of physical activity, is, as we will see, a major risk factor for weight gain.

Question3. Is exercise bashing and industry funding really a problem? From time to time, it becomes fashionable to ridicule the role of physical activity. An editorial in the British Journal of Sports Medicine wrote thus: “It is time to wind back the harms caused by the junk food industry’s public relation machinery. Let us bust the myth of physical inactivity and obesity. You cannot outrun a bad a diet”. I Sensationalist rubbish! An important peer-reviewed paper published recently in the leading journal (the American Journal of Clinical Nutrition) that I will now look at, was written by the top US researchers in the field of physical inactivity, health status and obesity. The study was supported by “an unrestricted research grant from the Coca Cola Company” and of course that led to considerable criticism. The fact that it was co-funded by the National Cancer Institute was of course ignored. The University of Colorado Medical School, where one of the leading authors works, recently returned a $1 million Coca Cola grant for physical inactivity research[1]. And of course, the Coke funding was likened to funding of the tobacco industry in the smoking area.

The main feature of the study that these authors published was that it looked at the long-term effects of. The authors go back in time to a very early study of low levels of physical activity in employees in the Ludlow Jute Company in Calcutta[2]. Those with low levels of physical activity included clerks, shopkeepers and supervisors whilst those with high physical activity included blacksmiths, coalmen and bale carriers. The authors of this 60 year old paper introduce their work with the following statement: “It has been stated-or implied-by many workers that the regulation of food intake functions with such flexibility that an increase in energy output due to exercise is automatically followed by an equivalent increase in caloric intake. This view, usually accompanied by a minimization of the energy expenditure due to exercise, has often led to the disparagement of physical activity as a factor in weight control. The fallacies inherent in such an attitude have been discussed.” These authors back in 1956 showed that the following: Body weight was highest among those with the lowest level of physical activity. However, as physical activity increased beyond that point, body weight remained constant. Research techniques have changed dramatically since then and the recent research re-visited this area. 421 subjects were recruited into this 1-year study. Accelerometers were used to repeatedly measure physical activity and subjects were classified into quintiles (fifths) of Moderate to Vigorous Physical Activity (MVPA). Energy intake was assessed by repeated dietary assessment combined with measurements in energy balance. Body fat mass was assessed using sophisticated X-ray technology. The two main findings of the study re-affirm what was shown 60 years ago: (1) above the lowest level of physical activity, there was a positive correlation between rising energy intake and rising physical activity. That was not so at the lowest level of physical activity. (2) The accumulation of fat mass was highest among the least physically active, while across the remaining fifths of physical activity, no changes in fat mass was seen. Both studies point to the dominant role of low levels of physical activity as the problem in body weight regulation. Beyond that lower level of physical activity, additional physical activity had no effect. So sitting as a couch potato has a much more important effect on long-term body weight regulation than pounding the pavement or gym. So what would a couch potato have to do to escape this gloomy fate? The more modern paper [3]can estimate this as steps per day since it measured these. The finding is that just over 7,000 steps per day would get the couch potato out of trouble. That is easily attainable in simple walking programmes of about 30 minutes duration. So to conclude:
  1. Physical inactivity is a global killer, actually ahead of obesity
  2. When we come to look at suitable end points of improved physical activity, improved cardio-respiratory fitness and improved management of body weight are best achieved in getting off the couch. Running marathons won’t yield a pro-rata improvement.
  3. Bashing physical activity and physical activity researchers because of industry funding, is a popular headline grabbing exercise. It particularly helps those who have the view that obesity is caused by large food corporations and who believe that any focus on physical activity detracts from that near criminal activity

[2] Mayer J et al (1956) Relation between Caloric Intake, Body Weight, and Physical Work: Studies in a West Bengal situation. Am J of Clin Nutr: 12,169-175

[3] Shook RP et al (2015) Low levels of physical activity are associated with dysregulation of energy intakes and fat mass gain over 1 year. Am J Clin Nutr e-pub ahead of print

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