The measurement of body composition (BC) represents a valuable tool to assess nutritional status in health and disease. The most used methods to evaluate BC in the clinical practice are based on bicompartment models and measure, directly or indirectly, fat mass (FM) and fat-free mass (FFM). Bioelectrical impedance analysis (BIA) and dual energy X-ray absorptiometry (DXA) (nowadays considered as the reference technique in clinical practice) are extensively used in epidemiological (mainly BIA) and clinical (mainly DXA) settings to evaluate BC. DXA is primarily used for the measurements of bone mineral content (BMC) and density to assess bone health and diagnose osteoporosis in defined anatomical regions (femur and spine). However, total body DXA scans are used to derive a three-compartment BC model, including BMC, FM, and FFM. Both these methods feature some limitations: the accuracy of BIA measurements is reduced when specific predictive equations and standardized measurement protocols are not utilized whereas the limitations of DXA are the safety of repeated measurements (no more than two body scans per year are currently advised), cost, and technical expertise. This review aims to provide useful insights mostly into the use of BC methods in prevention and clinical practice (ambulatory or bedridden patients). We believe that it will stimulate a discussion on the topic and reinvigorate the crucial role of BC evaluation in diagnostic and clinical investigation protocols.

BackgroundThis systematic review and meta-analysis summarized the most recent evidence on the efficacy of intermittent energy restriction (IER) versus continuous energy restriction on weight-loss, body composition, blood pressure and other cardiometabolic risk factors.MethodsRandomized controlled trials were systematically searched from MEDLINE, Cochrane Library, TRIP databases, EMBASE and CINAHL until May 2018. Effect sizes were expressed as weighted mean difference (WMD) and 95% confidence intervals (CI).ResultsEleven trials were included (duration range 8–24 weeks). All selected intermittent regimens provided ≤ 25% of daily energy needs on “fast” days but differed for type of regimen (5:2 or other regimens) and/or dietary instructions given on the “feed” days (ad libitum energy versus balanced energy consumption). The intermittent approach determined a comparable weight-loss (WMD: − 0.61 kg; 95% CI − 1.70 to 0.47; p = 0.87) or percent weight loss (WMD: − 0.38%, − 1.16 to 0.40; p = 0.34) when compared to the continuous approach. A slight reduction in fasting insulin concentrations was evident with IER regimens (WMD = − 0.89 µU/mL; − 1.56 to − 0.22; p = 0.009), but the clinical relevance of this result is uncertain. No between-arms differences in the other variables were found.ConclusionsBoth intermittent and continuous energy restriction achieved a comparable effect in promoting weight-loss and metabolic improvements. Long-term trials are needed to draw definitive conclusions.Electronic supplementary materialThe online version of this article (10.1186/s12967-018-1748-4) contains supplementary material, which is available to authorized users.

Background & aims: Bioelectrical impedance analysis-derived phase angle (PhA) has been gaining attention in the clinical evaluation of nutritional status because it is thought to be a proxy of water distribution and body cell mass; it is also associated to muscle strength and is an effective predictor of different clinical outcomes. Since an association may be expected between PhA and sarcopenia (defined by low skeletal muscle mass and impaired muscle function), the aim of this systematic review was to evaluate: a) changes in PhA due to sarcopenia; b) prevalence of sarcopenia according to PhA values; c) derivation of phase angle cutoffs for detecting sarcopenia; d) sarcopenia and PhA as predictors of clinical outcomes. Methods: A systematic research on electronic databases (PubMed, Embase, Scopus and Web of Science) from inception to January 31st, 2020 was performed according to PRISMA checklist. Using PICOS strategy, "P" corresponded to participants of any age, gender or ethnicity, "I" designated diagnosis of sarcopenia, "C" indicated subjects without sarcopenia, "O" corresponded to PhA, and "S" selected all study types. Methodological quality was assessed using the National Institute of Health (NIH) quality assessment tool. Results: Through the initial literature search and after removing duplicates and excluding papers by screening titles and abstracts, 79 potentially relevant studies were examined. Thirteen studies (7668 subjects) met the inclusion criteria. The overall risk of bias was low. Sarcopenia was associated with a significant lower PhA in seven studies out of eight, while five studies out of six reported a high prevalence of sarcopenia was in patients with low PhA. Different cutoff point values from 4.05 to 5.05 have been derived for the identification of sarcopenia. PhA and sarcopenia were independent predictors of survival in cancer patients and geriatric hospitalized patients. Conclusions: Data from the selected papers demonstrate that PhA is decreased in sarcopenic subjects and the prevalence of sarcopenia is higher in subjects with low PhA. Further studies are needed to determine to what extent PhA may be valuable in detecting low muscle quality and/or identifying sarcopenia.

Anorexia nervosa is a condition of low hemodynamic load that leads to low LVM. Even with adjustment for stroke work, however, LVM is lower than would be predicted by height, because of the effect of body weight reduction (ie, wasting of lean body mass).

Abstract-Despite current evidence suggesting that hemodynamic load is the fundamental stimulus to begin the sequence of biological events leading to the development of left ventricular hypertrophy, genotype, gender, body size, and less easily recognizable environmental factors may contribute to generate the cascade of molecular changes that eventually yield the increase in protein synthesis needed to increase left ventricular mass. However, even nonhemodynamic factors such as gender and body size eventually regulate the growth of left ventricular mass by at least in part influencing loading conditions. Consideration of measurable factors, such as gender, body size, and hemodynamic load, allows evaluation of individual echocardiographic left ventricular mass as the deviation from the level that would be required to face a gender-specific hemodynamic load at a given body size. Values of left ventricular mass that are inappropriately high for individual gender, body size, and hemodynamic load are associated with a high cardiovascular risk phenotype, even independent of the presence of arterial hypertension. Thus, the condition of inappropriately high left ventricular mass may be recognized as a more advanced stage of pathological structural changes initially induced by overload, going beyond the compensatory needs. The biological process that yields inappropriate left ventricular mass is probably linked to the protracted activity over time of biological mediators of left ventricular hypertrophy, such as proto-oncogenes and other growth factors, neurohormones, and cytokines, inducing structural modifications that initially compensate imposed overload but eventually change the structure of myocardial tissue and the composition of motor units. Key Words: hypertrophy Ⅲ gender Ⅲ genotype Ⅲ growth factors Ⅲ hemodynamics Ⅲ blood pressure M yocardial hypertrophy is the chronic adaptation of the left ventricle (LV) to increased cardiac load. Increased wall stress and strain provide a stimulus for signaling to cause mRNA transcription to increase muscular proteins. This prompt nuclear reaction is finalized to protect the myocardium from excessive wall tension by minimizing oxygen consumption and simultaneously producing sufficient strength to provide the body tissue with the required nutriment by maintaining or even increasing cardiac output. Thus, hemodynamic factors are at the basis of molecular changes that eventually yield the cascade of reactions needed to achieve those compensatory goals. [1][2][3][4] Studies and experiments performed on the pathways that lead to the increased protein synthesis that ultimately causes LV hypertrophy have provided the assumption that LV hypertrophy might also occur in the absence of clear-cut, recognizable changes in cardiac loading conditions. 5-9 Although this possibility appears to be true under experimental conditions in which direct exposures of cells to growth factors are investigated, independent of the hemodynamic factors known to be the stimuli for production of those substances...