Recent evidence demonstrates that tobacco smoking causes an imbalance in bone turnover, leading to lower bone mass and making bone vulnerable to osteoporosis and fracture. Tobacco smoke influences bone mass indirectly through alteration of body weight, parathyroid hormone-vitamin D axis, adrenal hormones, sex hormones, and increased oxidative stress on bony tissues. Also, tobacco smoke influences bone mass through a direct effect on osteogenesis and angiogenesis of bone. A RANKL-RANK-OPG pathway is an essential regulatory pathway for bone metabolism and its importance lies in its interaction with most of the pathophysiologic mechanisms by which smoking influences bone mass. Both first- and secondhand smoke adversely affect bone mass; smoking cessation seems to reverse the effect of smoking and improve bone health. Recent advances in research on bone turnover markers could advance scientific knowledge regarding the mechanisms by which smoking may influence bone mass.

This systematic review explored associations between smoking and health outcomes involving the musculoskeletal system. AMSTAR criteria were followed. A comprehensive search of PubMed, Web of Science, and Science Direct returned 243 articles meeting inclusion criteria. A majority of studies found smoking has negative effects on the musculoskeletal system. In research on bones, smoking was associated with lower BMD, increased fracture risk, periodontitis, alveolar bone loss, and dental implant failure. In research on joints, smoking was associated with increased joint disease activity, poor functional outcomes, and poor therapeutic response. There was also evidence of adverse effects on muscles, tendons, cartilage, and ligaments. There were few studies on the musculoskeletal health outcomes of secondhand smoke, smoking cessation, or other modes of smoking, such as waterpipes or electronic cigarettes. This review found evidence that suggests tobacco smoking has negative effects on the health outcomes of the musculoskeletal system. There is a need for further research to understand mechanisms of action for the effects of smoking on the musculoskeletal system and to increase awareness of healthcare providers and community members of the adverse effects of smoking on the musculoskeletal system.

We summarize the risk factors that may significantly contribute to racial disparities in pancreatic cancer, which is now the third leading cause of cancer deaths and projected to be second around 2030 in 12 years. For decades, the incidence rate of pancreatic cancer among Blacks has been 30% to 70% higher than other racial groups in the United States and the 5-year survival rate is approximately 5%. Diabetes and obesity have been identified as potentially predisposing factors to pancreatic cancer and both are more common among Blacks. Smoking continues to be one of the most important risk factors for pancreatic cancer and smoking rates are higher among Blacks compared to other racial groups. The overall risk of pancreatic cancer due to changes in DNA is thought to be the same for most racial groups; however, DNA methylation levels have been observed to be significantly different between Blacks and Whites. This finding may underlie the racial disparities in pancreatic cancer. Identification and prevention of these factors may be effective strategies to reduce the high incidence and mortality rates for pancreatic cancer among Blacks.

Few studies have examined the possibility that cachexia may affect men and women differently. This pilot study assessed gender differences in body composition in stomach, colorectal, and biliary cancer patients with cachexia. A sample of 38 participants (Female: Male = 17:21, mean age 57.4 years) were included if they were undergoing chemotherapy and experienced weight loss of 5% or more over a 6‐month period. Bioelectrical impedance analysis (BIA) was applied to measure body composition. Phase angle (PA) and levels of extra‐/intracellular water (ECW; ICW) were determined. Data were analyzed first by gender and then compared to age‐ and gender‐matched healthy controls from the NHANES‐III dataset. PA was lower (P < .01) in both genders compared with healthy controls, and PA was lower in female patients compared with male patients (P = .03). Male cancer patients with lower PA also had lower ICW levels compared with healthy controls (r = .98, P < .01). For female patients, PA and ICW were negatively correlated (r = .897, P < .01). A lower ECW/ICW ratio was highly correlated (r = .969 for men, r = .639 for women) with increased PA in cancer patients. ICW changes are gender‐specific in patients with GI cancer. ECW/ICW ratios and PA may be suitable surrogate markers for gender‐specific changes in cell composition and health status.

Vitamin C, well-established in immune function and a key factor in epigenetic inflammatory modifications, is only obtained through consistent dietary intake. Identifying individuals at risk for Vitamin C insufficiency may guide prevention and treatment, however, national surveillance has not been evaluated in the United States since 2006. A descriptive, cross-sectional secondary analysis was performed utilizing data from the 2003–2006 National Health and Nutrition Examination Surveys (NHANES) assessing non-institutionalized adults. Five categories of plasma Vitamin C were delineated: deficiency (<11 μmol/L), hypovitaminosis (11–23 μmol/L), inadequate (23–49 μmol/L), adequate (50–69 μmol/L), and saturating (≥70 μmol/L). Results indicated 41.8% of the population possessed insufficient levels (deficiency, hypovitaminosis, and inadequate) of Vitamin C. Males, adults aged 20–59, Black and Mexican Americans, smokers, individuals with increased BMI, middle and high poverty to income ratio and food insecurity were significantly associated with insufficient Vitamin C plasma levels. Plasma Vitamin C levels reveal a large proportion of the population still at risk for inflammatory driven disease with little to no symptoms of Vitamin C hypovitaminosis. Recognition and regulation of the health impact of Vitamin C support the goal of Nutrition and Healthy Eating as part of the Healthy People 2030.

Background: Unintentional weight loss is a major problem for patients with gastrointestinal (GI) cancers because it affects treatment, survival outcomes, and quality of life. To date, little is known about the trajectory of weight loss and the relationship between baseline body mass index (BMI), location of the cancer, and outcomes. The aims of this study were to investigate patterns of weight loss over time in patients with GI cancer according to BMI groups (low, normal, and high) and location of cancer.Methods: We examined de‐identified electronic medical record data of 801 adults (>21 years) with GI cancer using ICD‐9 codes (150–159). Descriptive statistics and linear mixed models were used to examine unintentional weight loss over time by BMI group (low, normal, and high) and to determine the effect of primary cancer site and patient characteristics on weight loss.Results: The mean age of patients was 66.5 ± 11.9 years (21–95 years), with 58% male and 86% White. Mean weight loss over 3 years was 21.39 kg. At the first observation point, 7.8% were in the low BMI group, 30.1% were in the normal, and 62% were in the high group. At the end of observation, a majority of deaths (35.5%) occurred in the low BMI group (BMI < 20 kg/m²). Significant weight loss was observed in patients with gastric (t = −5.11, P < 0.001), oesophageal (t = −4.18, P < 0.001), and pancreatic (35.8%, t = −3.58, P < 0.001) cancers. Predictors of weight change were gender (F = 64.93, P < 0.001), cancer stage (F = 7.28, P < 0.001), and site by days (F = 8.24, P < 0.001). Weight loss rates were similar among the three BMI groups, but patterns were different based on primary cancer type as a function of days within each group.Conclusions: Weight loss in patients with GI cancers has implications for survival. Patients with upper GI cancers experienced more weight loss and decreased survival rates compared with patients with lower GI cancers. Patients with a combination of upper GI cancer (oesophagogastric or pancreatic) and low baseline BMI had the fewest survival days and worst patient outcomes. Early intervention for weight management plays a critical role for improving the health outcomes and fatality rates of these patients.