Caloric intake and high blood pressure
A caloric intake that is in excess of the calories used during physical activity represents a crucial factor promoting hypertension. Since a high proportion of hypertensive persons is overweight, the designation "primary hypertension" is not justified and the term "overweight hypertension" appears more appropriate. These considerations represent also the basis for the generally accepted recommendation of a weight reduction when high blood pressure has been diagnosed. The blood pressure lowering effect of weight reduction is about 1 mm of Hg/kg body weight. In animal experiments using radio telemetry we have shown that an increased caloric intake is associated not only with a raised body weight but also with a rise in heart rate and blood pressure (1). The increase in heart rate and blood pressure is indicative of a raised sympathetic activity originating from the brain. This so-called "hyperkinetic hypertension" was reversible in animal experiments after changing the diet to a regular diet. In humans, a similar hyperkinetic hypertension has been observed particularly in young and young adult persons. This type of hypertension is typically not treated since it rarely exceeds the blood pressure (140 mm Hg/90 mm Hg) which, according to common guidelines, would require pharmacological treatment. This approach does not take into account that an established high blood pressure is associated with the deleterious process of vascular remodelling, e.g. increased media thickness, and more efforts should be made to prevent the early remodelling process.
    In view of many unsuccessful efforts in reducing body weight of overweight or obese persons, an initial rise in body weight should be avoided. One should also not argue that body weight should be reduced only when signs of illness occur. A further misconception refers to the commonly accepted view that disease relevant processes occur only when the body mass index (BMI) is greater than 28.
    As the number of overweight persons in Westernized societies increases constantly, a genetic basis of overweight appears unlikely while a genetic predisposition for overweight should not be dismissed. A prerequisite for the manifestation of overweight is - relative to the physical activity – a too high caloric intake. Generally acceptable recommendations regarding the daily caloric intake appear not to be justified, since there is an inter-individual variability in food utilization and resting metabolism.
    If one considers the fact that the incidence of hypertension correlates with the rise in body weight and appears to start with a body mass index of approx. 23, then the necessity arises to prevent a slight body weight gain and, as an adjunctive approach, to use pharmacological interventions which counteract the changes in the neuroendocrine status of overweight persons.
    The importance of overweight for the development of hypertension has been documented in numerous studies. In the Framingham Offspring Study, subscapular skinfold was, besides cigarette smoking, the major predictor of hypertension in men (2). Skinfold thickness can be measured by Harpenden calipers and is representative of body fat. A fold of skin and subcutaneous tissue is pinched between the operator’s thumb and forefinger (3).
    In the Framingham Offspring Study, also heart rate and alcohol consumed were independent predictors of hypertension. Since a raised sympathetic activity is associated with a higher heart rate, this association might not be unexpected. As regards alcohol, it has been shown that it raises sympathetic outflow of the brain.

1. Rupp H, Maisch B: Radiotelemetric characterization of overweight-associated rises in blood
pressure and heart rate. Am J Physiol 1999;277:H1540-5
2. Garrison RJ, Kannel WB, Stokes J, Castelli WP. Prev Med 1987;16:235-51
3. Jung RT: A colour atlas of obesity 1990,  Wolfe Medical Publications, London