Arya M. Sharma, MD

Regular readers may recall that I posed this question in a post earlier this year.

In it, I proposed that the positive impact of regular exercise on body weight has more to do with the positive effect of exercise on dietary caloric intake than on the number of calories ‘burnt’ - in other words, exercise is more about ‘calories in’ than ‘calories out’.

Following the rather enthusiastic response to this post, Jean-Philippe Chaput (a former CON Boot Camper and now an Assistant Professor at the Childrens’ Hospital of Eastern Ontario in Ottawa) and I co-authored an editorial on this topic for the British Journal of Nutrition.

The original post can be read here.

AMS
Edmonton, Alberta

As regular readers are well aware, one of the major dilemmas in obesity management is the fact that virtually any attempt at weight loss is counteracted by complex mechanisms that aim to restore the body back to initial weight.

So far, no one has discovered a way to reverse or ‘reset’ this mechanism so that, once weight is lost, the body ‘relaxes’ and ‘accepts’ that new, lower body weight again.

This is why, no matter what program, diet, exercise, medication or surgery you chose for weight loss, when you stop the program, diet, exercise, medication, or reverse the surgery, your weight comes back - there are almost no exceptions to this rule.

So how does weight gain lead to this apparently ‘permanent’ resetting of the body-weight ’set point’?

A recent paper by Tamas Horvath (Yale) together with colleagues from the US, Europe and Australia, published in the Proceedings of the US National Academy of Science, suggests that ‘micro-scarring’ of neurons that regulate hunger and satiety in the hypothalamus (the key homeostatic centre of eating behaviour) may play an important role in this process.

The researchers first studied the microscopic organisation of synapses (nerve-nerve contacts) in the anorexigenic (hunger-suppressing) proopiomelanocortin (POMC)-expressing nerve cells of the arcuate nucleus in lean rats that were vulnerable or resistant to diet-induced obesity.

There was a clear quantitative and qualitative difference in the synaptic organisaton of POMC cells between these animals, with a significantly greater number of inhibitory inputs in the POMC neurons in weight-gain susceptible rats compared with resistant rats.

Then, when given similar high-fat diets, the POMC cells of weight-gain resistant rats formed more connections whereas the susceptible animals actually lost synapses.

Importantly, this loss of synapses was associated with a process called ‘reactive astrogliosis’ or ‘glial-scarring’ whereby, in an ‘inflammatory’ response, astrocytes ensheath the POMC neurons, thereby making them ‘permanently’ inaccessible to new synapses (hence the use of the term ’scarring’).

In addition, this formation of glial ’scar’ tissue, also made the POMC cells less accessible to blood vessels (i.e. increased the blood-brain barrier).

As all ’scarring’ processes in the body, these micro-scars are in essence, irreversible, or in other words, permanent.

Thus, these findings clearly show how increased caloric intake in ‘obesity-prone’ rats (and humans?) can lead to permanent changes in the cell-architecture of the arcuate nucleus thereby essentially ‘locking in’ the new ’set point’.

Obviously, no diet, exercise, medication or surgery will undo the ’scarring’ in these key centres of the brain (in the same way that no diet, exercise, medication or surgery will undo a scar in your skin or anywhere else in your body) - which is perhaps why none of these interventions will ever lead to ‘permanent’ weight loss unless they are continued in the long-term.

Although this may sound very disappointing and discouraging, these findings may eventually lead to new treatment strategies that can help prevent the ‘resetting’ by reducing or preventing the ‘inflammation’ that promotes the formation of astrogliosis with weight gain.

Perhaps, as in rats, those ‘rare’ people who appear to be (genetically?) weight-gain resistant or have less problem losing weight and keeping it off, can do so simply because they have more synapses in their POMC neurons to start with, easily grow more synapses when exposed to excess calories, or simply do not develop the ‘micro-scarring’ in their brains with weight gain.

Of course, scar or no scar, none of this means that treatments don’t work - of course they do, as long as the treatments continue.

So, the runners, who lost weight running, will have to keep running, the dieters, who lost weight dieting, will have to keep dieting, the patients who had bariatric surgery, can expect weight regain if they ever reverse the surgery - when the ‘treatment’ stops, the weight comes back!

As I have said before, the first measure of success in obesity management is stopping the gain - less weight gain - less scarring?

Successful obesity management is prevention!

AMS
Edmonton, Alberta

Horvath TL, Sarman B, García-Cáceres C, Enriori PJ, Sotonyi P, Shanabrough M, Borok E, Argente J, Chowen JA, Perez-Tilve D, Pfluger PT, Brönneke HS, Levin BE, Diano S, Cowley MA, & Tschöp MH (2010). Synaptic input organization of the melanocortin system predicts diet-induced hypothalamic reactive gliosis and obesity. Proceedings of the National Academy of Sciences of the United States of America, 107 (33), 14875-80 PMID: 20679202

Despite all advances in gender equality, mothers overwhelmingly remain responsible for putting food on the family table.

Thus, any attempt at changing eating behaviours requires a sound understanding of the factors that determine mothers’ food choices for their families.

This issue is the topic of a study by Joyce Slater and colleagues from the University of Manitoba, published in Health Promotion International.

The researchers used qualitative methodology based on grounded theory to better understand the phenomena of food choice and food provisioning among employed middle-income mothers from Winnipeg.

All participants were born in Canada, were Caucasian, worked at least half-time at paid employment, lived with a male spouse working full-time, had at least one child between ages 5 and 12, had some post-secondary education and self-identified as having the primary responsibility for acquiring and preparing food for her family.

The methods consisted of extensive interviews and use of food choice maps to explore a wide range of determinants of food practices and choices.

Perhaps not surprisingly, the number one constraint that limited the preparation of healthy home cooked meals was lack of time!

As one participant put it:

“Life is far too rushed! Especially if you’re only getting home [from work] at, like anything after five is just a disaster. If you’re not home before quarter to five it’s like, you’re not going to make it! ‘Cause there’s evening events that are going to start and it’s like, oh man, now it’s the rush and a panic.”

The two main reasons for lack of time were employment and kids activities.

“All the women in this study described their family lives as being extremely busy due to their employment and children being engaged in multiple extracurricular events, which were felt to be important for their development. This contracted their food preparation time, however, resulting in the frequent use of convenience foods or take-away from restaurants, which also led to feelings of stress.”

The second major determinant of food choices were ‘picky eaters’:

“My daughter’s very picky, so who knows what she’ll eat what nights … it’s usually just a Pizza Pop or leftovers of a quick bowl of soup. We try to get her to eat what we eat, but it’s challenging. You don’t want it to be a battleground.”

While breakfast and lunch were rarely eaten together, most mothers appreciated the importance of having the family assembled for dinner - however, this also rarely happened due to busy and conflicting schedules.

Although mothers collectively perceived food as an important determinant of health,

“Many of the foods children preferred were perceived to be unhealthy by the mothers, but were frequently purchased because they knew they would be eaten, or it was believed that the children should have their way at least some of the time.”

Reasons for not eating enough fruits and vegetables boiled down to:

“…children not liking vegetables; they took too much time and work to prepare; it was not worth making them only for themselves and the women did not want to risk spending time making vegetables if they were going to be wasted.”

Although mothers appreciated that fathers may have a role to play - they preferred to make these choices themselves:

“Sometimes I wish he would help a bit more, but I still think I’m better off with the majority of it. Because, I said, I don’t think he would make as good of choices. He would give the kids Pizza Pops for lunch every day, and … vegetables?! Who cares? What do you need vegetables for!?”

“[Help with] groceries? No (laughter), not very often! I mean, you know, if I’m really really strapped he will go out but that’s not that often. He really doesn’t like grocery shopping.”

All of these findings have significant implications for improving population health:

“By purchasing and serving convenience foods over vegetables and healthier meals that take more preparation time, the women reinforce structural food norms within the family and within the retail grocery landscape that provides these foods for purchase. “

“Shifting norms surrounding the efforts put into food preparation are mutually reinforced by the women’s values, beliefs and identities, permitting the frequent use of these foods, thereby saving time. This is compounded by working outside the home and a busy family life, which leave considerably less time for preparing healthy foods and eating together. “

As the authors point out, educating mothers (or fathers) about healthy eating, although important, is insufficient to really change behaviour.

“Public health policy-makers should expand nutrition education initiatives to include … a more balanced discussion of domestic food work rather than perpetuating the current discourse on child obesity calling for greater ‘parental’ (maternal) responsibility. This could also include providing more flexibility for employees (male and female) to work part-time.

In addition, strategies to promote the uptake of more family food responsibility by male partners and children should be explored and promoted. A step towards this could be achieved through a re-introduction of school-based nutrition and food skills, not through traditional ‘home ec’ curriculum with gender-specific stereotypes, but teaching basic principles to feed young men and women, and their future families, within the current food environment.”

As I’ve discussed before, when trying to understand behaviours, it is far more important to explore the ‘why’ than the ‘what’.

This study certainly reminds us that for many, the key barrier to healthy eating is not lack of information on nutrients and food groups but rather having far too few minutes in your day.

Remember, the real problem with fast food is more the ‘fast’ than the ‘food’

AMS
Edmonton, Alberta

Slater J, Sevenhuysen G, Edginton B, & O’neil J (2011). ‘Trying to make it all come together’: structuration and employed mothers’ experience of family food provisioning in Canada. Health promotion international PMID: 21693474

If going on a diet or starting an exercise program resulted in persistent weight loss,  we would not have an obesity epidemic.

Unfortunately, as anyone who has tried this knows, maintaining a significant degree of weight loss requires daily dedication, motivation and a limitless supply of will power - nothing short of developing a compulsive obsession.

As readers will recall, the biology of the post-weight loss state is nothing like the biology of someone who has never lost weight. There are countless ways in which the psychoneurobiology, energy physiology and metabolism in anyone who has lost weight are remarkably different from someone ‘naturally’ of that weight.

Simply stated, someone who was 150 lbs and has lost 20 lbs cannot hope to maintain that weight loss by simply eating the same amount of food or doing the same amount of exercise as someone who is ‘naturally’ a 130 lbs.

The 150 lbs person who has lost 20 lbs, to maintain their new 130 lbs, has to actually now live like someone who is ‘naturally’ a 110 lbs; just eating like someone who is 130 lbs but has never lost weight, will simply result in rapid weight regain.

This is why just cutting out a few ‘extra’ calories or walking a few ‘extra’ steps is not an effective or sustainable strategy for maintaining weight loss - for any clinically meaningful weight loss (when indicated) - we are looking at cutting hundreds of calories from the diet and adding hours of serious exercise per week - forever!

A comprehensive and fascinating overview of the fundamental changes that occur with weight loss to ultimately make sustaining this new weight an ongoing challenge, is discussed by Paul Maclean and colleagues from the University of Denver Colorado, in a paper just published in the American Journal of Physiology.

The authors provide a detailed synthesis of data from a wide range of weight loss studies that include studies in clinically overweight and obese adults, in diet-induced, polygenic animal models of obesity, and with dietary (non-surgical) interventions involving an energy restricted low fat diet.

The consistent finding from all such studies is that all individuals or animals in a post-weight-loss state face considerable ‘homeostatic pressure’ that aims to drive their weight back to initial levels.

The paper extensively discusses how changes in biological signals of fat stores (e.g. leptin) elicit profound metabolic and behavioural adaptations - a topic that I dealt with extensively in previous posts.

The key findings of increased hunger and appetite, reduced satiety and substantially increased ‘fuel efficiency’ have very real underlying biological drivers - drivers powerful enough to ultimately wear down even the most persistent dieter.

As the authors point out - persistent dieting is so difficult because it requires maintaining a remarkably large ‘energy gap’:

“Because both sides of the energy balance equation are affected after weight loss, the biological pressure to gain weight is a consequence of both increased appetite and suppressed energy expenditure.

During weight maintenance after weight loss, this energy gap reflects the magnitude of the daily burden that thwarts cognitive efforts to maintain the reduced weight.

Regardless of which side of the energy balance equation is most affected, the energy gap imparts a substantial pressure to eat in excess of the energy requirements.

The magnitude of the energy gap is greatest at the nadir weight after weight loss. Likewise, this energy gap does not dissipate with time in weight maintenance. Rather, studies in DIO (diet induced obesity) models indicate that the magnitude of the energy gap gradually increases the longer they maintain their reduced weight with an energy restricted diet .

The implications from these observations are that the biological pressures may strengthen with time and the amount of lost weight, gradually increasing their perceived influence.”

The paper also extensively discusses some of the lesser known metabolic adaptations to weight loss including profound changes in gut biology that enhance caloric extraction from food as well as alterations in liver function, skeletal muscle and fat tissue that promote weight regain.

While all of this may seem hopeless to readers, the authors actually end on the rather positive note that:

“… only by acknowledging that these homeostatic pressures emerge, we can proactively develop and implement regain prevention strategies to counter their influence. To ensure success, the regain prevention strategies will likely need to be just as comprehensive, persistent, and redundant, as the biological adaptations they are attempting to counter.”

Obviously, it is also important to note, that no ‘weight-loss strategy” actually addresses the many complex reasons why people may gain weight in the first place.

Whoever said that treating obesity was simply a matter of ‘eating less and moving more’ (ELMM) probably also believes that they can live forever by simply breathing less.

AMS
Burlington, Ontario

Maclean PS, Bergouignan A, Cornier MA, & Jackman MR (2011). Biology’s Response to Dieting: the Impetus for Weight Regain. American journal of physiology. Regulatory, integrative and comparative physiology PMID: 21677272

Longtime readers may recall a post explaining why hunger makes you eat crap.

Understanding this, is an important principle to promote healthy eating and weight management (not necessarily the same).

To make this message somewhat easier to communicate, I produced this brief video, which hopefully brings this very simple but important point across (subscribers may have to visit my site to view this video).

Very much appreciate your comments and please feel free to repost.

AMS
Leipzig, Germany