Measurement of Muscle Strength in Haemodialysis Patients by Pinch and Hand Grip Strength and Comparison to Lean Body Mass Measured by Multifrequency Bio-Electrical Impedance

Background: Muscle weakness is a risk factor for mortality in haemodialysis (HD) patients; we wished to determine whether measuring the composition of the arm with bioimpedance was associated with arm muscle strength. Methods: We measured pinch strength (PS) and hand grip strength (HGS) in 250 adult HD patients with corresponding post-dialysis multifrequency bioelectrical assessments with segmental body analysis. Results: Mean age 64.0 ± 15.6, 66% male and 45.6% diabetic. The maximum HGS in the dominant or non-fistula arm was 18.9 ± 9.2 kg and PS 4.09 ± 1.96 kg respectively, with a correlation of r = 0.80, p < 0.001. HGS was associated with body cell mass (β 0.37, p < 0.001) and PS with appendicular muscle mass (β 0.06, p < 0.001). Both HGS and PS were independently associated with the ratio of extracellular water (ECW) to total body water (TBW); β -139.5, p = 0.024, β -44.8, p < 0.001 in the arm. The presence of an arterio-venous fistula increased the ECW/TBW ratio in the arm from 0.383 ± 0.009 to 0.390 ± 0.012, p < 0.05. Conclusion: Muscle strength measured by HGS and PS was associated with both markers of whole body and segmental body composition within the arm, particularly ECW/TBW. Bioimpedance measurements and assessment of muscle strength should be measured in the non-fistula arm

Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration

Alzheimer’s disease (AD) is a complex, multifactorial disease with a number of leading mechanisms, including neuroinflammation, processing of amyloid precursor protein (APP) to amyloid β peptide, tau protein hyperphosphorylation, relocalization and deposition. These mechanisms are propagated by obesity, the metabolic syndrome and type-2 diabetes mellitus. Stress, sedentariness, dietary overconsumption of saturated fat and refined sugars, and circadian derangements/disturbed sleep contribute to obesity and related metabolic diseases, but also accelerate age-related damage and senescence that all feed the risk of developing AD too. The complex and interacting mechanisms are not yet completely understood and will require further analysis. Instead of investigating AD as a mono- or oligocausal disease we should address the disease by understanding the multiple underlying mechanisms and how these interact. Future research therefore might concentrate on integrating these by systems biology approaches, but also to regard them from an evolutionary medicine point of view. The current review addresses several of these interacting mechanisms in animal models and compares them with clinical data giving an overview about our current knowledge and puts them into an integrated framework