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A double-blinded, randomized, parallel intervention to evaluate biomarker-based nutrition plans for weight loss: The PREVENTOMICS study.
Aldubayan, MA, Pigsborg, K, Gormsen, SMO, Serra, F, Palou, M, Galmés, S, Palou-March, A, Favari, C, Wetzels, M, Calleja, A, et al
Clinical nutrition (Edinburgh, Scotland). 2022;41(8):1834-1844
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Obesity, and particularly abdominal adiposity, is associated with various metabolic abnormalities. Diet has a vital role in preventing and managing obesity, but evidence from clinical studies demonstrates there is a great interindividual variability in response to the same dietary intervention, which likely indicates that no one diet is superior to another. The aim of this study was to examine the efficacy of the PREVENTOMICS (empowering consumers to PREVENT diet-related diseases through OMICS sciences) platform, incorporated in an e-commerce digital tool, for producing more favourable health outcomes over dietary plans based on general diet recommendations, in subjects with overweight or obesity and elevated waist circumference. This study is a 10-week randomised single-centre, parallel-group, double-blinded intervention study. Participants were allocated in a 1:1 ratio, stratified by cluster to either the intervention group (personalised plan) or the control group (generic recommendations). Results show that there isn’t any additional benefit of personalising dietary plans, over a generic approach, on the change in fat mass and body weight in individuals with overweight or obesity and elevated waist circumference. Accordingly, personalisation of the diet did not significantly improve health parameters beyond the changes induced by the control diet. Participants in both groups lost approximately 3 kg of body weight. Authors conclude that based on their findings evidence to translate personalised nutrition approaches into clinical practice is insufficient.
Abstract
BACKGROUND & AIMS Growing evidence suggests that biomarker-guided dietary interventions can optimize response to treatment. In this study, we evaluated the efficacy of the PREVENTOMCIS platform-which uses metabolomic and genetic information to classify individuals into different 'metabolic clusters' and create personalized dietary plans-for improving health outcomes in subjects with overweight or obesity. METHODS A 10-week parallel, double-blinded, randomized intervention was conducted in 100 adults (82 completers) aged 18-65 years, with body mass index ≥27 but <40 kg/m2, who were allocated into either a personalized diet group (n = 49) or a control diet group (n = 51). About 60% of all food was provided free-of-charge. No specific instruction to restrict energy intake was given. The primary outcome was change in fat mass from baseline, evaluated by dual energy X-ray absorptiometry. Other endpoints included body weight, waist circumference, lipid profile, glucose homeostasis markers, inflammatory markers, blood pressure, physical activity, stress and eating behavior. RESULTS There were significant main effects of time (P < 0.01), but no group main effects, or time-by-group interactions, for the change in fat mass (personalized: -2.1 [95% CI -2.9, -1.4] kg; control: -2.0 [95% CI -2.7, -1.3] kg) and body weight (personalized: -3.1 [95% CI -4.1, -2.1] kg; control: -3.3 [95% CI -4.2, -2.4] kg). The difference between groups in fat mass change was -0.1 kg (95% CI -1.2, 0.9 kg, P = 0.77). Both diets resulted in significant improvements in insulin resistance and lipid profile, but there were no significant differences between groups. CONCLUSION Personalized dietary plans did not result in greater benefits over a generic, but generally healthy diet, in this 10-week clinical trial. Further studies are required to establish the soundness of different precision nutrition approaches, and translate this science into clinically relevant dietary advice to reduce the burden of obesity and its comorbidities. CLINICAL TRIAL REGISTRY ClinicalTrials.gov registry (NCT04590989).
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Structured Long-Chain Omega-3 Fatty Acids for Improvement of Cognitive Function during Aging.
Mora, I, Arola, L, Caimari, A, Escoté, X, Puiggròs, F
International journal of molecular sciences. 2022;(7)
Abstract
Although the human lifespan has increased in the past century owing to advances in medicine and lifestyle, the human healthspan has not kept up the same pace, especially in brain aging. Consequently, the role of preventive health interventions has become a crucial strategy, in particular, the identification of nutritional compounds that could alleviate the deleterious effects of aging. Among nutrients to cope with aging in special cognitive decline, the long-chain omega-3 polyunsaturated fatty acids (ω-3 LCPUFAs) docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), have emerged as very promising ones. Due to their neuroinflammatory resolving effects, an increased status of DHA and EPA in the elderly has been linked to better cognitive function and a lower risk of dementia. However, the results from clinical studies do not show consistent evidence and intake recommendations for old adults are lacking. Recently, supplementation with structured forms of EPA and DHA, which can be derived natural forms or targeted structures, have proven enhanced bioavailability and powerful benefits. This review summarizes present and future perspectives of new structures of ω-3 LCPUFAs and the role of "omic" technologies combined with the use of high-throughput in vivo models to shed light on the relationships and underlying mechanisms between ω-3 LCPUFAs and healthy aging.
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Effect of Hesperidin on Cardiovascular Disease Risk Factors: The Role of Intestinal Microbiota on Hesperidin Bioavailability.
Mas-Capdevila, A, Teichenne, J, Domenech-Coca, C, Caimari, A, Del Bas, JM, Escoté, X, Crescenti, A
Nutrients. 2020;12(5)
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Cardiovascular diseases (CVDs) cause around 31% of all deaths worldwide. Certain dietary patterns have been associated with a reduction in CVDs and so the use of natural-based products has gained importance as a preventive strategy. Hesperidin is a bioactive compound found in high levels in citrus fruits. The reported beneficial properties include antitumor, antioxidant, anti-inflammatory; cholesterol and glucose lowering effects. Many animal studies show multiple beneficial effects but are inconclusive in human studies. The aim of this review is to describe the effects of hesperidin on CVD factors and to highlight the individual differences in its bioavailability and effectiveness. The gut bacteria play an important role in this. Hesperidin is not broken down by the normal digestive process and reaches the colon largely intact. It is the job of the gut bacteria to break it down into bioavailable substances that can be absorbed and utilised. The discrepancies observed in some of the results from human clinical trials may be partly due to individual differences, including that of the gut bacteria. Further clinical trials should be considered as well as classifying individuals according to individual differences in metabotypes.
Abstract
Recently, hesperidin, a flavonone mainly present in citrus fruits, has emerged as a new potential therapeutic agent able to modulate several cardiovascular diseases (CVDs) risk factors. Animal and in vitro studies demonstrate beneficial effects of hesperidin and its derived compounds on CVD risk factors. Thus, hesperidin has shown glucose-lowering and anti-inflammatory properties in diabetic models, dyslipidemia-, atherosclerosis-, and obesity-preventing effects in CVDs and obese models, and antihypertensive and antioxidant effects in hypertensive models. However, there is still controversy about whether hesperidin could contribute to ameliorate glucose homeostasis, lipid profile, adiposity, and blood pressure in humans, as evidenced by several clinical trials reporting no effects of treatments with this flavanone or with orange juice on these cardiovascular parameters. In this review, we focus on hesperidin's beneficial effects on CVD risk factors, paying special attention to the high interindividual variability in response to hesperidin-based acute and chronic interventions, which can be partly attributed to differences in gut microbiota. Based on the current evidence, we suggest that some of hesperidin's contradictory effects in human trials are partly due to the interindividual hesperidin variability in its bioavailability, which in turn is highly dependent on the α-rhamnosidase activity and gut microbiota composition.
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Detection of Early Disease Risk Factors Associated with Metabolic Syndrome: A New Era with the NMR Metabolomics Assessment.
Hernandez-Baixauli, J, Quesada-Vázquez, S, Mariné-Casadó, R, Gil Cardoso, K, Caimari, A, Del Bas, JM, Escoté, X, Baselga-Escudero, L
Nutrients. 2020;(3)
Abstract
The metabolic syndrome is a multifactorial disease developed due to accumulation and chronification of several risk factors associated with disrupted metabolism. The early detection of the biomarkers by NMR spectroscopy could be helpful to prevent multifactorial diseases. The exposure of each risk factor can be detected by traditional molecular markers but the current biomarkers have not been enough precise to detect the primary stages of disease. Thus, there is a need to obtain novel molecular markers of pre-disease stages. A promising source of new molecular markers are metabolomics standing out the research of biomarkers in NMR approaches. An increasing number of nutritionists integrate metabolomics into their study design, making nutrimetabolomics one of the most promising avenues for improving personalized nutrition. This review highlight the major five risk factors associated with metabolic syndrome and related diseases including carbohydrate dysfunction, dyslipidemia, oxidative stress, inflammation, and gut microbiota dysbiosis. Together, it is proposed a profile of metabolites of each risk factor obtained from NMR approaches to target them using personalized nutrition, which will improve the quality of life for these patients.
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Effects of EPA and lipoic acid supplementation on circulating FGF21 and the fatty acid profile in overweight/obese women following a hypocaloric diet.
Escoté, X, Félix-Soriano, E, Gayoso, L, Huerta, AE, Alvarado, MA, Ansorena, D, Astiasarán, I, Martínez, JA, Moreno-Aliaga, MJ
Food & function. 2018;(5):3028-3036
Abstract
FGF21 has emerged as a key metabolism and energy homeostasis regulator. Dietary supplementation with eicosapentaenoic acid (EPA) and/or α-lipoic acid (LIP) has shown beneficial effects on obesity. In this study, we evaluated EPA and/or LIP effects on plasma FGF21 and the fatty acid (FA) profile in overweight/obese women following hypocaloric diets. At the baseline, FGF21 levels were negatively related to the AST/ALT ratio and HMW adiponectin. The weight loss did not cause any significant changes in FGF21 levels, but after the intervention FGF21 increased in EPA-supplemented groups compared to non-EPA-supplemented groups. EPA supplementation decreased the plasma n-6-PUFA content and increased n-3-PUFAs, mainly EPA and DPA, but not DHA. In the LIP-alone supplemented group a decrease in the total SFA and n-6-PUFA content was observed after the supplementation. Furthermore, EPA affected the desaturase activity, lowering Δ4D and raising Δ5/6D. These effects were not observed in the LIP-supplemented groups. Besides, the changes in FGF21 levels were associated with the changes in EPA, n-3-PUFAs, Δ5/6D, and n-6/n-3 PUFA ratio. Altogether, our study suggests that n-3-PUFAs influence FGF21 levels in obesity, although the specific mechanisms implicated remain to be elucidated.
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Metabolic adaptation to cancer growth: from the cell to the organism.
Escoté, X, Fajas, L
Cancer letters. 2015;(2 Pt A):171-5
Abstract
Tumour cells proliferate much faster than normal cells; nearly all anticancer treatments are toxic to both cell types, limiting their efficacy. The altered metabolism resulting from cellular transformation and cancer progression supports cellular proliferation and survival, but leaves cancer cells dependent on a continuous supply of energy and nutrients. Hence, many metabolic enzymes have become targets for new cancer therapies. In addition to its well-described roles in cell-cycle progression and cancer, the cyclin/CDK-pRB-E2F1 pathway contributes to lipid synthesis, glucose production, insulin secretion, and glycolytic metabolism, with strong effects on overall metabolism. Notably, these cell-cycle regulators trigger the adaptive "metabolic switch" that underlies proliferation.