Obesity

Spotlight article

Obesity’s Origins May Extend Beyond Human Genetics

Authors of a review examining the evolutionary origins of obesity argues that no single theory adequately explains today’s epidemic. Earlier models include the “thrifty genotype” hypothesis, which proposes that efficient energy storage once supported survival during food scarcity; the “drifty” hypothesis, which attributes susceptibility partly to relaxed evolutionary pressure against higher body weight; and the thermogenic-capacity hypothesis, which considers adaptations to different climates and energy-expenditure demands. The authors also propose a newer “metaflammation” hypothesis: genetic variants that historically strengthened immune defenses against infectious disease may, in modern environments, contribute to chronic low-grade inflammation, insulin resistance, altered energy expenditure, and greater fat storage. These remain evolutionary hypotheses rather than established explanations for individual obesity risk.

 

The authors further argue that the gut microbiome should be incorporated into these models because microbial genes, host genetics, diet, environment, and immune signaling interact in ways that may influence metabolism and body weight. Human studies have identified differences in microbial diversity and composition associated with obesity, while microbial genetic variation has also been linked to body mass index. The authors propose that the microbiome may expand the host’s evolutionary and phenotypic variability and potentially modify “thrifty,” thermogenic, and metaflammatory pathways. Overall, obesity is presented as a highly polygenic, multifactorial condition shaped by human evolutionary history, environmental exposures, immune biology, and the gut microbiome, not by any single genetic or behavioral explanation.

 

Reference: Saad MJA, Santos A. The Microbiota and Evolution of Obesity. Endocr Rev. 2025 Mar 11;46(2):300-316. doi: 10.1210/endrev/bnae033.

Kristin Kamprath

MPAS, PA-C

Bariatric Surgery and Obesity Medicine Physician Associate, HCA Healthcare North Texas Division

Featured article

Obesity Care: Are Your Words Helping—or Hurting?

A June 2026 policy brief from The Obesity Society (TOS) emphasizes that the language clinicians use when discussing obesity can shape trust, treatment engagement, healthcare experiences, and willingness to seek care. TOS recommends using person-first, non-stigmatizing, scientifically accurate language that recognizes obesity as a complex, chronic, relapsing disease influenced by biological, environmental, social, and behavioral factors. The brief advises eliminating terminology that assigns blame or shame and instead using respectful, strengths-based communication that supports dignity and individualized care.

 

TOS also calls for broader efforts to reduce weight bias across healthcare, research, education, media, and policy, including bias-reduction training and greater attention to stigma in quality measures. One specific terminology change is to use “obesity medications” rather than “anti-obesity medications,” which TOS says can reinforce adversarial or stigmatizing framing. For clinical physician associates and nurse practitioners, the practical takeaway is that word choice is part of patient care: respectful communication can strengthen the therapeutic relationship, while stigmatizing language may contribute to reduced trust, delayed care, and poorer healthcare experiences.

 

Reference: The Obesity Society. Speaking the Language of Obesity: Guidance for Obesity-Related Conversations, Research, Education, and Publications. The Obesity Society. Published June 2026. Accessed August 25, 2026. https://www.obesity.org/wp-content/uploads/2026/06/M154_B_PolicyBrief_EWS_260602.pdf

Angela Ritten

DNP, ARNP, FNP-BC

Ketogenic Diet for Obesity: Long-Term Benefits Remain Uncertain

Authors of a review examining ketogenic diets (KDs) for obesity management suggest that carbohydrate restriction sufficient to produce nutritional ketosis may support weight loss through several mechanisms, including reduced appetite and energy intake, lower insulin exposure, increased fat oxidation, and decreased consumption of ultra-processed foods. Unlike a general low-carbohydrate diet, a therapeutic KD typically restricts carbohydrates to less than or equal to 50 g/day, although considerable variation exists across ketogenic protocols. Studies reviewed reported favorable changes in weight and metabolic measures, but differences in diet composition, ketone monitoring, study duration, and outcome measures make direct comparisons difficult.

 

For clinical practice, sustainability and safety remain important uncertainties. Potential concerns include loss of fat-free mass, effects on bone and renal health, low fiber intake and microbiome changes, and possible endocrine effects. This underscores the need for individualized patient selection, adequate protein and nutrient intake, and ongoing monitoring. Adherence may be supported by appetite suppression and improved eating behaviors, but long-term data on sustained weight loss remain limited. The authors conclude that properly implemented KDs have potential as a weight-management strategy, while emphasizing the need for larger, longer studies with standardized dietary protocols, consistent ketone and body-composition monitoring, and better assessment of long-term metabolic health and adherence.

 

Reference: Bachar A, Birk R. Ketogenic diet intervention for obesity weight-loss—a narrative review, challenges, and open questions. 2025 Mar 8;14:43. doi: 10.1007/s13668-025-00634-3.

HoChong Gilles

DNP, FNP-BC

Obesity: Is BMI Alone Enough?

A Lancet Diabetes & Endocrinology Commission proposes moving beyond body mass index (BMI) alone to distinguish clinical obesity from preclinical obesity. BMI remains useful for screening, but the Commission recommends confirming excess adiposity with at least one additional anthropometric measure—such as waist circumference, waist-to-hip ratio, or waist-to-height ratio—or direct body-fat measurement when available. Clinical obesity would then require evidence that excess adiposity is causing organ or tissue dysfunction, significant limitations in daily activities, or both. In contrast, preclinical obesity describes confirmed excess adiposity with preserved organ function, although affected individuals may still have increased risk of developing clinical obesity or other obesity-related diseases.

 

The distinction could change both assessment and treatment goals. Patients with clinical obesity should receive timely, individualized, evidence-based care aimed at improving or achieving remission of obesity-related clinical manifestations and preventing end-organ damage, not simply reaching a predetermined amount of weight loss. Patients with preclinical obesity generally require risk assessment, counseling, screening, and longitudinal monitoring, with more intensive interventions considered according to individual risk and coexisting conditions. The Commission also cautions clinicians to use differential diagnosis because organ dysfunction included in the proposed criteria is not specific to obesity and other causes should be reasonably excluded.

 

Reference: Rubino F, Cummings DE, Eckel RH, et al. Definition and diagnostic criteria of clinical obesity. Lancet Diabetes Endocrinol. 2025 Mar;13(3):221-262. doi: 10.1016/S2213-8587(24)00316-4. Epub 2025 Jan 14. Erratum in: Lancet Diabetes Endocrinol. 2025 Mar;13(3):e6. doi: 10.1016/S2213-8587(25)00006-3.

Kristin Kamprath

MPAS, PA-C

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