Senate Report on Obesity: Here’s What’s MIssing

Yesterday, I listed the 21 recommendations of the Canadian Senate Report on Obesity in Canada. Of the 21 recommendations, 12 essentially fall under the category “Eat-Less” (2,3,4,6,7,8,9,10,11,12,13,20) and 6 under the category “Move-More” (5,14,15,16,17,18). Of the remaining 3, two deal with surveillance and consultations (1,19) while recommendation 21 deals with comprehensive public awareness campaign on healthy active lifestyles. So there you have it. The Senate’s solution to obesity is pretty much “Eat-Less Move-More”, which, as someone who responded to me on yesterday’s blog post describes as, “…little more than a backhanded insult, a polite rephrasing of “Put down the fork, Fatty and move.” Now, in all fairness, the report does talk about social determinants of health. It does also vaguely mention genetics, epigenetics and pregnancies (but not antibiotics or environmental toxins or endocrine disrupters) – but none of this is deemed relevant enough to prompt any recommendations (not even, “we need more research”). Nothing about reigning in the commercial weight-loss industry with their false claims and promises – no mention of the fashion industry and media that promote unrealistic and harmful body images. However, what I find most alarming about the entire report is that it essentially writes off the 7,000,000 Canadians living with obesity as being beyond help. In view of the liberal use of the terms “lifestyle” and “choice” scattered throughout the report, one can truly sense that many involved in the report are likely of the opinion that 7,000,000 Canadians have simply “chosen their cake and should now eat it”. I simply cannot imagine another health “epidemic” where there would not be at least some call for providing better access to treatment. No mention of weight-bias or discrimination. No mention of encouraging provincial governments to reduce wait times for bariatric surgery. No mention of urging Health Canada to expedite reviews for novel obesity medications (an unmet medical need if there ever was one). No mention of legislation to ensure that benefit plans cover all evidence-based treatments for obesity. No mention of ensuring access to adequate equipment and professional services within Canada’s health system. Nothing, in fact, that would actually help improve the lives of the 7,000,000 Canadians living with obesity. And let me clear. I am not against the recommendations or policies in the report – all of these can, if implemented, potentially improve the health of Canadians – everyone can benefit from eating better and being more active – everyone! But… Read More »

100+ Putative Causes Of Obesity – Take Your Pick

Listening to (or reading the bestsellers written by) pundits, one may easily think that the entire obesity problem can be brought down to a couple of factors – sugar-sweetened beverages, fast food, sedentariness, screen-time, – take your pick. Now, Morgan Downey, former CEO of the Obesity Society on his blog – the Downey Obesity Report – provides an update of previous lists of putative causes of obesity – a list that now included 104 items. As he is careful to point out, “The links are not meant to be definitive or best study but merely a demonstration of the interest in the particular cause.” Given that many of these factors are implicated based largely on observational studies, which by their very nature cannot prove causality, some scepticism is in order. However, for many factors on this list there is biological plausibility, often backed by findings from animal or experimental studies. Here is Downey’s list of putative causes of obesity: 1. agricultural policies 2. air conditioning, 3. air pollution, 4. antibiotic usage at early age, 5. arcea nut chewing, 6. artificial sweeteners, 7.  Asian tiger mosquitos, 8. assortative mating, 9. being a single mother, 10. birth by C-section, 11. built environment, 12. celebrity chefs, 13. chemical toxins, (endocrine disruptors) 14. child maltreatment, 15. compulsive buying, 16. competitive food sales in schools, 17. consuming skim milk in preschool children, 18. consumption of pastries and chocolate (in Burkina Faso), 19. decline in occupational physical activity, 20. delayed prenatal care, 21. delayed satiety, 22. depression 23. driving children to school 24. eating away from home 25. economic development (nutrition transition) 26. entering into a romantic relationship, 27. epigenetic factors, 28. eradication of Helicobacter pylori, 29. family conflict, 30. family divorce, 31. first-born in family, 32. food addiction, 33. food deserts, 34. food insecurity, 35. food marketing to  children, 36. food overproduction, 37. friends, 38. genetics, 39. gestational diabetes, 40. global food system,(international trade policies) 41. grilled foods, 42. gut microbioata, 43. having children, for women, 44.  heavy alcohol consumption, 45.  home labor saving devices, 46. hormones (insulin,glucagon,ghrelin), 47. hunger-response to food cues, 48. high fructose corn syrup, 49. interpersonal violence, 50. lack of family meals, 51. lack of nutritional education, 52. lack of self-control, 53. large portion sizes, 54.  living in crime-prone areas, 55. low educational levels for women, 56. low levels of physical activity, 57. low Vitamin D levels, 58.  low socioeconomic status, 59. market economy, 60. marrying in later life 61. maternal employment, 62. maternal obesity, 63. maternal over-nutrition during pregnancy, 64. maternal smoking, 65. meat consumption, 66. menopause, 67. mental disabilities, 68. no or short term breastfeeding, 69. non-parental childcare 70. outdoor advertising, 71. overeating, 72. participation in Supplemental Nutrition Assistance Program (formerly Food Stamp Program) 73. perceived weight discrimination, 74. perception of neighborhood safety, 75. physical disabilities, 76. prenatal  maternal exposure to natural disasters, 77. poor emotional coping 78. sleep deficits, 79. skipping… Read More »

Transcriptional Control of Energy Regulation

To students of human physiology, the commonly held view that obesity is simply a matter of energy in and energy out is nothing short of laughable. Indeed, there are perhaps no other biological functions of more importance for survival of an organism, than those that regulate energy uptake, storage and expenditure – functions, without any form of life would be impossible. Thus, the finely tuned complex and often highly redundant pathways that have evolved to optimize energy metabolism have evolved to readily switch from states of feeding to starvation with shifts in substrate use (both qualitative and quantitative) – functions that are controlled by hundreds (if not thousands) of genes. Getting these genes to work in concert, requires a complex system of gene regulation, by which individual genes are switched on an off (to allow or stop protein synthesis) in various tissues to just the right amount at just the right time – a process known as transcriptional control. Now, a comprehensive review by Adelheid Lempradl and colleagues, published in Nature Genetics, summarizes the multitude of interlinked processes that control transcription of genes involved in energy homeostasis. As the authors explain, “Transcriptional control is the sum of the cellular events that select and dose gene transcription. In simple terms, these events converge on the regulation of gene locus accessibility and polymerase activity (including recruitment, pausing, processivity and termination).” “Energy homeostasis requires multi-layered regulation via dynamic, often periodic, expression of metabolic pathways to properly anticipate and respond to shifts in energy state.” “Transcription factors act by binding to specific regulatory DNA sequences, thus controlling the transcriptional output of defined target gene sets. They cooperate with co-regulators, which either promote (co-activators) or inhibit (co-repressors) transcription. Together, they build feedback networks and control the stability and responsiveness of energy homeostasis. Metabolic cells use receptors and metabolic machinery to generate specific signalling responses to endocrine inputs (for example, insulin, glucagon or leptin receptors) or metabolic inputs (for example, the primary energy metabolism machinery itself).” The papers goes on to discuss at length the various regulator, co-regulators and the plethora of epigenetic modifiers that determine how these factors do their job of activating or deactivating relevant genes throughout the body. Why is any of this important? “Rapid progress is currently being made in research on chromatin-based regulation of gene expression. Particular unknowns include the mechanisms that establish long-term set points or priming of gene expression. Identifying the processes that… Read More »

CON Co-Hosts the International Congress on Obesity in Vancouver

As Canada’s national representative in the World Obesity Federation (formerly IASO), the Canadian Obesity Network is proud to co-host the 13th International Congress on Obesity in Vancouver, 1-4 May 2016. The comprehensive scientific program will span 6 topic areas: Track 1: From genes to cells For example: genetics, metagenomics, epigenetics, regulation of mRNA and non–coding RNA, inflammation, lipids, mitochondria and cellular organelles, stem cells, signal transduction, white, brite and brown adipocytes Track 2: From cells to integrative biology For example: neurobiology, appetite and feeding, energy balance, thermogenesis, inflammation and immunity, adipokines, hormones, circadian rhythms, crosstalk, nutrient sensing, signal transduction, tissue plasticity, fetal programming, metabolism, gut microbiome Track 3: Determinants, assessments and consequences For example: assessment and measurement issues, nutrition, physical activity, modifiable risk behaviours, sleep, DoHAD, gut microbiome, Healthy obese, gender differences, biomarkers, body composition, fat distribution, diabetes, cancer, NAFLD, OSA, cardiovascular disease, osteoarthritis, mental health, stigma Track 4: Clinical management For example: diet, exercise, behaviour therapies, psychology, sleep, VLEDs, pharmacotherapy, multidisciplinary therapy, bariatric surgery, new devices, e-technology, biomarkers, cost effectiveness, health services delivery, equity, personalised medicine Track 5: Populations and population health For example: equity, pre natal and early nutrition, epidemiology, inequalities, marketing, workplace, school, role of industry, social determinants, population assessments, regional and ethnic differences, built environment, food environment, economics Track 6: Actions, interventions and policies For example: health promotion, primary prevention, interventions in different settings, health systems and services, e-technology, marketing, economics (pricing, taxation, distribution, subsidy), environmental issues, government actions, stakeholder and industry issues, ethical issues Early-bird registration is now open – click here Abstract submission deadline is November 30, 2015 – click here For more information including sponsorship and exhibiting at ICO 2016 – click here I look forward to welcoming you to Vancouver next year. @DrSharma Toronto, ON  

Are We More Susceptible to Obesity Than Before?

Regular readers will be familiar with my wariness of epidemiological data on diet and activity – especially, when these are self-reported. Nevertheless, for what it is worth, a publication by Ruth Brown and colleagues from York University, Toronto, published in Obesity Research and Clinical Practice, suggests that people today may be more susceptible to obesity than just a few decades ago. The study looks at self-reported dietary from 36,377 U.S. adults from the National Health and Nutrition Survey (NHANES) between 1971 and 2008 and physical activity frequency data from 14,419 adults between 1988 and 2006 (no activity data was available from earlier years). Between 1971 and 2008, BMI, total caloric intake and carbohydrate intake increased 10-14%, and fat and protein intake decreased 5-9%. Between 1988 and 2006, frequency of leisure time physical activity increased 47-120%. However, for a given amount of caloric intake, macronutrient intake or leisure time physical activity, the predicted BMI was up to 2.3kg/m2 higher in 2006 that in 1988. So unless there was some major systematic shift in what people were reporting (which seems somewhat unlikely) it is clear that factors other than diet and physical activity may be contributing to the increase in BMI over time – or in other words, it appears that people today, for the same caloric intake and physical activity, are more likely to have a higher BMI than people living a few decades ago. There are of course several plausible biological explanations for these findings including epigenetics, obesogenic environmental toxins, alterations in gut microbiota to name a few. If nothing else, these data support the notion that there is more to the obesity epidemic than just eating too much and not moving enough. @DrSharma Edmonton, AB