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Best of 2009

As 2009 is rapidly coming to a close, here are a selection of what may have been my most memorable posts of 2009:

January: Do High-Glycemic Foods Promote Food Addictions?

February: Weight Loss Miracles

March: Have Diabetes? Find a Surgeon!

April: Going to BAT for Obesity Solutions?

May: Like Father, Like Daughter

June: Does Weight Bias Promote Obesity?

July: Saying “I Do” Promotes Obesity

August: Is Weight-Loss Advice Unethical?

September: Why Weight Loss and Obesity Management Are Not the Same

October: Real Stories From Real People

November: Etiological Assessment of Obesity

December: Does White Hat Bias Confound Obesity Research?

Obviously, this is just a selection, admittedly a personally biased one.

Appreciate any comments on what you liked best or enjoyed the most.

Edmonton, Alberta


Smells Like I Am Full

An important aspect of enjoying food, in addition to the actual taste and mouth feel, is the complex sensory stimulation of the olfaction system. After the food enters the oral cavity, aroma molecules find their way to the sensitive olfactory nerve endings in the nose by making their way up the back of the throat into the nasal cavity (apparently the nose has a clever way of telling whether this aroma is coming from the food on your plate or from the food in your mouth).

This activation of specific brain areas by a retronasally sensed food odor is not only associated with the perception of the aroma of the food that is consumed but is also hypothesized to directly contribute to its satiating effect (sensory-related satiation).

A paper by Rianne Ruijschop and colleagues from The Netherlands, published in the Journal of Agricultural and Food Chemistry, provides a splendid overview of this fascinating area of research.

In this paper, Ruijschop and colleagues describe a series of experiments that examine a wide range of factors that can affect retronasal olfaction-related satiation.

Not surprisingly, solid and semisolid foods that required a greater amount of chewing and swallowing elicited a stronger and longer-lasting retronasal aroma release pattern than the rather short-lived spiked pattern observed with liquid foods. A higher extent of retronasal aroma release may therefore be one of the explanations why solid foods appear to be more satiating than liquid foods.

Indeed, the researchers did observe a negative trend between the extent of retronasal aroma release and the amount of ad libitum food intake. Subjects who had a higher extent of retronasal aroma release tended to consume less.

However, retronasal aroma release intensity and profile morphology appeared to be subject specific, which may support the hypothesis that subject differences in the extent of retronasal aroma release are linked to subject differences in sensory satiation and food intake behavior.

In further studies, the researchers found that certain aromas were better at eliciting a satiation response than others. Thus, aromas that suggest fat content (i.e., lactones) were less effective in creating a satiation response than aromas suggesting carbohydrate content (i.e., maltol) or the breakdown of protein (i.e., “animalic”). In a separate experiment, custard products with the addition of maltol or animalic at sensory detection threshold were able to increase subjects’ feeling of fullness significantly.

These results are in line with the observation that macronutrients have different satiating efficiencies, in which protein is more satiating, followed by carbohydrate and fat as least satiating.

Based on these studies, the authors suggest that these findings may provide the rational for developing strategies for prolonging the duration of retronasal aroma release during food consumption.

Examples could include food products with an increase of aftertaste or an increased or lingering aroma release via flavor delivery systems or encapsulation technology or the development of long-chewable food structures in beverages that evoke substantially more oral processing and an increase in transit time in the oral cavity.

Furthermore, a reduction in bite size by tailored packaging may support the “right” oral processing behavior in food products. Interestingly, as blogged previously, eating too fast has been previously associated with increased risk for obesity.

Differences in the extent of retronasal aroma release during consumption may be one of the reasons that people vary in their satiation characteristics, which may prevent them from overeating or not. Whether or not there is a difference in this effect between normal weight and obese people is not known.

As the authors point out, integration of these findings into novel food products may provide a new way to reduce food consumption.

While we wait for these new foods here are my retronasal olfaction-based satiation tips:

1) Take small bites
2) Chew your food thoroughly
3) Don’t drink your calories

Remember, the main problem with fast food is not the “food” – it’s the “fast”.

Happy Holidays,


p.s. As I am planning to take it easy for the next couple of days you are likely to see sporadic posts till the new year.


Is Fibre Overrated For Weight Control?

Nutrition literature abounds with odes to the many benefits of including liberal amounts of dietary fibre in your diet.

Apart from helping normalize bowel movements and reducing the risk for hemorrhoids and diverticulosis, more fibre may also reduce cholesterol levels, slow carbohydrate digestion, and perhaps even reduce risk for colon cancer (although the research on the latter remains disappointingly inconclusive).

Notably increasing fibre intake has also been promoted as a means to help manage body weight. Various mechanisms have been discussed for this, including increasing satiety, reducing the glycemic index of foods, and changing gut flora to favourably affect energy homeostasis.

But how effective is dietary fibre intake really in preventing weight gain?

This question was now examined in the perhaps largest study on this topic to date just published by Huaidong Du and colleagues from the National Institute for Public Health and the Environment, Bilthoven, Netherlands, in the American Journal of Clinical Nutrition.

The relationship between body weight and fibre intake was studied in a prospective cohort of 89,432 European participants, aged 20-78 y, who were free of cancer, cardiovascular disease, and diabetes at baseline and who were followed for an average of 6.5 y. Adjustments were made for follow-up duration, other dietary variables, and baseline anthropometric, demographic, and lifestyle factors.

Overall total fibre was inversely associated with subsequent weight and waist circumference change with a 10-g/day higher total fibre intake associated with about 40 g (~1.4 oz) less weight gain and 0.8 mm (~3/100 of an inch) less waist circumference per year. Interestingly most of this effect was apparently due to cereal fibre (largely insoluble) than to fruit or vegetable fibre (largely soluble).

The authors enthusiastically conclude that their study may support a beneficial role of higher intake of dietary fibre, especially cereal fibre, in prevention of body-weight and waist circumference gain.

I, in turn, am not looking to fibre as the next weight-loss panacea. Yes, eating lots of fibre may have some beneficial metabolic effects, but don’t count on it as the panacea for countering the obesity epidemic.

In fact, with beneficial effects of dietary fibre weighed in ounces and fractions of an inch, this fuss about fibre seems more like too much ado about nothing than a meaningful approach to weight management.

Obviously, the study tells us nothing about the effectiveness of using fibre in conjunction with a weight management program or about taking “pharmacological” doses of commercial fibre extracts often sold as weight-loss supplements – but I have yet to see totally convincing data on either.

For now, let’s stop obsessing about fibre intake for weight management and focus on what really matters: calories.

Edmonton, Alberta


Higher Leptin Levels Associated with Lower Risk of Alzheimer Disease?

Earlier this year, I blogged about a study that linked obesity to brain atrophy. Specifically, that study reported that in individuals with a BMI > 30, atrophy was found in the frontal lobes, anterior cingulate gyrus, hippocampus, and thalamus compared with individuals with a normal BMI (18.5-25). 

Now, a study by Wolfgang Lieb and colleagues from the Framingham Heart Study, just published in JAMA, suggests the opposite.

Admittedly, this study primarily looked at the relationship between plasma leptin levels and the incidence of dementia, based on findings from animal studies suggesting that leptin facilitates long-term potentiation and synaptic plasticity in the hippocampus, promotes β-amyloid clearance, and improves memory function in animal models of aging and Alzheimer disease (AD).

The researchers studied 785 persons from the Framingham original cohort including 198 dementia-free survivors, who also underwent volumetric brain MRI between 1999 and 2005, approximately 7.7 years after leptin was assayed. 

During a median follow-up of 8.3 years higher leptin levels were associated with a markedly lower risk of incident dementia and AD as well as higher total cerebral brain volume and lower temporal horn volume.

Obviously, as one of the major determinants of leptin levels is body mass index, it is therefore not surprising that there was a significant difference in BMI between the lowest (BMI=24) and highest (BMI=32) leptin quartiles.

As with all studies of this nature, associations do not prove causality, so although the authors appear delighted that their findings support their hypothesis, I believe we are far off from recommending that people gain weight to increase their leptin levels to, in turn, lower their risk for dementia.

As so often, further studies appear warranted…

Chicago, IL


OECD: Don’t Place All Your Bets on Obesity Prevention

A widely held view is that the best solution to the current obesity epidemic is to focus on prevention and that if we only talk enough about it, increase our efforts to promote healthy lifestyles, get phys-ed back into schools, ban pizza-fundraisers, reduce advertising to kids, and get everyone to be more active, we will soon no longer have an obesity crisis.

This is not what the OECD believes, at least according to a report co-published by the World Health Organisation (WHO) last month.

I am referring to OECD HEALTH WORKING PAPERS No. 48 presented by the Health Committee of the Directorate for Employment, Labour and Social Affairs, titled: “Improving Lifestyles, Tackling Obesity: The Health and Economic Impact of Prevention Strategies”.

This report should make for some very sobering reading to all prevention enthusiasts.

The following the summary taken directly from this report:

In an attempt to contain rising trends in obesity and associated chronic diseases, many governments have implemented a range of policies to promote healthy lifestyles. These efforts have been hindered by the limited availability of evidence about the effectiveness of interventions in changing lifestyles and reducing obesity. Evaluations of the cost-effectiveness and distributional impacts of such interventions are even fewer and narrower in terms of numbers of options considered.

An economic analysis was developed jointly by the OECD and the WHO with the aim of strengthening the existing evidence-base on the efficiency of interventions to tackle unhealthy diets and sedentary lifestyles. The analysis was broadly based on the WHO-CHOICE (CHOosing Interventions that are Cost-Effective) approach, and it aimed at assessing the efficiency of a range of policy options to tackle unhealthy lifestyles and related chronic diseases. Additionally, compared to the traditional CHOICE framework, the analysis assessed the distributional impacts of preventive strategies on costs and health outcomes.

Most of the preventive interventions evaluated as part of the project have favourable cost-effectiveness ratios, relative to a scenario in which no systematic prevention is undertaken and chronic diseases are treated once they emerge.

However, since the determinants of obesity are multi-factorial and affect all age groups and social strata, interventions tackling individual determinants or narrowly targeted to one groups of individuals will have a limited impact at the population level, and will not reduce significantly the scale of the obesity problem.

Although the most efficient interventions are found to be outside the health sector, health care systems can have the largest impact on obesity and related chronic conditions by focusing on individuals at high risk.

Interventions targeting younger age groups are unlikely to have significant health effects at the population level for many years. The cost-effectiveness profiles of such interventions may be favourable in the long-term, but remain unfavourable for several decades at the start of the interventions.

Preventive interventions do not always generate reductions in health expenditure, when the costs of treating a set of diseases that are directly affected by diet, physical activity and obesity are considered.

As I said, a very sobering read for anyone who thinks obesity is preventable anytime soon.

Chicago, IL

Hat tip to Nathalie for bringing this report to my attention