| 1. |
- Barber, R. M., et al.
(author)
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Healthcare access and quality index based on mortality from causes amenable to personal health care in 195 countries and territories, 1990-2015 : A novel analysis from the global burden of disease study 2015
- 2017
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In: The Lancet. - : Lancet Publishing Group. - 0140-6736 .- 1474-547X. ; 390:10091, s. 231-266
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Journal article (peer-reviewed)abstract
- Background National levels of personal health-care access and quality can be approximated by measuring mortality rates from causes that should not be fatal in the presence of effective medical care (ie, amenable mortality). Previous analyses of mortality amenable to health care only focused on high-income countries and faced several methodological challenges. In the present analysis, we use the highly standardised cause of death and risk factor estimates generated through the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) to improve and expand the quantification of personal health-care access and quality for 195 countries and territories from 1990 to 2015. Methods We mapped the most widely used list of causes amenable to personal health care developed by Nolte and McKee to 32 GBD causes. We accounted for variations in cause of death certification and misclassifications through the extensive data standardisation processes and redistribution algorithms developed for GBD. To isolate the effects of personal health-care access and quality, we risk-standardised cause-specific mortality rates for each geography-year by removing the joint effects of local environmental and behavioural risks, and adding back the global levels of risk exposure as estimated for GBD 2015. We employed principal component analysis to create a single, interpretable summary measure-the Healthcare Quality and Access (HAQ) Index-on a scale of 0 to 100. The HAQ Index showed strong convergence validity as compared with other health-system indicators, including health expenditure per capita (r=0·88), an index of 11 universal health coverage interventions (r=0·83), and human resources for health per 1000 (r=0·77). We used free disposal hull analysis with bootstrapping to produce a frontier based on the relationship between the HAQ Index and the Socio-demographic Index (SDI), a measure of overall development consisting of income per capita, average years of education, and total fertility rates. This frontier allowed us to better quantify the maximum levels of personal health-care access and quality achieved across the development spectrum, and pinpoint geographies where gaps between observed and potential levels have narrowed or widened over time. Findings Between 1990 and 2015, nearly all countries and territories saw their HAQ Index values improve; nonetheless, the difference between the highest and lowest observed HAQ Index was larger in 2015 than in 1990, ranging from 28·6 to 94·6. Of 195 geographies, 167 had statistically significant increases in HAQ Index levels since 1990, with South Korea, Turkey, Peru, China, and the Maldives recording among the largest gains by 2015. Performance on the HAQ Index and individual causes showed distinct patterns by region and level of development, yet substantial heterogeneities emerged for several causes, including cancers in highest-SDI countries; chronic kidney disease, diabetes, diarrhoeal diseases, and lower respiratory infections among middle-SDI countries; and measles and tetanus among lowest-SDI countries. While the global HAQ Index average rose from 40·7 (95% uncertainty interval, 39·0-42·8) in 1990 to 53·7 (52·2-55·4) in 2015, far less progress occurred in narrowing the gap between observed HAQ Index values and maximum levels achieved; at the global level, the difference between the observed and frontier HAQ Index only decreased from 21·2 in 1990 to 20·1 in 2015. If every country and territory had achieved the highest observed HAQ Index by their corresponding level of SDI, the global average would have been 73·8 in 2015. Several countries, particularly in eastern and western sub-Saharan Africa, reached HAQ Index values similar to or beyond their development levels, whereas others, namely in southern sub-Saharan Africa, the Middle East, and south Asia, lagged behind what geographies of similar development attained between 1990 and 2015. Interpretation This novel extension of the GBD Study shows the untapped potential for personal health-care access and quality improvement across the development spectrum. Amid substantive advances in personal health care at the national level, heterogeneous patterns for individual causes in given countries or territories suggest that few places have consistently achieved optimal health-care access and quality across health-system functions and therapeutic areas. This is especially evident in middle-SDI countries, many of which have recently undergone or are currently experiencing epidemiological transitions. The HAQ Index, if paired with other measures of health-system characteristics such as intervention coverage, could provide a robust avenue for tracking progress on universal health coverage and identifying local priorities for strengthening personal health-care quality and access throughout the world. Copyright © The Author(s). Published by Elsevier Ltd.
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| 2. |
- Kehoe, Laura, et al.
(author)
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Make EU trade with Brazil sustainable
- 2019
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In: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 364:6438, s. 341-
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Journal article (other academic/artistic)
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| 3. |
- Martin-Rincon, M., et al.
(author)
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Exercise mitigates the loss of muscle mass by attenuating the activation of autophagy during severe energy deficit
- 2019
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In: Nutrients. - : MDPI AG. - 2072-6643. ; 11:11
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Journal article (peer-reviewed)abstract
- The loss of skeletal muscle mass with energy deficit is thought to be due to protein breakdown by the autophagy-lysosome and the ubiquitin-proteasome systems. We studied the main signaling pathways through which exercise can attenuate the loss of muscle mass during severe energy deficit (5500 kcal/day). Overweight men followed four days of caloric restriction (3.2 kcal/kg body weight day) and prolonged exercise (45 min of one-arm cranking and 8 h walking/day), and three days of control diet and restricted exercise, with an intra-subject design including biopsies from muscles submitted to distinct exercise volumes. Gene expression and signaling data indicate that the main catabolic pathway activated during severe energy deficit in skeletal muscle is the autophagy-lysosome pathway, without apparent activation of the ubiquitin-proteasome pathway. Markers of autophagy induction and flux were reduced by exercise primarily in the muscle submitted to an exceptional exercise volume. Changes in signaling are associated with those in circulating cortisol, testosterone, cortisol/testosterone ratio, insulin, BCAA, and leucine. We conclude that exercise mitigates the loss of muscle mass by attenuating autophagy activation, blunting the phosphorylation of AMPK/ULK1/Beclin1, and leading to p62/SQSTM1 accumulation. This includes the possibility of inhibiting autophagy as a mechanism to counteract muscle loss in humans under severe energy deficit.
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| 6. |
- Calbet, J. A. L., et al.
(author)
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A time-efficient reduction of fat mass in 4 days with exercise and caloric restriction
- 2015
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In: Scandinavian Journal of Medicine and Science in Sports. - : Wiley. - 0905-7188 .- 1600-0838. ; 25:2, s. 223-233
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Journal article (peer-reviewed)abstract
- To determine whether a fast reduction in fat mass can be achieved in 4 days by combining caloric restriction (CR: 3.2kcal/kg body weight per day) with exercise (8-h walking+45-min arm cranking per day) to induce an energy deficit of approximate to 5000kcal/day, 15 overweight men underwent five experimental phases: pretest, exercise+CR for 4 days (WCR), control diet+reduced exercise for 3 days (DIET), and follow-up 4 weeks (POST1) and 1 year later (POST2). During WCR, the diet consisted solely of whey protein (n=8) or sucrose (n=7) (0.8g/kg body weight per day). After WCR, DIET, POST1, and POST2, fat mass was reduced by a mean of 2.1, 2.8, 3.8, and 1.9kg (P<0.05), with two thirds of this loss from the trunk; and lean mass by 2.8, 1.0, 0.5, and 0.4kg, respectively. After WCR, serum glucose, insulin, homeostatic model assessment, total and low-density lipoprotein cholesterol and triglycerides were reduced, and free fatty acid and cortisol increased. Serum leptin was reduced by 64%, 50%, and 33% following WCR, DIET, and POST1, respectively (P<0.05). The effects were similar in both groups. In conclusion, a clinically relevant reduction in fat mass can be achieved in overweight men in just 4 days by combining prolonged exercise with CR.
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| 7. |
- Calbet, Jose A. L., et al.
(author)
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Exercise Preserves Lean Mass and Performance during Severe Energy Deficit : The Role of Exercise Volume and Dietary Protein Content
- 2017
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In: Frontiers in Physiology. - : Frontiers Media SA. - 1664-042X. ; 8
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Journal article (peer-reviewed)abstract
- The loss of fat-free mass (FFM) caused by very-low-calorie diets (VLCD) can be attenuated by exercise. The aim of this study was to determine the role played by exercise and dietary protein content in preserving the lean mass and performance of exercised and non-exercised muscles, during a short period of extreme energy deficit (similar to 23 MJ deficit/day). Fifteen overweight men underwent three consecutive experimental phases: baseline assessment (PRE), followed by 4 days of caloric restriction and exercise (CRE) and then 3 days on a control diet combined with reduced exercise (CD). During CRE, the participants ingested a VLCD and performed 45 min of one-arm cranking followed by 8 h walking each day. The VLCD consisted of 0.8 g/kg body weight/day of either whey protein (PRO, n = 8) or sucrose (SU, n = 7). FFM was reduced after CRE (P < 0.001), with the legs and the exercised arm losing proportionally less FFM than the control arm [57% (P < 0.05) and 29% (P = 0.05), respectively]. Performance during leg pedaling, as reflected by the peak oxygen uptake and power output (Wpeak), was reduced after CRE by 15 and 12%, respectively (P < 0.05), and recovered only partially after CD. The deterioration of cycling performance was more pronounced in the whey protein than sucrose group (P < 0.05). Wpeak during arm cranking was unchanged in the control arm, but improved in the contralateral arm by arm cranking. There was a linear relationship between the reduction in whole-body FFM between PRE and CRE and the changes in the cortisol/free testosterone ratio (C/FT), serum isoleucine, leucine, tryptophan, valine, BCAA, and EAA (r = -0.54 to -0.71, respectively, P < 0.05). C/FT tended to be higher in the PRO than the SU group following CRE (P = 0.06). In conclusion, concomitant low-intensity exercise such as walking or arm cranking even during an extreme energy deficit results in remarkable preservation of lean mass. The intake of proteins alone may be associated with greater cortisol/free testosterone ratio and is not better than the ingestion of only carbohydrates for preserving FFM and muscle performance in interventions of short duration.
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| 8. |
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| 9. |
- Martin-Rincon, Macros, et al.
(author)
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Protein synthesis signaling in skeletal muscle is refractory to whey protein ingestion during a severe energy deficit evoked by prolonged exercise and caloric restriction
- 2019
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In: International Journal of Obesity. - : Springer Science and Business Media LLC. - 0307-0565 .- 1476-5497. ; 43:4, s. 872-882
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Journal article (peer-reviewed)abstract
- Background: Exercise and protein ingestion preserve muscle mass during moderate energy deficits. Objective: To determine the molecular mechanisms by which exercise and protein ingestion may spare muscle mass during severe energy deficit (5500 kcal/day).Design: Fifteen overweight, but otherwise healthy men, underwent a pre-test (PRE), caloric restriction (3.2 kcals/kg body weight/day) + exercise (45 min one-arm cranking + 8 h walking) for 4 days (CRE), followed by a control diet (CD) for 3 days, with a caloric content similar to pre-intervention while exercise was reduced to less than 10,000 steps per day. During CRE, participants ingested either whey protein (PRO, n = 8) or sucrose (SU, n = 7) (0.8 g/kg body weight/day). Muscle biopsies were obtained from the trained and untrained deltoid, and vastus lateralis.Results: Following CRE and CD, serum concentrations of leptin, insulin, and testosterone were reduced, whereas cortisol and the catabolic index (cortisol/total testosterone) increased. The Akt/mTor/p70S6K pathway and total eIF2α were unchanged, while total 4E-BP1 and Thr37/464E-BP1 were higher. After CRE, plasma BCAA and EAA were elevated, with a greater response in PRO group, and total GSK3β, pSer9GSK3β, pSer51eIF2α, and pSer51eIF2α/total eIF2α were reduced, with a greater response of pSer9GSK3β in the PRO group. The changes in signaling were associated with the changes in leptin, insulin, amino acids, cortisol, cortisol/total testosterone, and lean mass.Conclusions: During severe energy deficit, pSer9GSK3β levels are reduced and human skeletal muscle becomes refractory to the anabolic effects of whey protein ingestion, regardless of contractile activity. These effects are associated with the changes in lean mass and serum insulin, testosterone, and cortisol concentrations.
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| 10. |
- MARTIN-RINCON, M, et al.
(author)
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Upregulation of nicotinamide n-methyltransferase in skeletal muscle following prolongedexercise and caloric restriction
- 2017
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In: 22nd Annual Congress of the European College of Sport Science. - Cologne, Germany : DTP Publishing. - 9783981841404 ; , s. 186-
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Conference paper (peer-reviewed)abstract
- IntroductionExpression of Nicotinamide (NA) N-methyltransferase (NNMT), the enzyme responsible for the methylation of NA to methylnicotinamide (MNA), is reduced in obese and diabetic mice. In rodent liver, NNMT activity and plasma MNA levels are increased after 90min of swimming.NNMT knockdown in mice white adipose tissue increases energy expenditure, suggesting a protective role against diet-induced obesity and type-2 diabetes. The role that NNMT plays in human metabolism remains unknown. Thus, the aims of the study were 1) to determine in human skeletal muscle (sm) whether NNMT is upregulated by prolonged exercise and 2) to ascertain whether the expression of NNMT in sm is influenced by severe energy deficit.MethodsFifteen overweight men underwent to 4 days of caloric restriction (CR) (0.8 g/kg BW/day) in combination with prolonged exercise (PE) (8h walking + 45min single-arm cranking/day). Three sm biopsies (exercised/non exercised arm and one leg) were obtained before (PRE), after (PE+CR) and following 3 days of control diet (isoenergetic) and reduced exercise (CD) to measure the expression of key metabolic genes (e.g. PDK4, CPT2, PFKFB3, NNMT) (microarray), NNMT protein expression (WB) and circulating plasma MNA levels (LC-MS). Maximal fat oxidation (MFO) (indirect calorimetry) and body composition (DEXA) were measured. ANOVA repeated-measures was used.ResultsDuring PE+CR the energy deficit was 5000 kcal/d reducing fat mass by 2.8 (PE+CR) and 3.8 kg (CD). MFO was increased. CPT2, PDK4, PFKFB3 genes (CHO-to-fat metabolic shift) were differentially expressed (FDR<5%) in at least one sm. Compared to PRE, after CD, NNMT gene expression was upregulated in all sm (~3-5 fold). Protein NNMT increased ~13-fold (p<0.001), ~9-fold (p<0.01) and ~5-fold (p<0.001) for non-exercised and exercised arm (45min/day) and leg (8h/day), respectively. Circulating levels of MNA were augmented two-fold. The increase in NNMT expression from PRE to CD was associated with the increase in MFO (r=0.37, p=0.01,n=45).DiscussionThis findings reveal that NNMT is upregulated in human sm in response to a severe energy deficit, with a simultaneous increase of MNA plasma levels. However, this response was attenuated in the exercised sm. NNMT may have a role in facilitating fat oxidation. Caloric restriction elicits increased sirtuins expression and activity, coupled with the NAD+ breakdown into NA. Overexpression of NNMT probably prevents accumulation of NA, which would otherwise inhibit the sirtuins. Our data suggest sm as a plausible source of MNA, which may act as a myokine with a role in the adaptation to starvation.
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