New Study Confirms Breastfeeding Not Protective for Childhood Obesity

March 14th, 2013 1 comment »

A new study published in JAMA concludes that breastfeeding is unlikely to prevent the development of obesity in children up to 11 ½ years old. The study, involving 17, 046 breastfeeding mother-infant pairs,  contributes to the conclusion reached in an earlier posting, Breastfeeding and Obesity.

The Putative 82 Causes of Obesity

February 28th, 2013 5 comments »

I’ve been keeping track of the putative causes of obesity. I am now up to 82. I don’t allege they are all correct. But they do exist in the scientific or popular literature, usually both. The links will not take you to a definitive study but only to an example of the debate going on in that area. So, the questions are: 1. If a disease (condition) has 82 possible causes, can anyone say we know what THE CAUSE is? 2. Can all these putative causes be correct? In other words, can a diverse collection of events trigger a perturbation in the system to cause obesity? Alternatively, since each putative cause has some individuals with exposure who do not develop obesity, is there some kind of “master switch” which has to be tripped to cause excess adipose tissue accumulation? What possible prevention strategy could account for all these variables? Curious minds want to know.

1. agricultural policies

2. air conditioning,

3. air pollution,

4. antibiotic usage at early age

5. arcea nut chewing,

6. assortative mating,

7. being a single mother,

8. birth by C-section,

9. built environment,

10. chemical toxins,

11. child maltreatment,

12. competitive food sales in schools,

13. consumption of pastries and chocolate (in Burkina Faso),

14. decline in occupational physical activity,

15. delayed prenatal care,

16. delayed satiety,

17. depression

18. driving children to school

19. eating away from home

20. economic development

21. endocrine disruptors,

22. entering into a romantic relationship,

23. epigenetic factors,

24. family conflict,

25. first-born in family

26. food addiction

27. food deserts

28. food insecurity,

29. food marketing to  children

30. food overproduction

31. friends

32. genetics,

33. gestational diabetes,

34. global food system,

35. grilled foods

36. gut microbioata,

37. having children, for women,

38. heavy alcohol consumption,

39. home labor saving devices,

40. hunger-response to food cues,

41. international trade policies (globalization)

42. high fructose corn syrup,

43. lack of family meals,

44. lack of nutritional education,

45. lack of self-control,

46. large portion sizes,

47. living in the suburbs,

48. living in crime-prone areas,

49. low levels of physical activity,

50. low socioeconomic status,

51. market economy,

52. marrying in later life

53. maternal employment,

54. maternal obesity,

55. maternal over-nutrition during pregnancy,

56. maternal smoking,

57. meat consumption,

58. menopause,

59. mental disabilities,

60. no or short term breastfeeding,

61. non-parental childcare

62. overeating,

63. participation in Supplemental Nutrition Assistance Program (formerly Food Stamp Program)

64. perception of neighborhood safety,

65. physical disabilities,

66. prenatal  maternal exposure to natural disasters,

67. poor emotional coping

68. sleep deficits,

69. skipping breakfast,

70. snacking,

71. smoking cessation,

72. stair design

73. stress

74. sugar-sweetened beverages,

75. trans fats,

76. transportation policies,

77. television set in bedrooms

78. television viewing,

79. thyroid dysfunction

80. vending machines,

81. virus

82. weight gain inducing drugs.

 

Myths, Presumptions and Facts About Obesity

January 31st, 2013 No comments »

David Allison and 19 prestigious researchers have published an article in the New England Journal of Medicine on the Myths, Presumptions and Facts About Obesity. The myths they identify as being widely held are:

  1. Small, sustained changes in energy intake or expenditure will produce large, long-term weight changes.

  2. Setting realistic goals for weight loss is important, because otherwise patients will become frustrated and lose less weight.

  3. Large, rapid weight loss is associated with poorer long-term weight-loss outcomes, as compared with slow, gradual weight loss.

  4. It is important to assess the stage of change or diet in order to help patients who request weight-loss treatments.

  5. Physical education classes, in their current form, play an important role in reducing or preventing childhood obesity.

  6. Breast-feeding is protective against obesity.  (See my recent post on breastfeeding and obesity.)

  7. A bout of sexual activity burns 100 to 300 kcal for each participant.

They go on to identify six presumptions, which are widely accepted beliefs that have neither been proved nor disproved, so that we may move forward to collect solid data to support or refute them.

  1. Regularly eating (versus skipping) breakfast is protective against obesity.

  2. Early childhood is the period in which we learn exercise and eating habits that influence our weight throughout life.

  3. Eating more fruits and vegetables will result in weight loss or less weight gain, regardless of whether any other changes to one’s behavior or environment are made.

  4. Weight cycling (i.e. yo-yo dieting is associated with increased mortality.

  5. Snacking contributes to weight gain and obesity.

  6. The built environment, in terms of sidewalk and park availability, influences the incidence or prevalence of obesity.

They authors posit nine facts that we do know about obesity. The first two are:

  1. Although genetics plays a role, heritability is not destiny.

  2. Diets reduce weight but trying to go on a diet o recommending someone go on a diet generally does not work well in the long-term.

The remaining facts address specific tools: physical activity, maintenance, parent-child interventions, meal replacements, pharmacology and bariatric surgery.

An excellent discussion of the myth around how many calories does it take to make one overweight is the blog from Arya Sharma.

The article does not discuss a couple of observations. First, the media is a powerful tool in perpetuating many of these myths and presumptions. Second, policy-makers, especially at the federal level, repeat these myths when they know, or should know better. Third, it may be that our brains do not do a good job in analyzing data to overcome assumptions and stereotypical views.

We will have more on the myths and presumptions and role in policy-making in the days ahead.

 

Note to Mayor Bloomberg: It’s Harder than you think

September 27th, 2012 No comments »

On September 13, 2012, the New York City Board of Health enacted Mayor Michael Bloomberg’s proposal to limit the size of cups selling soda in New York City. The soda cup size ban over 16 oz only for facilities subject to inspection: restaurants, movie theatres, and stadium concession stands. Not covered are convenience stands, including 7-Elelven’s  (and its king-size Big Gulp drinks), vending machines and some newsstands. Also not affected are fruit juices, dairy-based  drinks like milkshakes or alcoholic beverages and non-caloric beverages. Fast food restaurants with self-service drink fountains would not be allowed to stock cups larger than 16 ounces. http://www.nytimes.com/2012/09/14/nyregion/health-board-approves-bloombergs-soda-ban.html.

There is no ban on  buying  two under 16oz cups of soda, selling ‘two for the price of one’, or free re-fills.

While most anti-obesity advocates shudder at the thought of sugar sweetened beverages, there is doubt over whether a ban on the size of the cup in which they are delivered is going to have much impact. Here’s why.

  1. Most sugar sweetened beverages (SSBs) are consumed by teenage boys, especially low income African-American and Hispanic. The ban rests on a hope that the consumers will voluntary switch from SSBs to some non- or low-caloric beverage. Yet, there is no educational campaign or subsidy to get them to substitute an SSB for another no/low-calorie drink. http://www.cdc.gov/nchs/data/databriefs/db71.pdf
  2. Males consume an average of 178 kcal from ssbs on any given day. Among males 12-19, consumption is highest at 273 kcal a day. This is still only a small  fraction of their total daily caloric intake. http://www.cdc.gov/nchs/data/databriefs/db71.pdf

At 273 kcal a day, a person would put on about 28 pounds a year. This is not happening, so the caloric intake is probably balanced to a large, if not full extent, by energy expenditure. The CARDIA study of 18-30 African-American and white men  and women   found that physical fitness changes were most strongly associated with weight changes over 7 years. Weight changes in this study range from 5.2kg in white women to 8.5 in African-American women.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1380845/pdf/amjph00503-0109.pdf

  1. Over half of sugar drink kilocalories, 52%, are consumed in the home, 92% having been purchased in stores. Presumably, the store-bought items are in cans and bottles, not in the cup sizes subject to the NYC ban. Of the 48% of kcal consumed away from home, 35.5% are purchased in fast-food restaurants and 1.4% in schools or daycare settings. 20% are consumed in vending machines, cafeterias, street vendors and community food programs. So, only about 1/3 of sugar drink consumption is in restaurants or fast-food outlets.   http://www.cdc.gov/nchs/data/databriefs/db71.pdf
  1. SSBs, while associated with increased daily caloric intake, are not the leading source. According to Harvard researchers Frank Hu and colleagues, the components most associated with increased intake are potato chips (1.69 lbs), potatoes (1.28 lbs), SSBs, (1 lb) unprocessed red meats (0.95 lb) and processed meats (0.93 lb), in that order. http://www.ncbi.nlm.nih.gov/pubmed/21696306.
  1. African-Americans need many changes to diet to affect CVD risk factors, including additional whole grains, vegetables and fish intake, reduction in saturated fat, sodium as well as sugar according to study by Carson et al in September 2012 Journal of the Academy of Nutrition and Dietetics. PubMed: Cardiovascular Health of Urban African Americans (I think this applies to all of us.)
  1. The most influential factor driving childhood obesity is parental weight, especially that of the mother, independent of the effect of socio-economic status. See Causes of Obesity also, http://www.ncbi.nlm.nih.gov/pubmed/19165162 A new study from Elmear Keane and  colleagues in Ireland provides further support for this. PubMed: Measured weight status and familial SES

To look at the combination of genetic pre-disposition to obesity and in the intake of SSBs, Qibin Qi  and colleagues at Harvard School of Public Health looked  at 32 genetic loci (called “risk alleles”) known to be associated with BMI.  They grouped the 32 loci into 3 groups and looked at prospective 4 year beverage intake data from two large studies. Participants who were obese at baseline were excluded.  They found a rising BMI from greater intake of SSBs. For every 10 risk alleles, the increases for BMI was 1.0 for one serving a month, 1.2 for one to four servings per week, and 1.85 for one or more servings per day. In a sub-analysis,  they excluded the FTO gene, known for its impact on body weight, and found similar results. They concluded that “persons with a greater genetic predisposition to obesity appeared to be more susceptible to the deleterious effects of sugar –sweetened beverages on BMI. PubMed: Sugar-Sweetened beverages and Genetic Risk of Obesity The implication of this article is that NYC may have overreached…applying a rule to all when only some are most affected.

Two intervention studies were published in the New England Journal of Medicine, along with the study above.  One, by Cara Ebbeling and colleagues, divided 224 overweight and obese adolescents into 2 groups. The first group received home delivery of non-caloric beverages and were followed for another year. The second group acted as controls. Consumption of SSBs in the first group declined significantly but at the end of 2 years there was not difference in BMI between the two groups.PubMed: Randomized Trial of SSB and Adolescent Weight

The other intervention study, by de Ruyter and colleagues, had a larger sample size (641 normal weight children from 4 yrs 10 months to 11 yrs 11 months) and was a double blind model.  Half received a sugar-free non-carbonated beverage and the other have a sugared non-carbonated drink.  26% dropped out of the study. If this were an obesity drug study, a great deal would be made of this. Evidently they dropped out because they no longer liked the taste of the beverage. The researchers assume they went back to consuming sugared beverages. They found that “masked” replacement of the SSB by a sugar-free beverage significantly reduced weight gain and fat accumulation in normal weight children. The difference was 1.01kg. However, the authors calculate that approximately 0.8kg of the differences in weight gain was due to fat mas and associated muscle and other tissues.  PubMed: Trial of sugar-free or sugar-sweetened beverages

You can listen to David Allison discuss the SSB issue and these studies at http://themixuab.blogspot.com/2012/09/do-sugar-sweetened-drinks-drive-obesity.html.

These studies were published in the New England Journal of Medicine September 21, 2012 edition.  Mayor Bloomberg could have looked at other recently published studies to see the difficulty of regulating consumption of SSBs.

Levy et al looked at school nutrition policies and price interventions directed at youth consumption of sugar sweetened beverages (SSBs). They found that school nutrition and price policies reduce SSB consumption and that reduced SSB consumption is associated with a reduction in energy intake that “can” influence Body Mass Index Their review of the literature found that the effects of nutrition policies on BMI were less conclusive, possibly due to the lack of adequate follow-up period or that reduced SSB consumption in school is compensated for by increased SSB consumption outside of schools. The authors’ concluded that, “The reduction in energy intake from even just one 8-oz serving of SSB appears enough to have important effects on the prevalence of overweight and obese youth if policies are started at early ages and maintained.”  PubMed: Review of the literature on policies youth consumption of SSB

Of course, the key word here is “if.” Some of the calculations of the benefits of reducing or eliminating SSBs, are premised on the assumption that the calories contained in SSB will not be compensated for by other caloric intake. PubMed: Effect of school district policy change on consumption of sugar An analysis of SSB consumption in middle schools compared students in states which reduced access and purchase with those that did not. The main finding was that SSB consumption was not associated with state policy, i.e. in-school access is reduced but overall consumption is not changed. PubMed: Banning all sugar-sweetened beverages in middle schools A study by Wang et al, calculated what a penny-per-ounce tax on SSBs would mean for health care costs and diabetes. They calculated that 40% of the calories in SSB would be replaced by other caloric intake and 60% of SSB calories would not be replaced. This would translate to a mean reduction of 0.9 pound in mean at the population level, with a greater impact on younger adults, a 1.5% reduction in the number of adults with obesity. This decline would further translate into a reduction of new cases of diabetes by 2.6% and cost savings over ten years of $17.1 billion. PubMed: Penny-per-ounce tax on sugar-sweetened beverages. However, the 40%-60% split was only an estimate, it wasn’t based on experimental or real world results.

News reports indicate 24 states and 5 localities which proposed taxes on sugar sweetened beverages failed in their attempts over the past 2 years. Industry resistance to taxes and regulation has been strong and effective. ( Reuters: Special Report: How Washington went soft on childhood obesity http://www.reuters.com/article/2012/04/27/us-usa-foodlobby-idUSBRE83Q0ED20120427, accessed April 28, 2012)

Worldwide, some 20 countries have banned all sugar-sweetened beverages from schools and about 12 have banned 100% fruit juice as well, according to Barry Popkin and colleagues. PubMed: Global Nutrition Transiiton and the Pandemic of  Obesity Hawkes and colleagues have found that 26 countries have made explicit statements on food marketing to children and 20 or so are developing explicit policies in the form of statutory guidelines or approved forms of self-regulation. PubMed: Regulationg the commercial promotion of food to children

Denmark last year became the first nation to tax sugar but has since rescinded its tax because it was hurting domestic businesses while Romania has introduced a lower value-added-tax on staple foods. New Zealand is researching taxing foods with little or no nutritional value at higher rates than more nutritious foods. Professor Sir Nicholas Wald, director of the Wolfson Institute of Preventive Medicine has proposed an all-embracing SASS (salt, sugar, alcohol and saturated fat) tax.  PubMed: Is a tax on junk food moving closer?

One alternative approach is to tax all SSB sales, whether in school or out of school. Researchers have pointed out that, in 2007, 34 states taxed soda sold in grocery stores and 39 taxed soda sold in vending machines at mean rates of 3.4% and 4.0% respectively. The tax was never greater than 10% of the price.  Several studies are cited which showed no effect on BMI from such taxes. PubMed: A review of the literature directed at the youth consumption of SSB Sturm et al point out the greater benefit of larger tax than a smaller tax to affect behavior. PubMed: Soda taxes, soft drink consumption, and children’s body mass index.

For an excellent discussion of food taxes, see these presentations from University College, Dublin.

The New York City experiment will be tested in court and then it will be tested in practice to see if it actually has an effect on reducing weight gain or causing weight loss. But there are other public policy options worth exploring. Mayor Bloomberg also proposed a waiver for the city from the Department of Agriculture to allow restrictions on the purchase of certain foods by families with SNAP benefits. SNAP is the Supplemental Nutrition Program for Women, Infants and Children. SNAP is a federal program designed to reduce hunger and food insecurity among low-income Americans.  In a study using store scanner data, Tatiana Andreyeva and colleagues at the Rudd Center for Food Policy and Obesity  looked at patterns in the New England states. They found on average that SNAP households purchased 689 oz of beverages per month, including 399 oz or 58% of SSBs. The researchers estimated that SNAP spends annually between $1.713 billion to $2.05 billion on SSBs. They note that no-calorie beverages and water were equally available and no more expensive. SNAP households appear to obtain more total energy from SSBs than the general, higher-income population. PubMed: Grocery Store Beverage Choices by Participants in Federal food

So there are other public policy options. But this debate over SSBs show the problem with over-simplifying obesity to one source, fashioning a simplistic response, only to see the “solutions” fail. This stuff is difficult and we need to appreciate how difficult it truly is.

 

A New Understanding of Body Weight Regulation

September 17th, 2012 No comments »

John Blundell and colleagues have come out with an interesting new paper, “Role of resting metabolic rate and energy expenditure in hunger and appetite control: A New Formulation.” The paper provides a fascinating insight into human body weight regulation, appetite and the recurring drive to eat. The  resting metabolic rate (RMR) refers to the energy needed to keep our bodies functioning. Of all of the components of energy expenditure, it is the largest, accounting for about 50%-70% of total energy expenditure.  The liver contributes about 20% to the RMR, the brain another 20%, the heart 11%, the GI tract 9% and skeletal muscle another 20%. The drive to eat is predicated on getting enough energy to these systems to keep them running.

Blundell and colleagues’ paper explores a long-running research question as to the influence energy expenditure has on energy intake. As many people know, one of the problems with the ‘eat less, exercise more’ prescription is that exercising often leads to greater hunger, then to more eating, negating or lessening the weight-related benefits of exercise in the first place.  They noted previous research that found that exercise caused a significant increase in levels of hunger but this was highly variable between individuals. However, they also observed an increase in post-feeding satiety signalling. What the researchers found was that fat-free body mass but not fat mass or BM is strongly correlated with meal size and daily energy intake. The write, “The strong implication of this relationship is that some privileged molecules arising from FFM (fat free mass) or some physiological consequences that reflect the activity of FFM, act as a signal to drive food intake.” They note, further, that RMR is positively associated with meal size and daily energy expenditure. It is also a strong predictor of fasting levels of hunger and influences the daily profile of hunger. Ergo, RMR is the driver of food intake. They suggest three components of appetite regulation: a drive for food arising from the physiological demand for energy; an inhibition of eating arising from signals of energy storage, primarily adipose tissue; and additional inhibitory signals arising from the mouth and GI tract.

Regarding weight management, the authors note that their observations bring additional dissatisfaction with the Body Mass Index (BMI) as a measure of excess weight. They note that persons with obese, as well as people with large muscle mass, would have a higher tendency to consume larger meals just to maintain their RMR and greater difficulty in tolerating dietary restrictions. RMR is not the cause of obesity; it is the mechanism for preserving body weight. The amount of food actually consumed is determined by energy density. A high RMR could influence weight gain by maintaining a high level of hunger but a positive energy balance (i.e. gaining additional weight) would “depend on the energy density and palatability of the diet.” Increasing fat-free mass and RMR would increase the drive to eat “meaning that weight gain becomes part of a positive, rather then a negative, feedback system. Increasing body weight therefore could facilitate further weight gain and increase the difficulty of weight loss or maintenance.” See PubMed: Role of Resting Metabolic rate and Energy Expenditure

The universal call to “maintain a healthy weight”, “avoid weight gain” and “eat less to lose weight” begs the question, “How many calories should I be consuming?” The answer is your resting metabolic rate. Going well below that rate induces strong hunger signals and a return to earlier calorie consumption levels. Almost all diet advice tries to get dieters to consume just about their RMR to encourage weight loss and avoid triggering hunger cues. RMR can be measure in the laboratory using very sophisticated tools. But most consumers will look to web-based calculators. And this is a sorry story indeed.

 

Time for a reappraisal

September 14th, 2012 No comments »

I have a blog on the STOP Obesity Alliance website on the latest research on the effectiveness of public policy interventions to prevent obesity.

See:  http://www.stopobesityalliance.org/blog/time-for-a-reappraisal-of-public-policy-interventions-on-obesity

 

 

Our Genes Are Changing: New Evidence

August 23rd, 2012 1 comment »

As readers of these pages know, I always react when people, in discussing obesity, dismiss genetics as a cause with the statement to the effect, ‘our genes just don’t change.’ On other pages, I recite evidence that this just isn’t true. Our genes do change. I also notice that you never hear a genetics expert make this claim. And for a good reason, our knowledge of genetics changes every week.

Now comes a new study using genomic databases from Iceland. The study of 78 trios of mother, father and child, looking for mutations in the child’s genes which were not present in either parent and therefore must have arisen spontaneously in the egg, sperm or embryo. Fathers passed on nearly four times as many new mutations as mothers, 55 v. 14. The older the father, the greater the number of mutations. Most of the mutations may be harmless but some are linked to conditions like autism and schizophrenia. NatureNews:Fathers bequeath more mutations as they age

Maternal obesity and metabolic conditions have been linked to autism in their offspring PubMed: Maternal Metabolic Conditions and risk of autism. Likewise, schizophrenia has been linked to obesity, diabetes and inflammation PubMed: Schizophrenia, metabolic syndrrome and inflammation

Bottom line: while the increasing age of the father may be relevant for autism research, the point for obesity genetics may be that both mothers and fathers pass on spontaneous mutations to their child. Our genes are changing.

 

Another cause?

August 22nd, 2012 No comments »

Another putative cause of obesity was just published…the use of antibiotics in children. How many does that make? PubMed: Antibiotic use in children and obesity