Does Measuring Your Food Add Up?

diet journalMeasuring and monitoring your food intake – a strategy that may involve counting points or calories, weighing and measuring your food and drink, paying attention to food labels or calories on menu boards, obsessing about added fat or sugar, and excluding or limiting certain foods, are the backbone of virtually all weight management strategies.

Indeed, there is enough evidence in the literature to show that most “successful” dieters develop a somewhat obsessive relationship to accounting for every bite they put in their mouths – measuring, counting, adding, journaling, avoiding and restricting become part of their daily routine. For some it becomes so automatic a behaviour, that they are no longer even conscious of doing it (nor do many stop to realise just how “abnormal” such a behaviour actual is).

If this helps them better manage their weight – good for them. As a strategy for the population – or in other words when measured in terms of “effectiveness” – such an approach is bound to fail. This is because most people are simply not going to live their lives that way (and who can blame them?).

That said, it turns out that calorie counting (in whatever form) may indeed be the only behavioural weight management strategy that actually works (albeit with rather modest results).

This is apparent from a new meta-analysis by J. Hartmann-Boyce and colleagues from a UK-based Behavioural Weight Management Review Group, published in Obesity Reviews.

The rather painstaking systematic review, meta-analysis and meta-regression included 37 randomized controlled trials of multicomponent behavioural weight management programmes in over 16,000 overweight and obese adults.

While the overall effect of these interventions at 12 months was a rather meagre 2.8 Kg weight loss, the authors went to great lengths to try to dissect out what worked and what did not.

Thus, for e.g. there was no evidence that supervised physical activity, frequency of contact (rather surprisingly), or in-person contact were related to overall effectiveness.

In fact, the meta-regression analysis found only three factors that had a somewhat greater impact:

1) Calorie-counting (-3.3 Kg)

2) Contact with a dietitian (-1.5 Kg)

3) Behaviour change techniques that compare one participant’s behaviour to others (-2.9 Kg)

Thus, the authors conclude that programs involving some form of calorie-counting and contact with a dietitian may be the most effective. I would add to the list interventions that include group settings where participants can compare notes.

But with all of this said, the real message is  just how modest the outcomes of behavioural approaches to obesity actually are – in fact the finding from this analysis fly in the face of what most people (health professionals included) are convinced is possible based on anecdotes (“success stories”) and from what  commercial and non-commercials programs  so often claim (with virtually no published or otherwise publicly accessible data to support these claims).

Indeed, if I were to tell my patients that they need to start counting calories so that they can lose an additional 5 lbs, most would probably be walking out of my office never to return.

Thus, if anything, this analyses should conclusively lay to rest the notion that for most people, clinically meaningful weight loss can be achieved (and maintained) through behavioural interventions alone.

This is not to say that behavioural interventions in obese individuals (including physical activity) are not beneficial – they are, just not for weight loss.

As I have said before (and restate every time I get a chance) – improving health behaviours can certainly lead to a healthier you – whether that you is leaner or not is an entirely different (and less important?) question.

It turns out that getting your cortex to run your hypothalamus is far more difficult that you may think.

As discussed in  earlier posts, the key problem with these behavioural approaches is that they are designed to change behaviour – what we need are behavioural approaches designed to change physiology – that is a very different order.

@DrSharma
Edmonton, AB

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Obesity Weekend Roundup, March 28, 2014

As not everyone may have a chance during the week to read every post, here’s a roundup of last week’s posts:

And, If you haven’t done so already, please consider supporting this anti-weight bullying Children’s tale.

Have a great Sunday! (or what is left of it)

@DrSharma
Edmonton, AB

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Why Watching Your Kid’s Media Use May Affect Their Weight

sharma-obesity-family-watching-tvElectronic media consumption has been linked to childhood obesity – but does monitoring your kid’s media use affect their body weight?

This question was now addressed by Tiberio and colleagues in a paper published in JAMA Pediatrics.

The researchers examined longitudinal data from a community sample in the US Pacific Northwest that indluced 112 mothers, 103 fathers and their 213 kids aged five to nine years old.

The data included what parents reported on their general monitoring of their children (whereabouts and activities), specific monitoring of child media exposure, children’s participation in sports and recreational activities, children’s media time (hours per week), household annual income, and educational level as well as parental BMI was recorded.

It turns out that maternal (but not paternal) reports of monitoring their kid’s media exposure was associated with lower BMI z scores at age seven as well as less weight gain between five and seven years of age.

These findings remained significant even after adjustment for several other variables including total media time as well as sports and recreational activities.

From these findings, the authors conclude that,

Parental behaviors related to children’s media consumption may have long-term effects on children’s BMI in middle childhood.

And that these finding,

“…underscore the importance of targeting parental media monitoring in efforts to prevent childhood obesity.”

I would not go quite that far for several reasons.

Firstly, associations do not prove causation. In addition, we don’t know much about other aspects of parenting style from this study that may well also have impacted body weight.

Thus, we could well speculate that moms who monitor their kid’s media consumption may also be more adamant about bed times, healthy eating, or even just spending more time talking to or listening to their kids – all of which may well have positive effects on their kid’s weight.

This is why simply getting parents to be stricter about monitoring their kid’s media consumption may not result in better weights at all.

As always, I  find it disconcerting when epidemiological data is used to predict what may or may not happen when interventions target a proposed “cause”.

Nevertheless, for anyone interested in this topic, the following event may be of interest:

Details:

On May 1, 2014 the Alberta Teachers’ Association, in partnership with the Alberta Centre for Child, Family and Community Research, is pleased to invite Dr. Michael Rich and Dr. Valerie Steeves to Edmonton for a discussion on how technology is impacting children, youth and society. This is a continuation of our series of evening public lectures with world renowned and distinguished speakers that has included Sir Ken Robinson, Sherry Turkle, Yong Zhao, Jean Twenge, and Carl Honore.

Dr. Valerie Steeves, Associate Professor, University of Ottawa, and principal investigator of the largest Canadian research study on children & teens’ online habits.

Young Canadians in a Wired World (2013) – Explore the highlights of Dr. Steeves’ pioneering Canadian research on children & teens’ online habits.

Ø  Cyberbullying: Dealing with Online Meanness, Cruelty and Threats

Ø  Online Privacy, Online Publicity 

Ø  Life Online

Dr. Michael Rich, Associate Professor of Pediatrics at Harvard Medical School and Associate Professor of Society, Human Development, and Health at Harvard School of Public Health, Boston, United States.

Ø Centre on Media and Child Health – Explore Dr. Rich’s extensive work on behalf of Children’s Hospital Boston, Harvard Medical School and the Harvard School of Public Health:

Ø CBC national panel discussion on Youth and Technology (February 2014):

Ø Ask the “Mediatrician” a question

There will also be a public lecture on Thursday evening May 1, 2014 entitled “Connected or Disconnected? Technology and Canadian Youth”.

Who: Dr. Michael Rich (Harvard University) and Dr. Valerie Steeves (University of Ottawa)

When: Thursday Evening, May 1, 2014

Where: Barnett House, Alberta Teachers’ Association, 11010 – 142 street NW Edmonton, Alberta

•6:00 pm Registration and reception (hors d’oeuvre and no host bar)

•7:00 pm to 9:30 pm Public lectures and discussions

Order Tickets ($10) Online at http://www.event-wizard.com/promiseperil2014/0/register/

For further information or any questions about this event please email karin.champion@ata.ab.ca or call 1-800-232-7208.

@DrSharma
Edmonton, AB

ResearchBlogging.orgTiberio SS, Kerr DC, Capaldi DM, Pears KC, Kim HK, & Nowicka P (2014). Parental Monitoring of Children’s Media Consumption: The Long-term Influences on Body Mass Index in Children. JAMA pediatrics PMID: 24638968

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Three Essential Ways in Which Melatonin Links to Energy Balance

sharma-obesity-pineal-glandAs a regular reader, you will be quite familiar with the emerging recognition of sleep (or rather lack thereof) as an important determinant of weight gain.

Melatonin, an evolutionary ancient molecule that, in mammals, is secreted from the pineal gland, is a hormone that plays a major role as a key regulator of the circadian cycle, along which  virtually all metabolic activities are coordinated.

A paper by José Cipolla-Neto and colleagues, published in the Journal of Pineal Research, provides a fascinating overview of how melatonin plays a significant role in energy metabolism.

Its first role relates to insulin secretion and action. Thus, melatonin is not only necessary for the proper synthesis and secretion of insulin, it also plays a role in the insulin-signalling pathway through its effects on GLUT4 receptors.

Secondly, as a powerful chronobiotic, it helps coordinate various metabolic processes so that the activity/feeding phase of the day is associated with higher insulin sensitivity whereas the rest/fasting phase is synchronized to lower insulin sensitivity.

Thirdly, melatonin plays an important role in regulating energy flow to and from fat stores and directly regulating the energy expenditure through the activation of brown adipose tissue and participating in the browning process of white adipose tissue.

The paper discusses how the reduction in melatonin production, as seen during aging, shift-work or night-time light exposure can induce insulin resistance, glucose intolerance, sleep disturbance and metabolic circadian disorganization, which together can lead to weigh gain.

Thus, the available data supports the notion that melatonin replacement therapy may provide a novel strategy to influence metabolism, at least in people with disruptions in their melatonin system.

Clearly, these notions need to be tested in well-controlled randomised trials but there certainly appears to be ample data to suggest that such a trial may well be worthwhile.

If you have taken melatonin or prescribed it to your patients, I’d certainly like to hear about your experience.

@DrSharma
Edmonton, AB

Hat tip to Sukie for pointing me to this article.

ResearchBlogging.orgCipolla-Neto J, Amaral FG, Afeche SC, Tan DX, & Reiter RJ (2014). Melatonin, Energy Metabolism and Obesity: a Review. Journal of pineal research PMID: 24654916

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How The FTO Gene Affects Body Weight

sharma-obesity-dna_molecule9Body weight is one of the most heritable of physiological traits – in fact (believe it or not), it is just as heritable as body height.

Among the many genes associated with body weight, data for the FTO gene have been most consistent.

But these finding have puzzled researchers, as genetic manipulations of the coding regions of the FTO gene have large effects on body weight, without any apparent change in the function of this gene.

Now, a paper by Scott Smemo and colleagues, published in NATURE, suggests a mechanism for how variants of the FTO gene may affect body composition.

The answer lies in the way that the region of the FTO gene associated with obesity directly interacts with another gene IRX3, located a few megabases away on the same chromosome. This interaction appears conserved across species all the way back to the zebrafish.

Consistent with this finding, it turns out that the obesity-associated single nucleotide polymorphisms of the FTO gene are associated with changes in the expression of IRX3, but not FTO, in human brains.

Also consistent with this idea is the fact that IRX3-deficient mice have a 30% lower body weight, primarily due to less fat mass and an increase in basal metabolic rate with browning of white adipose tissue. The animals also appear resistant to the effects of a high-fat diet and appear protected against diabetes.

Furthermore, expression of a dominant-negative form of IRX3 in the hypothalamus reproduces the metabolic phenotypes of Irx3-deficient mice.

Thus, these findings suggest that FTO exerts its effect on body weight through its functional impact on the IRX3 gene, a gene that has so far not been linked to body weight regulation.

This is of particular significance, as IRX3 appears to be a “master gene” that controls the expression of other genes in many tissues including the brain and fat cells.

Given that variants of the FTO gene are frequent in the population and consistently linked to obesity (and type 2 diabetes), these findings may take us one step closer to a molecular target for anti-obesity interventions.

@DrSharma
Edmonton, AB
ResearchBlogging.orgSmemo S, Tena JJ, Kim KH, Gamazon ER, Sakabe NJ, Gómez-Marín C, Aneas I, Credidio FL, Sobreira DR, Wasserman NF, Lee JH, Puviindran V, Tam D, Shen M, Son JE, Vakili NA, Sung HK, Naranjo S, Acemel RD, Manzanares M, Nagy A, Cox NJ, Hui CC, Gomez-Skarmeta JL, & Nóbrega MA (2014). Obesity-associated variants within FTO form long-range functional connections with IRX3. Nature, 507 (7492), 371-5 PMID: 24646999

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