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placebo. Resting and postprandial energy metabolism, and carbohydrate and fat oxidation did not differ significantly before and after supplementation in both groups. In muscle, postprandial glucose uptake and aerobic glucose oxidation were significantly higher for verum. In addition, verum significantly increased serum magnesium concentrations.
Four weeks of protein-rich diet did not significantly influence acid-base balance. However, alkaline supplementation improved systemic and tissue acid-base parameters and oxidative glucose metabolism.
Four weeks of protein-rich diet did not significantly influence acid-base balance. However, alkaline supplementation improved systemic and tissue acid-base parameters and oxidative glucose metabolism.
Medically supervised fasting has long tradition and broad acceptance in some European countries. The exact amount to which ketone bodies are produced as well as their possible contribution to beneficial effects in this procedure are open.
Open-label observational trial with in-patients undergoing medically supervised fasting with supplementation of approximately 40 g/d carbohydrates as part of an established routine care. Daily finger-stick blood samples for measurement of glucose and ß-hydroxybutyrate. Descriptive analysis for all data.
Complete sets of data of 17 patients (5 m, mean age 63.1) could be evaluated. Mean concentrations of ß-hydroxybutyrate rose continuously to a mean maximum of 3.6 mmol/L with an individual maximum of 5.1 mmol/L, while glucose decreased within normal range. Two patients with type 2 diabetes produced significantly less ß-hydroxybutyrate. Courses for ß-hydroxybutyrate and glucose showed a weak inverse correlation, while no serious adverse effects could be observed.
Medically supervised fasting with definite small amounts of carbohydrates by fluid intake may lead to limited increases of ketone bodies in their biopositive range, as known e.g. from epileptology or sports medicine. Clinical consequences deserve further research.
Medically supervised fasting with definite small amounts of carbohydrates by fluid intake may lead to limited increases of ketone bodies in their biopositive range, as known e.g. from epileptology or sports medicine. Clinical consequences deserve further research.
Age-related decline in skeletal muscle mass and strength, loss of bone density, and increased risk of osteoporotic fractures are important public health issues. Systemic acid-base balance is affected by dietary intake and may be relevant to these conditions. We therefore investigated associations of dietary acid-base load with skeletal muscle mass, bone density status, and fracture risk.
We analysed the European Prospective Investigation into Cancer and Nutrition-Norfolk cohort of >25,000 individuals, 39-79 years at baseline. Potential renal acid load (PRAL) was calculated from 7-day food diary data. LTGO-33 research buy As a proxy for skeletal muscle mass, we estimated fat-free mass from bioelectrical impedance analysis and scaled this for BMI (FFM
). Bone density status was assessed by heel-bone broadband ultrasound attenuation (BUA), and fracture rates were obtained from health-care records. Multivariable regression was used to test musculoskeletal outcomes across sex-specific quintiles of PRAL.
PRAL in quintiles wasnegative association between PRAL and musculoskeletal health in middle to older age men and women, and thus supports the rationale for a less acidic dietary load.Consuming a lower acid (and particularly lower phosphate) diet and/or supplementing the diet with base precursors, such as bicarbonate, might have a number of mitigating effects on the aging process. These include (1) slowing progression of fibrosis by reduction of high endogenous acid production to preserve net acid excretion and minimize the degree of systemic acidosis; (2) avoiding the downregulation of klotho, a membrane and soluble factor associated with aging. Klotho declines when constant high dietary phosphate intake leads to an increase in FGF23 production; and (3) increasing activity of the enzyme telomerase, an important factor in maintaining telomere length, another factor associated with longer lifespan. Current evidence is based on studies in invertebrate and small animal models. These results, and extrapolations of associated human studies, suggest that low acid-producing diets, or neutralization of the low grade metabolic acidosis seen in humans with age-related renal dysfunction could potentially lead to a longer, healthier lifespan.Long-term exposure to high dietary acid load has been associated with insulin resistance and type 2 diabetes in epidemiological studies. However, it remains unclear whether the acid load of the diet translates to mild metabolic acidosis and whether it is responsible for the impairment in glucose regulation in humans. Previously, in a cross-sectional study we have reported that dietary acid load was not different between healthy individuals with normal weight and those with overweight/obesity, irrespective of insulin sensitivity. However, 4-week high acid load diet increased plasma lactate (a small component of the anion gap) and increased insulin resistance in healthy participants. The change in plasma lactate correlated significantly with the change in insulin resistance. Because cause-and-effect could not be evaluated in these settings, we sought to directly test the effect of an alkalizing treatment preload on postprandial glucose regulation. In a randomized placebo-controlled study with a crossover design, we administered sodium bicarbonate (NaHCO3, 1.68 g) prior to high acid load meal to healthy individuals. We found that while the bicarbonate preload attenuated the post meal decrease in pH observed with placebo, no effect on postprandial glucose regulation (glucose, insulin, and C-peptide) was observed. Following 3-month treatment of nondiabetic individuals with bicarbonate, others have reported no change in insulin resistance markers, consistent with our findings. Together, studies in human suggest that insulin resistance associated with longstanding obesogenic diet may be mediated by mild metabolic acidosis. However, buffering the Western diet with bicarbonate and increasing body pH does not change glucose homeostasis in nondiabetic individuals. Further studies are required to shed light on the role of body acid-base balance and glucose homeostasis in health and disease.
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