The DASH to lower blood pressure

• Published in: Canadian Medical Association journal (CMAJ) Vol. 157; no. 12; pp. 1657 - 1658
• Main Author: Hoffer, L J
• Format: Journal Article
• Language: English
• Published: Canada CMA Impact, Inc 15.12.1997
• Series: Clinical nutrition
• Subjects: 1997; Adult; Blood pressure; Calcium, Dietary - therapeutic use; Diet; Dietary Fiber - administration & dosage; Humans; Hypertension - drug therapy; Magnesium - therapeutic use; Potassium - therapeutic use; Research Design; Review; Year end reviews
• ISSN: 0820-3946; 1488-2329

During 1997 epidemiologic studies continued to show that an elevated serum blood homocysteine concentration increases the risk of coronary artery disease. People carrying the gene for homocystinuria have the highest concentrations of serum homocysteine, but milder increases occur far more frequently and (in the absence of renal failure) are most often due to inadequate vitamin B12 and, especially, folic acid nutriture. Indeed, levels of serum homocysteine and methylmalonic acid the latter is selectively increased in people with vitamin B,2 deficiency - are emerging as better tests of vitamin B,2 and folic acid status than are blood levels of the vitamins themselves. Research continues in an attempt to find whether a common mutation in methylenetetrahydrofolate reductase, an enzyme that enables folate to metabolize homocysteine, constitutes a disease risk factor in increasing the folic acid requirement. Although the control diet had no consistent effect on blood pressure, the combined diet reduced systolic and diastolic blood pressure by 5.5 and 3.0 mm Hg, respectively, compared with concurrently measured controlgroup values. The fruits-and-vegetables diet reduced blood pressure to a lesser extent. Of particular interest to physicians, the blood-pressure-lowering impact of diet was greatest for subjects with the highest initial blood pressures. Thus, among the 133 subjects with a blood pressure of 140/90 mm Hg or higher, the combination diet reduced the systolic and diastolic blood pressure by 11.4 and 5.5 mm Hg more respectively than the control diet. This effect is similar in magnitude to single-drug therapy for mild primary hypertension. It is unlikely, however, that the current crop of antioxidant trials will either establish or discredit nutritional antioxidant therapy for chronic disease. For one thing we still don't know what forms, doses and combinations of nutrients to test. For another, there is still much to learn about the pathophysiology of the diseases being considered for treatment by using nutritional approaches. For example, consider the recent, widely publicized trial involving the use of vitamin E and selegiline in treating Alzheimer's disease (AD). That trial tested a biologically improbable hypothesis - that vitamin E alone can dramatically reduce the rate of cognitive decline in established AD - and it obtained an implausible result: no effect on cognitive function but, after adjustments for baseline mental status, a delay in the time to hard primary outcomes such as severe mental decline, institutionalization because of loss of function, or death.4