Hypertension is a risk factor for cardiovascular disease and its cause is not fully understood, but both environmental and genetic factors are thought to contribute to its development. While it might be considered that genetic factors are beyond the control of the individual, recent advances in epigenetics suggests that genes liked to disease often have environmental triggers. The known environmental causes of hypertension centre around diet and exercise, with low quality food coupled to a sedentary lifestyle being particularly important risk factors. Until recently dietary advice regarding hypertension involved reducing salt intake, however the role of salt in hypertension is controversial. In contrast, The dietary approach to stop hypertension (DASH) dietary pattern is characterised by a high fruit and vegetable intake, coupled with low intakes of diary, saturated and total fat and sweetened beverages. In other words, the DASH diet attempts to improve the quality of the individuals nutrition.
Researchers1 have investigated the effects of the DASH diet on hypertension in 20 unmediated hypertensive adults with a mean age of 43 years. The subjects consumed a control diet for one week and were then randomly assigned to receive either the control diet or the DASH diet for a further two weeks. At baseline the mean systolic and diastolic blood pressure was 144 and 89 mmHg, respectively. During the two week intervention period, only those on the DASH diet experienced a fall in blood pressure. Systolic blood pressure fell by 11 and 10mmHg and diastolic blood pressure fell by 6.0 and 9.0mmHg, in weeks one and two, respectively. Subjects consuming the DASH diet had changes in urinary sodium to potassium excretion ratio that was shown through regression analysis to be associated with the fall in blood pressure. In addition, plasma nitrite levels rose suggesting that nitric oxide metabolism may have been upregulated.
The DASH diet is high in potassium, supplementation of which has been shown to be effective at causing excretion of sodium (natriuresis) within 4 days. Although it was not detected at the end of week 1, evidence that natriuresis had occurred prior to measurement was the raised levels of plasma aldosterone and rennin. This hormonal response was likely a post natriuretic event to prevent further sodium loss and increase excretion of potassium. The increase plasma nitrite levels could reflect upregulation of nitric oxide. Oxidative stress and vascular dysfunction have been implicated in hypertension, via suppression of nitric oxide activity. The DASH diet contains nuts which are a good source of the nitric oxide precursor arginine, and a good source of antioxidants. Antioxidants may decrease oxidative stress in the endothelium and arginine allow adequate production of nitric oxide, which would then allow relaxation of the vasculature and a subsequent decrease in blood pressure.
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