Metabolism is the set of biochemical processes that determine how efficiently the body converts food into energy, stores or mobilizes nutrients, and maintains homeostasis. The social claim that “two people eating the same amount” will “react totally different” aligns with well-established mechanisms: individuals vary in resting energy expenditure, diet-induced thermogenesis, substrate partitioning, gut physiology, and hormonal signaling. These differences mean that identical burger intake can yield different trajectories of fat storage, glycogen storage, insulin sensitivity, inflammation, and appetite-driven intake over time.
Resting metabolic rate (RMR) and total daily energy expenditure (TDEE) differ substantially between people. RMR reflects the energy cost of maintaining vital functions (cardiovascular work, thermoregulation, cellular turnover). It is influenced by lean body mass, genetics, age, sex, and endocrine status. Higher lean mass generally increases RMR because muscle is metabolically active compared with fat. Conversely, reduced lean mass from sedentary behavior or illness can lower RMR, shifting the energy balance toward storage even when perceived dietary intake is similar.
Diet-induced thermogenesis (DIT) describes the rise in energy expenditure after eating, driven by digestion, absorption, and nutrient processing. Protein typically produces a higher thermic effect than carbohydrates and fats. However, the magnitude of DIT varies with meal composition, habitual diet, gut microbiota, and adaptive metabolic responses. Some people show a stronger DIT response and therefore burn more energy after meals, while others experience less postprandial energy loss, increasing the likelihood of net positive energy balance.
Fuel partitioning—how nutrients are directed toward oxidation versus storage—also differs. Insulin signaling affects glucose uptake into muscle and adipose tissue and suppresses lipolysis. In insulin-sensitive individuals, carbohydrates are more likely to be used for energy storage (e.g., glycogen) and oxidation. In insulin-resistant states, a greater fraction may be stored as triglycerides, raising fat mass over time. Insulin sensitivity is modulated by genetics, visceral adiposity, sleep quality, stress hormones (notably cortisol), and physical activity patterns.
Exercise is often discussed as a universal solution, but its impact depends on compensatory behaviors. When people increase activity, they may unconsciously eat more (increased hunger or reward-driven intake) or reduce non-exercise activity thermogenesis (NEAT), such as fidgeting and routine movement. Additionally, “exercise helps” is true primarily by improving insulin sensitivity, increasing muscle mass over time, and raising energy expenditure; however, net effects depend on intensity, frequency, total energy intake, and adherence.
Non-exercise factors are particularly important. The gut microbiome can influence energy harvest from food and produce metabolites (e.g., short-chain fatty acids) that affect host metabolism and appetite regulation. Chronic stress and inadequate sleep can increase appetite via ghrelin/leptin dysregulation and elevate cortisol, promoting central fat deposition and impairing glucose tolerance. Medications such as antipsychotics and some antidepressants can contribute to weight gain through appetite changes and metabolic effects, including insulin resistance.
Genetic variation affects appetite, nutrient absorption, and metabolic pathways. Polymorphisms can influence energy expenditure, fat oxidation capacity, and signaling through pathways such as AMPK and mTOR that regulate cellular energy balance. While genetics is not destiny, it helps explain why “same quantity” does not guarantee “same outcome.”
The discussion of “fat jabs” likely refers to injectable weight-related treatments or metabolic therapies; regardless of the specific product, pharmacologic interventions work only when aligned with the individual’s physiology and goals. Modern evidence-based pharmacotherapy for weight management—such as incretin-based agents (GLP-1 receptor agonists and dual agonists)—can improve satiety, slow gastric emptying, and enhance insulin secretion, thereby reducing appetite-driven intake and improving metabolic markers. The effectiveness varies among patients due to differences in baseline insulin resistance, dietary patterns, and adherence. Importantly, these therapies are not interchangeable with lifestyle changes; they are typically adjuncts requiring monitoring for adverse effects.
Finally, time horizon matters. Acute meal responses (blood glucose, insulin, postprandial lipemia) may differ even if long-term weight change appears similar. Over months, small differences in energy balance compounded by metabolic adaptations—like changes in RMR and NEAT—can lead to divergent fat gain patterns. Therefore, education should focus on personalized assessment: body composition, dietary pattern, activity and sleep, metabolic health (waist circumference, HbA1c, lipid panel), and medication review.
In summary, metabolism is not a single trait but an interactive system determining how energy intake becomes energy expenditure, nutrient oxidation, and fat storage. Identical portions can produce different outcomes due to inter-individual differences in RMR, DIT, hormonal regulation, insulin sensitivity, gut microbiota, genetics, and compensatory eating or movement. Consequently, “metabolism matters” is an oversimplification only in tone; mechanistically, it is highly accurate.
Source: @mikepriestley13 (from the provided X post)
MIKE!: Alison is right, if she ate 2 burgers and Tom ate 2 burgers it would react totally different to both of them… metabolism has a lot to do with it.. people will say exercise helps, not always.. if it was there wouldn’t be a need for fat jabs to be available #ThisMorning. #breaking
— @mikepriestley13 May 1, 2026
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