If you have diabetes or are at risk for it, you've probably heard conflicting advice about what to eat. Cut carbs. Count calories. Avoid processed foods. But why is there so much disagreement? The answer lies in a fascinating scientific debate about how weight gain actually works—and understanding this debate can help you make better decisions for your metabolic health.
Since 1975, worldwide obesity rates have tripled, and type 2 diabetes has followed a similar trajectory. Despite decades of public health campaigns urging people to "eat less and move more," the problem keeps getting worse. This has led researchers to question whether we truly understand what drives weight gain and metabolic disease.
Two competing scientific models are at the center of this debate, each with profound implications for how we think about diabetes prevention and management.
The Traditional View: The Energy Balance Model
The Energy Balance Model (EBM) has dominated nutrition science since the 1950s. Its core principle is straightforward: weight gain occurs when you consume more calories than you burn. Think of your body like a bank account—if deposits exceed withdrawals, your balance grows.
This model has evolved significantly over time. Modern proponents acknowledge that not all calories are created equal. A hundred calories from sugary soda affects your body differently than a hundred calories from chicken breast. However, EBM supporters maintain that total calorie intake remains the most important factor for weight management.
How the EBM Explains Modern Obesity
The updated Energy Balance Model points to ultra-processed foods as the primary culprit behind rising obesity and diabetes rates. These foods—think chips, cookies, frozen dinners, and sugary beverages—are:
- Inexpensive and convenient
- Packed with calories in small volumes
- Engineered to be hyperpalatable (intensely pleasurable to eat)
- Potentially addictive, activating brain reward centers similar to opioids
Research shows these foods may literally rewire your brain. Mouse studies have demonstrated that high-fat diets can alter neural pathways, causing the brain to prefer and actively seek out these foods. This emerging science on gut-brain interactions helps explain why it's so difficult to resist processed foods once you start eating them.
Supporting the EBM, studies comparing high-carbohydrate, low-fat diets to low-carbohydrate, high-fat diets show negligible differences in weight loss when calories are controlled. This suggests that total calorie intake matters more than macronutrient composition.
The Problems with This Model
Despite its dominance, the EBM faces serious criticism. Harvard Medical School professor David Ludwig and science journalist Gary Taubes argue that:
It hasn't worked: Decades of "eat less, move more" messaging haven't reduced obesity rates
It's descriptive, not explanatory: The model describes what happens (calorie imbalance) but not the underlying physiological mechanism driving it
Studies may be too short: Many feeding studies last only weeks or months, potentially missing long-term metabolic adaptations
It's too complex to be useful: With so many variables, the model struggles to generate clear, testable hypotheses or practical interventions
The Alternative View: The Carbohydrate-Insulin Model
The Carbohydrate-Insulin Model (CIM) flips conventional thinking on its head. Instead of overeating causing weight gain, the CIM proposes that something about modern food—specifically high-glycemic carbohydrates—hormonally programs your body to store fat, which then drives overeating.
This is particularly relevant for people with diabetes or prediabetes, as it centers on insulin—the hormone you're already familiar with.
How the CIM Works
According to this model, here's what happens when you eat high-glycemic carbohydrates (white bread, white rice, sugary foods, potatoes):
Blood sugar spikes rapidly: These foods break down quickly into glucose
Insulin surges: Your pancreas releases large amounts of insulin to manage the glucose
Energy gets locked away: High insulin levels signal your liver and muscles to store glucose, with excess converted to triglycerides and stored in fat cells
Fat burning stops: When insulin is elevated, your body cannot readily access stored fat for energy
Hunger increases: With energy locked in storage, your brain perceives an energy shortage and signals hunger, driving you to eat more
The CIM frames obesity as a "calorie distribution problem" rather than simply an overconsumption problem. Your body is storing too much energy in fat tissue and not making it available for use, creating a vicious cycle.
For people with type 2 diabetes, this model resonates because insulin resistance—a hallmark of the condition—means your body needs to produce even more insulin to manage blood sugar, potentially worsening the fat storage problem.
Why Scientists Are Skeptical
Despite its intuitive appeal, the CIM faces significant scientific challenges:
The cultural contradiction: Many populations consume high-carbohydrate diets but have low obesity rates. The Kitavans of Papua New Guinea eat a diet of 70% carbohydrates, mostly from sweet potatoes and fruit, yet obesity is virtually non-existent. Japan's traditional high-rice diet correlated with low obesity rates for decades.
Glycemic index doesn't matter much: Studies show that low-glycemic diets aren't significantly better for long-term weight loss than higher-glycemic diets when calories are equal.
Animal studies refute it: Surprisingly, mice on high-glycemic diets actually ate fewer calories and gained less weight despite higher insulin levels—the opposite of what the CIM predicts.
The missing phase: The CIM proposes a "dynamic phase" of obesity development where blood glucose and fatty acids are reduced, but this phase has never been observed in actual studies.
Genetic evidence points elsewhere: Research suggests genes influencing body weight are more related to brain function and appetite regulation than insulin signaling or fat cell metabolism.
Moving goalposts: The latest version of the CIM has backed away from its central claim that insulin action on fat cells drives hunger and weight gain, instead proposing a vague "integrated, multiorgan, multihormone" explanation that lacks clear mechanisms.
Where Does This Leave Us?
In 2022, top obesity researchers gathered at a Royal Society meeting to discuss these competing models. The honest conclusion? The science remains uncertain. Both camps called for more research—better studies to understand obesity mechanisms and longer, better-funded trials of different dietary approaches.
Interestingly, the two sides are moving closer together. Most researchers now acknowledge that both the amount and type of calories likely play important roles in weight gain and metabolic health.
What This Means for Your Diabetes Management
While scientists debate mechanisms, several practical truths have emerged that can guide your daily decisions:
Ultra-Processed Foods Are the Real Problem
Both models agree: ultra-processed foods are strongly associated with obesity, type 2 diabetes, and metabolic disease. These foods are engineered to override your natural satiety signals, making it easy to overconsume calories. Minimizing processed foods and focusing on whole foods—vegetables, fruits, whole grains, legumes, nuts, seeds, fish, and lean meats—is one of the few universally agreed-upon recommendations.
Blood Sugar Stability Matters
Whether or not insulin is the primary driver of weight gain, high insulin levels do prevent fat burning. For people with diabetes, maintaining stable blood sugar levels through balanced meals, adequate protein and fiber, and avoiding rapid glucose spikes supports both weight management and glycemic control.
The Foundations Still Work
Regardless of which model is correct, certain lifestyle factors consistently support metabolic health:
- Regular physical activity: Exercise improves insulin sensitivity, helps regulate appetite, and supports weight management
- Quality sleep: Poor sleep disrupts hormones that regulate hunger and blood sugar
- Stress management: Chronic stress elevates cortisol, which can worsen insulin resistance and promote abdominal fat storage
- Consistent meal timing: Regular eating patterns support metabolic rhythms and blood sugar control
Personalization Is Key
The debate between these models highlights an important truth: different approaches work for different people. Some individuals with diabetes thrive on lower-carbohydrate diets, experiencing better blood sugar control and easier weight management. Others do well on higher-carbohydrate diets that emphasize whole food sources.
Working with your healthcare team to find the approach that works for your body, preferences, and lifestyle is more important than adhering to any single dietary dogma.
The Bottom Line
The scientific debate about what drives weight gain and metabolic disease remains unsettled, but this uncertainty shouldn't paralyze us. The obesity and diabetes epidemics are urgent public health crises that demand action even as research continues.
What we know for certain is that the dramatic rise in ultra-processed food consumption parallels the rise in obesity and diabetes. We know that these foods are designed to be overconsumed. And we know that returning to a dietary pattern centered on whole, minimally processed foods consistently improves metabolic health outcomes.
Rather than waiting for scientists to settle their debate, focus on what you can control: choose real food over processed products, stay physically active, prioritize sleep and stress management, and work with your healthcare providers to monitor your blood sugar and overall metabolic health.
The perfect diet that works for everyone may not exist. But a diet built on whole foods, balanced nutrients, and sustainable habits can work for you—regardless of which scientific model eventually proves most accurate.
References
Ludwig, D. S., Aronne, L. J., Astrup, A., de Cabo, R., Cantley, L. C., Friedman, M. I., Heymsfield, S. B., Johnson, J. D., King, J. C., Krauss, R. M., Lieberman, D. E., Taubes, G., Volek, J. S., Westman, E. C., Willett, W. C., Yancy, W. S., Jr, & Ebbeling, C. B. (2021). The carbohydrate-insulin model: a physiological perspective on the obesity pandemic. The American Journal of Clinical Nutrition, 114(6), 1873–1885.
Hall, K. D., Guo, J., Courville, A. B., Boring, J., Brychta, R., Chen, K. Y., Darcey, V., Forde, C. G., Gharib, A. M., Gallagher, I., Howard, R., Joseph, P. V., Milley, L., Ouwerkerk, R., Raisinger, K., Rozga, I., Schick, A., Stagliano, M., Torres, S., Walter, M., … Chung, S. T. (2021). Effect of a plant-based, low-fat diet versus an animal-based, ketogenic diet on ad libitum energy intake. Nature Medicine, 27(2), 344–353.
