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1.
Blueberry anthocyanin intake attenuates the postprandial cardiometabolic effect of an energy-dense food challenge: Results from a double blind, randomized controlled trial in metabolic syndrome participants.
Curtis, PJ, Berends, L, van der Velpen, V, Jennings, A, Haag, L, Chandra, P, Kay, CD, Rimm, EB, Cassidy, A
Clinical nutrition (Edinburgh, Scotland). 2022;(1):165-176
Abstract
BACKGROUND & AIMS Whilst the cardioprotective effects of blueberry intake have been shown in prospective studies and short-term randomized controlled trials (RCTs), it is unknown whether anthocyanin-rich blueberries can attenuate the postprandial, cardiometabolic dysfunction which follows energy-dense food intakes; especially in at-risk populations. We therefore examined whether adding blueberries to a high-fat/high-sugar meal affected the postprandial cardiometabolic response over 24 h. METHODS A parallel, double-blind RCT (n = 45; age 63.4 ± 7.4 years; 64% male; BMI 31.4 ± 3.1 kg/m2) was conducted in participants with metabolic syndrome. After baseline assessments, an energy-dense drink (969 Kcals, 64.5 g fat, 84.5 g carbohydrate, 17.9 g protein) was consumed with either 26 g (freeze-dried) blueberries (equivalent to 1 cup/150 g fresh blueberries) or 26 g isocaloric matched placebo. Repeat blood samples (30, 60, 90, 120, 180, 360 min and 24 h), a 24 h urine collection and vascular measures (at 3, 6, and 24 h) were performed. Insulin and glucose, lipoprotein levels, endothelial function (flow mediated dilatation (FMD)), aortic and systemic arterial stiffness (pulse wave velocity (PWV), Augmentation Index (AIx) respectively), blood pressure (BP), and anthocyanin metabolism (serum and 24 h urine) were assessed. RESULTS Blueberries favorably affected postprandial (0-24 h) concentrations of glucose (p < 0.001), insulin (p < 0.01), total cholesterol (p = 0.04), HDL-C, large HDL particles (L-HDL-P) (both p < 0.01), extra-large HDL particles (XL-HDL-P; p = 0.04) and Apo-A1 (p = 0.01), but not LDL-C, TG, or Apo-B. After a transient higher peak glucose concentration at 1 h after blueberry intake ([8.2 mmol/L, 95%CI: 7.7, 8.8] vs placebo [6.9 mmol/L, 95%CI: 6.4, 7.4]; p = 0.001), blueberries significantly attenuated 3 h glucose ([4.3 mmol/L, 95%CI: 3.8, 4.8] vs placebo [5.1 mmol/L, 95%CI: 4.6, 5.6]; p = 0.03) and insulin concentrations (blueberry: [23.4 pmol/L, 95%CI: 15.4, 31.3] vs placebo [52.9 pmol/L, 95%CI: 41.0, 64.8]; p = 0.0001). Blueberries also improved HDL-C ([1.12 mmol/L, 95%CI: 1.06, 1.19] vs placebo [1.08 mmol/L, 95%CI: 1.02, 1.14]; p = 0.04) at 90 min and XL-HDLP levels ([0.38 × 10-6, 95%CI: 0.35, 0.42] vs placebo [0.35 × 10-6, 95%CI: 0.32, 0.39]; p = 0.02) at 3 h. Likewise, significant improvements were observed 6 h after blueberries for HDL-C ([1.17 mmol/L, 95%CI: 1.11, 1.24] vs placebo [1.10 mmol/L, 95%CI: 1.03, 1.16]; p < 0.001), Apo-A1 ([1.37 mmol/L, 95%CI: 1.32, 1.41] vs placebo [1.31 mmol/L, 95%CI: 1.27, 1.35]; p = 0.003), L-HDLP ([0.70 × 10-6, 95%CI: 0.60, 0.81] vs placebo [0.59 × 10-6, 95%CI: 0.50, 0.68]; p = 0.003) and XL-HDLP ([0.44 × 10-6, 95%CI: 0.40, 0.48] vs placebo [0.40 × 10-6, 95%CI: 0.36, 0.44]; p < 0.001). Similarly, total cholesterol levels were significantly lower 24 h after blueberries ([4.9 mmol/L, 95%CI: 4.6, 5.1] vs placebo [5.0 mmol/L, 95%CI: 4.8, 5.3]; p = 0.04). Conversely, no effects were observed for FMD, PWV, AIx and BP. As anticipated, total anthocyanin-derived phenolic acid metabolite concentrations significantly increased in the 24 h after blueberry intake; especially hippuric acid (6-7-fold serum increase, 10-fold urinary increase). In exploratory analysis, a range of serum/urine metabolites were associated with favorable changes in total cholesterol, HDL-C, XL-HDLP and Apo-A1 (R = 0.43 to 0.50). CONCLUSIONS For the first time, in an at-risk population, we show that single-exposure to the equivalent of 1 cup blueberries (provided as freeze-dried powder) attenuates the deleterious postprandial effects of consuming an energy-dense high-fat/high-sugar meal over 24 h; reducing insulinaemia and glucose levels, lowering cholesterol, and improving HDL-C, fractions of HDL-P and Apo-A1. Consequently, intake of anthocyanin-rich blueberries may reduce the acute cardiometabolic burden of energy-dense meals. CLINICAL TRIAL REGISTRY NCT02035592 at www.clinicaltrials.gov.
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2.
Relative energy deficiency in sports (RED-S): elucidation of endocrine changes affecting the health of males and females.
Dipla, K, Kraemer, RR, Constantini, NW, Hackney, AC
Hormones (Athens, Greece). 2021;(1):35-47
Abstract
The purpose of this review is to present a different perspective of the relative energy deficiency syndrome, to improve understanding of associated endocrine alterations, and to highlight the need for further research in this area. The term "female athlete triad" was coined over 25 years ago to describe three interrelated components: disordered eating, menstrual dysfunction, and low bone mass. The syndrome's etiology is attributed to energy intake deficiency relative to energy expenditure required for health, function, and daily living. Recently, it became clear that there was a need to broaden the term, as the disorder is not an issue of only three interrelated problems but of a whole spectrum of insults resulting from low energy availability (LEA; i.e., insufficient energy availability to cover basic physiological demands) that can potentially affect any exerciser, irrespective of gender. The new model, termed relative energy deficiency in sport (RED-S), has received greater scrutiny in sports medicine due to its effects on both health and performance in athletes of both sexes. RED-S results from low-energy diets (intentional or unintentional) and/or excessive exercise. Energy deficiency reduces hypothalamic pulsatile release of gonadotropin-releasing hormone, this impairing anterior pituitary release of gonadotropins. In women, reduced FSH and LH pulsatility produces hypoestrogenism, causing functional hypothalamic amenorrhea and decreased bone mass. In men, it reduces testosterone and negatively affects bone health. Moreover, LEA alters other hormonal pathways, causing physiological consequences, such as alteration of the thyroid hormone signaling pathways, leptin levels, carbohydrate metabolism, the growth hormone/insulin-like growth factor-1 axis, and sympathetic/parasympathetic tone. This review explains and clarifies the effects of RED-S in both sexes.
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3.
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.
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4.
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.
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5.
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.
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6.
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.
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7.
The long-term influence of orlistat on dietary intake in obese subjects with components of metabolic syndrome.
Svendsen, M, Helgeland, M, Tonstad, S
Journal of human nutrition and dietetics : the official journal of the British Dietetic Association. 2009;(1):55-63
Abstract
BACKGROUND Orlistat is a lipase inhibitor that reduces the intestinal absorption of fat and may enhance the effects of dietary and behavioural therapy on weight loss and maintenance. The present study examined the effect of orlistat on dietary intake, especially fat intake, during long-term weight maintenance. METHODS Subjects comprised 44 men and women (aged 18-63 years; body mass index 37.5 +/- 4.3 kg m(-2)) included in the Scandinavian Multicenter study of Obese subjects with the metabolic syndrome, a 3-year clinical trial of orlistat or placebo following an 8-week, very low energy diet (VLED). Two months after the end of the trial when the use of orlistat was optional, 33 subjects remained in the study. A dietary interview based on a validated food frequency questionnaire was conducted before the VLED, after 1 year of treatment with orlistat or placebo and 2 months after the end of the trial. RESULTS At 1 year, dietary intake did not differ between the orlistat and placebo group. Energy percent (E%) fat was reduced and E% carbohydrate was increased within both groups. Two months after the end of the trial, E% fat was 32.6% (SD 6.2%) in subjects that chose to take orlistat and 27.7% (SD 5.5%) in subjects not taking orlistat [between group difference -5.0% (95% confidence interval -9.2 to -0.7); P = 0.021]. CONCLUSIONS The use of orlistat compared with placebo in a lifestyle modification programme does not appear to influence dietary intake. Subjects that chose to take orlistat after the end of the programme did not comply with dietary recommendations and this may hamper the effect of the drug.
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8.
Unlimited energy, restricted carbohydrate diet improves lipid parameters in obese children.
Dunlap, BS, Bailes, JR
Metabolic syndrome and related disorders. 2008;(1):32-6
Abstract
BACKGROUND Childhood obesity is a leading health concern. We have previously demonstrated the effectiveness of a restricted-carbohydrate, unlimited energy diet for weight reduction in elementary school-aged children. To our knowledge, there are no studies that have looked at the effect of this diet on lipid profiles in elementary school-aged children. Therefore, the objective of this pilot study was to examine the effect of a restricted-carbohydrate, unlimited protein, unlimited energy diet on lipid profiles in obese children 6 to 12 years of age. METHODS Overweight children (body mass index >97%) referred to our obesity clinic were treated with a restricted-carbohydrate (<30 grams daily), unlimited protein, and unlimited energy diet. Weight, height, body mass index, and fasting lipid profiles were obtained at baseline and at 10 weeks on each patient. RESULTS Twenty-seven patients were enrolled in our study, with a total of 18 patients returning for our 10 week follow-up (67%). The study group included 10 males and 8 females, with an age range of 6 to 12 years. Both total serum cholesterol and triglyceride levels showed a significant reduction; 24.2 (P = 0.018) and 56.9 (P = 0.015) mg/dL, respectively. CONCLUSIONS We have demonstrated a significant decrease in total cholesterol and triglycerides in elementary school-aged children after 10 weeks of a restricted-carbohydrate, unlimited protein, and unlimited energy diet. We suggest that this diet may decrease cardiovascular risk factors in obese children. Long-term studies will be needed to substantiate these data.
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9.
Evidence-based nutrition recommendations for the treatment and prevention of type 2 diabetes and the metabolic syndrome.
Mann, JI
Food and nutrition bulletin. 2006;(2):161-6
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10.
Cancer-associated cachexia and underlying biological mechanisms.
Baracos, VE
Annual review of nutrition. 2006;:435-61
Abstract
Cancer metastases (spread to distant organs from the primary tumor site) signify systemic, progressive, and essentially incurable malignant disease. Anorexia and wasting develop continuously throughout the course of incurable cancer. Overall, in Westernized countries nearly exactly half of current cancer diagnoses end in cure and the other half end in death; thus, cancer-associated cachexia has a high prevalence. The pathophysiology of cancer-associated cachexia has two principal components: a failure of food intake and a systemic hypermetabolism/hypercatabolism syndrome. The superimposed metabolic changes result in a rate of depletion of physiological reserves of energy and protein that is greater than would be expected based on the prevailing level of food intake. These features indicate a need for nutritional support, metabolic management, and a clear appreciation of the context of life-limiting illness.