Key result
In patients with type 2 diabetes, every 100 mmol rise in 24-h urinary sodium excretion was associated with a 28% lower risk of all-cause mortality (95% CI 6-45%; P=0.02).
Why the study?
Does dietary salt intake affect all-cause and cardiovascular mortality in patients with type 2 diabetes?
Cohort (n=638)
No
Does dietary salt intake affect all-cause and cardiovascular mortality in patients with type 2 diabetes?
In patients with type 2 diabetes, lower dietary salt intake is paradoxically associated with increased all-cause and cardiovascular mortality, challenging current guidelines that advocate for salt restriction in this population.
Answers are grounded in this paper and cite their sources.
Challenges strict sodium restriction in type 2 diabetes; leaves open causal effects pending trials.
OBJECTIVE: Many guidelines recommend that patients with type 2 diabetes should aim to reduce their intake of salt. However, the precise relationship between dietary salt intake and mortality in patients with type 2 diabetes has not been previously explored. RESEARCH DESIGN AND METHODS: Six hundred and thirty-eight patients attending a single diabetes clinic were followed in a prospective cohort study. Baseline sodium excretion was estimated from 24-h urinary collections (24hU(Na)). The predictors of all-cause and cardiovascular mortality were determined by Cox regression and competing risk modeling, respectively. RESULTS: The mean baseline 24hU(Na) was 184 ± 73 mmol/24 h, which remained consistent throughout the follow-up (intraindividual coefficient of variation [CV] 23 ± 11%). Over a median of 9.9 years, there were 175 deaths, 75 (43%) of which were secondary to cardiovascular events. All-cause mortality was inversely associated with 24hU(Na), after adjusting for other baseline risk factors (P < 0.001). For every 100 mmol rise in 24hU(Na), all-cause mortality was 28% lower (95% CI 6-45%, P = 0.02). After adjusting for the competing risk of noncardiovascular death and other predictors, 24hU(Na) was also significantly associated with cardiovascular mortality (sub-hazard ratio 0.65 [95% CI 0.44-0.95]; P = 0.03). CONCLUSIONS: In patients with type 2 diabetes, lower 24-h urinary sodium excretion was paradoxically associated with increased all-cause and cardiovascular mortality. Interventional studies are necessary to determine if dietary salt has a causative role in determining adverse outcomes in patients with type 2 diabetes and the appropriateness of guidelines advocating salt restriction in this setting.
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Ekinci et al. (2011) conducted a cohort in Type 2 Diabetes (n=638). 24-h urinary sodium excretion (dietary salt intake) vs. Lower sodium excretion was evaluated on all-cause mortality (28% lower, 95% CI 6-45%, p=0.02). In patients with type 2 diabetes, every 100 mmol rise in 24-h urinary sodium excretion was associated with a 28% lower risk of all-cause mortality (95% CI 6-45%; P=0.02).
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