Body weight

BMI is the standard measure in population studies because it needs only a scale and a height measurement. Its limits are well known: two people with the same BMI can differ widely in muscle mass and in the amount of fat stored around the abdominal organs (visceral fat). Diabetes also occurs at lower BMI in some groups, and US screening guidance uses a BMI of 23 rather than 25 as the threshold for Asian American adults [1].

Waist circumference measures fat around the abdomen. A pooled analysis of 11 studies of 650,386 white adults aged 20 to 83, followed for a median of 9 years, found a strong linear association between waist size and all-cause mortality (death from any cause) after accounting for BMI, smoking, alcohol and physical activity. Men with a waist of 110 cm or more had a hazard ratio (the risk in one group relative to another; 1.52 means 52% higher) of 1.52 compared with men under 90 cm, and women with a waist of 95 cm or more had a hazard ratio of 1.80 compared with women under 70 cm. Each 5 cm increase was associated with 7% higher risk in men and 9% in women, at every BMI from 20 to 50, and the association was stronger for heart and respiratory disease than for cancer [4].

The Prospective Studies Collaboration pooled 57 studies, mostly from western Europe and North America, and excluded the first 5 years of follow-up to limit the effect of illness causing weight loss. Above a BMI of about 25, each 5-unit higher BMI was associated with about 30% higher overall mortality (hazard ratio 1.29, 95% CI 1.27 to 1.32), 40% higher vascular mortality and 60 to 120% higher mortality from diabetes, kidney and liver disease. The authors judged the excess mortality above this range to be mainly due to vascular disease and probably largely causal [3].

The Global BMI Mortality Collaboration analysed 239 studies of 10.6 million people on four continents and restricted its main analysis to 3,951,455 never-smokers without chronic disease at recruitment. Mortality was lowest at a BMI of 20 to 25 and rose throughout the overweight range, with hazard ratios of 1.45 for obesity grade 1 (BMI 30 to 35), 1.94 for grade 2 (35 to 40) and 2.76 for grade 3 (40 to 60). The increase per 5 BMI units was larger in men than in women and larger when BMI was measured at ages 35 to 49 than at ages 70 to 89 [8]. In UK primary care records of 3.6 million adults, life expectancy at age 40 was 4.2 years shorter in men and 3.5 years shorter in women with obesity than in those of healthy weight [2].

Excess weight also raises the risk of the diseases through which it shortens life. In 18 prospective studies, adults with obesity had 7.19 times the risk of type 2 diabetes of normal-weight adults [10]; the metabolic effects are described under metabolic health and type 2 diabetes, and the effects on the heart under cardiovascular disease and blood pressure.

Low body weight is also associated with higher mortality. Among never-smokers in the Global BMI Mortality Collaboration, the hazard ratio was 1.13 at a BMI of 18.5 to 20 and 1.51 at 15 to 18.5 [8]. In the UK study, life expectancy at age 40 was 4.3 years shorter in underweight men and 4.5 years shorter in underweight women than in people of healthy weight, and the BMI with the lowest risk was higher in older than in younger adults [2]. In the Prospective Studies Collaboration, the excess mortality below a BMI of 22.5 was mainly from smoking-related diseases and was stronger in smokers, and the authors noted it was not fully explained [3].

In older adults low weight often reflects loss of muscle, which is itself associated with mortality. In the PURE study of 139,691 adults aged 35 to 70 in 17 countries, each 5 kg lower grip strength was associated with 16% higher all-cause mortality, and grip strength predicted death more strongly than systolic blood pressure [12]. Muscle loss with age is described under muscle mass.

Physical fitness changes the mortality risk associated with body weight. A meta-analysis (a study that pools the results of earlier studies) of 10 prospective studies that measured both fitness and BMI found that unfit adults had about twice the mortality of fit, normal-weight adults regardless of BMI, while fit adults who were overweight or had obesity had mortality similar to fit, normal-weight adults [5]. Fitness is described under VO2 max. The finding concerns mortality only, and excess weight remains strongly associated with diabetes [10].

The length of time spent with obesity also matters. Among 5,036 participants of the Framingham Heart Study followed every 2 years for up to 48 years, and after adjustment for BMI, adults who had obesity for 1 to 4.9 years had 1.51 times the mortality of those never obese, rising to 1.94 for 5 to 14.9 years, 2.25 for 15 to 24.9 years and 2.52 for 25 years or more. Each additional 2 years with obesity was associated with 6% higher all-cause mortality and 7% higher cardiovascular mortality [11].

Modest weight loss has measurable effects on disease. In the Diabetes Prevention Program, 3,234 adults with raised glucose (mean BMI 34.0) were assigned to a lifestyle programme aiming for at least 7% weight loss and 150 minutes of weekly activity, to metformin, or to placebo; the lifestyle programme cut new cases of diabetes by 58% over an average of 2.8 years [6]. Diet composition affects how much is eaten: in an inpatient trial, 20 adults ate 508 more calories a day on an ultra-processed diet than on an unprocessed diet and gained 0.9 kg in two weeks, and lost 0.9 kg on the unprocessed diet [13]. Dietary approaches are described under dietary patterns.

Drug treatment now has evidence on cardiovascular outcomes. In the SELECT trial, 17,604 adults aged 45 or older with established cardiovascular disease and a BMI of 27 or more but no diabetes were assigned to weekly semaglutide, a GLP-1 receptor agonist (a drug that mimics a gut hormone that reduces appetite), or placebo. Over a mean of 39.8 months, the combined rate of cardiovascular death, heart attack and stroke was 6.5% with semaglutide and 8.0% with placebo (hazard ratio 0.80, 95% CI 0.72 to 0.90); 16.6% of the semaglutide group stopped treatment because of adverse events, compared with 8.2% on placebo [7].

Weight-loss (metabolic-bariatric) surgery has the largest association with survival. A pooled analysis of 16 matched cohort studies and one controlled trial, with 174,772 participants and 7,712 deaths, found 49.2% lower all-cause mortality after surgery than with usual care. Median life expectancy was 6.1 years longer overall, 9.3 years longer in people with diabetes and 5.1 years longer in those without, and the effect did not differ between gastric bypass, banding and sleeve gastrectomy [9].

Full deep dive: Body weight and lifespan.

Most evidence linking body weight to mortality is observational (it comes from tracking people rather than assigning them to a weight). Illness and smoking both lower body weight, so thin people include some who are already ill; the large collaborations excluded early deaths, smokers or people with chronic disease to reduce this bias, but the excess risk at low BMI was not fully explained [3, 8]. The waist study included only white adults [4], and the Framingham analysis of obesity duration was a single US population [11].

The surgery evidence comes mostly from matched cohort studies rather than randomised trials, so people who chose surgery may have differed from controls in ways that were not measured [9]. SELECT enrolled only people with existing cardiovascular disease, was funded by the drug's manufacturer, and did not report life expectancy [7]. The Diabetes Prevention Program measured new cases of diabetes rather than death [6].