Publications by authors named "Owen J Kelly"

This is the third review in our series examining the connection between osteosarcopenic adiposity/obesity (OSA/OSO) syndrome and health impairments. The objective here was to examine whether there is a causal and/or bidirectional relationship between OSA and some chronic diseases. The search (in PubMed, Scopus, and WoS), screened for articles from their inception to the end of February 2024.

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Over the millennia, patterns of food consumption have changed; however, foods were always whole foods. Ultra-processed foods (UPFs) have been a very recent development and have become the primary food source for many people. The purpose of this review is to propose the hypothesis that, forsaking the evolutionary dietary environment, and its complex milieu of compounds resulting in an extensive metabolome, contributes to chronic disease in modern humans.

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The objectives were to examine if there is a causal relationship between osteosarcopenic adiposity (OSA) syndrome (coexistence of osteopenia/osteoporosis, sarcopenia, and excess adiposity) and cardiometabolic disorders or if these disorders initiate the development of OSA and its worsening. The search was conducted in PubMed, Scopus, and Web of Science to include articles up to the end of 2023. Of n=539 articles retrieved, n=15 met the eligibility criteria.

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Adiposity is central to aging and several chronic diseases. Adiposity encompasses not just the excess adipose tissue but also body fat redistribution, fat infiltration, hypertrophy of adipocytes, and the shifting of mesenchymal stem cell commitment to adipogenesis. Bone marrow adipose tissue expansion, inflammatory adipokines, and adipocyte-derived extracellular vesicles are central to the development of osteopenic adiposity.

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A low-protein diet (LPD) is recommended to patients with non-dialysis advanced chronic kidney disease (CKD) for delaying renal function decline. However, this approach potentially prevents an adequate calorie and micronutrient intake. We examined the influence of an LPD including a renal-specific oral nutrition supplement (RONS) on the nutrition status of patients with stage 3b-5 CKD.

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Type 2 diabetes is associated with an increased risk for sarcopenia. Moreover, sarcopenia correlates with increased risk for falls, fractures, and mortality. This study aimed to explore relationships among nutrient intakes, diet quality, and functional limitations in a sample of adults across levels of glycemic control.

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Background: Obesity and chronic disease risk are significantly related to healthy lifestyle behavior, including dietary intakes. Further, the interrelated etiology of many chronic conditions supports the comorbidity in US adults to manage multiple diagnoses. The purpose of this study was to assess diet quality across varying numbers of existing conditions, including obesity, hypercholesterolemia, hyperglycemia, and hypertension.

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The present study investigated the meal patterns across demographic characteristics in middle-aged and older US adults. Study participants were noninstitutionalized participants from the 2005-2016 National Health and Nutrition Examination Survey, an observational cross-sectional study. Data from 17,361 adults were categorized into 45-59 years ( = 7366), 60-70 years ( = 5348), and 71+ years ( = 4647) to compare demographics, nutrient intakes, and meal patterns.

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Several studies have investigated the possibility of dairy foods and calcium (Ca) mediating weight and body composition, but a consensus has not been reached. We aimed to investigate weight-loss-related outcomes during intervention with low-fat dairy foods or Ca + vitamin D supplements, both as complements to hypocaloric diets. Overweight/obese Caucasian, early-postmenopausal women ( = 135) were recruited for a 6 month energy-restricted weight loss study complemented with either low-fat dairy foods (D; 4-5 servings/day), or Ca + vitamin D supplements (S); both to amount a total of ~1500 mg/day and 600 IU/day of Ca and vitamin D, respectively, or placebo pills (C).

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Osteosarcopenic obesity (OSO) syndrome describes the simultaneous deterioration of bone, muscle and excess fat, resulting in reduced functionality and systemic metabolic dysregulation. The key component contributing to this may be ectopic fat in the viscera, bone and muscle. OSO research to date is summarized, and the revised criteria for its identification for research purposes are reviewed and proposed, including new criteria to assess visceral fat in males and females.

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We recently showed that using micronutrient ratios in nutritional research might provide more insights into how diet affects metabolism and health outcomes, based on the notion that nutrients, unlike drugs, are not consumed one at a time and do not target a single metabolic pathway. In this paper, we present a concept of macronutrient ratios, including intra- and inter-macronutrient ratios. Macronutrient intakes from food only, from the What We Eat in America website (summarized National Health and Nutrition Examination Survey data) were transposed into Microsoft Excel to generate ratios.

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The 2015 US dietary guidelines advise the importance of good dietary patterns for health, which includes all nutrients. Micronutrients are rarely, if ever, consumed separately, they are not tissue specific in their actions and at the molecular level they are multitaskers. Metabolism functions within a seemingly random cellular milieu however ratios are important, for example, the ratio of adenosine triphosphate to adenosine monophosphate, or oxidized to reduced glutathione.

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In vascular diseases, including hypertension and atherosclerosis, vascular endothelial dysfunction (VED) occurs secondary to altered function of endothelial nitric oxide synthase (eNOS). A novel redox regulated pathway was identified through which eNOS is uncoupled due to -glutathionylation of critical cysteine residues, resulting in superoxide free radical formation instead of the vasodilator molecule, nitric oxide. In addition, the redox sensitive cofactor tetrahydrobiopterin, BH, is also essential for eNOS coupling.

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Loss of muscle mass during periods of disuse likely has negative health consequences for older adults. We have previously shown that β-hydroxy-β-methylbutyrate (HMB) supplementation during 10 days of strict bed rest (BR) attenuates the loss of lean mass in older adults. To elucidate potential molecular mechanisms of HMB effects on muscle during BR and resistance training rehabilitation (RT), we examined mediators of skeletal muscle mitochondrial dynamics, autophagy and atrophy, and intramyocellular lipids.

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Aging affects almost all physiological processes, but changes in body composition and body phenotype are most observable. In this review, we focus on these changes, including loss of bone and muscle and increase in body fat or redistribution of the latter, possibly leading to osteosarcopenic obesity syndrome. We also address low-grade chronic inflammation, prevalent in aging adults and a cause of many disorders including those associated with body composition.

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Osteosarcopenic obesity syndrome (OSO) has recently been identified as a condition encompassing osteopenia/osteoporosis, sarcopenia and obesity. OSO is especially deleterious in older adults (even if they are not obese by conventional measures), due to age-related redistribution of fat and its infiltration into bone and muscle. Osteoporosis and bone fractures in elderly increase the risk of sarcopenia, which, through decreased mobility, increases the risk of more falls and fractures, creating a vicious cycle.

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Conditions related to body composition and aging, such as osteopenic obesity, sarcopenia/sarcopenic obesity, and the newly termed osteosarcopenic obesity (triad of bone muscle and adipose tissue impairment), are beginning to gain recognition. However there is still a lack of definitive diagnostic criteria for these conditions. Little is known about the long-term impact of these combined conditions of osteoporosis, sarcopenia, and obesity in older adults.

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Background: Aging, chronic inflammation and/or many chronic conditions may result in loss of bone, loss of muscle and increased adiposity, manifested either overtly (overweight) or furtively as fat infiltration into bone and muscle. This combined condition has been identified as osteosarcopenic obesity. Micronutrients are required, not just to prevent deficiency diseases, but for optimal health and metabolic homeostasis.

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Background: Osteosarcopenic obesity, the combined deterioration of bone, muscle and fat tissues, could become the ultimate trajectory of aging. Aging stem cells are deregulated by low-grade chronic inflammation and possibly by diet. The metabolic shift of stem cells towards adipogenesis results in osteo obesity, sarco obesity and obesity.

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Background: Body composition changes occur with aging; bone and muscle mass decrease while fat mass increases. The collective term for these changes is osteosarcopenic obesity. It is known that conventional resistance exercise programs build/maintain lean mass and reduce fat mass.

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Some of the universal characteristics of pre-agricultural hominin diets are strikingly different from the modern human diet. Hominin dietary choices were limited to wild plant and wild animal foods, while the modern diet includes more than 70 % of energy consumed from refined sugars, refined vegetable oils, and highly processed cereals and dairy products. The modern diet, with higher intake of fat has also resulted in a higher ratio of omega-6 (n-6) to omega-3 (n-3) polyunsaturated fatty acids (PUFA), contributing to low-grade chronic inflammation (LGCI) and thus promoting the development of many chronic diseases, including obesity and osteoporosis.

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While sarcopenia and sarcopenic obesity have been recognized in the last decade, a combined concept to include decreased muscle mass and strength, as well as decreased bone mass with coexistence of adiposity is discussed here. We introduce a new term, osteopenic obesity, and operationalize its meaning within the context of osteopenia and obesity. Next, we consolidate osteopenic obesity with the already existing and more familiar term, sarcopenic obesity, and delineate the resulting combined condition assigning it the term osteosarcopenic obesity.

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The overconsumption of n-6 polyunsaturated fatty acids (PUFA), resulting in a high ratio of n-6 to n-3 PUFA, may contribute to the increased pathogenesis of obesity and osteoporosis by promoting low-grade chronic inflammation (LGCI). As evidence suggests, both obesity and osteoporosis are linked on a cellular and systemic basis. This review will analyze if a relationship exists between LGCI, fat, bone, and n-3 PUFA.

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Whole fat milk and dairy products (although providing more energy compared to low- or non-fat products), are good sources of α-linolenic acid (ALA), conjugated linoleic acid (CLA) and calcium, which may be favorable in modulating bone and adipose tissue metabolism. We examined individual and/or synergistic effects of ALA, CLA and calcium (at levels similar to those in whole milk/dairy products) in regulating bone and adipose cell growth. ST2 stromal, MC3T3-L1 adipocyte-like and MC3T3-E1 osteoblast-like cells were treated with: (a) linoleic acid (LNA):ALA ratios = 1-5:1; (b) individual/combined 80-90 % c9, t11 (9,11) and 5-10 % t10, c12 (10,12) CLA isomers; (c) 0.

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