With two-thirds of the population now overweight or obese, we must accept that primary prevention has failed, the obesity horses are out of the the barn, there is no longer any point in locking the doors.
Rather, it’s now time to move on to secondary prevention; so let’s round up a posse and chase after the horses to catch them before they gallop off a cliff.
In developed countries around the world (including the US), we are beginning to see rates of overweight and obesity leveling off. This is not because these countries have now implemented strict measures to prevent obesity or to be taken as evidence that any such measures are working. I believe that the leveling off in the rates of overweight and obesity simply means that everyone in the Western world, who can be overweight or obese is now overweight or obese. The remaining third, that still has a normal weight, is overweight resistant and will never become obese, so let’s stop worrying about them.
Epidemiologists know, that in every epidemic comes a time when everyone who can be affected is affected. Even during the worst flu epidemic, a significant number of people will not come down with the flu no matter how much they are sneezed on or or how close they live to those who are affected. Yes, they may even have the virus circulating in their blood, but will yet have no sign of clinical disease nor will they develop it.
Obesity is no different. We are all exposed to the same societal factors that drive obesity. We are all surrounded by food (mostly unhealthy), we are all deprived of sleep, we all have sedentary jobs, we are all short of time, less than 5% of us eat the recommended diets or receive the recommended amount of daily activity. So why are we not all overweight or obese?
Because some of us are simply obesity resistant. For whatever reason (genetics, different metabolisms, distinct gut bugs, more brown fat, exercise addiction, etc.), some of us are either simply not obesity prone or are managing well to keep it at bay. Even if circumstances were to become more obesogenic, this proportion of our population would still not gain substantial amounts of weight – they are either truly (genetically) resistant, or would simply double their efforts to ward off those unwanted pounds – these people (I often refer to them as the “mutants”) will simply never become obese baring a catastrophe (e.g. an immobilising injury or illness, being put on an obesogenic drug, post-traumatic stress, severe depression, losing their income, etc.).
These are not the people we need to worry about. Educating them about the merits of eating healthier or being more active is a waste of time and resources – they are already eating just fine (or are resistant to their junk food diets) and are already getting plenty of exercise (or simply don’t need exercise because they are “natural-born” fidgeters). Any dollar spent on educating or incentivising them (e.g. tax breaks) is a dollar wasted.
Rather, it is now time to switch gears, time to call a spade a spade, and time to move on to secondary prevention. As my epidemiologist colleagues are well aware, in contrast to primary prevention, secondary prevention is not about preventing anyone from getting the condition; it is about ensuring that the problem does not get worse in the people who already have the problem.
Normally, in secondary prevention, you focus your efforts solely on the people who have the problem. However, when two-thirds of the population have it, you may as well treat the whole population, because making exceptions for those who don’t have the problem may simply not be practical. When most people have iodine deficiency, supplementing foods with iodine makes sense, even if this means that some people who do not need more iodine will get more iodine (thereby slightly increasing their risk for hyperthyroidism).
But moving to secondary prevention also means using different and more intense interventions. Thus in the secondary prevention of heart attacks, it is no longer simply enough to cut out the salt and add 20 mins of exercise to your day. After that first heart attack, you definitely want to make sure that your blood pressure and cholesterol levels are well controlled, even if this means increasing your dose of medications. And we are no longer talking about smoking less – no, after that heart attack, smoking is an absolute “no-no”.
Similarly, in the secondary prevention of obesity, simply eating more fruit and vegetables or walking more steps will not be enough. It is likely going to take far more drastic changes to your diet and to your activity levels to halt progression or reverse your condition. Effective weight management is neither easy nor simple (if it was simple for you, you’d be in the weight-resistant category in the first place). Now that you already have the problem, you will need special attention, special dedication, perhaps even special treatments to stop gaining more weight and hopefully lose some of that excess weight and keep it off. To some readers, secondary prevention may sound much more like treatment than prevention – this is because secondary prevention is in fact far closer to treatment than prevention.
Indeed, moving to secondary prevention requires a drastic rethinking in how we address the overweight and obesity epidemic at a population level. The question no longer is, how to help thin people stay thin. The question now is, how to help overweight and obese people not gain any more weight and perhaps receive treatments that will help them lose some of that excess weight and keep it off.
This may still mean we need to rebuild our neighbourhoods, deal with food insecurity, improve our diets, promote physical activity, and everything else that we should have done years ago at the first sign of the epidemic. But, because today we should no longer be worrying about primary prevention (which may have been easier had we actually done it), we will need far greater resolve and efforts to support far more radical changes at a societal level (not dissimilar the lengths we go to to remove peanuts from schools) to begin seeing clinically significant changes in weight at a population level – I purposely use the term “clinical”, because we now talking of disease control rather than disease prevention.
Skeptics may ask, “But what about the children? Is there not still time for primary prevention there?” To them my answer is that I do not for an instant believe that we will make a dent in the childhood obesity epidemic without first (or at least concurrently) addressing adult obesity (see previous post on this). Thus, probably the best primary prevention for childhood obesity simply takes us back to more secondary prevention for their parents.
Simply distributing more condoms in a population where most people already carry HIV is a waste of perfectly good condoms. It’s now time to put the anti-retrovirals in the drinking water.