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Components of the renin–angiotensin–aldosterone system (RAAS) are present on bone cells. One measure of RAAS activity, the aldosterone-renin-ratio (ARR), is used to screen for primary aldosteronism. Associations between ARR and bone mineral density are conflicting. This study investigated associations between ARR and peripheral quantitative computed tomography (pQCT) and impact microindentation (IMI). Male participants (n = 431) were from the Geelong Osteoporosis Study. “Likely” primary aldosteronism was defined as ARR ≥ 70 pmol/mIU. Another group, “possible” primary aldosteronism, was defined as either ARR ≥ 70 pmol/mIU or taking a medication that affects the RAAS, but not a beta blocker, and renin < 15 mU/L. Using pQCT, images at 4% and 66% of radial (n = 365) and tibial (n = 356) length were obtained. Using IMI measurements, bone material strength index (BMSi; n = 332) was determined. Associations between ARR or likely/possible primary aldosteronism and IMI or pQCT-derived bone parameters were tested using median regression. ARR and aldosterone values were not associated with any of the pQCT-derived bone variables in either unadjusted or adjusted analyses. Men with likely primary aldosteronism (n = 16), had lower adjusted total bone area (radial 66% site, − 12.5%). No associations were observed for men with possible primary aldosteronism (unadjusted or adjusted). No associations with BMSi were observed (p > 0.05). There were no associations between ARR or aldosterone and pQCT-derived bone parameters. Men with likely primary aldosteronism had lower bone area, suggesting clinically high levels of ARR may have a negative impact on bone health.

Stroke is a leading cause of death and disability and is responsible for a significant economic burden. Sarcopenia and cognitive dysfunction are common consequences of stroke, but there is less awareness of the concurrency of these conditions. In addition, few reviews are available to guide clinicians and researchers on how to approach sarcopenia and cognitive dysfunction as comorbidities after stroke, including how to assess and manage them and implement interventions to improve health outcomes. This review synthesises current knowledge about the relationship between post-stroke sarcopenia and cognitive dysfunction, including the physiological pathways, assessment tools, and interventions involved.

Dynapenia is a key contributor to physical frailty. Cognitive impairment and dementia accompany frailty, yet links between skeletal muscle and neurocognition are poorly understood. We examined the cross-sectional relationship between lower limb muscle strength and global cognitive function. Participants were 127 women aged 51–87 years, from the Geelong Osteoporosis Study. Peak eccentric strength of the hip-flexors and hip abductors was determined using a hand-held dynamometer, and dynapenia identified as muscle strength t-scores < −1. Cognition was assessed using the Mini-Mental State Examination (MMSE), and MMSE scores below the median were rated as low. Associations between dynapenia and low cognition were examined using logistic regression models. Hip-flexor dynapenia was detected in 38 (71.7%) women with low cognition and 36 (48.7%) with good cognition (p = 0.009); for hip abductor dynapenia, the pattern was similar (21 (39.6%) vs. 9 (12.2%); p < 0.001). While the observed difference for hip-flexor strength was attenuated after adjusting for age and height (adjusted Odds Ratio (OR) 1.95, 95%CI 0.86–4.41), low cognition was nearly 4-fold more likely in association with hip abductor dynapenia (adjusted OR 3.76, 95%CI 1.44–9.83). No other confounders were identified. Our data suggest that low strength of the hip abductors and low cognition are associated and this could be a consequence of poor muscle function contributing to cognitive decline or vice versa. As muscle weakness is responsive to physical interventions, this warrants further investigation.

Sarcopenia is the loss of skeletal muscle mass and function with advancing age. It involves both complex genetic and modifiable risk factors, such as lack of exercise, malnutrition and reduced neurological drive. Cognitive decline refers to diminished or impaired mental and/or intellectual functioning. Contracting skeletal muscle is a major source of neurotrophic factors, including brain-derived neurotrophic factor, which regulate synapses in the brain. Furthermore, skeletal muscle activity has important immune and redox effects that modify brain function and reduce muscle catabolism. The identification of common risk factors and underlying mechanisms for sarcopenia and cognition may allow the development of targeted interventions that slow or reverse sarcopenia and also certain forms of cognitive decline. However, the links between cognition and skeletal muscle have not been elucidated fully. This review provides a critical appraisal of the literature on the relationship between skeletal muscle health and cognition. The literature suggests that sarcopenia and cognitive decline share pathophysiological pathways. Ageing plays a role in both skeletal muscle deterioration and cognitive decline. Furthermore, lifestyle risk factors, such as physical inactivity, poor diet and smoking, are common to both disorders, so their potential role in the muscle–brain relationship warrants investigation.

Obesity is characterised by excessive body fat and is associated with several detrimental health conditions, including cardiovascular disease and diabetes. There is some evidence that people who are obese have structural and functional brain alterations and cognitive deficits. It may be that these neurophysiological and behavioural consequences are underpinned by altered plasticity. This study investigated the relationship between obesity and plasticity of the motor cortex in people who were considered obese (n = 14, nine males, aged 35.4 ± 14.3 years) or healthy weight (n = 16, seven males, aged 26.3 ± 8.5 years). A brain stimulation protocol known as continuous theta burst transcranial magnetic stimulation was applied to the motor cortex to induce a brief suppression of cortical excitability. The suppression of cortical excitability was quantified using single-pulse transcranial magnetic stimulation to record and measure the amplitude of the motor evoked potential in a peripheral hand muscle. Therefore, the magnitude of suppression of the motor evoked potential by continuous theta burst stimulation was used as a measure of the capacity for plasticity of the motor cortex. Our results demonstrate that the healthy-weight group had a significant suppression of cortical excitability following continuous theta burst stimulation (cTBS), but there was no change in excitability for the obese group. Comparing the response to cTBS between groups demonstrated that there was an impaired plasticity response for the obese group when compared to the healthy-weight group. This might suggest that the capacity for plasticity is reduced in people who are obese. Given the importance of plasticity for human behaviour, our results add further emphasis to the potentially detrimental health effects of obesity.

Dementia comprises a wide range of progressive and acquired neurocognitive disorders. Obesity, defined as excessive body fat tissue, is a common health issue world-wide and a risk factor for dementia. The adverse effects of obesity on the brain and the central nervous system have been the subject of considerable research. The aim of this review is to explore the available evidence in the field of body–brain crosstalk focusing on obesity and brain function, to identify the major research measurements and methodologies used in the field, to discuss the potential risk factors and biological mechanisms, and to identify the research gap as a precursor to systematic reviews and empirical studies in more focused topics related to the obesity–brain relationship. To conclude, obesity appears to be associated with reduced brain function. However, obesity is a complex health condition, while the human brain is the most complicated organ, so research in this area is difficult. Inconsistency in definitions and measurement techniques detract from the literature on brain–body relationships. Advanced techniques developed in recent years are capable of improving investigations of this relationship.

Background: Sarcopenic obesity refers to age-related loss of skeletal muscle mass and function, in the face of obesity. We aimed to examine the association of falls with sarcopenic obesity and its components, among elderly individuals in the population. Methods: Participants were 353 men and 245 women aged 65-98 yr of the Geelong Osteoporosis Study. Body fat and lean mass were measured using dual energy X-ray absorptiometry; body fat mass was expressed as a percentage of weight (%BF) and appendicular lean mass was adjusted for height (rALM, kg/m2). Poor physical performance was assessed using the timed up-&-go (TUG) test. Sarcopenic obesity referred to low-rALM (Tscore<- 1), poor physical performance (TUG>10 s) and obesity (%BF >25% for men, >35% for women). Fallers were identified by self-report as having had at least one fall in the previous 12 mo. Associations between sarcopenic obesity (and its components) and falls were determined using logistic regression after adjusting for age and sex. Results: In total, 219 (36.6%) had low-rALM, 205 (34.2%) had poor physical performance, 466 (77.9%) were obese and 69 (11.5%) had all three thereby meeting our criteria for sarcopenic obesity. There were 170 (28.4%) fallers; falls were more common for those with sarcopenic obesity than without (28 (40.6%) vs 142 (26.8%); p=0.017). The likelihood of a fall in association with sarcopenic obesity and its components were: sarcopenic obesity OR=1.65 (95%CI 0.96-2.85), sarcopenia OR=1.52 (0.93-2.47), poor physical performance and obesity OR=1.74 (1.16-2.61), low-rALM OR=1.41 (0.96-2.06), poor physical performance OR=1.88 (1.26-2.80), obesity OR=0.88 (0.57-1.35). Conclusion: While obesity per se was not associated with falls, there was an increased risk of falls individuals with sarcopenic obesity that was of borderline statistical significance and this appears to be largely a consequence of poor physical performance.