The research by Rebecca Reynolds, professor of metabolic medicine, and colleagues at the University of Edinburgh publishing in the British Medical Journal yesterday reinforces the findings of a British Nutrition Foundation Task Force Report published in May.
Reynolds noted that the findings highlighted the urgent need for strategies to prevent obesity in women of childbearing age and the need to assess the offspring of obese mothers for their cardiovascular risk.
In the study of 37,709 people born since 1950 on the Aberdeen Maternity and Neonatal databank linked to the death and hospital admission for cardiovascular problems up to January 1 2012 in offspring aged 34–61 using the body mass index (BMI) of the mothers as a measure, the results showed that mortality increased “significantly” in the offspring of mothers with a BMI >30, compared with those of normal BMI once adjustments for other risk factors had been taken into account.
The researchers concluded:“Maternal obesity is associated with an increased risk of premature death in adult offspring. As one in five women in the United Kingdom is obese at antenatal booking, strategies to optimise weight before pregnancy are urgently required.” They added that these findings were independent of socioeconomic status of those studied.
Among the 37,709 offspring there were 6,551 deaths from “any cause”. The leading cause of death was cardiovascular disease (24% of deaths in men and 13% in women) and cancer (26% of deaths in men and 42% in women).
Reynolds and her team proposed possible physiological mechanisms for the findings. They referred to research by J E Ramsay et al from 2002, which found that pregnant overweight women had increased circulating concentrations of inflammatory cytokines, non-esterified fatty acids, and amino acids and increased insulin resistance. Reynolds concluded as a result there was a potential for increased nutrient supply to the developing foetus, with compensatory foetal hyperinsulinaemia and increased foetal adiposity.
Animal studies have indicated that these changes could permanently influence appetite control and body metabolism of food later in life, said the researchers.
However, they issued a caveat on their findings: “We cannot separate the direct effects of maternal obesity on the developing child from shared genetic and postnatal lifestyle influences in childhood and adulthood on obesity and cardiovascular risk.” In other words, other influences – including environmental factors such as obesity, unhealthy diets, and lack of exercise in families – were also likely to have some impact on the results.
They also noted that the study did not take account of paternal obesity either, and added “there is now some evidence of programming of obesity through the paternal line”.