Resting energy expenditure has been recently reported to mediate the body mass effect on blood pressure in normal-weight Siberians, normal-weight Africans, and over-weight African-Americans. The current study extends the previous findings, in that REE appears to mediate the body mass effect on BP in a sample of normal-weight African-American and European-American women who reside in Birmingham, AL. Furthermore, the current findings support the strength of this relationship, as it is independent of many of the commonly reported anthropometric/demographic variables and, additionally, a marker of sympathetic tone.
Epidemiological reports have consistently demonstrated a myriad of chronic disease outcomes with advancing BMI [9
]. This has often led to a working hypothesis that obesity, per se, is the primary causal feature or risk factor for metabolic aberrations and overt chronic disease conditions with down-stream consequences on metabolic processes. The present analysis along with other reports would suggest that alterations in metabolic and neuro-humoral processes may precede, act in concert with, or be entirely independent of body weight [9
]. Although the inherent difficulty of parsing out the causal features and the temporal relationship between indentified actors and averse health outcomes remains very challenging, the present confirmation that REE is associated with BP, independent of body weight, in normal-weight, healthy women confirms that the association between BMI and BP may be considerably confounded by REE. As Kunz et al [9
] and Luke et al [10
] eluded to in previous reports, REE is most likely serving as a proxy for other correlated neuro-humoral processes and/or systemic oxidative stress that are direct actors on BP, and body weight in of itself is not a primary determinant of BP, but may serve as an exacerbating factor during the process of adding additional body weight, primarily adipose tissue, as a result of positive energy balance. Additionally, variation in brown adipose tissue quantity and activity may be an underlying contributing factor that affects metabolic rate, thermogenesis, and sympathetic tone [22
The role of catecholamines, insulin, and leptin are all considered primary neurohormonal factors in obesity-related HTN. Although methodological complications are still present and reports are mixed about the relationship between epinephrine and norepinephrine with body weight, Ward et al [23
] in the Normative Aging Study found that in 752 non-diabetic men urinary norepinephrine excretion levels were strongly related to BP. In a similar study Masuo et al [24
] reported in a cross-sectional sample of 724 Japanese men that urinary norepinephrine was an independent predictor of BP. Our finding in the current study that urinary norepinephrine is not a predictor of BP should be interpreted cautiously. In both of the previous reports, the participants had a wide range of BMIs, ranging from normal to obese; whereas, our cohort were all in the normal BMI category, with a small range of BMIs. According to the Landsberg [25
] hypothesis of obesity, elevated SNS activity is a compensatory mechanism in response to obesity that acts to increase metabolic rate to offset the positive energy balance and prevent further weight gain. As a result of this, the well known effects of elevated SNS activity on the heart, kidneys, and vasculature are unfortunately impacted as well and have a deleterious consequence on BP. In our cohort, due to the normal BP and BMI, although urinary norepinephrine was not predictive of BP, this does not necessarily provide evidence that SNS activity is not an important contributing factor to obesity-related elevations in BP or overt HTN, as previous reports have linked SNS over-activity to higher HR and metabolic factors such as hyperinsulinemia, insulin resistance, hyperleptinemia, and obesity-related HTN [26
In summary, this report extends previous findings that REE may be an important mediator of BP. Body mass accounts for the preponderance of the inter-individual variation in REE, and the remaining variation in REE is likely due to other metabolic processes that may serve as intermediaries in the REE/BP association. The collective findings from our report along with other recent findings provide compelling evidence that the BMI-independent variation in REE is capturing an underlying metabolic process that is likely a pathway involved in obesity-related HTN. Although, the current report offers little insight into the underlying mechanisms, the proxy features of REE on the BP/HTN relationship clearly warrant further investigation, as this may be an important addition to the conceptual framework of obesity-related HTN.