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Background: Age-related declines in taste and smell function are widely assumed to contribute to the decrease in appetite and the development of undernutrition in older adults., Objectives: Here we aim to assess the associations of both taste and smell function with several nutrition-related outcomes in a single study, with poor appetite and undernutrition as primary outcomes., Methods: This is a cross-sectional cohort study of 359 community-dwelling Dutch older adults, aged 65-93 y. Taste function was measured for all 5 basic tastes. Smell function was assessed with 3 tests: for odor identification, discrimination, and threshold. Self-reported taste and smell, appetite, energy (kcal/d) and macronutrient (% energy) intake, and covariates were assessed with extensive questionnaires. Dietary quality was calculated using the Dutch Healthy Diet index 2015, Alternative Healthy Eating Index 2010, and Mediterranean Diet Score. Body measurements included body weight (current and 2 y prior), height, and body impedance analysis. Data were analyzed via multiple logistic and linear regression., Results: Of our sample, 9.2% had poor taste and 17.0% poor smell, 6.1% had poor appetite, and 21.4% were undernourished. Self-reported poor taste (OR: 8.44; 95% CI: 1.56, 45.56; P = 0.013) was associated with poor appetite, but no other taste or smell score was associated with either poor appetite or undernutrition. Some associations were found of individual taste and smell scores with macronutrient intake and dietary quality. Self-reported poor taste and smell were both consistently associated with poorer dietary quality., Conclusions: In community-dwelling older adults, specific taste and smell impairments may have diverse consequences for appetite, food intake, or dietary quality. However, this does not necessarily result in undernutrition. The consistent associations of self-reported poor taste and smell with poor dietary quality do underline the usefulness of this information when screening for nutritional risk., (© The Author(s) 2021. Published by Oxford University Press on behalf of the American Society for Nutrition.)

Background & Aims: Lower birth weight is associated with an increased risk of cardiovascular and metabolic disease. These associations may, at least in part, be explained by alterations in dietary intake in later life. The aim of this study is to examine whether lower birth weight is associated with alterations in dietary intake in later life, and whether this association is due to intrauterine environmental or genetic factors., Methods: In this observational study birth weight and dietary intake were investigated in 78 dizygotic (DZ) and 94 monozygotic (MZ) adolescent same-sex twin subjects. Birth weight was obtained from the mothers. Dietary intake was assessed by two-day dietary records., Results: In the total group of twins, lower birth weight was associated with higher intake of saturated fat after adjustment for current weight (1.2 per cent of total energy intake (E%) per kg increase in birth weight, P < 0.01). Intra-pair analysis in all twin pairs demonstrated that twins with the lower birth weight had a 115 kcal higher total energy intake and a 0.7 E% higher saturated fat intake compared to their co-twins with the higher birth weight (P < 0.05). Intra-pair differences in birth weight were negatively associated with differences in energy intake and differences in intake of saturated fat after adjustment for differences in current weight (P = 0.07 and P < 0.05, respectively). Intra-pair differences in birth weight were positively associated with intra-pair differences in intake of dietary fibres (P < 0.05). These intra-pair differences and associations were similar for DZ and MZ twins (P for difference > 0.6)., Conclusions: Lower birth weight was related with higher intake of energy and saturated fat within twin pairs, and these associations were independent of zygosity, suggesting that the association between birth weight and alterations in dietary intake in later life is explained by intrauterine environmental rather than genetic factors., (Copyright © 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.)

Low birth weight is associated with an increased risk of atherothrombosis, which may be related in part to the association between low birth weight and high plasma fibrinogen. The association between birth weight and fibrinogen may be explained by intrauterine, socio-economic or genetic factors. We examined birth weight and fibrinogen in 52 dizygotic and 56 adolescent monozygotic (genetically identical) twin pairs. The dizygotic but not the monozygotic twins with the lowest birth weight from each pair had a fibrinogen level that was higher compared with their co-twins with the highest birth weight [dizygotic twins: 2.62 +/- 0.46 g L(-1) vs. 2.50 +/- 0.41 g L(-1) (P = 0.04); monozygotic twins: 2.42 +/- 0.45 g L(-1) vs. 2.49 +/- 0.39 g L(-1) (P = 0.2)]. These findings suggest that the association between birth weight and plasma fibrinogen is abolished after the elimination of genetic influences and therefore that this association has genetic causes. Improvement of intrauterine nutrition may not lower fibrinogen levels in later life.

Central obesity is increasingly recognized as a risk factor for atherosclerosis and type 2 diabetes mellitus. Here we present a hypothesis that may explain the excess atherosclerosis, endothelial dysfunction and progressive beta-cell failure. Central obesity is associated with increased cytosolic triglyceride stores in non-adipose tissues such as muscles, liver and pancreatic beta-cells. A high cytosolic triglyceride content is accompanied by elevated concentrations of cytosolic long-chain acyl-CoA esters, the metabolically active form of fatty acids. These esters inhibit mitochondrial adenine nucleotide translocators, resulting in an intramitochondrial ADP deficiency. In vitro, such ADP deficiency is a potent stimulator of mitochondrial oxygen free radical production, and we assume that this mechanism is also active in vivo. The decline of organ function with normal ageing is thought to be due, at least partly, to a continuous low-grade mitochondrial oxygen free radical production. In tissues containing increased cytosolic triglyceride stores this process will be accelerated. Tissues with a high-energy demand or poor free radical scavenging capacity, such as pancreatic beta-cells, are likely to be more susceptible to this process. This is how we explain their gradual dysfunctioning in central obesity. Likewise we propose that the enhanced production of oxygen free radicals in endothelial cells, or vascular smooth muscle cells, leads to the increased subendothelial oxidation of LDL and atherosclerosis, as well as to the endothelial dysfunction and microalbuminuria.