Obesity Shows Minimal Energy Change from Acute Cold
In recent years, cold exposure has emerged as a popular topic within the realms of weight management and metabolic health, often hailed as a natural and accessible method to enhance energy expenditure and curtail appetite. The theory underpinning this interest revolves around the body’s physiological response to cold stimuli, which may stimulate thermogenesis—the process of […]

In recent years, cold exposure has emerged as a popular topic within the realms of weight management and metabolic health, often hailed as a natural and accessible method to enhance energy expenditure and curtail appetite. The theory underpinning this interest revolves around the body’s physiological response to cold stimuli, which may stimulate thermogenesis—the process of heat production in organisms—and theoretically lead to increased calorie burning. However, whether acute cold exposure translates into meaningful changes in both energy intake and expenditure, especially among individuals living with obesity, has remained an unresolved question. A groundbreaking 2025 study by McInnis et al., published in the International Journal of Obesity, rigorously examines this precise issue, unveiling findings that challenge some of the prevalent assumptions about cold exposure’s role in weight control.
The human body’s response to cold is complex and multifaceted, involving an interplay of systems aimed at preserving core temperature. Traditionally, this response is characterized by shivering thermogenesis, where muscle contractions generate heat, and non-shivering thermogenesis, primarily orchestrated by brown adipose tissue (BAT). BAT, abundant in infants and present to a lesser extent in adults, is metabolically active and can increase energy expenditure by oxidizing fatty acids and glucose. This mechanism initially suggested cold exposure as a promising strategy to combat obesity. However, comprehensive data on how acute cold exposure influences the entire energy balance—considering both energy expenditure and appetite-driven energy intake—has been conspicuously scant.
McInnis and colleagues addressed this crucial gap by enrolling individuals living with obesity into a controlled experimental setup, where acute cold exposure protocols were applied while meticulously monitoring changes in metabolic parameters. Their sophisticated approach involved indirect calorimetry to measure resting energy expenditure, activity monitors to control for physical movement, and precisely quantified dietary intake assessments pre- and post-exposure to cold environments. This multi-modal and objective methodology allowed for a nuanced evaluation of how the challenges posed by cold translate into physiological and behavioral changes.
Contrary to the expectation that cold exposure would robustly increase caloric burn and suppress appetite, the study revealed that the acute cold stimulus led to only marginal modulations in total energy expenditure among participants living with obesity. These findings suggest that the thermogenic response in this population might be blunted or less responsive than previously thought, potentially due to variations in brown fat activity or other metabolic adaptations linked with obesity. This nuance is essential because it indicates that cold-triggered thermogenesis alone may not constitute a potent weight loss strategy for all individuals.
Furthermore, the researchers observed minimal impact on energy intake following cold exposure sessions. Appetite regulation is governed by a highly integrated network of hormonal signals and neural pathways, often influenced by environmental cues and metabolic status. The anticipated anorexigenic effect—that is, the reduction of hunger and decreased food consumption—was not significantly evident in the study participants. This challenges the notion that brief encounters with cold temperatures could serve as a practical means to limit caloric intake, at least in the context of obesity.
One possible explanation for the muted appetite response lies in the complexities within central appetite control centers in the brain, such as the hypothalamus, which integrate peripheral signals including leptin, ghrelin, and other gut hormones. Obesity is known to alter the sensitivity and signaling dynamics within these pathways, potentially blunting hunger suppression triggered by diverse stimuli. Hence, while cold exposure might elicit a physiological stress response capable of increasing energy demands, the corresponding behavioral adaptation in terms of reduced food intake may be impaired.
The study also highlights the importance of considering individual variability in the metabolic response to cold. Not all bodies react uniformly to environmental stressors, and genetics, body composition, and prior cold acclimatization might modulate the effectiveness of cold as a metabolic stimulant. For instance, lean individuals with higher brown fat activity may demonstrate more pronounced increases in energy expenditure and appetite changes compared to their obese counterparts.
From a methodological standpoint, the research exemplifies rigor by addressing potential confounders such as physical activity levels, circadian influences, and ambient temperature control, which often cloud interpretation in studies of energy metabolism. The controlled acute cold exposure sessions ensured that observed outcomes were indeed attributable to cold stimuli rather than extraneous factors, reinforcing the validity of the conclusions.
Beyond the immediate findings, this investigation raises important questions about the long-term applicability of cold exposure in weight management protocols. While acute interventions may have limited effects, chronic or repeated cold exposure might induce adaptive changes, potentially enhancing brown fat activity or modulating energy homeostasis. Future longitudinal studies will be critical to unravel these possibilities and to identify whether specific cold exposure regimens could be harnessed effectively.
Moreover, the study refocuses attention on the multifactorial aspects of obesity treatment, underscoring that simplistic solutions such as cold exposure alone are unlikely to suffice. Obesity is a complex, systemic condition influenced by genetics, environment, physiology, and behaviors. Effective interventions will likely necessitate holistic strategies addressing diet, physical activity, psychological health, and possibly metabolic modulation.
Importantly, McInnis et al.’s findings inject a note of caution into the enthusiasm surrounding cold exposure as a “quick fix” for weight loss. Marketing narratives and popular media often emphasize the perceived ease and immediacy of cold-induced fat burning. This study urges the scientific community and the public to critically appraise such claims and recognize the nuanced realities revealed by empirical data.
The minimal changes in energy expenditure and unaltered appetite observed in individuals living with obesity during acute cold exposures also prompt a reevaluation of the mechanisms underlying metabolic dysfunction in obesity. It suggests possible impairments in thermogenic pathways and appetite regulation that extend beyond mere excess adiposity, warranting deeper mechanistic research at cellular and molecular levels.
Furthermore, this research contributes to the broader understanding of human adaptive physiology. The ability to maintain energy balance via thermoregulation is critical for survival, and understanding its modulation in pathological states such as obesity informs both clinical practice and evolutionary biology paradigms. Insights from such studies may guide novel therapeutic avenues, including pharmacologic or lifestyle interventions designed to sensitize thermogenic tissues or recalibrate appetite control circuits.
In conclusion, while the potential of cold exposure to influence weight control remains an intriguing concept, the 2025 study by McInnis and colleagues firmly establishes that acute cold exposure exerts only minimal impact on energy intake and expenditure in individuals living with obesity. This nuanced perspective reshapes ongoing conversations and future research directions in obesity management and metabolic health. It advocates for a balanced view grounded in scientific evidence, tempered enthusiasm for quick solutions, and a commitment to exploring comprehensive, individualized approaches in tackling the obesity epidemic.
Subject of Research: Energy intake and energy expenditure responses to acute cold exposure in individuals living with obesity.
Article Title: Energy intake and energy expenditure are minimally impacted by acute cold exposure in individuals living with obesity.
Article References:
McInnis, K., Larocque, A., Beauregard, N. et al. Energy intake and energy expenditure are minimally impacted by acute cold exposure in individuals living with obesity. Int J Obes (2025). https://doi.org/10.1038/s41366-025-01809-2
Image Credits: AI Generated
DOI: https://doi.org/10.1038/s41366-025-01809-2
Tags: acute cold exposure effectsappetite regulation and coldbrown adipose tissue functioncalorie burning through cold exposurecold exposure and weight managementenergy expenditure and cold stimuliInternational Journal of Obesity study findingsmetabolic health and obesityphysiological response to coldshivering and non-shivering thermogenesisthermogenesis in obesityweight control mechanisms
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