1.
How much does reduced food intake contribute to cancer-associated weight loss?
Martin, L, Kubrak, C
Current opinion in supportive and palliative care. 2018;(4):410-419
Abstract
PURPOSE OF REVIEW An international consensus group defined cancer cachexia as a syndrome of involuntary weight loss, characterized by loss of skeletal muscle (with or without fat loss), which is driven by a variable combination of reduced food intake and altered metabolism.This review presents recent studies that evaluated the contribution of reduced food intake to cancer-associated weight loss. RECENT FINDINGS Four studies examined food intake in relation to weight loss. Heterogeneity among studies rendered aggregation and interpretation of results challenging. Despite these limitations, reduced food intake had consistent significant, independent associations with weight loss. However, reduced food intake did not explain all the variation in weight loss; and limited data suggests factors related to alterations in metabolism (e.g. increased resting energy expenditure, systemic inflammation) are also contributing to weight loss. SUMMARY Reduced food intake is a significant contributor to cancer-associated weight loss. Understanding the magnitude of the association between food intake and weight loss may improve when it is possible to account for alterations in metabolism. Efforts to align clinical assessments of food intake to reduce heterogeneity are needed.
2.
Inadequate dietary energy intake associates with higher prevalence of metabolic syndrome in different groups of hemodialysis patients: a clinical observational study in multiple dialysis centers.
Duong, TV, Wong, TC, Chen, HH, Chen, TW, Chen, TH, Hsu, YH, Peng, SJ, Kuo, KL, Liu, HC, Lin, ET, et al
BMC nephrology. 2018;(1):236
Abstract
BACKGROUND Metabolic syndrome (MetS) has been established as a risk for cardiovascular diseases and mortality in hemodialysis patients. Energy intake (EI) is an important nutritional therapy for preventing MetS. We examined the association of self-reported dietary EI with metabolic abnormalities and MetS among hemodialysis patients. METHODS A cross-sectional study design was carried out from September 2013 to April 2017 in seven hemodialysis centers. Data were collected from 228 hemodialysis patients with acceptable EI report, 20 years old and above, underwent three hemodialysis sessions a week for at least past 3 months. Dietary EI was evaluated by a three-day dietary record, and confirmed by 24-h dietary recall. Body compositions were measured by bioelectrical impedance analysis. Biochemical data were analyzed using standard laboratory tests. The cut-off values of daily EI were 30 kcal/kg, and 35 kcal/kg for age ≥ 60 years and < 60 years, respectively. MetS was defined by the American Association of Clinical Endocrinologists (AACE-MetS), and Harmonizing Metabolic Syndrome (HMetS). Logistic regression models were utilized for examining the association between EI and MetS. Age, gender, physical activity, hemodialysis vintage, Charlson comorbidity index, high sensitive C-reactive protein, and interdialytic weight gains were adjusted in the multivariate analysis. RESULTS The prevalence of inadequate EI, AACE-MetS, and HMetS were 60.5%, 63.2%, and 53.9%, respectively. Inadequate EI was related to higher proportion of metabolic abnormalities and MetS (p < 0.05). Results of the multivariate analysis shows that inadequate EI was significantly linked with higher prevalence of impaired fasting glucose (OR = 2.42, p < 0.01), overweight/obese (OR = 6.70, p < 0.001), elevated waist circumference (OR = 8.17, p < 0.001), AACE-MetS (OR = 2.26, p < 0.01), and HMetS (OR = 3.52, p < 0.01). In subgroup anslysis, inadequate EI strongly associated with AACE-MetS in groups of non-hypertension (OR = 4.09, p = 0.004), and non-cardiovascular diseases (OR = 2.59, p = 0.012), and with HMetS in all sub-groups of hypertension (OR = 2.59~ 5.33, p < 0.05), diabetic group (OR = 8.33, p = 0.003), and non-cardiovascular diseases (OR = 3.79, p < 0.001). CONCLUSIONS Inadequate EI and MetS prevalence was high. Energy intake strongly determined MetS in different groups of hemodialysis patients.
3.
AMPK activation--protean potential for boosting healthspan.
McCarty, MF
Age (Dordrecht, Netherlands). 2014;(2):641-63
Abstract
AMP-activated kinase (AMPK) is activated when the cellular (AMP+ADP)/ATP ratio rises; it therefore serves as a detector of cellular "fuel deficiency." AMPK activation is suspected to mediate some of the health-protective effects of long-term calorie restriction. Several drugs and nutraceuticals which slightly and safely impede the efficiency of mitochondrial ATP generation-most notably metformin and berberine-can be employed as clinical AMPK activators and, hence, may have potential as calorie restriction mimetics for extending healthspan. Indeed, current evidence indicates that AMPK activators may reduce risk for atherosclerosis, heart attack, and stroke; help to prevent ventricular hypertrophy and manage congestive failure; ameliorate metabolic syndrome, reduce risk for type 2 diabetes, and aid glycemic control in diabetics; reduce risk for weight gain; decrease risk for a number of common cancers while improving prognosis in cancer therapy; decrease risk for dementia and possibly other neurodegenerative disorders; help to preserve the proper structure of bone and cartilage; and possibly aid in the prevention and control of autoimmunity. While metformin and berberine appear to have the greatest utility as clinical AMPK activators-as reflected by their efficacy in diabetes management-regular ingestion of vinegar, as well as moderate alcohol consumption, may also achieve a modest degree of health-protective AMPK activation. The activation of AMPK achievable with any of these measures may be potentiated by clinical doses of the drug salicylate, which can bind to AMPK and activate it allosterically.
4.
Fructose, exercise, and health.
Johnson, RJ, Murray, R
Current sports medicine reports. 2010;(4):253-8
Abstract
The large daily energy intake common among athletes can be associated with a large daily intake of fructose, a simple sugar that has been linked to metabolic disorders. Fructose commonly is found in foods and beverages as a natural component (e.g., in fruits) or as an added ingredient (as sucrose or high fructose corn syrup [HFCS]). A growing body of research suggests that excessive intake of fructose (e.g., >50 g.d(-1)) may be linked to development of the metabolic syndrome (obesity, dyslipidemia, hypertension, insulin resistance, proinflammatory state, prothrombosis). The rapid metabolism of fructose in the liver and resultant drop in hepatic adenosine triphosphate (ATP) levels have been linked with mitochondrial and endothelial dysfunction, alterations that could predispose to obesity, diabetes, and hypertension. However, for athletes, a positive aspect of fructose metabolism is that, in combination with other simple sugars, fructose stimulates rapid fluid and solute absorption in the small intestine and helps increase exogenous carbohydrate oxidation during exercise, an important response for improving exercise performance. Although additional research is required to clarify the possible health-related implications of long-term intake of large amounts of dietary fructose among athletes, regular exercise training and consequent high daily energy expenditure may protect athletes from the negative metabolic responses associated with chronically high dietary fructose intake.