Effects Of Undernutrition Research Articles

Early-life undernutrition and depression later in life: a systematic review.

Early adverse experience can have a long-term effect on growth and development and negative repercussions into adulthood. Among the various consequences of undernutrition is depression. The present work aimed to evaluate the relationship between early-life undernutrition and depression in adult life. Data were obtained from the PubMed, SCOPUS, and Web of Science databases in November 2021 and were selected using the systematic bibliographic review manager program State of the Art Through Systematic Review. Data were extracted using the State of the Art Through Systematic Review program. Of the 559 articles that were identified, 114 were duplicates, and 426 were excluded after inclusion and exclusion criteria were applied to the title and abstract. One other relevant study was included. From the 20 remaining articles, 8 were excluded after the full-text screening. Finally, 12 articles remained for review in the present work. The studies described in these articles investigated humans, rats, or mice, and correlated early-life malnutrition and depression in adulthood as the principal outcome. Undernutrition in early life and later depression are linked. Furthermore, the knowledge that the risk factors for depression start at the beginning of life points to public health policies starting in intrauterine life and extending throughout childhood and adolescence.

Building better barriers: how nutrition and undernutrition impact pediatric intestinal health.

Chronic undernutrition is a major cause of death for children under five, leaving survivors at risk for adverse long-term consequences. This review focuses on the role of nutrients in normal intestinal development and function, from the intestinal epithelium, to the closely-associated mucosal immune system and intestinal microbiota. We examine what is known about the impacts of undernutrition on intestinal physiology, with focus again on the same systems. We provide a discussion of existing animal models of undernutrition, and review the evidence demonstrating that correcting undernutrition alone does not fully ameliorate effects on intestinal function, the microbiome, or growth. We review efforts to treat undernutrition that incorporate data indicating that improved recovery is possible with interventions focused not only on delivery of sufficient energy, macronutrients, and micronutrients, but also on efforts to correct the abnormal intestinal microbiome that is a consequence of undernutrition. Understanding of the role of the intestinal microbiome in the undernourished state and correction of the phenotype is both complex and a subject that holds great potential to improve recovery. We conclude with critical unanswered questions in the field, including the need for greater mechanistic research, improved models for the impacts of undernourishment, and new interventions that incorporate recent research gains. This review highlights the importance of understanding the mechanistic effects of undernutrition on the intestinal ecosystem to better treat and improve long-term outcomes for survivors.

Exploring the prevalence of multiple forms of malnutrition in children 6–18 years living in the Eastern Cape, South Africa

Background: The existence of multiple forms of malnutrition is a growing problem in developing countries. Children living in the Eastern Cape have a relatively high prevalence of cardiovascular disease (CVD) risk factors and food insecurity, suggesting the possibility of the several coexisting forms of malnutrition. Due to the negative long-term consequences of undernutrition, overnutrition and, to a greater extent, a combination of both, it is important for this issue to be identified early in children and addressed. Aim: This study was undertaken to investigate the prevalence of the different forms of malnutrition in children living in the Eastern Cape province. Methods: Secondary analysis of a cross-sectional sample of 237 school-aged children, aged 6–18 years, in the Eastern Cape province of South Africa was conducted. The variables included in the analysis were the demographic data, anthropometric data and biochemical data, specifically blood profiles related to micronutrient deficiencies and CVD risk factors. Fisher’s exact test was used to compare the prevalence rates of several coexisting forms of malnutrition in the children. All data analysis was conducted in R version 4.0.3 and statistical significance was set at 0.05. Results: In children with overweight/obesity, 13.6% had a micronutrient deficiency, while 37.71% of the children within the normal weight range had coexisting micronutrient deficiencies and CVD risk factors. The prevalence of folate deficiency was 73.0%, iron deficiency 6.3%, and hyperglycaemia was at 10.6%. Fisher’s exact test was used to compare the prevalence rates between genders and no statistically significant differences were observed. Conclusion: Further research is needed to understand the relatively high prevalence of CVD risk factors in these children within the normal weight range and to investigate how dietary intake contributes to the overall double burden of malnutrition in children.

Altered White Matter Connectivity in Young Acutely Underweight Patients With Anorexia Nervosa

Reductions of gray matter volume and cortical thickness in anorexia nervosa (AN) are well documented. However, findings regarding the integrity of white matter (WM) as studied via diffusion weighted imaging (DWI) are remarkably heterogeneous, and WM connectivity has been examined only in small samples using a limited number of regions of interest. The present study investigated whole-brain WM connectivity for the first time in a large sample of acutely underweight patients with AN. DWI data from predominantly adolescent patients with acute AN (n= 96, mean age= 16.3 years) and age-matched healthy control participants (n= 96, mean age= 17.2 years) were analyzed. WM connectivity networks were generated from fiber-tractography-derived streamlines connecting 233 cortical/subcortical regions. To identify group differences, network-based statistic was used while taking head motion, WM, and ventricular volume into account. Patients with AN were characterized by 6 WM subnetworks with abnormal architecture, as indicated by increased fractional anisotropy located primarily in parietal-occipital regions and accompanied by reduced radial diffusivity. Group differences based on number of streamlines reached only nominal significance. Our study reveals pronounced alterations in the WM connectome in young patients with AN. In contrast to known reductions in gray matter in the acutely underweight state of AN, this pattern does not necessarily indicate a deterioration of the WM network. Future studies using advanced MRI sequences will have to clarify interrelations with axonal packing or myelination, and whether the changes should be considered a consequence of undernutrition or a vulnerability for developing or maintaining AN.

Using intervention mapping to develop an outpatient nursing nutritional intervention to improve nutritional status in undernourished patients planned for surgery

BackgroundUndernutrition in surgical patients leads to a higher risk of postoperative complications like infections and delayed recovery of gastrointestinal functions, often resulting in a longer hospital stay and lower quality of life. Nurses at outpatient clinics can deliver nutritional care during outpatient preoperative evaluation of health status to ensure that patients are properly fed in preparation for hospital admission for surgery. However, nutritional nursing care was not determined in research yet. This paper describes the structural development of an Outpatient Nursing Nutritional Intervention (ONNI).MethodsA project group followed the steps of the Intervention Mapping. The needs assessment included assessment of delivery of nutritional care and nutritional care needs at two anaesthesia outpatient clinics of an academic and a teaching hospital. Also, outpatient clinic nurses and patients at risk for undernutrition were interviewed. Determinants resulted from these methods were matched with theories on behaviour change and nutritional support.ResultsBoth patients and nurses were unaware of the consequences of undernutrition, and nurses were also unaware of their roles with regard to nutritional support. The intervention goals were: 1) enabling surgical patients to improve or maintain their nutritional status before hospital admission for surgery, and 2) enabling nurses to deliver nutritional support. The ONNI was developed for outpatients at risk for or with undernutrition. A training was developed for nurses. The ONNI included the five following components: 1) identification of the causes of undernutrition; 2) provision of a nutritional care plan including general and individually tailored advice; 3) self-monitoring of nutrient intake; 4) counselling and encouragement; and 5) support during a telephone follow-up meeting. The intervention and training were tested. A multifaceted implementation strategy was used to deliver the intervention in daily practice.ConclusionsDespite the unique position of the nurses at outpatient clinics, nurses were unaware of their role with regard to nutritional care. The ONNI was developed and implemented along with a training program for nurses. The test confirmed that the training can improve nurses’ knowledge, skills, and sense of responsibility for nutritional support. The intervention may empower patients to actively improve their nutritional status.

Current nutritional status assessment tools for metabolic care and clinical nutrition.

The aim of this report is to critically review existing questionnaires and tools to assess nutritional status in different populations and pathological conditions. A total of 16 instruments to evaluate nutritional status were recorded, which were based on anthropometrical determinations, biochemical markers, clinical examinations and subjective questionnaires, depending on the nutritional assessment focus, involving different concepts: screening of the risk, diagnosis and severity of malnutrition, as well as the consequences of undernutrition or overnutrition. A variety of questionnaires, equations and tools were found with ability to assess nutritional status for metabolic care or clinical nutrition purposes, but apparently there is no optimal, universal and reliable nutritional status screening system for all metabolic conditions. Novel assessment instruments should provide high sensibility and specificity, be precise and reliable as well as inexpensive and simple, in order to avoid the additional burden of excessive loads of costs, work and time while dynamically overcoming the influence of disease diversity.

Neuroprotection Induced by Energy and Protein-Energy Undernutrition Is Phase-Dependent After Focal Cerebral Ischemia in Mice

Malnutrition predisposes to poor stroke outcome. In animal models, undernutrition protected against ischemic injury in some, but not in other studies. In view of diverse stroke models and food restriction paradigms, the consequences of undernutrition are poorly understood. Herein, we exposed mice to energy-reduced and protein-energy-reduced diets for 7–30 days and subsequently induced intraluminal middle cerebral artery occlusion. Undernutrition phase dependently influenced ischemic injury. Short-lasting 7 days of protein-energy undernutrition, but not energy undernutrition, decreased post-ischemic brain leukocyte infiltration and microglial activation and reduced brain Il-1β mRNA, but did not protect against ischemic injury. Fourteen days of energy and protein-energy undernutrition, on the other hand, reduced ischemic injury despite absence of anti-inflammatory effects. Anti-oxidant genes (Sod-1, Sod-2, and Cat mRNAs) were regulated in the liver and, to a lesser extent, the ischemic brain, indicating an adapted, compensated stage. Conversely, 30 days of energy and protein-energy undernutrition caused progressive animal exhaustion associated with post-ischemic hypoperfusion, rise of metabolic markers (Sirt-1 and Glut-1 mRNAs, Sirt-1 protein) in the ischemic brain, and reregulation of pro- and anti-oxidant markers (now also Nox-4 and Gpx-3 mRNAs) in the liver. In the latter condition, no neuroprotection was noted. Our study suggests an adaptation of metabolic systems that provides neuroprotection in a circumscribed time window.

Socio‐cultural and economic determinants and consequences of adolescent undernutrition and micronutrient deficiencies in LLMICs: a systematic narrative review

AbstractAdolescent undernutrition is a persisting public health problem in low and lower middle income countries (LLMICs). Nutritional trajectories are complexly interrelated with socio‐cultural and economic (SCE) trajectories. However, a synthesis of the SCE determinants or consequences of undernutrition in adolescents is lacking. We undertook a narrative review of published literature to provide a narrative overview of the SCE determinants and consequences associated with undernutrition among adolescents in LLMICs. We identified 98 articles from PubMed, SCOPUS, and CAB‐Abstracts on determinants and consequences of undernutrition as defined by stunting, underweight, thinness, and micronutrient deficiencies. At the individual level, significant determinants included age, sex, birth order, religion, ethnicity, educational and literacy level, working status, and marital status. At the household level, parental education and occupation, household size and composition, income, socioeconomic status, and resources were associated with undernutrition. Only a few determinants at the community/environmental level, including residence, sanitation, school type, and seasonality, were identified. The consequences of adolescent undernutrition were mostly related to education and cognition. This review underscores the importance of the broad range of context‐specific SCE factors at several levels that influence adolescent nutritional status and shows that further research on SCE consequences of undernutrition is needed.

Global disability-adjusted life-year estimates of long-term health burden and undernutrition attributable to diarrhoeal diseases in children younger than 5 years.

SummaryBackgroundDiarrhoea is a leading cause of death and illness globally among children younger than 5 years. Mortality and short-term morbidity cause substantial burden of disease but probably underestimate the true effect of diarrhoea on population health. This underestimation is because diarrhoeal diseases can negatively affect early childhood growth, probably through enteric dysfunction and impaired uptake of macronutrients and micronutrients. We attempt to quantify the long-term sequelae associated with childhood growth impairment due to diarrhoea.MethodsWe used the Global Burden of Diseases, Injuries, and Risk Factors Study framework and leveraged existing estimates of diarrhoea incidence, childhood undernutrition, and infectious disease burden to estimate the effect of diarrhoeal diseases on physical growth, including weight and height, and subsequent disease among children younger than 5 years. The burden of diarrhoea was measured in disability-adjusted life-years (DALYs), a composite metric of mortality and morbidity. We hypothesised that diarrhoea is negatively associated with three common markers of growth: weight-for-age, weight-for-height, and height-for-age Z-scores. On the basis of these undernutrition exposures, we applied a counterfactual approach to quantify the relative risk of infectious disease (subsequent diarrhoea, lower respiratory infection, and measles) and protein energy malnutrition morbidity and mortality per day of diarrhoea and quantified the burden of diarrhoeal disease due to these outcomes caused by undernutrition.FindingsDiarrhoea episodes are significantly associated with childhood growth faltering. We found that each day of diarrhoea was associated with height-for-age Z-score (–0·0033 [95% CI −0·0024 to −0·0041]; p=4·43 × 10−14), weight-for-age Z-score (–0·0077 [–0·0058 to −0·0097]; p=3·19 × 10−15), and weight-for-height Z-score (–0·0096 [–0·0067 to −0·0125]; p=7·78 × 10−11). After addition of the DALYs due to the long-term sequelae as a consequence of undernutrition, the burden of diarrhoeal diseases increased by 39·0% (95% uncertainty interval [UI] 33·0–46·6) and was responsible for 55 778 000 DALYs (95% UI 49 125 400–62 396 200) among children younger than 5 years in 2016. Among the 15 652 300 DALYs (95% UI 12 951 300–18 806 100) associated with undernutrition due to diarrhoeal episodes, more than 84·7% are due to increased risk of infectious disease, whereas the remaining 15·3% of long-term DALYs are due to increased prevalence of protein energy malnutrition. The burden of diarrhoea has decreased substantially since 1990, but progress has been greater in long-term (78·7% reduction [95% UI 69·3–85·5]) than in acute (70·4% reduction [95% UI 61·7–76·5]) DALYs.InterpretationDiarrhoea represents an even larger burden of disease than was estimated in the Global Burden of Disease Study. In order to adequately address the burden of its long-term sequelae, a renewed emphasis on controlling the risk of diarrhoea incidence may be required. This renewed effort can help further prevent the potential lifelong cost on child health, growth, and overall potential.FundingBill & Melinda Gates Foundation.

Maternal undernutrition during early pregnancy inhibits postnatal growth of the tibia in the female offspring of rats by alteration of chondrogenesis

Epidemiological research has suggested that birth weights are correlated with adult leg lengths. However, the relationship between prenatal undernutrition (UN) and postnatal leg growth remains controversial. We investigated the effects of UN during early pregnancy on postnatal hindlimb growth and determined whether early embryonic malnutrition affects the functions of postnatal chondrocytes in rats.Undernourished Wistar dams were fed 40% of the daily intake of rats in the control groups from gestational days 5.5–11.5, and femurs, tibias, and trunks or spinal columns were morphologically measured at birth and at 16 weeks of age in control and undernourished offspring of both sexes. We evaluated cell proliferation and differentiation of cultured chondrocytes derived from neonatal tibias of female offspring and determined chondrocyte-related gene expression levels in neonatal epiphysis and embryonic limb buds.Tibial lengths of undernourished female, but not male, offspring were longer at birth and shorter at 16 weeks of age (p < .05) compared with those of control rats. In chondrocyte culture studies, stimulating effects of IGF-1 on cell proliferation (p < .01) were significantly decreased and levels of type II collagen were lower in female undernourished offspring (p < .05). These phenomena were accompanied by decreased expression levels of Col2a1 and Igf1r and increased expression levels of Fgfr3 (p < .05), which might be attributable to the decreased expression of specificity protein 1 (p < .05), a key transactivator of Col2a1 and Igf1r.In conclusion, UN stress during early pregnancy reduces postnatal tibial growth in female offspring by altering the function of chondrocytes, likely reflecting altered expression of gene transactivators.

Neonatal leptin treatment reverses the bone-suppressive effects of maternal undernutrition in adult rat offspring

Alterations in the early life environment, including maternal undernutrition (UN) during pregnancy, can lead to increased risk of metabolic and cardiovascular disorders in offspring. Leptin treatment of neonates born to UN rats reverses the programmed metabolic phenotype, but the possible benefits of this treatment on bone tissue have not been defined. We describe for the first time the effects of neonatal leptin treatment on bone in adult offspring following maternal UN. Offspring from either UN or ad libitum-fed (AD) rats were treated with either saline or leptin (2.5 µg/ g.d on postnatal days (D)3–13) and were fed either a chow or high fat (HF) diet from weaning until study completion at D170. Analysis of micro-tomographic data of the left femur showed highly significant effects of UN on cortical and trabecular bone tissue indices, contributing to inferior microstructure and bone strength, almost all of which were reversed by early leptin life treatment. The HF fat diet negatively affected trabecular bone tissue, but the effects of only trabecular separation and number were reversed by leptin treatment. The negative effects of maternal UN on skeletal health in adult offspring might be prevented or attenuated by various interventions including leptin. Establishment of a minimal efficacious leptin dose warrants further study.

Cancer and nutrition - a paradigma shift

Substantial international differences in the prevalence of cancer disease suppose that nutrition may be an important factor in the development of cancer. Many experts believe, that nutritional factors may contribute up to 35 % to the development of malignant tumors. Many patients have lost substantial body weight already at the time of the diagnosis of the disease as consequence of undernutrition and malnutrition, respectively. During the course of the disease the nutritional status often is deteriorating further. Caused by both the cancer disease itself and the treatment, loss of appetite, changes in taste, nausea and vomiting may additionally contribute to undernutrition. Undernutrition is a relevant factor for the outcome of the disease and for the tolerance of the treatment as well. Therefore, supporting the heavily impaired patients in nutritional intake is of paramount importance and an urgent task for physicians and nurses. In view of physiology, pathophysiology, genetics and molecular biology, metabolic processes in cancer are highly complex regulated and there is increasing evidence that a diet rich in fat and protein is favourable. This, however, implies a paradigma shift away from the "healthy" balanced diet rich in fruit, vegetable and complex carbohydrates. So far, the evidence based data of this new concept is, however, a controversial issue.

Eating disorders and bone metabolism in women.

Eating Disorders are psychiatric disorders associated with a high risk for low bone mineral density (BMD) and fractures. Low BMD is a consequence of undernutrition, changes in body composition, and hormonal alterations. This review summarizes recent findings regarding novel strategies for assessing bone outcomes in patients with eating disorders, factors contributing to altered bone metabolism, and possible therapeutic strategies. Emerging research in this field suggests that not only anorexia nervosa, but also bulimia nervosa results in lower BMD compared to controls. To date studies of bone structure, and all randomized controlled trials examining the impact of various therapies on bone outcomes in anorexia nervosa, have focused on adolescent girls and women. We discuss the impact of anorexia nervosa on bone structure, and associations of resting energy expenditure, marrow adipose tissue (including the ratio of saturated to unsaturated fat), and cold activated brown adipose tissue with BMD and bone structure. Promising strategies for treatment include physiological estrogen replacement (rather than oral contraceptives) in adolescent girls with anorexia nervosa, and bisphosphonates, as well as teriparatide, in adult women with anorexia nervosa. Recent data on (i) BMD and bone structure in adolescent girls and women with eating disorders, (ii) factors that contribute to altered bone metabolism, and (iii) randomized controlled trials reporting positive effects of physiologic estrogen replacement, bisphosphonates and teriparatide on bone health, provide us with a greater understanding of the impact of eating disorders on bone and novel management strategies.

Impact of Nutritional State on Critical Limb Ischemia Early Outcomes (DENUCRITICC Study)

Despite current progress, the prognosis of critical limb ischemia (CLI) remains poor. The ageing of the population, the increasing prevalence of diabetes mellitus, and the stability of tobacco use will increase the prevalence of CLI. CLI patients have risk factors for malnutrition, and the impact of malnutrition on morbidity and mortality has been demonstrated in the general population. However, we have little information on the consequences of undernutrition in the CLI population. The aim of this study is to assess the impact of malnutrition on the early outcomes in CLI patients. This is a double-center prospective study that included all consecutive hospitalized patients with CLI. All patients were screened for malnutrition and divided into 2 groups: severe malnourished patients (group A) and moderate malnourished and well-nourished (group B). This distribution was based on age-indexed clinical and biological data and the patient's general condition: the Nutritional Risk Index for patients younger than 75years, the Mini Nutritional Assessment, or the Geriatric Nutritional Risk Index for those older than 75years. The primary end point was defined as the rate of 30-day death. Outcomes were compared in a univariate analysis. Stepwise logistic regression was used for the multivariate analysis. Variables with a P value <0.2 in the univariate analysis were introduced in the multivariate model. We included 106 patients. The prevalence of malnutrition was 75.5%, divided into moderate malnutrition (51.9%) and severe malnutrition (23.6%). Six patients (24%) died in group A compared with 8 in group B (4.9%) (P=0.01). By univariate analysis, severe malnutrition was the only factor associated with death at 30days. By stepwise logistic regression, severe malnutrition (odds ratio 6.1, 95% confidence interval 1.6-23.7, P=0.006) was found to be the significant risk factors for death at 30days. This study is the first to demonstrate prospectively the major importance of malnutrition in the early prognosis of CLI patients.

Diet-Regulated Anxiety

A substantial proportion of noncommunicable disease originates in habitual overconsumption of calories, which can lead to weight gain and obesity and attendant comorbidities. At the other end of the spectrum, the consequences of undernutrition in early life and at different stages of adult life can also have major impact on wellbeing and quality of life. To help address some of these issues, greater understanding is required of interactions with food and contemporary diets throughout the life course and at a number of different levels: physiological, metabolic, psychological, and emotional. Here we review the current literature on the effects of dietary manipulation on anxiety-like behaviour. This evidence, assembled from study of preclinical models of diet challenge from gestation to adult life, supports a role for diet in the important connections between psychology, physiology, and behaviour. Analogous processes in the human population in our current obesogenic environment are likely to contribute to individual and societal challenges in this area.

Cardiac responses of rats submitted to postnatal protein restriction

Undernutrition during critical stages of development and childhood has important effects on cardiovascular homeostasis. The present study was undertaken to evaluate the in vivo and ex vivo cardiac function of rats submitted to postnatal protein restriction. Male Wistar rats (28 days old) were fed a regular (20%) or low-protein (6%) diet over 5 weeks. After this period, cardiac function was analyzed by echocardiography and isolated heart preparation. Furthermore, the density of cardiac noradrenergic fibers and hematological profile were evaluated. We found that malnourished rats exhibited elevated arterial blood pressure, increased fractional shortening (echocardiography), increased systolic tension, increased ±dT/dt (isolated heart technique), impaired diastolic function characterized by a slight increase in the left ventricular end-diastolic diameter (echocardiography) and decreased diastolic tension (isolated heart technique), and cardiac hypertrophy evidenced by augmentation of the posterior left ventricular wall and discrete hematological changes. In addition, malnourished rats exhibited increased noradrenergic fiber density in their hearts (0.08% ± 0.02% area in control rats vs. 0.17% ± 0.03% area in malnourished rats). Our current data demonstrate that postnatal protein restriction causes cardiac adaptation characterized by an early overworking heart. This is at least in part mediated by an increase in the efferent sympathetic fibers to the heart. These findings provide important information for efforts to prevent and manage the consequences of undernutrition in the human population.

Biofortification in China: policy and practice

Micronutrient deficiency undernutrition, due to insufficient levels of vitamins and minerals in the diet, remains one of the most prevalent and preventable nutritional problems in the world today. Micronutrient undernutrition is the most common form of malnutrition. Compared to the 180 million children with protein-energy malnutrition, 3.5–5 billion persons are iron-deficient, and 140–250 million persons are vitamin A-deficient. Micronutrient deficiencies diminish physical, cognitive, and reproductive development. Undernutrition is both a cause and a result of poor human health and achievement.Middle-income nations, such as China, also suffer from micronutrient undernutrition's effects. In China's poor western provinces, despite supplementation and fortification efforts, stunting and underweight (symptoms of micronutrient undernutrition) remain common. In recent decades, nutritional adequacy, in terms of available food energy, improved immensely, as the government made food security a top priority. A potential next step for China could be to address specifically micronutrient undernutrition. The paper aims to provide a discussion of policy issues relevant to biofortification, if China were to consider the implementation of this intervention in its rural provinces.Traditional nutritional interventions currently employ four main strategies: dietary modification, supplementation, commercial fortification, and biofortification. Biofortification, a relatively new technique, involves selectively breeding staple plant varieties to increase specific nutrient levels in plant tissues. Biofortification has the potential to provide benefits to humans, plants, and livestock; nourish nutrient-depleted soils; and help increase crop yields per acre. Biofortification methods include selective breeding, reducing levels of anti-nutrients, and increasing levels of substances that promote nutrient absorption.If China were to implement biofortification programs, with help from government agencies and international organizations, several policy questions would need to be addressed. The paper discusses several policy questions that pertain to the relationship between biofortified and genetically modified crops, human health and safety concerns, labeling of biofortified crops for consumers, consumer rights, potential environmental impacts, intellectual property rights, seed disbursement, government investment, private-sector research, and additional agricultural and commercial regulations. Biofortification has the potential to help alleviate the suffering, death, disability, and failure to achieve full human potential that results from micronutrient undernutrition-related diseases.

Obesity as a consequence of undernutrition

The role of early undernutrition as a risk factor for adult obesity is supported by data from epidemiologic, clinical, and animal studies. In experimental animals, maternal energy restriction results in pups of reduced body size but with increased fat depots and hyperphagia. Similarly, reduced lean mass with relative increase in fat mass in the newborn have been described in gestational energy restriction in human populations. When coupled with the appropriate environmental conditions (widely available energy-dense foods, low energy expenditure) those factors predispose a person to excess weight gain and body fat accumulation in adult life. This combination of early biologic factors with environmental factors is best exemplified in the situation of populations from developing countries undergoing economic and nutritional transition, where high prevalence of low birth weight now is combined with an urban, sedentary lifestyle and increased access to low-cost, energy-dense foods. Thus reducing the prevalence of intrauterine growth retardation and early undernutrition should be an important component of our effort to control the worldwide obesity epidemic.

Failure to Thrive: A Consequence of Undernutrition

1. Sheila Gahagan, MD, MPH 1. *Clinical Professor, Department of Pediatrics and Communicable Diseases; Assistant Research Scientist, Center for Human Growth & Development, University of Michigan, Ann Arbor, Mich After completing this article, readers should be able to: 1. Recognize three common presentations in the physician’s office of failure to thrive. 2. Identify three principal mechanisms that lead to a mismatch between caloric intake and caloric expenditure. 3. Understand the complex interaction between psychosocial and biomedical risks that may lead to failure to thrive. 4. Review the diagnostic approach based on three different growth presentations. 5. Discuss the role of the physician in identifying psychosocial factors in failure to thrive and in referring families to mental health professionals. Failure to thrive (FTT) is not a disease, but a sign that is better thought of as a final common pathway of many medical, psychosocial, and environmental processes that lead to poor growth in a young child. Although FTT once was conceptualized as either organic or nonorganic, it now is understood to be the result of interaction between the environment and the child’s health, development, and behavior. The evaluation of a young infant who is growing slowly, or not at all, is truly the ultimate test of the pediatrician’s ability to evaluate simultaneously biomedical and psychosocial information obtained from the medical history and the physical examination. The stakes are high during the diagnostic phase because the child could have a life-threatening disease or be in a life-threatening psychosocial environment. Fortunately, these dire scenarios are exceedingly rare. Most cases of FTT are due to inadequate nutrition that results from biologic and environmental factors that intersect in such a way as to preclude adequate nourishment of the child. It is essential to take a developmental approach to poor growth because the causes of this condition change with development. Two case histories are presented to illustrate examples of medical and psychosocial conditions leading to inadequate growth. Management must be tailored to the child, taking into account medical, psychological, family …

Nutrition as a determinant of functional autonomy and quality of life in aging: a research program

With the aging of the Canadian population, functional autonomy and quality of life among seniors are now important public health issues. We hypothesized that nutrition is an important determinant of the quality of aging because of its potential to modulate the transitions from vulnerability to frailty and dependence. Over the past 15 years, our research program addressed the prevalence, the determinants, and the consequences of undernutrition among seniors, especially the free-living frail elderly. Very low energy and nutrient intakes were observed as well as a high prevalence of involuntary weight loss. These chronic conditions were associated with early institutionalization and increased mortality rates. Intervention strategies were then developed and evaluated, including the Nutrition Screening Program and the Nutrition Support Program. The effectiveness of these programs was shown with respect to improvement of nutritional status. However, this improvement was not sufficient to produce significant changes in functional autonomy or quality of life. Methodological issues related to the conduct of intervention studies in this specific population were addressed. A conceptual framework of nutritional intervention is currently being validated. A large longitudinal study that is being undertaken will further contribute to our understanding of the aging process as determined by a modifiable factor such as nutrition.