Obese Folks: on Your Feet!

One of the most common accusations faced by people with weight problems is that they are simply lazy and just lack the motivation to be active (the other one is that they simply eat too much!).

It turns out that some obese people may in fact be less active than lean individuals. For e.g., a recent study by Darcy Johannsen and colleagues from Iowa State University published in OBESITY, used state-of-the-art activity monitoring technology (IDEAA) to examine in detail the activity patterns of 20 free-living lean and obese women over 14 days. Total energy expenditure was measured using doubly labeled water, body composition was measured using dual energy X-ray absorptiometry.

The main finding was that even after correction for increased body mass, obese women on average expended around 300 KCal less in physical activity per day than their lean counterparts. Overall, obese women sat 2.5 hrs more each day and stood 2 hrs less than the lean women. They also spent only half the time being physically active compared to lean women.

This finding is not new. Previous studies have noted that obese individuals spend less time on their feet and expend less energy through non-exercise thermogenesis (fidgeting). Importantly, intervention studies have shown that this is not corrected by weight loss - rather, the tendency to be less active appears to be innate, i.e. not due to the excess weight.

Well, as usual, Johannson and colleagues conclude their paper with the profound insight that if only obese women adopted the activity pattern of lean women, they wouldn't be obese - and that is where the logic breaks down.

In fact, this is very much like saying that, "if only depressed people could be less sad and, like "normal" people, show more interest in things, they'd be so less depressed".

The issue is not whether or not obese people move less - the question is why they do so. If the tendency to be less physically active and spend less time on their feet is innate - i.e. a character trait that is determined largely by genetics, then trying to get someone with this trait to be more physically active is likely to be difficult.

Perhaps one way of thinking about this is to reverse the argument. If, for a moment, we assumed that being lean was really the problem, then we'd have to teach lean people to really try to sit down more and to focus on being less active, so that they could gain weight. Anyone who believes that it would probably be difficult to teach lean people to sit still, to stop fidgeting and to simply be less active, should realise that for exactly the same reasons it may be unreasonable to expect the opposite of people with excess weight.

Not to say it is impossible - but in both cases it would take a special focus, a lot of resolve and perhaps constant reminding as it goes against their "natural" disposition.

While in today's obesogenic environment the natural disposition to fidget and rush around works to the advantage of lean people, the natural disposition to sit down and not rush around (indeed a "sensible" behaviour in a calorically frugal environment) is a handicap.

Again, the results of such studies should not be interpreted in the sense of: "Aha, so now we know what is "wrong" with people who have obesity - they are indeed lazy!". Rather they should be interpreted in the sense of: "Aha, so that is why people with obesity have such a hard time keeping their weight off - they are simply "programmed" against a senseless waste of energy".

This of course is not an excuse to do nothing - it just means that we must appreciate the extra effort that is required.

In other words, when lean people run around - that's just their nature, they can't help it - it's not because they are extra smart or better people. In fact, now that we have seen this research we should realise that when people who have obesity run around (even a little) this is certainly highly commendable, as we now know that they have to consciously make this extra effort despite their innate tendency to preserve energy.

Creating an environment that fosters time on your feet will serve everyone - the lean people will love it (or not care), those with weight problems will benefit without having to make a conscious effort. Time for more stand-up meetings?

AMS

Out on a Binge

Anyone running an obesity clinic is well aware of the surprisingly large number of patients who have Binge Eating Disorder (BED). Some reports put the number at around 30% of patients with severe obesity who seek help for their weight.

But you have to ask the right questions to make the diagnosis:

Do you ever, especially when you are alone and are not even really hungry, rapidly eat vast amounts of food that is not really a proper meal (e.g. a bag of chips followed by a box of cookies followed by a loaf of bread followed by all the cheese you can find followed by a bag of nuts followed by a pot of ice cream followed by..........you get the picture!) till you get uncomfortably full (or run out of food) and then end up feeling quite disgusted about yourself for having done it again but have no idea why you are doing this or how to stop yourself from doing it again?

If this behaviour occurs at least a couple of times a week over at least six months, this patient probably has BED, a well described eating disorder listed in the appendix of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV).

To me, the most important differential diagnosis is overeating because of true hunger (homeostatic hyperphagia) or as part of a planned social event (e.g. a birthday, a festival, a special treat, etc.).

Typically homeostatic hyperphagia occurs when you have not eaten enough during the day and your body craves calories so that when you finally allow yourself (or find the time) to eat, you end up eating the wrong things too fast till you vastly overshoot your actual caloric requirements. Also, overeating at social events, especially when there is plenty of great-tasting food (and alcohol), i.e. "pigging out at the buffet" - does not mean you have binge eating disorder.

The key differences are that the patient with BED is not eating because of any "need for calories" or physical hunger, is not eating as part of a regular meal or social event, and ends up feeling quite troubled and disgusted at the lack of control (unlike the "hedonic overeater" who truly enjoys splurging on tasty foods and actually feels quite happy and content after a large scrumptious meal).

Diagnosing BED (which, despite popular belief, occurs as commonly in men as in women!) is essential, as this condition is actually made worse by dieting and patients usually have long-standing histories of weight cycling (usually with the help of commercial weight loss programs). Given that patients have little control over their behaviour, recidivism of weight gain is extraordinarily high and long-term maintenance of weight loss is virtually impossible without addressing the pscychopthology specific to this condition.

Fortunately, BED is highly responsive to psychotherapy (e.g. cognitive behavioural therapy, group interpersonal therapy, etc.) with various investigators reporting upto 95% reduction in the frequency of binge-eating episodes with almost 80% of patients becoming completely free from binging. Pharmacotherapy also appears to provide some relief.

The bottom line is: "true" BED is common and needs to be treated as a separate and distinct psychiatric disorder before hoping to make any progress in weight management.

Luckily this is possible.

AMS

Sifting Through Obesity Research

There is no doubt, obesity research is hot!

With over 100 new obesity publications appearing in the literature every month, it is impossible to keep up.

This is where the Canadian Obesity Network's OBESITY+ service comes in.

Based on McMaster University’s Health Information Research Unit's unique secondary peer rating system, OBESITY+ provides access to the current best evidence about the causes, course, diagnosis, prevention, treatment, and economics of obesity and its related mental, metabolic and mechanical complications.

Every week, the best evidence relevant for clinical practice in the fields of medicine, nursing, dietetics, and rehabilitation is identified from over 130 premier clinical journals with a focus on or strength in obesity.

All citations are pre-rated for quality by research staff, then rated for clinical relevance and interest by at least 3 members of a worldwide panel of practising health professionals with an interest in obesity.

The service includes a searchable database of the best evidence from the health care literature and features a customizable email alerting system.

Only the best research makes it through the rigorous review process - reducing "noise" by 98%

A related service Pre-OBESITY+ provides a broader overview for researchers - this service is less rigorous about the methodological criteria and therefore also includes studies that may not be ready for prime time, but are nevertheless of interest.

And best of all - both services are absolutely free to subscribers.

Click here to sign up for OBESITY+ (for health professionals)

Click here to sign up for Pre-OBESITY+ (for researchers)

AMS

Googling Guggul for Weight Loss

Guggul, or rather guggulsterone, is the active ingredient in an age-old Indian Ayurvedic remedy derived from the gum resin of the guggul tree (Commiphora mukul), which has been shown to lower lipid and cholesterol levels. Claims have also been made regarding its usefulness as an antiobesity drug, although the data on this is far from consistent.

A recent paper by Yang and colleagues from the University of Georgia, published in a recent issue of OBESITY, demonstrates that guggelsterone in fact does substantially inhibit adipogenic differentiation of cultured 3T3-L1 cells (a widely used in vitro model of fat cells). In this model, guggulsterone also promotes lipolysis as well as induces apoptosis of fat cells, albeit at higher concentrations. (link to abstract)

Together, these findings appear to provide a biological mechanism to support the anti-obesity health claims for this compound.

However, this does not mean that we now have a new natural "solution" to the obesity problem (although, as a brief excursion to Google confirms, guggul is already widely promoted and available for exactly that).

Here are my reservations:

1) Fat cells are the safest place to store excess calories. Limiting the growth or destroying fat cells, without also targeting the state of caloric excess raises the issue of where those extra calories should go. Because they are in excess of what the body needs, they are not simply "burnt off". Rather, the body now has to store them somewhere else, i.e. in non-fat tissue (for e.g. liver, muscle, etc.) - also referred to as "ectopic" fat deposition. There is now ample evidence that it is in fact this ectopic fat that causes the metabolic problems (e.g. diabetes) that are often associated with obesity. So if guggul prevents the formation of fat cells or destroys them (by apoptosis) the big question is: what happens with all the excess energy? If this now ends up in the form of fat stores in other organs like your liver or muscle, you are more likely to cause harm rather than reap any benefits.

2) Obviously, extrapolating from an in vitro finding to clinical benefits in patients is a long shot. While the data on guggul's clinical antilipid effects appears well-documented, I am not convinced of any weight-loss effects thus far. Destroying fat cells, to me does not necessarily translate into weight loss unless the extra calories stored in those cells are actually burnt. For that guggul would either have to promote burning of calories, for which to my knowledge there is no indication. Alternatively, guggul would have to also reduce energy intake for which I have also seen no evidence.

The bottom line is that, despite this elegant laboratory work demonstrating biological action of guggelsterone in vivo, health claims should be based on demonstration of clinically significant health benefits in rigorously conducted clinical trials. As the issue in obesity treatment is not short-term weight loss but rather long-term weight-loss maintenance, these studies would have to be long enough (i.e. 12 months or longer).

Is this going to stop people from selling and buying guggul because of its now "proven ability to destroy fat cells"?

Not likely.

Will I be recommending guggulsterone as obesity treatment to my patients?

Definitely not!

AMS

Replacing Meals Beats Skipping Them

One of the basic principles in weight management is not to let yourself get hungry.

This is based on the simple rationale that when you are hungry, your hypothalamus "kicks in", essentially overriding any "sensible" choices you may have intended to make.

For one, when you are hungry you are more likely to eat energy-dense foods.

But hunger also makes you eat faster, in turn making you more likely to overshoot your actual caloric requirements before satiety sets in. I have previously referred to this as ""homeostatic hyperphagia"".

Skipping meals is perhaps the most common reason for people to get hungry. The meals most likely to be skipped are breakfast and lunch, resulting in the evening "binge".

If the reason for skipping breakfast and lunch is lack of time and an irregular hectic schedule, commercial meal replacements can come in handy. The convenience of quickly drinking a shake or eating a bar is hard to beat.

Sure, a proper balanced meal prepared with fresh wholesome ingredients enjoyed in a relaxing setting would be best, but the reality is that that is rarely the reality.

Therefore, I would rather see my patients eating a meal replacement than skipping a meal. Meal replacements also promote portion control. Not least, meal replacements are cheap - costing as little as a couple of dollars per meal.

Because I have seen this strategy work over and over again, I was not at all surprised by the results of a recent randomised-controlled trial from John Hopkins (Baltimore), where a diet using portion-controlled meal replacements yielded significantly greater initial weight loss and less regain after 1 year of maintenance than a standard, self-selected, food-based diet in patients with type 2 diabetes (click here for abstract).

Obviously, this is not a strategy for people who "hate" meal replacements. And, like any weight-management strategy, it only works as long as you stick with it.

But for those who embrace it, using meal replacements to replace meals that they'd otherwise skip may prove a viable long-term strategy to regain control of their hypothalamus and their diet.

AMS

Are Obese People Fit to Parent?

Yesterday's headline in the Toronto Star was about a case where an Ontario family court judgment cited obesity as a reason for removing a child from the parental home, after determining the mother was contributing to her child's weight gain and was oblivious to the required medical regime. The article cites other cases where obesity was a factor in rulings regarding parenting and foster care. (Click here to read the article)

The question is: can parents, who are actively contributing to their child's excessive weight gain or are not doing enough to ensure a healthy eucaloric diet, be accused of chid abuse or neglect?

My take on this is that the situation is probably no different from other circumstances, where parents are endagering the health of their children by exposing them to potential health risks (e.g. passive smoking, not using a child seat, etc.).

Obviously the rulings will have to depend on the extent of the actual risk. Clearly, there is a substantial difference between feeding your otherwise healthy active child the occasional French fry versus letting your child with a peanut allergy enjoy a couple of nuts.

I do not envy the folks, who have to make these rulings and are called upon to decide where the limit is of what is acceptable parental discretion and what constitutes abuse or neglect.

In the end however, there is no special case for obesity - it needs to be treated like any other condition based on the actual risk to the child and on the extent to which the parental behaviour is deemed a significant contributor.

Tough call - I am glad that it is not mine to make.

AMS

Is Obesity Critical in Critical Care?

Although obesity is now well-recognized as a risk factor for the development of many chronic diseases, its role in acute situations is less clear.

So while one might assume that severe obesity in critical ill patients is a predictor of poor outcomes, this hypothesis was not confirmed in a recent meta-analysis of studies comparing outcomes in obese (BMI > 30 kg/m2) critically ill patients in intensive care settings published by Akinnusi and colleagues from the University of Buffalo School of Medicine in the January issue of Critical Care Medicine (for Abstract click here).

Fourteen studies with 15,347 obese patients met inclusion criteria. Surprisingly, obesity was not associated with an increased risk of intensive care unit mortality, albeit duration of mechanical ventilation and intensive care unit length of stay were statistically but not remarkably longer in the obese group.

Interestingly, in a subgroup analysis, an improved survival was observed in obese patients with body mass index ranging between 30 and 39.9 compared with nonobese patients (relative risk, 0.86; 95% Cl, 0.81-0.91; p < .001). This latter finding is reminiscent of the "obesity survival paradox" alluded to in previous blogs.

Clearly, obesity is not a significant risk factor for poor survival outcomes in critical care. Whether or not this also applies to the subset of extremely obese patients that are now increasingly seen in hospital settings remains to be seen.

AMS