Think sweet ~ stay slim

Think sweet ~ stay slim

Notwithstanding the overwhelming evidence that an excess of calorie intake per se, irrespective of the source of calories, causes obesity, there remains a populist and a policy view that sugar, rather than fat is the primary culprit. Although the biological argument that not all calories are equal and that carbohydrate calories are more fattening has been debunked by sound experimental evidence[1], the case moves more to appetite as the causative factor. Since people don’t eat what they don’t like, an understanding of the “liking” of particular foods becomes important.

To study this phenomenon, two approaches are possible. One is to use a ‘cross sectional’ approach which seeks to compare obese persons and lean persons for their food preferences at a single moment in time. The problem here is that the obese persons may have acquired a view of what putatively ‘causes’ obesity and in so doing, they may bias their response to any study questionnaires. Thus obese subjects at a given point in time might express a lower liking for sugar-sweetened beverages compared to diet beverages because that is what they are conditioned by society to believe. Moreover, obese subjects may in fact use sugar free beverages to manage their weight. The alternative to this approach is to complete a ‘prospective’ study in which people’s likings for food are measured at a single point in time and the group subsequently followed over several years to see who gets obese and who stays slim. That way, the presence of obesity is independent of the answers to the original questionnaire.

A recent paper from the French research consortium “NutriSanté” has examined the effect of liking for fat, sugar and salt on subsequent development of obesity[2]. The NutriSanté study is an internet-based study, initiated in 2009, with a current enrolment of some 65,683 volunteers. Data is gathered at the point of recruitment on many aspects of health such as diet, physical activity, weight, smoking and alcohol habits, weight management and so on and is repeated annually.  Each month, volunteers are invited to complete questionnaires related among other things to food behaviour.  The questionnaire covered salt (11 questions) and sweet (21 questions) tastes plus preferences of fat-and-salt (31 questions) and fat and sweet sensations (20 items).  Some 49,066 subjects agreed to answer these questions. However, when the data were cleaned up to ensure that all respondents had completed every aspect of the overall NutriSanté study, there were full data on 24,776 subjects.

In the 4 years of follow up, 24,112 subjects remained non-obese while 664 subjects became obese. The key sensory findings are thus:

Sensory liking scores	Non-obese subjects	Obese subjects	Statistical conclusions
Liking for fat	3.79	4.03	Highly different
Liking for sweet	3.73	3.66	No difference
Liking for salt	3.77	3.93	Highly different

Those who gained weight had a higher preference for fat and salt but not for sugar.  Another approach to the data analysis is to look across the “liking” score data and to divide subjects according to their ranking, starting at the “low liking” (lowest quarter or ‘quartile’) right up to the “highest liking”  (highest quartile). These data are controlled statistically for all known confounding variables.

	Statistical difference in risk of developing obesity between lowest and highest quartiles of “liking”
	Men	Women
Fat liking	Yes, up 85%	Yes, up 49%
Fat + salt liking	Yes, up 106%	No
Fat + sweet liking	No	Yes, up 37%
Sweet liking	Yes, down 59%	No
Natural sweetness liking	No	Yes, down 69%

The authors also looked at baseline food intake (as opposed to liking) and observed no association between sugary food intake and obesity. Indeed, the evidence was that those who did not develop obesity had higher sugar intakes at baseline. The results are summarised below.

Food group intake g/d	Non-obese subjects	Obese subjects	Statistical conclusions
Fruits	279	234	Highly different
Meat	45	57	Highly different
Processed meat	3.77	3.93	Highly different
Milk and yogurts	169	192	Highly different
Cheese	38	36	Not different
Oil	9.3	8.1	Highly different
Whole grain products	36	28	Highly different
Sugar and products	24	19	Highly different
Fatty sweet products	69	65	Not different
Sugar-sweetened soft drinks	39	41	Not different

The authors conclude thus: “This prospective study reinforced results from cross sectional studies, by highlighting that fat liking was prospectively associated with an increased risk of obesity and diet appeared to substantially explain this relationship. Results have also shown that sweet liking is associated with a decreased risk of obesity, and there is no significant association between salt liking and obesity risk”.

Once again, we have a fully public funded comprehensive and prospective study from a highly reputable group, with the study suitably powered for optimal statistical analysis, which challenges conventional wisdom. It will be ignored but, you see, it won’t go away and one day, when the false gods of the demonic sugar sect are reduced to clay, these papers will come back to haunt the high priests of public health nutrition. I wanna be there!!!

By the way, the blog stands now at 231,325 views. Thank you all and a happy New Year to all of you.

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[1] See blogs of November 21^st 2016 and of August 14^th, 2015.

[2] Lampuré et al. International Journal of Behavioral Nutrition and Physical Activity (2016) 13:74

Diet and poverty: Mind over money?

Diet and poverty: Mind over money?

Obesity is popularly linked with low-income groups and with a low socio-economic status (SES). This relationship is frequently explained by a lack of money, a lack of understanding of healthy nutrition, a general disdain for healthy eating and both isolation from supermarkets and proximity to convenience and fast food outlets. I won’t argue with this except to say that while obesity is more prevalent in low SES, there are a lot of fat judges, mayors, prime ministers, presidents elect, ex-sportsmen, doctors, nurses and others for whom the putative drivers of obesity in poverty are generally absent. New research[1] on obesity and SES has recently been published by scientists from Singapore’s A*STAR and published in the prestigious journal, The Proceedings of the National Academy of Sciences. The key question they asked was thus: Irrespective of your true SES, if you were made to think you were of a low SES, would that influence your food habits?

They started their thinking process with reference to the animal kingdom where in any social organisation, those that are marginalized for whatever reason (too slow, too weak, too fussy), also tend to overeat and gain weight. This might be a precaution for survival in the event that they might one day be in fact ousted from the group. They cite a hamster study where a smallish hamster living in harmony with other small hamsters is placed alone in a cage into which a larger hamster is admitted. The latter will assert itself as dominant within less than a minute and the  “defeated” smaller hamster is left to sulk. The plot of body weight over time comparing those hamsters subject to defeat against those spared this ignominy shows that the defeated hamsters, stigmatized and “psychologically” marginalised, get fatter.

Against that background from the animal kingdom of which the hamster data is merely illustrative of so many such studies, they set out to study if an “imagined” low SES could alter food habits.

The human volunteers were placed in a private room and the study was conducted in what were effectively laboratory conditions. They were shown a ladder with the following instructions:

Think of this ladder as representing where people stand in Singapore. Now, please compare yourself to the people at the very top of the ladder. These are the people who are the best off—those who have the most money, most education, and most respected jobs. In particular, we’d like you to think about how YOU ARE DIFFERENT FROM THESE PEOPLE in terms of your own income, educational history, and job status. Where would you place yourself on this ladder relative to these people at the very top? Please select the number that corresponds to the rung where you think you stand in relation to these people.

 A second group was similarly treated but they compared themselves to people at the bottom of the ladder: poor, less education and rotten jobs. To emphasise the mental induction of subjective higher or lower SES, subjects had to write down in detail how a conversation might go with the group above or below themselves and to suggest how such a conversation might flow. Now, suitably indoctrinated into a feeling of subjective high or low SES, the experiments began and the easiest way to communicate the studies is to simply focus on the results.

• When asked to select the foods they might be subsequently included in a meal, those who subjectively thought of themselves as lower SES, chose higher energy dense foods and overall indicated an intention to eat more calories than those who were attuned to think of themselves as higher SES
• When asked to rate foods according to descriptors such as pleasant (e.g., tasty, delicious, wonderful) and unpleasant (e.g., disgusting, nasty, awful) those in the lower SES subjective state chose the higher energy density foods as the most pleasant
• In a third study, the subjects viewed a short documentary video while freely eating three snacks (potato chips, M&M candies, and California raisins) from separate bowls. Those with the lower SES frame of mind ate more calories and they more or less favoured the chips and M&Ms over the raisins.
• Finally, the subjects were given access to a meal in the form of noodles and asked to eat to appetite. For completeness, a control group who did not take part in the imagined SES ranking exercise was included. The outcome showed that those who subjectively rated themselves as lower SES ate significantly more then the other two groups.

These studies were carefully designed and the analysis took statistical account of all key variables (age, gender, weight etc.) including the actual SES of the subjects. The results could be interpreted thus: When induced to think they are of a low SES, people overeat because that’s what they think those of low SES actually do. However, there are a few reasons to downplay this potential explanation. First, each experiment involved different volunteers so there could be no sense of training. Secondly, food was not portrayed as a central element of the study but rather the self-imposition of a state of mind. Finally, and most importantly, those induced to imagine themselves as low SES, were comparing themselves to those at the top of the social ladder who were the economic elite.

So, once again, we see what we refer to as the “mind” playing a driving role in one of nature’s most powerful biological drives, the drive to eat[2].

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[1] Cheon BK & Hong Y-Y (2016) Mere experience of low subjective socioeconomic status stimulates appetite and food intake Proceedings of the National Academy of Sciences (Early edition) www.pnas.org/cgi/doi/10.1073/pnas.1607330114

[2] Mind over matter: Perceived time as opposed to real time on blood glucose in type 2 diabetes: Blogged October 14^th 2016

Dieting and the appetite battle

I have previously written that if slimming were a drug, it wouldn’t be allowed for sale given that after 5 years of treatment, less than 5% would be successful in their weight loss. This is worse than the cure rate for the worst cancer.[1] To many in public health nutrition, this relapse tendency is utterly ignored as some arcane piece of physiology, which quite simply is inconvenient to their strategy and, anyway, not as important as is made out to be. Indeed “Look at all the people who have lost weight” they cry, while all the time ignoring the far greater numbers who weren’t so lucky. A new paper from the NIH National Institute for Diabetes and Digestive and Kidney diseases, led by Prof Kevin Hall who is doing stalwart work in this field, throws strong light on this issue of relapse and is well worth reflecting on.

When we organise experimental weight loss programmes, we use dietary advice on weight loss and comparable expert advice on physical activity. There can be no placebo. We can have a control group who receive little structured and certainly not personalised or customised advice, but until now, the experimental advantages of a placebo controlled diet is almost impossible to achieve, Until now that is. A drug, with the silly name Canagliflozin, which, as the lawyers say, hereinafter is known as the “drug treatment” has been used in this study.[2] It is presently available for the management of type 2 diabetes and leads to a sizeable excretion of glucose each day. That means that the subjects pee out a lot of untapped calories and therefore this drug leads to some weight loss.  The key question the researchers set out to address was that in a placebo controlled blind trial using this drug, how did subjects respond in terms of compensating energy intake to the weight loss anticipated from the drug.

As is seen from the attached figure, the drug did lead to weight loss but it reached a plateau. The daily drug-induced loss of untapped calories from urinary glucose remained for the 54 weeks but the initial weight loss was checked by a compensatory rise in energy intake. Normally energy intake is measured using dietary assessment methods but in this case the change in energy intake was related back to changes in bodyweight using a complex equation that had been previously shown to be valid[3] against very robust biomarkers (doubly labeled stable isotope water along with multiple dual-energy X-ray absorptiometry scans).  The authors estimated that the energy intake compensation was 100 kcal per day per kg of weight loss. Adaptations in terms of changes in energy expenditure were minimal.

In this study, half the subjects (153 Type 2 diabetics) received the drug and half the placebo and there was no advice on weight loss. So there was no psychological effect of the intervention on weight loss or on appetite. As weight was shed, appetite responded to a strong and lasting effect, which minimised the process of weight loss. As the authors point out, those who successfully diet and who achieve significant and prolonged weight loss, battle by ‘heroic and vigilant efforts’ against the powerful effect of this compensatory rise in appetite. Maybe there is a threshold of weight change below which the body choses to ignore in which case we can win limited success in mass weight loss programmes. But if as this study shows, weight loss is not minimal (>3kg average), then we will need to have a much better understanding of how to motivate people for that long term battle against compensatory weight loss. May I end this blog by once again citing the Sir David King FRS formerly Chief Scientific Adviser to HM Government, and Head of the Government Office for Science who in the UK Foresight Report on Obesity wrote: “What quickly becomes apparent to anyone who examines the body of evidence from several different disciplinary sources is that the answers are neither straightforward nor, as is popularly supposed, necessarily known. Although a great deal of research has been done into the problem, much of the evidence is not integrated”.  What is the threshold of weight loss for energy intake compensation? What aspects of appetite adaptation are most affected by the most and least successful dieters? What are likely to be the most helpful strategies to those who want to lose weight and must battle this enhanced appetite phenomenon? There are no simple answers.

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[1] Ever seen a fat fox ~ human obesity explored (2016). UCD Press My new book on obesity

[2] Polidori D et al (2016) Obesity, 24, 2288

[3] Sanghvi A et al (2015) Am J Clin Nutr 102, 353

Fat calories count most in obesity ~ new study

Conventional wisdom, at least from the media and the high priests of public health nutrition, tells us that sugar causes obesity and all its ailments to the point where it is likened to tobacco in its sinister provenance and its foul health implications. Sugar is to be taxed and restricted in every way and politicians of all persuasions win popular support for their call for yet more extreme measures to decry the putative effects of sugar. And all the time, this conventional wisdom is promoted by the media and by celebrity chefs and diet gurus.. So it should come as no surprise that when a study from a high quality group using high quality data, publish a high quality paper in a high quality journal, which flies in the face of conventional wisdom, that this fine data, is simply ignored.

The paper[1] is based on data from the UK Biobank database that tracks individuals over time (2011 and 2012). It uses direct measures of body weight and height and classified the 132,479 subjects into underweight, normal weight, overweight and obese with obesity further divided into grades I, II and III obesity. Data were also obtained for each subject on % body fat and on waist circumference. Dietary data was collected using four 24-hour recalls over 2011 and 2012. Subjects were excluded from the study if there was any possibility that their diet or weight might be compromised in some way. For example, smokers, who tend to be under-weight, were excluded, as were those with a reported energy intake deemed by international norms to indicate under-reporting of calorie intake.

The bottom line in the findings was that moving across increasing grades of either body weight or body fat, energy intake, as in calories per day, also increased. As I have previously paraphrased US President Bill Clinton in his election campaign: “It’s the calories, stupid!” Compared with normal BMI, obese participants had 11.5% higher total energy intake and 15%, 14%, 10% and 5% higher intake from fat, protein, starch and sugar, respectively. Hence, the proportion of energy derived from fat was higher (34.3 v. 33.4) but from sugar was lower (22.0 v. 23.4).

This simply tells us there is a direct positive association between calorie intake and rising levels of overweight. A key question remains as to the contribution of fat and carbohydrate (with sugar specifically in mind) to obesity when we statistically control for the calorie intake. The authors thus transformed the data to control for the following: sex, ethnicity, physical activity and calorie intake.  This allows us look at data where fat intake and sugar intake are examined for their links to obesity where caloric intake is controlled to a common level. Now we see that when sugar intake and starch intake (all carbohydrates) are compared across rising levels of obesity, they actually fall. In contrast, fat rises. This isn’t anything new because when energy intake is fixed at a constant point, as one contributor to caloric intakes rise (e.g. fat) others, (carbohydrates including sugar) falls, a fact recorded so many times (the sugar-fat see-saw) and so repeatedly ignored by the anti-sugar lobby.  The figures below are taken from the journal where quintiles if nutrient intake are compared to BMI.

The authors conclude as follows from their research:

 Key Messages

• Adiposity is associated with higher intake of sugar; but the association is stronger for fat intake and strongest for total energy intake.

• Fat is the largest contributor to overall energy intake.

• There is only a weak correlation between absolute energy derived from sugar and from fat. Therefore, targeting high sugar consumers will not necessarily target high consumers of fat and overall energy.

• Focusing public health messages on sugar consumption may mislead the public on the need to reduce fat intake and overall energy intake.

This was a study funded by a University of Glasgow internal grant and was not funded by the sugar lobby nor have the authors any conflict of interest to report. But it doesn’t conform to conventional wisdom so it will largely remain ignored by the media and senior policy makers will find it awkward reading, if at all, because they have already followed the herd of the anti-sugar lobby.

 

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[1] Andersen JJ (2016) Adiposity among 132 479 UK Biobank participants; contribution of sugar intake vs other macronutrients. International Journal of Epidemiology, 2016, 1–10