Commentary: Sodium and Blood Pressure: Never Too Late to Reduce Dietary Intake
He, Jiang; Kelly, Tanika
From the Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA.
Correspondence: Jiang He, Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA. E-mail: firstname.lastname@example.org.
“Hence if too much salt is used for food, the pulse hardens …”
Huang Ti Nei Ching Su Wen, 2698–2598 BC
(The Yellow Emperor’s Classic of Internal Medicine)
Ancient Chinese medical literature reported nearly 5000 years ago that a high intake of dietary salt could produce a “hardened pulse,” or hypertension. The first modern scientific evidence for this association was published by Dahl in 1960.1 Dahl described a remarkable linear relationship between average sodium intake and prevalence of hypertension across five population groups. Since then, a consensus on the causal association between dietary sodium intake and high blood pressure has emerged from animal experiments, observational epidemiological studies, and randomized controlled clinical trials.2,3
Most observational studies on the association between dietary sodium intake and blood pressure are cross-sectional, whereas randomized controlled trials on sodium reduction are short-term.2,3 In this issue of EPIDEMIOLOGY, Batis and colleagues4 report a positive dose-response association between recent sodium intake and incidence of hypertension among 6578 adults enrolled in the China Health and Nutrition Survey, with a median of 11 years of follow-up. Although recent sodium intake was important, the baseline and mean intake during follow-up were inconsistently associated with hypertension.
The risk of hypertension was almost halved among those with consistently low sodium intake (sodium <3.7 g/day) at the baseline and at most recent measurement, compared with those who consistently had high sodium intake (>8.7 g/day). More interesting, those whose recent diet was low in sodium had half the risk of hypertension compared with those whose recent diet was high in sodium, regardless of baseline intake. These data suggest that reducing dietary sodium or maintaining a low sodium diet can lower the risk of hypertension in this Chinese population.
Limitations of the study must be taken into account to appropriately interpret these results. Among 13,764 eligible study participants, only half (6,578) were included in the final analysis because of various exclusion criteria. Those included differed from those excluded on several important covariables. Dietary sodium intake was estimated based on a combination of three consecutive 24-hour recalls at the individual level and a food inventory at the household level performed over the same 3-day period. The Chinese food composition table did not include all processed foods available in China. This oversight in the estimation of dietary sodium intake may have contributed to the unusual observation of a lower sodium intake in people living in the north compared with the south. Previous studies using multiple measures of 24-hour urinary sodium excretion have consistently documented a higher sodium intake in the northern Chinese population.2,5–7 Furthermore, a cumulative average dietary sodium intake giving more weight to the most recent diet should be more informative than a simple average.8 Finally, a pooled logistic regression analysis may be more appropriate because the exact time-to-event was unknown for most hypertensive cases in this cohort.9 If a time-to-event analysis was conducted, age might be a more appropriate timescale for these survey data.10 However, it is not obvious that alternative approaches in data analysis would change these study findings.
High dietary sodium intake is a major risk factor for hypertension and stroke in the Chinese general population, where the prevalence of hypertension is high and increasing. The study by Batis and colleagues4 adds new justification for promoting reduced dietary sodium consumption in China and in other populations with high sodium intake.
ABOUT THE AUTHORS
JIANG HE is a Professor and Joseph S. Copes, M.D., Chair in the Department of Epidemiology at Tulane University. He has more than 20 years of experience in studying the health effects of dietary sodium intake in the population. He is a member of the Institute of Medicine Committee on the Consequences of Sodium Reduction in Populations. TANIKA KELLY is an Assistant Professor of Epidemiology at Tulane University. She has extensively studied the interaction of dietary sodium intake and genetic variants on blood pressure.
1. Dahl LKCottier P, Bock KD. Possible role of salt intake in the development of essential hypertension. In: Essential Hypertension—An International Symposium. 1960 Berlin Springer-Verlag:53–65
2. Elliott P, Stamler J, Nichols R, et al. Intersalt revisited: further analyses of 24 hour sodium excretion and blood pressure within and across populations. BMJ. 1996;312:1249–53
3. Sacks FM, Svetkey LP, Vollmer WM, et al.DASH-Sodium Collaborative Research Group. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. N Engl J Med. 2001;344:3–10
4. Batis C, Gordon-Larsen P, Cole SR, Du S, Zhang B, Popkin B. Sodium intake from various time frames and incident hypertension among Chinese adults. Epidemiology. 2013;24:410–418
5. Kesteloot H, Huang DX, Li YL, Geboers J, Joossens JV. The relationship between cations and blood pressure in the People’s Republic of China. Hypertension. 1987;9:654–659
6. Liu LS, Xie JX, Fang WQ. Urinary cations and blood pressure: a collaborative study of 16 districts in China. J Hypertens Suppl. 1988;6:S587–S590
7. Zhao L, Stamler J, Yan LL, et al.INTERMAP Research Group. Blood pressure differences between northern and southern Chinese: role of dietary factors: the International Study on Macronutrients and Blood Pressure. Hypertension. 2004;43:1332–1337
8. Hu FB, Stampfer MJ, Rimm E, et al. Dietary fat and coronary heart disease: a comparison of approaches for adjusting for total energy intake and modeling repeated dietary measurements. Am J Epidemiol. 1999;149:531–540
9. D’Agostino RB, Lee ML, Belanger AJ, Cupples LA, Anderson K, Kannel WB. Relation of pooled logistic regression to time dependent Cox regression analysis: the Framingham Heart Study. Stat Med. 1990;9:1501–1515
10. Korn EL, Graubard BI, Midthune D. Time-to-event analysis of longitudinal follow-up of a survey: choice of the time-scale. Am J Epidemiol. 1997;145:72–80
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