Weight Gain in Early Adult Life Linked to Adverse Cardiac Function, Structure in Older Age

Excess weight gain during young adulthood and middle age is associated with reduced cardiac function and adverse cardiac remodeling in later adult life, according to new research, suggesting a legacy effect of early adulthood adiposity and highlighting an essential role for effective preventive interventions. The findings were published in the European Heart Journal.

Citing the known association between obesity and poor cardiac function yet a paucity of data on the effect of excess weight early in life on later cardiac structure and function, researchers led by Alun Hughes, professor of cardiovascular physiology and pharmacology at UCL in London, set out to investigate the relationship of body mass index/waist-to-hip ratio (BMI/WHR) as proxy for adiposity over the adult lifespan with cardiac structure and function at age 60 to 64 years.

The team tapped longitudinal data from Britain’s National Survey of Health and Development initiated in 1946), creating a final cohort of 1690 participants who had repeated adiposity measurements throughout adulthood (age 20, 26, 36, 43, 53, and 60–64 years ) and echocardiography obtained between 60 and 64 years of age. The cohort had a mean age of 63.2 years and 48% were women when outcome measurements were taken.

They looked specifically at the impact of early weight gain on left ventricular mass (LVM), LV internal diameter in diastole (LVIDd), relative wall thickness (RWT), maximum left atrial volume (LAVi) .

FINDINGS

The investigators reported that increased BMI from age 20 years onwards was associated with greater LVM and LIVIDd, independent of confounding variables. For LVIDd, the associations remained independent of current BMI and for LVM were independent at ages 26, 43, and 53 years. Increased BMI after age 43 years, they found, was linked with greater RWT, but not after controlling for BMI at age 60 to 64 years. They found an association between increased BMI at ages 26, 36, and 53 years and reduced left ventricular ejection fraction and with adiposity from age 20 years onward for lower myocardial contraction fraction, but neither association was independent of BMI at age 60 to 64 years.

Hughes and colleagues reported an association between elevated BMI from 20 years onwards and poorer diastolic function, an association that remained independent after controlling for confounding variables. Positive associations between BMI and LAVi indexed to body surface area persisted from 26 years onward after investigators adjusted for BMI at age 60 to 64 years. When they considered WHR, they observed similar relationships from age 43 years forward.

Greater LVM at age 60 to 64 years was associated with high BMI at any time from age 20 years onward, even after adjusting for BMI in that age group. The authors present an example. For an average 43-year-old, a 5-unit higher BMI corresponded with a 15% or 27-gram increase in LVM. The middle-aged weight gain leads to cardiovascular damage over and above the effects of increased adiposity later in life.

In a discussion of the study’s limitations, Hughes et al emphasize that the findings cannot be generalized beyond the White British population of similar age, given the sample used is representative of native-born adults living in England, Scotland, and Wales. They also note the potential for unmeasured or residual confounding variables and the possibility of “false discovery” inherent in the examination of multiple associations.

“Our data suggest lasting effects of adiposity on cardiac structure and function and reinforce calls for system approaches to the obesity syndemic. Early prevention of excessive adiposity gain may be important to prevent future cardiac target organ damage in later life. This possibility should be explored in future studies, including in more diverse populations,” the team wrote.

In an accompanying editorial Leonardo Roever, MHS, PhD, from the Brazilian Evidence-Based Health Network, Uberlândia, Brazil and colleagues write: “… this study poignantly summarises the temporal and dimensional continuum of cardiac injury associated with abnormal BMI, and provides compelling evidence that being overweight or obese, even at a younger age, translates into an unfavourable cardiovascular risk profile …” They noted in particular a temporal dose-response relationship between increasing BMI and adverse cardiac sequelae, ie, greater injury observed at higher levels of adiposity, and “even minor increases in such parameters were associated with adverse cardiac effects.”

They added: “… it is likely that improvements in BMI over several decades, such as in a patient who was obese when young but has now successfully lost weight due to dieting and exercising, may translate into significant clinical benefits from prevention or reversal of cardiac injury or dysfunction.”

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