OPINION:
“I have more flesh than another man, and therefore more frailty.”
— Falstaff, “Henry IV, Part I”
The self-deprecating jest of Shakespeare’s Falstaff character resonates today, as excess “flesh” (i.e., obesity) has become emblematic of a deeper frailty in modern America. Approximately 88% of U.S. adults are metabolically unhealthy, grappling with obesity-derived conditions such as insulin resistance, hypertension and infertility. This isn’t merely a cosmetic concern; it’s a pressing public health crisis.
Unsurprisingly, in our search for answers, weight loss drugs have taken center stage. None more so than Ozempic and its GLP-1 agonist relatives. The mechanism is elegant: These drugs mimic glucagonlike peptide-1 (GLP-1), a hormone naturally released from the gut in response to food. Among the hormone’s many effects is that it acts on the brain to suppress appetite, particularly curbing cravings, a welcome ally in the modern war against overconsumption.
What do we overconsume? A 1996 study revealed that some people have a muted GLP-1 response to carbohydrate ingestion. This suggests that even when they eat carbohydrates, they don’t feel full the way others do. The result: persistent cravings and overeating, particularly processed carbohydrates, the kind that come in a bag or a box with a barcode.
These processed foods dominate the American plate. In fact, carbohydrates account for nearly 60% of daily caloric intake, with a significant portion coming from refined sources. Carbohydrates, not fat or protein, are the most commonly abused macronutrient. They are overconsumed not because of hunger but rather hedonic drive. GLP-1 agonists, then, may be best viewed not as weight loss drugs but as tools to retrain the brain’s response to carbohydrates. When used wisely, they can suppress those pathological cravings long enough for a person to reestablish control over their food environment and habits.
Unfortunately, current clinical practice is overcorrecting. Standard doses of GLP-1 drugs are aggressive. Although they certainly lower weight, they don’t discriminate. Indeed, roughly 40% of the weight lost on GLP-1 therapy is from fat-free mass, which includes muscle and bone. This carries long-term consequences: frailty and increased risks of falls and fractures, especially in older adults.
Mental health is another area of concern. Recent evidence indicates that patients on high-dose GLP-1 agonists experience increased rates of depression and suicidal ideation. Thus, at currently used doses, curbing cravings for carbohydrates may simply reflect a reduction in cravings for other things a person used to enjoy. To amplify this concern, even efficacy declines over time. After two years, many users report a full return of sweet cravings despite ongoing use of the drug. The satiety signal weakens, the neurochemical adaptations wear off, and the patient is left relying once again on willpower, a resource already proved insufficient in the current food landscape.
It doesn’t have to be this way.
Instead of treating GLP-1 drugs as a lifelong solution, we should consider them short-term, cyclical tools. Much like cognitive behavioral therapy, the goal is not indefinite pharmacological intervention but strategic use to retrain behavior.
We propose a model of “microdosing” GLP-1 agonists: using the lowest effective dose to suppress cravings, not to induce dramatic weight loss, and conducting regular clinical check-ins to assess control over carbohydrate intake. Patients could cycle off the drug once their habits stabilize. If carb cravings return, they could reinitiate treatment at the minimum dose necessary, maintaining metabolic progress without the side effects of chronic pharmacotherapy.
This approach aligns the tool with the target. It also honors the biology of GLP-1, respects the risks of overtreatment and centers the discussion where it belongs: not on weight but on metabolic function and food addiction, particularly to refined carbohydrates. The path to better metabolic health won’t be found in shrinking numbers on a scale alone but rather in reclaiming control over the most abused macronutrient in our modern diet. GLP-1 agonists have opened a door not just to appetite suppression but also to behavioral reset.
Still, tools are only as useful as the hands that wield them. These drugs should not be seen as permanent fixtures in a person’s life but rather as scaffolding, or temporary supports, while the more enduring structure of habit and self-regulation is built.
By using the lowest effective dose, monitoring responses to carbohydrate cravings and cycling treatment in a way that prioritizes long-term dietary change over short-term weight loss, we can avoid the pitfalls of muscle loss, mental health decline and eventual relapse.
Metabolic health is not a number; it’s a pattern of eating, moving and living that resists the tides of processed food culture. GLP-1 drugs, when used judiciously, can help people find that rhythm again. However, the goal must always be independence, not dependence.
• The authors are professors in the Department of Cell Biology and Physiology at Brigham Young University in Provo, Utah. To learn more, visit benbikman.com.
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