The Association Between Weight Gain Up to Midlife, 30-Year Mortality, and Quality of Life in Older Men FREE

A recent editorial¹ and articles^2- 3 in the Archives investigated the complex relationships between obesity, mortality, and disability, and studies that take into account the dynamic history of body weight over one's life span were called for. In the follow-up of the Helsinki Businessmen Study, we have combined these aspects (weight gain in midlife, mortality, and health-related quality of life [HRQOL] in old age⁴). We report herein the extended follow-up (now up to 30 years) of these relationships.

This was a prospective cohort study of a socioeconomically homogeneous sample of 1657 men (born 1919-1934) who had attended health checks during the 1960s, were free of cardiovascular disease and diabetes in 1974, had no use of regular medication, and could recall their weight at the age of 25 years.⁴ Weight gain from age 25 years up to midlife in 1974 was calculated and divided as follows: (1) loss or no change (n = 188), (2) 0.1 kg to 4.9 kg (n = 246); (3) 5.0 kg to 9.9 kg (n = 419); (4) 10.0 kg to 14.9 kg (n = 379); (5) greater than 14.9 kg (n = 425). Baseline examinations in 1974 included laboratory, clinical, and lifestyle data (body mass index [BMI] [calculated as weight in kilograms divided by height in meters squared], smoking, and alcohol use). The men were also asked to self-rate their health and physical fitness with a 5-step scale. At baseline in 1974, only 6.8% (n = 113) of the men were obese (BMI ≥30), which should be borne in mind when comparing our results with the present US population with more prevalent obesity in midlife.

In 2003, survivors were assessed with mailed questionnaires about lifestyle, body weight, and the RAND-36 (Medical Outcomes Study 36-Item Short-Form Health Survey⁵) HRQOL instrument. In the RAND-36, a difference of 3 to 5 points has often been considered clinically meaningful.⁵ Mortality was ascertained from nationwide registers. Outcome measures were total mortality between 1974 and 2004 and HRQOL of the survivors in 2003. Cox proportional hazards analysis was used to compare mortality (adjusted for age, BMI at age 25 years, smoking, and alcohol use at baseline in 1974), and analysis of covariance was used to compare HRQOL in 2003.

During the 30-year follow-up, 534 men (32.2% of the initial 1974 cohort) died. Mortality was 29.6%, 24.8%, 31.9%, 29.3%, and 40.7% from the lowest to the highest midlife weight gain group. Body mass index at age 25 years did not predict mortality. Using the group with weight gain of 0.1 kg to 4.9 kg as reference, we determined that the adjusted mortality risk was significantly (P = .001) increased only in the highest (>14.9 kg) weight gain group (relative risk, 1.63; 95% confidence interval, 1.21-2.20); the 95% confidence interval of the group with no weight gain up to midlife included unity.

In 2003, 837 men (72.2% of eligible participants; median age, 77 years [interquartile range, 73-80 years]) responded to the questionnaire survey including the RAND-36 instrument. The pattern of weight gain from age 25 years to midlife in 1974 was similar among responders and nonresponders. Analyses of the association between the midlife weight gain and the RAND-36 scales in 2003 were extensively adjusted (age, variables measured in 1974, body weight both at age 25 years and in 2003) (Figure). The adjusted analyses showed that a larger midlife weight gain was associated with lower RAND-36 scores (suggesting worse HRQOL) in old age in 2003.

In this homogeneous, mainly nonobese white male cohort followed up to old age, only the largest weight gain (>14.9 kg) from 25 years of age to midlife was associated with a significantly (P = .001) higher long-term mortality. Those with the smallest weight gain (<5 kg) tended to have the best prognosis. Importantly, weight gain up to midlife was sensitively associated with HRQOL later in life. The men with no or minimal weight gain up to midlife consistently had the best HRQOL; a larger weight gain was associated with clearly poorer HRQOL in old age. As the editorial rightly pointed out, weight reduction in old age is a complex issue.¹ However, prevention of overweight earlier in life seems justified also (and especially) from the geriatric point of view.

Correspondence: Dr T. E. Strandberg, Department of Public Health Science and General Practice, University of Oulu and University Hospital, Unit of General Practice, Aapistie 1, PO Box 5000, Oulu FIN-90014, Finland (timo.strandberg@oulu.fi).

Author Contributions: Study concept and design: T. E. Strandberg and Salomaa. Acquisition of data: T. E. Strandberg and Miettinen. Analysis and interpretation of data: T. E. Strandberg, A. Strandberg, Salomaa, Pitkälä, Tilvis, and Miettinen. Drafting of the manuscript: T. E. Strandberg, A. Strandberg, and Tilvis. Critical revision of the manuscript for important intellectual content: T. E. Strandberg, Salomaa, and Pitkälä. Statistical analysis: T. Strandberg, Salomaa, and Tilvis. Obtained funding: T. E. Strandberg. Administrative, technical, and material support: Tilvis. Study supervision: A. Strandberg, Pitkälä, and Miettinen.

Financial Disclosure: None reported.

Funding/Support: This study was supported by the Academy of Finland, the Päivikki and Sakari Sohlberg Foundation, the Helsinki University Central Hospital, and the Finnish Foundation for Cardiovascular Research.

Role of the Sponsor: The sponsors had no role in the design or conduct of the study; collection, management, analysis, and interpretation of the data; or preparation, review, or approval of the manuscript.