Adeola Olowu, MD

Lambert EA, Esler MD, Schlaich MP, Dixon J, Eikelis N, Lambert GW. Obesity-Associated Organ Damage and Sympathetic Nervous Activity: A Target for Treatment? Hypertension. 2019;73:1150–1159.

The authors of this review focused on obesity and a potential target for treatment. Obesity and increased body mass index are risk factors for diseases such as stroke, cardiovascular disease, and other medical conditions. This brief review focused on cardiovascular studies, studies demonstrating an association between weight gain with blood pressure, cardiovascular abnormalities, renal function, and endothelial dysfunction and its relationship with biochemical sympathetic nervous activity.

Being overweight or obese is a growing medical condition worldwide. Obesity is unique to other cerebrovascular risk factors because it may be the sole risk factor an individual may have for quite some time. However, the lack of other cerebrovascular risk factors such as hypertension and diabetes does not make being overweight or obese harmless. The studies reviewed showed hypertension prevalence to be at least 16% higher in the obese population compared to the normal-weight population in the United States. Pre-hypertension was found in approximately 40% of obese men and 30% in obese women in China. Observational studies demonstrated elevated plasma norepinephrine and increased MSNA with weight gain.

Cardiovascular changes occur in the setting of obesity. Studies have found left ventricular dysfunction and hypertrophy, cardiac failure, and mortality within the obese population without cardiac medical conditions such as hypertension and coronary artery disease. The relationship between obesity, cardiovascular changes, and sympathetic activity is not clearly established. However, there may be a link between renin angiotensin system and increased sympathetic nervous system activity.

Renal function is changed in the setting of obesity with increased glomerular filtration. This is important due to glomerular hyperfiltration occurring before renal dysfunction. This observation of glomerular hyperfiltration associated with obesity occurs in individuals without hypertension. The studies found increased creatinine clearance associated with increased muscle sympathetic nerve activity (MSNA) in their obese population. 

Endothelial dysfunction affects arterial vasodilation capabilities. This occurs prior to atherosclerosis and has been found in the metabolically normal obese population. MSNA and blood pressure values could predict endothelial function in healthy overweight individuals.

Obesity affects various organ systems with increased sympathetic activity, thus making sympathetic activity a great target for cerebrovascular risks in individuals with obesity. Since overweight status or being obese is not always present with other cerebrovascular risk factors, obesity could be considered an independent risk factor. A mix of studies, such as prospective and retrospective studies, were used for this review. The studies reviewed were performed in various countries and may be applicable to our population here in the U.S. A methods section was not provided, as this was not a systematic review. There are no prospective clinical trials involving the obese population without comorbidities and antiadrenergic hypertensive agents. A clinical trial with this population would positively impact primary and secondary stroke prevention in those with obesity.