Sarcopenia, the age-related decline in skeletal muscle mass and function, is one of the main contributors to morbidity and physical disability (1). In women, menopause may contribute to sarcopenia, which not only affects very old wom-en but can also have impact on middle-aged adults (2). Changes in the gonadal hormones dur-ing the menopause transition appear to be a strong determinant of skeletal muscle mass in women. . . .

Background: Acid-base homeostasis impacts bone health. Acidosis is associated with negative calcium balance and directly enhances osteoclast activity and bone resorption. The study aimed to ascertain whether dietary acidity (dietary protein intake to potassium intake ie, estimate of net endogenous noncarbonic acid production (NEAP)) is associated with femoral and spine bone density as well as bone turnover in postmenopausal women with osteopenia.Methods: The present cross-sectional study was carried out on 51 healthy postmenopausal women aged 45-60 years.Bone mineral density (BMD) was measured by Dual Energy XDownloaded ray Absorptiometry at lumbar spine and total hip. All women were osteopenic according to WHO criteria. Dietary intake was assessed using 2 days 24 hours food recalls. Bone resorption was calculated by measuring carboxy-terminal telopeptide of type I collagen (crosslaps) and bone formation by measuring serum osteocalcin. NEAP was estimated using the following algorithm: NEAP (mEq/d)= -10.2+54.5 (Pro/K).Results: Mean±SD of NEAP was 44.6±18.4 mEq/d. After adjustment for energy intake,higher NEAP was correlated with lower spine and femoral BMD (r= -0.3,p<0.05,for both). No significant correlation was seen for bone turnover markers.Conclusion: These findings provide evidence of a link between a ratio of lower protein to higher potassium dietary intake (ie, less dietary acid) and skeletal integrity.

Background: Premature menopause is characterized by amenorrhea before age of 40 years, markedly raised serum luteinizing hormone (LH) level, follicle-stimulating hormone (FSH) level and reduced serum level of estradiol. Genome-wide analysis suggested several loci associated with premature menopause. Here, we aimed to analyze association of variants at the MCM8, FNDC4, PRRC2A, TLK1, ZNF346 and TMEM150B gene loci with premature menopause. Materials and Methods: In this cross-sectional study, a total of 117 women with premature menopause were compared to 183 healthy women. Anthropometric indices were measured in all participants: height, weight, body mass index (BMI), waist circumference (WC) and wrist circumference. Eight single-nucleotide polymorphisms (SNPs) of the indicated genes (rs16991615, rs244715, rs451417, rs1046089, rs7246479, rs4806660, rs10183486 and rs2303369) were identified from the literature. Genotyping was performed using tetra-ARMS polymerase chain reaction (PCR) and ASO-PCR methods. Results: T allele of the rs16991615, rs1046089, rs7246479 and rs10183486, C allele of rs244715, rs451417 and rs4806660 as well as TT genotype of rs2303369 were associated with an increased risk of premature menopause, likely causing susceptibility to primary ovarian insufficiency (POI) in comparison with C allele. We also found an association between the rs16991615 SNP with premature menopause. Frequency of the minor allele in cases was increased for all SNPs in comparison with controls. All minor alleles, except for rs2303369, showed a statistically significant increased odds ratio (OR). However, after Bonferroni correction for multiple testing, none of the P values were remained significant. Conclusion: The selected polymorphisms in MCM8, FNDC4, PRRC2A, TLK1, ZNF346 and TMEM150B genes may potentially affect susceptibility to premature menopause, although replication of the results in larger cohort could clarify this.