The Hidden Dangers of Appetite Suppression
And the real solution to obesity that most overlook
GLP-1 agonists have become mainstream. From an explosive excitement in 2022-2023, the use of Wegovy and similar drugs for weight loss has now been normalised to an extent where many people consider them a natural part of modern human life and a necessary tool for controlling bodyweight in the era of abundance.
It really seems as though humanity has finally found the root-cause solution to one of its major problems: obesity—and with it a potential cure for the swathe of debilitating chronic diseases that follow, at least partially, from this common cause. Users experience unparalleled improvements in life quality, and commentators predict wide societal benefits of what seems to be our final win against one of our greatest opponents in the modern era.
While one can only celebrate that this injection of hope has finally broken the coping mechanism that was the fat acceptance discourse and replaced it with the implicit recognition that being fat is undesirable, we should be wary of the long-term consequences of pharmacological appetite suppression.
There is no doubt that these drugs have been life-changing for many users, and the societal benefits of lowering obesity rates are unquestionable. Obesity is truly the root cause of many costly, chronic diseases.
But is it really so obvious that we should use pharmacology to treat something that used to be recognised as the result of lifestyle?
And do we understand the role of appetite in human health sufficiently well to conclude that the clinical trials would have surfaced all relevant side effects of appetite suppressants? That the safety profile of these drugs is therefore well-elucidated?
Or should we pause our celebration for a moment and consider that our appetite perhaps—just perhaps—is there for a reason and that overriding it pharmacologically may produce unintended consequences in the long run?
To begin this investigation, it is useful to lay out the theories of appetite that could underpin a positive outlook for their suppression and which many commentators seem to subscribe to—implicitly or explicitly.
The Case for Appetite Suppression
Two theories of appetite are frequently raised to explain the modern obesity epidemic. They are:
- Our appetite is poorly adapted to a life of abundance
- Our appetite can handle abundance but not hyper-palatable, ultra-processed foods
The first argument goes roughly as follows: Human beings evolved under conditions of scarcity. Food availability was unreliable and unpredictable. As a result, we evolved to pursue a hypercaloric diet whenever food was available so we could survive starvation when it was not. Today, food is always abundant, and we are therefore trapped in an unrelenting biological drive towards over-eating and weight gain.
Under this premise, GLP-1 agonists are the obvious and even necessary solution. If our bodies have no endogenous mechanism for regulating food intake, we must impose it exogenously. Historically, the exogenous regulator was food availability. With this environmental guardrail removed, we must replace it with a pharmacological one. Appetite suppressants are merely helping the body navigate in conditions it never had the chance to adapt to.
The second theory is similar in spirit but puts the blame on food engineering specifically rather than food availability itself. It holds that we do, in principle, have the capacity for regulating our food intake but that modern, hyper-palatable, ultra-processed foods are designed to circumvent this mechanism. If they make up any significant part of the diet, therefore, our tendency will be to eat more food than we truly need.
Under this premise, GLP-1 agonists are a protection not against the fundamental dysfunction of the human body but of deliberate attempts at tricking or hacking its biological wiring. We do not truly need to eat as much as we do, but we cannot help ourselves because we are surrounded by food that is so addictive. We fight fire with fire: We meet engineered addiction with pharmacological self-control.
These two theories differ in their degree of damnation of the human body, but they agree on an important conclusion and prediction: Our hunger drive is stronger than it should be in our environment, so we eat more than we need to. Pharmacologically induced satiety merely restores the balance.
Both theories imply that there is no reason to suspect harmful side effects of appetite suppression as such, since our excess food intake is clearly unnecessary for health. There may be side effects of particular drugs used to achieve appetite suppression, as for drugs used for any other purpose, so the challenge is merely to engineer a compound that suppresses appetite with minimal non-specific effects. A drug that affects appetite and appetite only would be the golden bullet we need.
But what if the greatest risk from pharmacological appetite suppression comes not from the potential side effects of the drugs themselves but from the thing that makes them successful: Getting us to eat less? What if there is a good reason why many people feel ravenously hungry and end up eating more than they seemingly need? What if this is a rational response to our environment rather than a maladaptation? What if appetite suppressants could, therefore, cause more harm than good—not despite their effectiveness towards appetite control and weight loss but because of it?
An Alternative Theory of Appetite
I propose a theory of human appetite that frames it not as an outdated mechanism adapted to a different age (theory 1), nor something we can trick and circumvent (theory 2), but as a rational protector of bodily needs under any and all conditions—though one we can decide to misinterpret.
This theory predicts that we can satisfy our hunger without over-eating even in the modern environment, and that overriding it pharmacologically is a band-aid solution that may work in the short term but produces predictable undesirable side effects in the long term.
This theory starts from the premise that appetite exists to regulate our total nutritional needs, which goes beyond ensuring an adequate supply of energy. To maintain our bodily functions we need not only fuel to burn (carbohydrates and fat) but also building blocks (protein, minerals, and certain essential fatty acids), and various compounds that support the many biochemical processes involved in metabolism (vitamins).
From this vantage point, it seems that if our needs for essential nutrients are met (protein, essential fatty acids, vitamins, minerals), there should be little reason to accumulate body fat beyond a level that will secure an adequate supply of energy over such periods of scarcity as we would have had to deal with historically. There is hardly an evolutionary advantage to becoming ever more obese, even had the food supply made it possible.
In other words, given an adequate supply of essential nutrients, we should expect the body to have a so-called set point for body fat; an equilibrium body composition that we will tend to towards and which it would require persistent and ever-increasing effort to deviate from—both in the direction of fat loss and accumulation. Appetite would gradually increase when we eat below our energetic needs and decrease when we eat in excess of them. Any bodybuilder who has gone through a cycle of bulking and cutting will recognise this well.
At the same time, since appetite exists not only to regulate body composition but also to ensure that needs for essential nutrients are met, if the latter cannot be achieved at a food intake that keeps us at our natural set point, we should expect hunger to drive us to eat more than required for energy expenditure alone. This, I believe, explains the modern obesity epidemic.
Obesity and the Dangers of Appetite Suppression
If one’s diet contains an inadequate ratio of essential nutrients (protein, vitamins, minerals) to energy substrates (fat and carbohydrates), the body has no way to maintain its set point without facing nutrient deficiencies. Since the detrimental effects to health of deficiencies are probably greater than those of excess, the rational response and the optimal solution is to maintain hunger at a level that will ensure nutritional sufficiency, even though this sacrifices the set point and leads to fat accumulation.
The culprit is, of course, our modern, ultra-processed foods, such as seed oils, sugar, refined grains, and all the many junk foods and snacks made from them. But in contrast to theory 2 which defends pharmacological appetite suppressants as protectors against food engineering, I do not conclude that these foods lead us to eat more than we need. Rather, I hold that we eat exactly the right amount for that second purpose which many seem to ignore when discussing appetite—to satisfy our needs for essential nutrients—and that the only way to do this when junk food and snacks make up a significant part of our diet is to eat in excess of our energy needs.
This difference between my theory and theory 2 may sound subtle, but it has significant implications for the safety profile of suppressing one’s appetite via pharmacological intervention. If processed foods lead to superfluous food intake, i.e. a food intake in excess of our needs, then suppressing it is presumably harmless—you simply bring your intake back to what it should be. But if the excess energy intake that comes from including processed foods in one’s diet is driven by the body’s real need for essential nutrients, then reducing that intake must inevitably lead to such needs being increasingly unmet—nutritional deficiency.
This, then, is my prediction. If human appetite is neither dysfunctional nor circumvented by food engineering, but protects us against malnutrition in a nutrient deficient environment, then suppressing this appetite may eventually cause more harm than good. We may break the obesity curve for a while, but we could be substituting it for a plethora of diseases with pharmacologically induced nutrient deficiencies as their common cause.
The real solution to obesity is not pharmacological intervention but a return to a diet that is satiating and therefore must be nutritious. Any food item that one can continue to eat, seemingly without bounds, or which satisfies you for no more than a few hours, is a food item to be avoided, for it does not provide you with the nutrients your body needs and it will push you away from your set point. The proof of the pudding is in the eating, as they say.