Guidelines have recommended significant reductions in dietary sodium intake to improve cardiovascular health. However, these dietary sodium intake recommendations have been questioned as emerging evidence has shown that there is a higher risk of cardiovascular disease with a low sodium diet, including in individuals with type 2 diabetes. This may be related to the other pleotropic effects of dietary sodium intake. Therefore, despite recent review of dietary sodium intake guidelines by multiple organizations, including the dietary guidelines for Americans, American Diabetes Association, and American Heart Association, concerns about the impact of the degree of sodium restriction on cardiovascular health continue to be raised. This literature review examines the effects of dietary sodium intake on factors contributing to cardiovascular health, including left ventricular hypertrophy, heart rate, albuminuria, rennin–angiotensin–aldosterone system activation, serum lipids, insulin sensitivity, sympathetic nervous system activation, endothelial function, and immune function. In the last part of this review, the association between dietary sodium intake and cardiovascular outcomes, especially in individuals with diabetes, is explored. Given the increased risk of cardiovascular disease in individuals with diabetes and the increasing incidence of diabetes worldwide, this review is important in summarizing the recent evidence regarding the effects of dietary sodium intake on cardiovascular health, especially in this population.

Objective: Low sodium intake may trigger sympathetic nervous system (SNS) activation and endothelial dysfunction. Studies have not explored these associations along the glucose continuum. Accordingly, we compared endothelial function and SNS activity in individuals with low sodium intake and differing categories of metabolic risk along the glucose continuum. We hypothesized that low sodium intake is associated with (1) impairment of endothelial function and (2) higher SNS activity in individuals with higher metabolic risk. Research Design and Methods: In this prospective observational study, participants (n=54) with low sodium intake (single 24 hours urine sodium excretion <150 mmol/24 hours) were categorized based on oral glucose tolerance testing as: normal glucose tolerance (NGT, n=10), impaired glucose tolerance (IGT, n=15), treatment naive type 2 diabetes (T2D−) (n=12) or treated type 2 diabetes (T2D+) (n=17). We assessed endothelial function using pulse amplitude tonometry (PAT) derived reactive hyperemic index and PAT ratio; arterial stiffness via augmentation index; muscle sympathetic nerve activity (MSNA) using microneurography; cardiac baroreflex; heart rate; blood pressure; glycosylated hemoglobin A1c (HbA1c) and lipid profile. Results: Mean (SD) sodium excretion was 110.6 (26) mmol/24 hours. Compared with NGT, IGT and T2D−, the T2D+ group had lower MSNA (p=0.005), PAT ratio (p=0.04) and baroreflex sensitivity (p=0.0002) and an augmented heart rate (p=0.02). The T2D+ group had appropriate mean (SD) glycemic (HbA1c 7.2 (1.72)%), total cholesterol (4.2 (1.0) mmol/L), low-density lipoprotein (2.2 (1.0) mmol/L) and blood pressure (systolic 136 (13), diastolic 78 (12)) (mm Hg) control. Conclusions: Individuals with T2D+ have impaired endothelial and baroreflex function, despite low sodium intake, appropriately managed cardiometabolic risk factors and lower SNS activity, compared with others along the glucose continuum. Whether low sodium intake is associated with modulation of the sympathovascular profile in T2D requires further investigation.

Aim: To generate pilot data regarding acceptance, safety, and function of a novel long-term CGM. Methods: The investigational CGM (Eclipse 3, GlySens, San Diego, CA) was surgically inserted superficial to the rectus sheath in 8 type 1 diabetes adults (4 Female; Mean [SD] age 56 [7]; BMI 25 [3]). CGM data were masked to participants and processed retrospectively in simulated real-time with one capillary blood glucose calibration per day. Monthly visits evaluated: user acceptance by standardised questionnaire; health of implantation sites; safety by anti-glucose oxidase and anti-catalase antibodies; and performance benchmarked against YSI during standardised meal tests. Bluetooth communication between the sensor and an Apple iPhone was assessed continuously. Results: One sensor was removed at 4 months (participant withdrawal) due to impacted implant environment. There were no SAE’s. User acceptance remained high for the study duration. (Figure 1) Antibody levels did not rise. The lag corrected (23.3minutes) MARD (Median [range]) of 12.4% (1401 paired readings) was stable from month 1 (13.1%) to month 10 (14.0%). CGM readings within 20/20% and 30/30% of YSI values were 85% and 96%, respectively. The App received 95% of sensor data within 10 minutes. Conclusions: Our results provide initial data supporting participant acceptance, and safety of Eclipse 3. Further sensor refinement will reduce lag and improve performance. Disclosure A.Butler: Employee; GlySens Incorporated. J.Tan: None. D.N.O'neal: None. L.Robinson: None. V.R.Obeyesekere: None. H.Jones: None. Y.W.Kong: None. C.Yuan: None. K.Bertsch: Employee; GlySens Inc. T.L.Routh: Employee; GlySens Incorporated. S.L.Martha: Employee; GlySens Incorporated.

Context Lower sodium intake is paradoxically associated with higher mortality in type 2 diabetes (T2D). Objective To determine whether sympathetic nervous system (SNS) activation and endothelial dysfunction contribute to these observations, we examined the effect of salt supplementation on these systems in people with T2D with habitual low sodium. We hypothesized that salt supplementation would lower SNS activity and improve endothelial function compared to placebo. Design We conducted a randomized, double-blinded, placebo-controlled crossover trial. Setting The study took place in a tertiary referral diabetes outpatient clinic. Participants Twenty-two people with T2D with habitual low sodium intake (24-hour urine sodium &lt;150 mmol/24h) were included. Intervention Salt supplementation (100 mmol NaCl/24h) or placebo for 3 weeks was administered. Main outcome measures The primary outcome of SNS activity and endothelial function was assessed as follows: Microneurography assessed muscle sympathetic nerve activity (MSNA), pulse amplitude tonometry assessed endothelial function via reactive hyperemic index (RHI), and arterial stiffness was assessed via augmentation index (AI). Secondary outcomes included cardiac baroreflex, serum aldosterone, ambulatory blood pressure monitoring (ABPM), heart rate variability (HRV), and salt sensitivity. Results Compared to placebo, salt supplementation increased MSNA (burst frequency P = .047, burst incidence P = .016); however, RHI (P = .24), AI (P = .201), ABPM (systolic P = .09, diastolic P = .14), and HRV were unaffected. Salt supplementation improved baroreflex (slope P = .026) and lowered aldosterone (P = .004), and in salt-resistant individuals there was a trend toward improved RHI (P = .07). Conclusions In people with T2D and low habitual sodium intake, salt supplementation increased SNS activity without altering endothelial function or blood pressure but improved baroreflex function, a predictor of cardiac mortality. Salt-resistant individuals trended toward improved endothelial function with salt supplementation.

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