Advanced cardiovascular physiology in an individual with type 1 diabetes after 10-year ketogenic diet.

Adults with type 1 diabetes (T1D) have an elevated risk for cardiovascular disease (CVD) compared with the general population. HbA1c is the primary modifiable risk factor for CVD in T1D. Fewer than 1% of patients achieve euglycemia (<5.7% HbA1c). Ketogenic diets (KD; ≤50 g carbohydrate/day) may improve glycemia and downstream vascular dysfunction in T1D by reducing HbA1c and insulin load. However, there are concerns regarding the long-term CVD risk from a KD. Therefore, we compared data collected in a 60-day window in an adult with T1D on exogenous insulin who consumed a KD for 10 years versus normative values in those with T1D (T1D norms). The participant achieved euglycemia with an HbA1c of 5.5%, mean glucose of 98 [5] mg/dL (median [interquartile range]), 90 [11]% time-in-range 70-180 mg/dL (T1D norms: 1st percentile for all), and low insulin requirements of 0.38 ± 0.03 IU/kg/day (T1D norms: 8th percentile). Seated systolic blood pressure (SBP) was 113 mmHg (T1D norms: 18th percentile), while ambulatory awake SBP was 132 ± 15 mmHg (T1D target: <130 mmHg), blood triglycerides were 69 mg/dL (T1D norms: 34th percentile), low-density lipoprotein was 129 mg/dL (T1D norms: 60th percentile), heart rate was 56 beats/min (T1D norms: >1SD below the mean), carotid-femoral pulse wave velocity was 7.17 m/s (T1D norms: lowest quartile of risk), flow-mediated dilation was 12.8% (T1D norms: >1SD above mean), and cardiac vagal baroreflex gain was 23.5 ms/mmHg (T1D norms: >1SD above mean). Finally, there was no indication of left ventricular diastolic dysfunction from echocardiography. Overall, these data demonstrate below-average CVD risk relative to T1D norms despite concerns regarding the long-term impact of a KD on CVD risk.NEW & NOTEWORTHY Adults with type 1 diabetes (T1D) have a 10-fold higher risk for cardiovascular disease (CVD) compared with the general population. We assessed cardiovascular health metrics in an adult with T1D who presented with a euglycemic HbA1c after following a ketogenic diet for the past 10 years. Despite concerns about the ketogenic diet increasing CVD risk, the participant exhibited below-average CVD risk relative to others with T1D when considering all outcomes together.

Acute nasal breathing lowers diastolic blood pressure and increases parasympathetic contributions to heart rate variability in young adults.

There is growing interest in how breathing pace, pattern, and training (e.g., device-guided or -resisted breathing) affect cardiovascular health. It is unknown whether the route of breathing (nasal vs. oral) affects prognostic cardiovascular variables. Because nasal breathing can improve other physiological variables (e.g., airway dilation), we hypothesized that nasal compared with oral breathing would acutely lower blood pressure (BP) and improve heart rate variability (HRV) metrics. We tested 20 adults in this study [13 females/7 males; age: 18(1) years, median (IQR); body mass index: 23 ± 2 kg·m-2, means ± SD]. We compared variables between nasal- and oral-only breathing (random order, five min each) using paired, two-tailed t tests or Wilcoxon signed-rank paired tests with significance set to P < 0.05. We report the median (interquartile range) for diastolic BP and means ± SD for all other variables. We found that nasal breathing was associated with a lower mean BP (nasal: 84 ± 7 vs. oral: 86 ± 5 mmHg, P = 0.006, Cohen's d = 0.70) and diastolic BP [nasal: 68(8) vs. oral: 72(5) mmHg, P < 0.001, Rank-biserial correlation = 0.89] but not systolic BP (nasal: 116 ± 11 vs. oral: 117 ± 9 mmHg, P = 0.48, Cohen's d = 0.16) or heart rate (HR; nasal: 74 ± 10 vs. oral: 75 ± 8 beats·min-1, P = 0.90, Cohen's d = 0.03). We also found that nasal breathing was associated with a higher high-frequency (HF) contribution to HRV (nasal: 59 ± 19 vs. oral: 52 ± 21%, P = 0.04, Cohen's d = 0.50) and a lower low frequency-to-HF ratio at rest (nasal: 0.9 ± 0.8 vs. oral: 1.2 ± 0.9, P = 0.04, Cohen's d = 0.49). These data suggest that nasal compared with oral breathing acutely 1) lowers mean and diastolic BP, 2) does not affect systolic BP or heart rate, and 3) increases parasympathetic contributions to HRV.NEW & NOTEWORTHY There is growing interest in how breathing pace, pattern, and training (e.g., device-guided or -resisted breathing) affect prognostic cardiovascular variables. However, the potential effects of the breathing route on prognostic cardiovascular variables are unclear. These data suggest that nasal compared with oral breathing 1) lowers mean and diastolic blood pressure (BP), 2) does not affect systolic BP or heart rate (HR), and 3) increases parasympathetic contributions to heart rate variability (HRV). These data suggest that acute nasal breathing improves several prognostic cardiovascular variables.