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Diet and physical activity are two major lifestyle factors that play a role in the prevention or management of debilitating conditions affecting older people. Both under- and overnutrition predispose to diseases. Low sodium and high potassium intakes, as well as the consumption of fruits and vegetables are associated with a reduction of hypertension and diseases arising from hypertension such as stroke and dementia. Dietary patterns (consumption of quantity and types of fats, cholesterol, vegetable oils, fish) are important in the prevention of coronary heart disease. Calcium and vitamin D intakes are important factors in the development of osteoporosis, while various dietary factors have been linked to the development of cancer. Physical activity is important in the prevention of functional decline and increased survival, reduced incidence of falls and fractures, and has various cardiovascular health benefits. Apart from prevention of diseases, exercise also has an important role in improving function in some chronic diseases such as heart failure or chronic obstructive pulmonary disease. Both diet and exercise interact, so that public health recommendations often take the form of lifestyle modification advice in the prevention of disease and disability.
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PMID:Relationships among diet, physical activity and other lifestyle factors and debilitating diseases in the elderly. 1104 Oct 86

Diabetes mellitus, hyperlipidemia, hypertension and atherosclerotic diseases have recently defined as typical life style-related diseases. A common background of these life style-related diseases is overnutrition and its consequence, obesity. Recent advances in the biology of adipose tissue have revealed that adipose is not simply an energy storage organ but it also secretes a variety of molecules which affect the metabolism of the whole body. Through a systematic search of active genes in adipose tissue, we found that adipose tissue, especially visceral fat expressed numerous genes for secretory proteins. Among them, plasminogen activator inhibitor-1(PAI-1) was over expressed in the visceral fat in an animal model of obesity. Plasma level of PAI-1 was closely correlated with visceral adiposity in human. Thus, PAI-1 secreted from visceral fat may play an important role in vascular disease in visceral obesity. Adiponectin, a novel adipose-specific gene product, is abundantly presented in human plasma. This molecule has been shown to have protective roles against atherosclerotic vascular changes and its plasma level is negatively correlated with visceral adiposity. In conclusion, dysregulated secretion of these adipose-specific secretory proteins(adipocytokines) may have important roles in the development of life style-related diseases, especially atherosclerotic diseases.
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PMID:[Life style-related disease]. 1119 54

Undernutrition is being rapidly reduced in India and China. In both countries the diet is shifting toward higher fat and lower carbohydrate content. Distinct features are high intakes of foods from animal sources and edible oils in China, and high intakes of dairy and added sugar in India. The proportion of overweight is increasing very rapidly in China among all adults; in India the shift is most pronounced among urban residents and high-income rural residents. Hypertension and stroke are relatively higher in China and adult-onset diabetes is relatively higher in India. Established economic techniques were used to measure and project the costs of undernutrition and diet-related noncommunicable diseases in 1995 and 2025. Current WHO mortality projections of diet-related noncommunicable diseases, dietary and body composition survey data, and national data sets of hospital costs for healthcare, are used for the economic analyses. In 1995, China's costs of undernutrition and costs of diet-related noncommunicable diseases were of similar magnitude, but there will be a rapid increase in the costs and prevalence of diet-related noncommunicable diseases by 2025. By contrast with China, India's costs of undernutrition will continue to decline, but undernutrition costs did surpass overnutrition diet-related noncommunicable disease costs in 1995. India's rapid increase in diet-related noncommunicable diseases and their costs projects similar economic costs of undernutrition and overnutrition by 2025.
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PMID:Trends in diet, nutritional status, and diet-related noncommunicable diseases in China and India: the economic costs of the nutrition transition. 1176 8

When the fetus growth in an unfavorable intrauterine environment, this process has implications in the adult life, that predisposes to suffer metabolic abnormalities as obesity, hypertension and non-insulin dependent diabetes mellitus. The unfavorable intrauterine environment includes the pregnancy with diabetes mellitus, pregnancy with gestational diabetes, and pregnancy with maternal undernutrition. Multiple epidemiological studies developed in North America and Europe appear to broadly confirm the association of the low birth weight in babies borne at term, with the glucose metabolism impairments in the adult life. An implication of metabolic impairments on high birth weight for the gestational age has been founded. This alteration could start when there are changes in nutritional habits in migrate populations, having number and function of the pancreatic islets altered, maybe because during fetal life they were faced to blood fluid decreased, and nutrients also decrease as well as the differentiation of cells was modified, as an important intent for fetal survival. The prevalence of type 2 diabetes has been reported in 13 to 25% for low birth weight. On the other hand, maternal hyperglycemia leads to beta-cell hyperplasia in the fetus, by a constant stimulus over the insulin production which stimulates the use of glucose as nutrients, leading to the increase in fetal weight and determining genetic changes. In overnutrition conditions, the prevalence of type 2 diabetes has been reported of 8 to 18%. Growth of tissues has critical periods at different times and intrauterine environment can be one mechanism for may permanently changes in pancreas structure and hormonal secretion patterns. Thus, the hypothesis that autoprotective fetal changes during the intrauterine life occur, took place, specially during the critical period of development, leaves to permanent changes called "programmed changes", including an endocrine disturbance of pancreatic functions, appearing in adult life. Further molecular studies of pancreatic islets are necessary in order to determine the mechanisms for lifelong changes and insulin metabolism due to intrauterine growth.
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PMID:[Fetal weight at weight as predisposing risk factor for type 2 diabetes in adulthood]. 1181 27

The underlying determinants of cardiovascular risk are governed by both genetic and lifestyle factors. One of the major adverse outcomes of unhealthy lifestyles is obesity, the genesis of which begins in childhood. Obesity, an important risk factor for atherosclerotic cardiovascular disease, type 2 diabetes, and hypertension, persists (tracks) strongly from adolescent years to adulthood. Secular trends toward increased obesity in the past 25 years have occurred in children and adults alike. Of interest, baseline adiposity precedes hyperinsulinemia in all age groups, independently of race, sex, and baseline insulin levels. Adiposity is an independent predictor of the risk of developing the cluster of risk variables of the metabolic syndrome X, beginning in childhood. Exposure to a multiple risk factor burden over time enhances the development of coronary atherosclerosis and hypertensive cardiovascular disease. In fact, autopsy studies in youths have shown that the extent of fibrotic atherosclerotic plaques in coronary arteries, measured antemortem, increases markedly with the presence of syndrome X risk variables. Further, in overweight children, insulin levels are associated with left ventricular mass. In young people, overnutrition, coupled with physical inactivity, leads to weight gain. Since obesity, unhealthy dietary habits, and a sedentary lifestyle are interrelated and modifiable, prevention and intervention must begin in early life. (c)2001 CHF, Inc.
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PMID:Emergence of obesity and cardiovascular risk for coronary artery disease: the Bogalusa Heart Study. 1182 87

During the last five decades the metabolic syndrome has turned into an epidemic in countries with overnutrition and low levels of physical activity. About 15% of the population aged 40-75 in these countries exhibit exhibit the 'metabolic syndrome' cluster diseases. We define the metabolic syndrome as a cluster of diseases with at least three of the following components diagnosed in any one subject: ITG/type 2 diabetes, android obesity, dyslipidemia, hypertension, hyperuricemia, albuminuria and atherosclerosis. Insulin resistance was found in more than 80% of both the clinical type 2 diabetics and the subjects with IGT in the RIAD study. Intra-abdominal obesity and lipotoxicity are other important causes. Today the metabolic syndrome is--and for the near future will continue to be--the most important source of new diabetics, as well as a major cause of coronary heart disease.
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PMID:[The metabolic syndrome and its epidemiologic dimensions in historical perspective]. 1201 62

Early life nutrition impacts on subsequent risk of obesity and hypertension. Several brain chemicals responsible for both feeding and cardiovascular regulation are altered in obesity. We examined effects of early postnatal overnutrition on blood pressure, brain neuropeptide Y (NPY), and adiposity markers. Rat pup litters were adjusted to either 3 or 12 male animals (overnutrition and control, respectively) on day 1 of life. After weaning, rats were given either a palatable high-fat diet or standard chow. Smaller litter pups were significantly heavier by 17 days of age. By 16 wk, the effect of litter size was masked by that of diet, postweaning. Small and normal litter animals fed a high-fat diet had similar increases in body weight, plasma insulin, leptin, and adiponectin concentrations, leptin mRNA, and fat masses relative to chow-fed animals. An increase in 11beta-hydroxysteroid dehydrogenase-1 mRNA in white adipose tissue, and a decrease in uncoupling protein-1 mRNA in brown adipose tissue in both small litter groups at 16 wk of age, may represent a programming effect of the altered litter size. NPY concentration in the paraventricular nucleus of the hypothalamus was reduced in high fat-fed groups. Blood pressure was significantly elevated at 13 wk in high-fat-fed animals. This study demonstrates that overnourishment during early postnatal development leads to profound changes in body weight at weaning, which tended to abate with maturation. Thus the effects of long-term dietary intervention postweaning can override those of litter size-induced obesity.
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PMID:Early dietary intervention: long-term effects on blood pressure, brain neuropeptide Y, and adiposity markers. 1564 56

The aim of this editorial was to discuss evidence indicating a role for low-grade inflammation as a pathogenetic event of the metabolic syndrome. The metabolic syndrome has emerged as an important cluster of risk factors for atherosclerotic disease. Common features are central (abdominal) obesity, insulin resistance, hypertension, and dyslipidemia, namely high triglycerides and low high-density lipoprotein cholesterol. According to the clinical criteria developed by ATP III, it has been estimated that 1 out of 4 adults living in the United States merits the diagnosis. The presence of the metabolic syndrome is highly prognostic of future cardiovascular events. Chronic inflammation may represent a triggering factor in the origin of the metabolic syndrome: stimuli such as overnutrition, physical inactivity, and ageing would result in cytokine hypersecretion and eventually lead to insulin resistance and diabetes in genetically or metabolically predisposed individuals. Alternatively, resistance to the anti-inflammatory actions of insulin would result in enhanced circulating levels of proinflammatory cytokines resulting in persistent low-grade inflammation. A generally enhanced adipose tissue derived cytokine expression may be another plausible mechanism for the inflammation/metabolic syndrome relationship. The role of adipose tissue as an endocrine organ capable of secreting a number of adipose tissue-specific or enriched hormones, known as adipokines, is gaining appreciation. Although the precise role of adipokines in the metabolic syndrome is still debated, an imbalance between increased inflammatory stimuli and decreased anti-inflammatory mechanisms may be an intriguing working hypothesis. The proinflammatory state that accompanies the metabolic syndrome associates with both insulin resistance and endothelial dysfunction, providing a connection between inflammation and metabolic processes which is highly deleterious for vascular functions.
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PMID:The metabolic syndrome and inflammation: association or causation? 1567 55

In this review, we attempt to deduce teleologically the physiological mission of leptin. Because overnutrition and diet-induced obesity are the only known causes of hyperleptinemia, we contrast the differences in overnutrition in normally leptinized rodents, in which the added lipids are confined to adipocytes, with those of unleptinized rodents, in which the added lipids are distributed in liver, pancreatic islets, and heart and skeletal muscle, causing organ dysfunction and cell death with a disease cluster resembling metabolic syndrome. We focus here on lipid-induced cardiac dysfunction and the remarkable ability of hyperleptinemia to prevent it. We conclude that the hyperleptinemia of overnutrition prevents the ectopic lipid deposition by: (1) acting on hypothalamic appetite centers to limit the caloric surplus to fit the available adipocyte storage capacity and, (2) upregulating of fatty acid oxidation and downregulating lipogenesis in peripheral tissues to minimize ectopic lipid deposition. The causes of failure of this system and its clinical consequences are discussed.
Hypertension 2005 Jun
PMID:Hyperleptinemia: protecting the heart from lipid overload. 1589 72

Obesity induced by a high-fat diet was associated with increased tail-cuff blood pressure in adult rats. The mechanisms underlying obesity-related hypertension are unclear, but increased sympathetic activation most probably plays a role. Neuroendocrine alterations observed in obesity may influence both feeding patterns and blood pressure. Work from our laboratory has shown that chronic overfeeding in rats leads to changes in neuropeptide Y (NPY) and alpha-melanocyte stimulating hormone (alphaMSH) in the hypothalamus. These peptides have central effects on blood pressure, indicating that obesity-related changes in the CNS may impact on cardiovascular function. Population studies suggest that nutrition in early life can influence the subsequent risk of obesity and high blood pressure. To examine the impact of early postnatal overnutrition on blood pressure and adipose-derived mediators, we adjusted rat litters to 3 or 12 pups (overnutrition and control, respectively). Pups raised in small litters were 15% heavier at weaning, and this intervention was associated with a modest elevation of blood pressure and body weight as adults (16 weeks). Animals raised in small litters had increased 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) mRNA in white adipose tissue as adults, which may impact on cardiovascular function. Adjustment of diet after weaning, to 30% fat diet or standard chow, allowed comparison of the impact of different periods of overnourishment. Implementation of a high-fat diet at weaning overcame the effect of litter size on body weight from 10 weeks of age. Blood pressure rose progressively with high-fat feeding and was positively correlated with leptin and body weight. Chronic consumption of a high-fat diet led to marked increases in leptin and insulin and modest increases in blood pressure, and impacts on brain transmitters implicated in the regulation of both appetite and blood pressure. Overnourishment during early postnatal development led to profound changes in body weight at weaning, which tended to abate with maturation. It also led to long-term changes in some adipose-derived mediators, possibly increasing cardiovascular risk.
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PMID:Central and peripheral contributions to obesity-associated hypertension: impact of early overnourishment. 1610 38


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