Main findings here are a direct association of SSB consumption with BP, and direct associations of fructose and glucose intake with BP, stronger among individuals with higher urinary sodium excretion.
Observed direct associations of SSB with BP are compatible with the findings of the PREMIER intervention trial, where reduction in SSB consumption by 355 ml/day was associated with systolic/diastolic BP lower by 1.8/1.1 mm Hg, 0.7/0.4 mm Hg with adjustment for change in body weight[30
] For diet beverages, findings similar to INTERMAP, i.e., inverse, non-significant in multivariate models; and caffeine, no association. In INTERMAP, SSB-BP associations were independent of caffeine, and caffeine intake was inversely associated with SSB consumption. While some SSBs, e.g., cola, are important sources of caffeine, it is likely that SSB consumption displaced coffee and tea consumption (main dietary sources of caffeine) for many individuals. In analyses of women from the Nurses Health Studies (NHS) I and II, sugared and diet cola consumption, but not caffeine consumption, were associated with risk of incident hypertension.[37
] Among adolescents of the National Health and Nutrition Examination Survey (NHANES) 1999-2004, sugar-sweetened beverage intake was associated with systolic BP and serum uric acid concentration (see below).[28
To our knowledge, no observational studies have reported associations of glucose intake with BP. Forman et al.[27
] found no link between fructose intake (assessed by food frequency questionnaire) and incident hypertension among >200,000 women and men of the Nurses’ Health Study I and II, and the Health Professionals Follow-up Study; Jalal et al. [29
] reported a direct association between fructose intake and odds of elevated BP in cross-sectional analysis of 4,528 adults from NHANES 2003-2006.
The direct associations reported here for SSB/fructose intake and BP are consistent with the hypothesized effect on the uric acid pathway. Fructose consumption may lead to increased serum uric acid via phosphorylation of fructose by hepatocytes and generation of adenosine diphosphate, which is metabolized to uric acid [38
]; raised serum uric acid may influence BP by reducing levels of nitric oxide, a potent vasodilator.[39
] Sugar consumption has also been linked to enhanced sympathetic nervous system activity and sodium retention.[21
] Detection of significant interaction with sodium excretion, i.e., direct fructose- and glucose-BP associations stronger for individuals with higher urinary sodium excretion, is compatible with the findings of several animal studies.[41
] He et al. [45
] reported that SSB consumption was directly associated with salt intake (assessed by 7 day dietary record) in UK children and adolescents. Here, sodium excretion was not associated with SSB consumption in US and UK adults; however urinary sodium/potassium ratio was directly associated with SSB. Significant interaction with BMI, i.e., direct SSB-BP associations weaker for individuals with higher BMI, could be due to greater misclassification of SSB intake in this subgroup due to differential under-reporting of SSB intake. [46
Limitations of the INTERMAP findings include: their cross-sectional nature; underestimation of effect size, attributable to limited reliability in the measurement of nutrients (i.e., regression dilution bias, despite repeated measures – although observed BP differences were of similar magnitude to the PREMIER intervention trial); possible systematic bias (likely minimized by observer training, standardization, multi-pass methods, open non-leading questioning, and extensive ongoing quality control); and possible residual confounding. There was little evidence from multiple sensitivity analyses to indicate substantial bias. SSB-, glucose- and fructose-BP associations were reduced with control for weight and height. Interpretation of this finding is problematic: If intakes of SSB/sugars act on BP through positive energy balance and increased body mass, then body mass is in the causal pathway, and statistical control for weight (standardized for height) is over-adjustment [34
]. Findings adjusted for BMI (not presented here) were quantitatively similar to those adjusted for weight and height. We are presently unable to quantify high-fructose corn syrup (HFCS), however SSB intake may be a good proxy, as HFCS is the most common caloric sweetener used by the US beverage industry.[14
] Fructose intake was higher, urinary potassium and fiber intake lower for participants consuming >1 serving/day SSB, compared to those consuming ≤1 serving/day, indicating that higher fructose intake in SSB consumers likely reflects HFCS consumption rather than fruit intake. Since INTERMAP was designed primarily as a study of individual-level diet-BP associations the samples were not intended to be nationally representative, but – given the heterogeneity of the 8 USA samples particularly, and the similarity of USA and UK SSB-BP associations – it is reasonable to infer that findings may be applicable to middle-aged USA and UK men and women.
Higher intake of SSB was associated with more adverse overall nutritional quality, and there were independent direct associations of SSB, fructose, glucose with BP; sugar-BP associations were stronger among higher sodium consumers. These findings are consistent with recent trial data [30
] and lend support to recommendations for reducing intake of SSB/added sugars/salt, for the improvement cardiovascular health.