eing overweight may significantly increase the risk of a number of diseases. In particular, individuals with a body mass index of over ~27 kg/m2 are at an increased risk of cardiovascular disease. The exact relationship between cardiovascular disease and obesity is not fully understood, but weight gain is known to cause blood pressure rises, which can significantly increase the risk of cardiovascular disease. For example in one study1, the association between pre-hypertension, defined as a slightly elevated blood pressure (systolic blood pressure 120-130 mmHg and diastolic blood pressure 80 to 89 mmHg) and weight gain was investigated in a group of women. The cross sectional study of 36075 women measured blood pressure changes since 20 years of age and correlated them with changes in weight. The results showed that the increase in hypertension risk associated with 1 kg weight gain was similar to that experienced with 1 year of increasing age.
The authors concluded that weight gain in early adulthood increased the risk of high blood pressure to a greater extent than weight gain in later adulthood. These results are broadly consistent with other studies that have shown blood pressure raises with increasing weight. The link between obesity and blood pressure is complex and not fully understood. However, weight gain might not be detrimental to health if the adipose tissue is sequestered in subcutaneous fat tissue. In fact recent evidence suggests that weight itself is not unhealthy, unless central adiposity is present. Central adiposity is an indicator of the presence of the metabolic syndrome (syndrome X). Characterised by insulin resistance, central adiposity is the accumulation of visceral fat, likely as a result of nutrient overload on the liver. This results in metabolic changes, including insulin and leptin resistance, that increases the risk of cardiovascular disease.
So what mechanism can explain the increase in blood pressure associated with central adiposity? Interestingly fructose is thought to be the primary driver of the insulin resistance that causes metabolic syndrome in mammals, and fructose may be able to cause rises in blood pressure (here). Fructose is able to cause blood pressure increases for 2 hours postprandially because it can increase sympathetic nervous activation. Glucose too can cause sympathetic nervous system activation postprandially, but glucose also causes the release of insulin. Because insulin dilates peripheral tissues such as in skeletal muscle, glucose consumption does not cause blood pressure rises. The sympathetic nervous activation caused by fructose ingestion however, combined with no peripheral dilation because fructose does not stimulate insulin release, causes rises in blood pressure. The association between weight gain and hypertension may therefore be explained by dietary fructose.