Sarcopenia is the decline in muscle mass that occurs with normal aging. Sarcopenia is a major cause of frailty, disability, and loss of independence in the elderly [1]. It is not a disease and is seen even in master athletes as they age. However, exercise can reverse many of the effects of sarcopenia, and even make elderly people stronger than sedentary young ones. Exercise is also known to have beneficial effects on mood, which is often depressed in people with sarcopenia, and it may have psychological as well as physiological benefits in this population.
{"title":"Exercise, sarcopenia, cognition, and mood.","authors":"Ronenn Roubenoff","doi":"10.1159/000061864","DOIUrl":"https://doi.org/10.1159/000061864","url":null,"abstract":"Sarcopenia is the decline in muscle mass that occurs with normal aging. Sarcopenia is a major cause of frailty, disability, and loss of independence in the elderly [1]. It is not a disease and is seen even in master athletes as they age. However, exercise can reverse many of the effects of sarcopenia, and even make elderly people stronger than sedentary young ones. Exercise is also known to have beneficial effects on mood, which is often depressed in people with sarcopenia, and it may have psychological as well as physiological benefits in this population.","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"6 ","pages":"151-9; discussion 160-2"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000061864","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26309058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In the struggle for life, humans as every mammal and other living species, have to face two main dangers: (1) the competition against other individuals or other living species, including parasites, bacteria and viruses, and (2) the extreme toxicity of oxygen. The so-called ‘degenerative diseases’, which include the process of aging, are also related to both oxygen toxicity and immune defense against other living species, although some specific genetic characteristics may also be involved. The existence of a family of chemical compounds, called free radicals, has long been recognized as well as their harmful effects on biological molecules [1–5]. But, despite very active research concerning this field of reactive oxygen species (ROS) and extended work in both basic and clinical fields, we are still facing severe morbidity probably related to abnormalities on this pathway [6–12]. Several experimental studies have reported successful attempts to prevent or to counteract the deleterious effects of ROS [13–18] but, aside from important exceptions, the results so far have not produced the degree of evidence we are expecting [6, 19–25]. This relative lack of efficacy of the therapeutic approaches regarding oxidative stress and antioxidant treatments is probably related to the high degree of complexity of the ROS pathway and the antioxidant family, as well as the limitations for investigating oxidative stress and antioxidant status in patients. Besides several pharmacological approaches to such disorders [6, 22–26], which could be very promising, nutritional intake represents the most important way of providing an adequate antioxidant status in daily clinical practice.
{"title":"How valid is the concept of antioxidants and cell injury?","authors":"Xavier M Leverve, Cécile Batandier, Eric Fontaine","doi":"10.1159/000067511","DOIUrl":"https://doi.org/10.1159/000067511","url":null,"abstract":"In the struggle for life, humans as every mammal and other living species, have to face two main dangers: (1) the competition against other individuals or other living species, including parasites, bacteria and viruses, and (2) the extreme toxicity of oxygen. The so-called ‘degenerative diseases’, which include the process of aging, are also related to both oxygen toxicity and immune defense against other living species, although some specific genetic characteristics may also be involved. The existence of a family of chemical compounds, called free radicals, has long been recognized as well as their harmful effects on biological molecules [1–5]. But, despite very active research concerning this field of reactive oxygen species (ROS) and extended work in both basic and clinical fields, we are still facing severe morbidity probably related to abnormalities on this pathway [6–12]. Several experimental studies have reported successful attempts to prevent or to counteract the deleterious effects of ROS [13–18] but, aside from important exceptions, the results so far have not produced the degree of evidence we are expecting [6, 19–25]. This relative lack of efficacy of the therapeutic approaches regarding oxidative stress and antioxidant treatments is probably related to the high degree of complexity of the ROS pathway and the antioxidant family, as well as the limitations for investigating oxidative stress and antioxidant status in patients. Besides several pharmacological approaches to such disorders [6, 22–26], which could be very promising, nutritional intake represents the most important way of providing an adequate antioxidant status in daily clinical practice.","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"7 ","pages":"67-81; discussion 81-5"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000067511","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22155688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
For the purpose of this article, ‘specialized nutrition support’ means using nutrient formulations that have particular adaptations deemed either to alter the inflammatory response or correct a conditional deficiency. The term ‘immunonutrition’ is widely used. For ‘whom’ requires an understanding of the pathological processes patients are undergoing and ‘when’ implies there is some optimal intervention window. However, implicit in both is the need to understand the objectives of the nutritional intervention and the balance between the benefits and risks involved and how these relate to outcome. The focus will be on the survival of critically ill patients and how we can make decisions that are of practical consequence for the general clinician.
{"title":"Specialized nutrition support in the critically ill: for whom and when?","authors":"Richard D Griffiths","doi":"10.1159/000067499","DOIUrl":"https://doi.org/10.1159/000067499","url":null,"abstract":"For the purpose of this article, ‘specialized nutrition support’ means using nutrient formulations that have particular adaptations deemed either to alter the inflammatory response or correct a conditional deficiency. The term ‘immunonutrition’ is widely used. For ‘whom’ requires an understanding of the pathological processes patients are undergoing and ‘when’ implies there is some optimal intervention window. However, implicit in both is the need to understand the objectives of the nutritional intervention and the balance between the benefits and risks involved and how these relate to outcome. The focus will be on the survival of critically ill patients and how we can make decisions that are of practical consequence for the general clinician.","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"7 ","pages":"199-214; discussion 214-7"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000067499","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22155696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In a 70-kg man, skeletal muscle accounts for 40–50% of the total body mass. A loss of the muscle mass due to the net breakdown of muscle proteins is a common feature of many acute and long-term illnesses. During the initial flow phase, patients with an acute critical illness (multiple trauma and sepsis) lose 1–2 kg muscle mass per day and up to half the muscle mass in periods of 1–2 weeks [1]. Many chronic diseases that impair the function of the lungs, liver, kidney and heart including cancer and AIDS (affecting multiple systems) are attended by a generally slower, gradual loss of muscle mass. A very slow, but in the end substantial, loss of muscle mass is also observed during aging (sarcopenia) [2]. The reduction in muscle mass in all these conditions is the major component of the reduction in lean body mass. Impairments are also seen in muscle function, with a reduction in strength and endurance capacity being most evident [2, 3]. This again limits the ability of the patients to walk and perform normal activities of daily living. In some of the chronic diseases, the reduction in muscle function forms a serious disability or even handicap that dramatically reduces their quality of life [3]. This limitation in physical performance and continuous subjective feelings of fatigue are experienced as the most distressing phenomenon of many acquired chronic diseases [3, 4]. In patients with multiple trauma and sepsis, the loss of muscle mass and functions leads to life-threatening complications (e.g. respiratory failure) and is a major cause of death [5]. In clinical nutrition practice, the traditional approach to try and combat excessive rates of muscle protein breakdown is to give the patient more
{"title":"The primary target of nutritional support: body composition or muscle function?","authors":"Anton J M Wagenmakers","doi":"10.1159/000067500","DOIUrl":"https://doi.org/10.1159/000067500","url":null,"abstract":"In a 70-kg man, skeletal muscle accounts for 40–50% of the total body mass. A loss of the muscle mass due to the net breakdown of muscle proteins is a common feature of many acute and long-term illnesses. During the initial flow phase, patients with an acute critical illness (multiple trauma and sepsis) lose 1–2 kg muscle mass per day and up to half the muscle mass in periods of 1–2 weeks [1]. Many chronic diseases that impair the function of the lungs, liver, kidney and heart including cancer and AIDS (affecting multiple systems) are attended by a generally slower, gradual loss of muscle mass. A very slow, but in the end substantial, loss of muscle mass is also observed during aging (sarcopenia) [2]. The reduction in muscle mass in all these conditions is the major component of the reduction in lean body mass. Impairments are also seen in muscle function, with a reduction in strength and endurance capacity being most evident [2, 3]. This again limits the ability of the patients to walk and perform normal activities of daily living. In some of the chronic diseases, the reduction in muscle function forms a serious disability or even handicap that dramatically reduces their quality of life [3]. This limitation in physical performance and continuous subjective feelings of fatigue are experienced as the most distressing phenomenon of many acquired chronic diseases [3, 4]. In patients with multiple trauma and sepsis, the loss of muscle mass and functions leads to life-threatening complications (e.g. respiratory failure) and is a major cause of death [5]. In clinical nutrition practice, the traditional approach to try and combat excessive rates of muscle protein breakdown is to give the patient more","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"7 ","pages":"219-34; discussion 234-8"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000067500","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22155697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mitochondria contain the only extra-nuclear source of DNA. Under evolutionary pressure mitochondrial DNA (mtDNA) has adapted from genomes containing over 1,000 kb containing significant quantities of non-coding DNA to the highly compact mammalian mtDNA. In humans, the mitochondrial genome consists of a small (16.5 kb) double-stranded circular genome constituting less than 1% of the total cellular nucleic acid, yet its role is essential for the survival and function of the mitochondria and hence the cell (Fig. 1). Human mtDNA is a highly efficient structure in terms of expressed DNA containing no introns. It encodes for 37 genes, all of which are involved in synthesising subunits of the respiratory chain complex, either directly as 13 essential polypeptide components, or indirectly as the 22 transfer RNAs and the 2 ribosomal RNAs of the mitochondrial protein synthesis machinery (Fig. 1b). Human cells contain several hundred to many thousand mitochondria, with each mitochondrion having 2–10 copies of mtDNA [1]. Therefore several thousand copies of mtDNA can be present within a single cell. Both mutated and wild-type (normal) mtDNA can co-exist in any proportion, a situation termed heteroplasmy. The level of mutant mtDNA can vary considerably between mitochondria, cells and even tissues within the same individual. The mitochondrial genome mutates at a faster rate than its nuclear counterpart for several reasons. Firstly mitochondria lack nucleotide excision and recombination DNA repair mechanisms [2]. Secondly mtDNA lacks the structurally DNA stabilising proteins known as histones. Thirdly mtDNAs reside and replicate close to the inner mitochondrial membrane and hence are exposed
{"title":"The mitochondrial genome, aging and neurodegenerative disorders.","authors":"D A Cottrell, D M Turnbull","doi":"10.1159/000061856","DOIUrl":"https://doi.org/10.1159/000061856","url":null,"abstract":"Mitochondria contain the only extra-nuclear source of DNA. Under evolutionary pressure mitochondrial DNA (mtDNA) has adapted from genomes containing over 1,000 kb containing significant quantities of non-coding DNA to the highly compact mammalian mtDNA. In humans, the mitochondrial genome consists of a small (16.5 kb) double-stranded circular genome constituting less than 1% of the total cellular nucleic acid, yet its role is essential for the survival and function of the mitochondria and hence the cell (Fig. 1). Human mtDNA is a highly efficient structure in terms of expressed DNA containing no introns. It encodes for 37 genes, all of which are involved in synthesising subunits of the respiratory chain complex, either directly as 13 essential polypeptide components, or indirectly as the 22 transfer RNAs and the 2 ribosomal RNAs of the mitochondrial protein synthesis machinery (Fig. 1b). Human cells contain several hundred to many thousand mitochondria, with each mitochondrion having 2–10 copies of mtDNA [1]. Therefore several thousand copies of mtDNA can be present within a single cell. Both mutated and wild-type (normal) mtDNA can co-exist in any proportion, a situation termed heteroplasmy. The level of mutant mtDNA can vary considerably between mitochondria, cells and even tissues within the same individual. The mitochondrial genome mutates at a faster rate than its nuclear counterpart for several reasons. Firstly mitochondria lack nucleotide excision and recombination DNA repair mechanisms [2]. Secondly mtDNA lacks the structurally DNA stabilising proteins known as histones. Thirdly mtDNAs reside and replicate close to the inner mitochondrial membrane and hence are exposed","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"6 ","pages":"1-13; discussion 13-6"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000061856","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26309048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
It is becoming increasingly apparent that the early environment both before birth and in infancy has profound effects on aging and long-term health. This is due to environmental programming whereby influences acting at critical periods of growth and development can permanently change structure and function with lifelong consequences. Many biological characteristics of the adult can be affected including the maximum size attained, the structure and function of different systems and the response to stimuli [1]. Nutrition is the most widely researched cause of environmental programming but other agents include physical factors such as temperature, light and noise.
{"title":"Early life effects on aging.","authors":"Avan Aihie Sayer, Cyrus Cooper","doi":"10.1159/000061857","DOIUrl":"https://doi.org/10.1159/000061857","url":null,"abstract":"It is becoming increasingly apparent that the early environment both before birth and in infancy has profound effects on aging and long-term health. This is due to environmental programming whereby influences acting at critical periods of growth and development can permanently change structure and function with lifelong consequences. Many biological characteristics of the adult can be affected including the maximum size attained, the structure and function of different systems and the response to stimuli [1]. Nutrition is the most widely researched cause of environmental programming but other agents include physical factors such as temperature, light and noise.","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"6 ","pages":"33-44; discussion 44-8"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000061857","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26309050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Normal aging is often described as a continuous process characterized by a decrease in lean body mass, an increase in fat, and a decrease in total body water. However, it has been pointed out that many older people, especially those aged 75 years and over, may feel healthy in spite of a chronic illness [1]. Thus, both nutrition and hydration may be altered by chronic diseases, infection, as well as by changes in functional status, mobility disorders, confusion, impaired sensory perception, medication effects and difficulties in drinking, swallowing and eating because of the absence of teeth or ill-fitting dentures. For water balance, two factors place the elderly at risk for dehydration: a decreased fluid intake and an increased fluid loss. In the human, the normal pattern of drinking is intermittent while water is continuously lost by various routes so that dehydration occurs. Dehydration is the most common cause of fluid and electrolyte imbalance and is frequently reported in residents, hospitalized and community-dwelling elderly people. It has been stated that one of the greatest threats to the survival of any terrestrial animal, including man, is that of dehydration [2]. In this chapter we review the factors which may disturb fluid balance and predispose elderly to dehydration, the mechanisms involved and the changes in body water compartments. The possible health consequences of dehydration and the new recommendations of fluid intake in elderly populations are also discussed.
{"title":"Age-related changes in hydration.","authors":"Maurice J Arnaud","doi":"10.1159/000061866","DOIUrl":"https://doi.org/10.1159/000061866","url":null,"abstract":"Normal aging is often described as a continuous process characterized by a decrease in lean body mass, an increase in fat, and a decrease in total body water. However, it has been pointed out that many older people, especially those aged 75 years and over, may feel healthy in spite of a chronic illness [1]. Thus, both nutrition and hydration may be altered by chronic diseases, infection, as well as by changes in functional status, mobility disorders, confusion, impaired sensory perception, medication effects and difficulties in drinking, swallowing and eating because of the absence of teeth or ill-fitting dentures. For water balance, two factors place the elderly at risk for dehydration: a decreased fluid intake and an increased fluid loss. In the human, the normal pattern of drinking is intermittent while water is continuously lost by various routes so that dehydration occurs. Dehydration is the most common cause of fluid and electrolyte imbalance and is frequently reported in residents, hospitalized and community-dwelling elderly people. It has been stated that one of the greatest threats to the survival of any terrestrial animal, including man, is that of dehydration [2]. In this chapter we review the factors which may disturb fluid balance and predispose elderly to dehydration, the mechanisms involved and the changes in body water compartments. The possible health consequences of dehydration and the new recommendations of fluid intake in elderly populations are also discussed.","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"6 ","pages":"193-205; discussion 205-6"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000061866","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26309060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Efficacy of nutritional support can be defined in two main ways: the first relates to the production of new body tissue or the prevention of loss of existing tissue, this could either be growth in a child or repair or maintenance in an adult, and the second relates to how well the various body tissues are functioning. So the issue raised in the title of this chapter can be crystallized into ‘How do trace elements affect the amount and function of body tissues?’
{"title":"Trace elements: contribution to the efficacy of nutritional support.","authors":"Alan Shenkin","doi":"10.1159/000067515","DOIUrl":"https://doi.org/10.1159/000067515","url":null,"abstract":"Efficacy of nutritional support can be defined in two main ways: the first relates to the production of new body tissue or the prevention of loss of existing tissue, this could either be growth in a child or repair or maintenance in an adult, and the second relates to how well the various body tissues are functioning. So the issue raised in the title of this chapter can be crystallized into ‘How do trace elements affect the amount and function of body tissues?’","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"7 ","pages":"133-45; discussion 145-9"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000067515","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22155692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aging is associated with predictable alterations in body fat that are thought to have an important impact on health. From early adult life through middle age there is a substantial increase in body fat [1, 2], while after 65–70 years of age body fat typically decreases, even in healthy individuals [1, 2]. Unexplained weight loss becomes relatively common after the age of 65 [3, 4] and 30–50% of institutionalized elderly are reported to suffer from proteinenergy malnutrition [3, 4]. This loss of body fat in later years is associated with several adverse factors including micronutrient deficiencies, frailty, increased hospital admission, an increased risk of disability from falls, delayed recovery from injury and premature death [5–8]. As reviewed elsewhere [9–12], negative energy balance resulting from low energy intake relative to total energy expenditure is suggested to be the usual cause of the loss of body fat in old age and, consistent with this suggestion, nationwide studies have suggested that low dietary energy intake is widespread even among healthy elderly adults [13]. However, the underlying determinants of low energy intake remain uncertain. There are several factors, such as reductions in the sensations of taste and smell, poor dentition, prescription medications, depression and social isolation that may possibly promote inadequate energy intake [14–17]. In addition, an impairment in the ability to regulate food intake, termed the ‘anorexia of aging’ [15], is speculated to be important. This chapter synthesizes recent results and reviews [9–12] on changes in the regulation of food intake in old age and the possible underlying mechanisms.
{"title":"Impaired regulation of energy intake in old age.","authors":"Susan B Roberts","doi":"10.1159/000061858","DOIUrl":"https://doi.org/10.1159/000061858","url":null,"abstract":"Aging is associated with predictable alterations in body fat that are thought to have an important impact on health. From early adult life through middle age there is a substantial increase in body fat [1, 2], while after 65–70 years of age body fat typically decreases, even in healthy individuals [1, 2]. Unexplained weight loss becomes relatively common after the age of 65 [3, 4] and 30–50% of institutionalized elderly are reported to suffer from proteinenergy malnutrition [3, 4]. This loss of body fat in later years is associated with several adverse factors including micronutrient deficiencies, frailty, increased hospital admission, an increased risk of disability from falls, delayed recovery from injury and premature death [5–8]. As reviewed elsewhere [9–12], negative energy balance resulting from low energy intake relative to total energy expenditure is suggested to be the usual cause of the loss of body fat in old age and, consistent with this suggestion, nationwide studies have suggested that low dietary energy intake is widespread even among healthy elderly adults [13]. However, the underlying determinants of low energy intake remain uncertain. There are several factors, such as reductions in the sensations of taste and smell, poor dentition, prescription medications, depression and social isolation that may possibly promote inadequate energy intake [14–17]. In addition, an impairment in the ability to regulate food intake, termed the ‘anorexia of aging’ [15], is speculated to be important. This chapter synthesizes recent results and reviews [9–12] on changes in the regulation of food intake in old age and the possible underlying mechanisms.","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"6 ","pages":"49-60; discussion 60-1"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000061858","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26309051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nutritional surveys in elderly populations have pointed to low energy and nutrient intake. This is of particular concern among the homebound or frail population groups [1–5] as reflected by considerable involuntary weight loss, including net protein loss [6, 7] leading to muscle wasting [8]. Inadequate intake of a number of nutrients has been associated with decreased body strength, lower resistance to infection and poorer indicators of quality of life [9–11]. Both an inadequate body weight for height and weight loss are associated with hip fractures, reduced autonomy, early institutionalization and increased mortality rates [12–21]. Low muscle mass was shown to be a significant independent risk factor for falls in elderly women after adjustment for age, balance and gait, medications, physical activity, proportion of body fat, and health status [22]. Preservation of muscle function is paramount for the maintenance of autonomy until advanced age. Since age-related decreases in functional ability are neither inevitable nor uniform [23], efforts have been made to identify factors associated with muscle function or functional status in general in many studies over the last decade. Two candidates for modifiable determinants, nutrition and physical activity, have been consistently studied in the context of observational and experimental designs. This chapter will focus on the manner in which nutritional status contributes to the preservation or deterioration of muscle function in the elderly. For this purpose, an epidemiological perspective rather than a mechanistic one will be adopted. Results from cross-sectional and longitudinal observations as well as from experimental studies will be presented and
{"title":"Known related effects of nutrition on aging muscle function.","authors":"Hélène Payette","doi":"10.1159/000061863","DOIUrl":"https://doi.org/10.1159/000061863","url":null,"abstract":"Nutritional surveys in elderly populations have pointed to low energy and nutrient intake. This is of particular concern among the homebound or frail population groups [1–5] as reflected by considerable involuntary weight loss, including net protein loss [6, 7] leading to muscle wasting [8]. Inadequate intake of a number of nutrients has been associated with decreased body strength, lower resistance to infection and poorer indicators of quality of life [9–11]. Both an inadequate body weight for height and weight loss are associated with hip fractures, reduced autonomy, early institutionalization and increased mortality rates [12–21]. Low muscle mass was shown to be a significant independent risk factor for falls in elderly women after adjustment for age, balance and gait, medications, physical activity, proportion of body fat, and health status [22]. Preservation of muscle function is paramount for the maintenance of autonomy until advanced age. Since age-related decreases in functional ability are neither inevitable nor uniform [23], efforts have been made to identify factors associated with muscle function or functional status in general in many studies over the last decade. Two candidates for modifiable determinants, nutrition and physical activity, have been consistently studied in the context of observational and experimental designs. This chapter will focus on the manner in which nutritional status contributes to the preservation or deterioration of muscle function in the elderly. For this purpose, an epidemiological perspective rather than a mechanistic one will be adopted. Results from cross-sectional and longitudinal observations as well as from experimental studies will be presented and","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"6 ","pages":"135-47; discussion 147-50"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000061863","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26309057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：