Nutritional Experience Research Articles

Metabolic Programming Due to Alterations in Nutrition in the Immediate Postnatal Period1–3

Altered nutritional experiences such as undernutrition, overnutrition, and modified milk formula in the immediate postnatal life via the phenomenon of metabolic programming have been identified as one of the components in the etiology of metabolic syndrome. We have developed a rat model in which an altered dietary experience in the form of a high-carbohydrate (HC) milk formula in the immediate postnatal life of rat pups results in chronic hyperinsulinemia and adult-onset obesity in these rats. The HC dietary modification causes functional alterations in pancreatic islets and the hypothalamus during the period of the dietary modification. These early adaptations in islets (supporting hyperinsulinemia) and the hypothalamus (supporting hyperphagia and increased body weight gain) persist in the postweaning period despite withdrawal of the HC milk formula at the time of weaning. In female rat pups receiving the HC milk formula, metabolic programming effects translate into an adverse (hyperinsulinemic, hyperleptinemic, and obese) intrauterine environment during pregnancy, causing spontaneous transfer of the maternal phenotype to the progeny (generational effect). Our results suggest that alterations in feeding practices for babies (early introduction of cereals, fruits, etc.) and babies born to obese/hyperinsulinemic mothers may be contributing factors for the obesity epidemic prevalent in developed and developing countries.

AAHA Nutritional Assessment Guidelines for Dogs and Cats

The American Animal Hospital Association recommends these nutritional assessment guidelines because good nutrition enhances pets’ quality and quantity of life, and is integral to optimal animal care. Incorporating nutritional assessment into regular animal care is critical for maintaining pets’

Molecular and Sensory Basis of a Food Related Two-State Behavior in C. elegans

Most animals display multiple behavioral states and control the time allocation to each of their activity phases depending on their environment. Here we develop a new quantitative method to analyze Caenorhabditis elegans behavioral states. We show that the dwelling and roaming two-state behavior of C. elegans is tightly controlled by the concentration of food in the environment of the animal. Sensory perception through the amphid neurons is necessary to extend roaming phases while internal metabolic perception of food nutritional value is needed to induce dwelling. Our analysis also shows that the proportion of time spent in each state is modulated by past nutritional experiences of the animal. This two-state behavior is regulated through serotonin as well as insulin and TGF-beta signaling pathways. We propose a model where food nutritional value is assessed through internal metabolic signaling. Biogenic amines signaling could allow the worm to adapt to fast changes in the environment when peptide transcriptional pathways may mediate slower adaptive changes.

Maternal capital and the metabolic ghetto: An evolutionary perspective on the transgenerational basis of health inequalities

There is particular interest in understanding socioeconomic and ethnic variability in health status. The developmental origins of disease hypothesis emphasize the importance of growth patterns across the life-course in relation to noncommunicable disease risk. The physiological components of cardiovascular risk, collectively termed the metabolic syndrome, derive in part from a disparity between the homeostatic "metabolic capacity" of vital organs and the "metabolic load" induced by large tissue masses, a rich diet and sedentary behavior. From an evolutionary perspective, the risk of such disparity is decreased by maternal physiology regulating offspring growth trajectory during gestation and lactation. Maternal capital, defined as phenotypic resources enabling investment in the offspring, allows effective buffering of the offspring from nutritional perturbations and represents the environmental niche initially occupied by the offspring. Offspring growth patterns are sensitive to the magnitude of maternal capital during early windows of plasticity. Offspring life-history strategy can then respond adaptively to further factors across the life-course, but only within the context of this initial maternal influence on growth. Maternal somatic capital is primarily gained or lost across generations, through variable rates of fetal and infant growth. I argue that the poor nutritional experience of populations subjected to colonialism resulted in a systematic loss of maternal capital, reflected in downward secular trends in stature. Accelerating the recovery of somatic capital within generations overloads metabolic capacity and exacerbates cardiovascular risk, reflected in increased disease rates in urbanizing and emigrant populations. Public health policies need to benefit metabolic capacity without exacerbating metabolic load.

Grasping the nutritional situation: a grounded theory study of patients’ experiences in intensive care

The aim of this study was to provide a theoretical understanding of nutritional experiences for patients with enteral nutrition (EN) during their stay in the intensive care unit (ICU). It is well known that EN can result in underfeeding for patients in ICUs. How the patients experience their nutritional care during their stay in the ICU remains somewhat unclear. In this study, a grounded theory approach was chosen to conduct and analyse 14 interviews with patients and 21 observations of nutritional care during the patients' stay in an ICU. The core category 'grasping nutrition during the recovery process' was reflected in, and related to, the categories 'facing nutritional changes', 'making sense of the nutritional situation' and 'being involved with nutritional care'. While grasping the nutrition, the patients were emotionally shifting between worry, fear and failure, and relief and hope. Turning points were having the appetite back, getting rid of the feeding tube and regaining a functioning gut. The patients' views of nutritional care during their stay in the ICU may contribute to understanding of how patients make sense of their nutritional changes and how they are involved in their nutritional care. This study shows that grasping the nutrition can be a way to regain some control in a situation where the patients are highly dependent on professional care. Further research is needed to develop this substantive theory in other intensive care settings to support patients' nutritional journey in intensive care. Nurses can promote patients' abilities to grasp their nutritional situation during their recovery process. There is a need to focus not only on the patients' physical needs but also on their emotional and social needs.

Maternal and fetal determinants of adult diseases.

Recent epidemiologic studies in the United Kingdom have led to the hypothesis that adverse nutritional experiences in utero have a powerful influence on the development of degenerative diseases in adulthood. Poor fetal growth as measured by weight, length, head, chest, and abdominal circumferences is a strong predictor of hypertension, diabetes, hyperlipidemia, alteration in clotting factors, Syndrome X,* and mortality from cardiovascular and chronic obstructive airways disease. The theory of fetal origins of adult disease proposes that early defects in the development, structure, and function of organs lead to a programmed susceptibility, which interacts with later diet and environmental stresses to cause overt disease many decades after the original insult.

Retirement Intentions of the Public Health Nutrition Workforce

High retirement rates are anticipated throughout public health as baby boomers (those born between 1946 and 1964) near retirement. Predicting retirement intention would aid workforce planning. Participants were nutrition professionals/paraprofessionals 45 years and older in nutrition programs under official health agencies' authority who participated in a census enumeration and released their data for research. Secondary data analysis was conducted using selected factors from Beehr's Model of Retirement Behavior to determine whether significant (P < or = .05) differences exist for and can be used to predict retirement intention (within 10 years) and years until intended retirement. Of the 4,460 individuals, 47.2% intended to retire within 10 years. Retirement intention was predicted by age category, years of experience in nutrition/dietetics and public health nutrition, agency type, retirement and vacation benefits, time in direct services, US Department of Health and Human Services region, and full-time/part-time status. Years until intended retirement was predicted by age category, years of nutrition/dietetics and public health nutrition experience, required training, and time in direct services. Results suggest retirement rates similar to the public health workforce overall. Findings can be used by managers/administrators to prepare their organizations for worker retirement or to influence retirement intention. Further research is necessary to determine other factors impacting retirement decision.

Metabolic programming: Role of nutrition in the immediate postnatal life

Although genes and dietary habits are generally implicated in the aetiology of the prevailing obesity epidemic, the steep increase in the incidence of obesity within a relatively short span of time suggests that other contributing factors may be at play. The role of nutritional experience during the very early periods of life is increasingly being recognized as contributing to growth and metabolic changes in later life. Epidemiological data and studies from animal models have established a strong correlation between an aberrant intrauterine environment and adult-onset disorders in offspring. The nutritional experience in the immediate postnatal life is another independent factor contributing to the development of metabolic diseases in adulthood. Although studies on the small-litter rat model have shown that overnourishment during the suckling period results in adult-onset metabolic disorders, our studies have shown that a change in the quality of calories-specifically, increased carbohydrate intake by newborn rat pups in the immediate postnatal period-results in chronic hyperinsulinaemia and adult-onset obesity. Several functional alterations in islets and in the hypothalamic energy homeostatic mechanism appear to support this phenotype. Remarkably, female rats that underwent the high-carbohydrate dietary modification as neonates spontaneously transmitted the obesity phenotype to their offspring, thus establishing a vicious generational effect. The high-carbohydrate diet-fed rat model has particular relevance in the context of the current human infant feeding practices: reduction in breast feeding and increase in formula feeding for infants, accompanied by early introduction of carbohydrate-enriched baby foods.

Developmental Changes of Gut Microflora and Enzyme Activity in Rat Pups Exposed to Fat‐rich Diet

The aim of this study was to investigate the effect of a high-fat (HF)/energy diet on the intestinal microbiota, the alkaline phosphatase (AP) activity, and related parameters of growth and obesity during the suckling and weaning periods in male Sprague-Dawley rats. From birth, nutrition in suckling pups was manipulated by feeding rat dams either HF or a standard diet, and then after weaning, by exposure of experimental pups to the HF, and control rats to normal diet. On days 15, 20, 40 the numbers of 2 microbial groups, i.e., Bacteroides/Prevotella (BAC) and the Lactobacillus/Enterococcus (LAB) in the jejunum, were determined by fluorescent in situ hybridization technique, and the AP activity was assayed histochemically. During all investigated periods HF pups gained body fat more rapidly than control animals, but from weaning they displayed significantly stunted growth resulting in final body weight loss. Obesity in HF rats was also accompanied by higher LAB and lower numbers of BAC and with permanently higher AP activity. Correlation of these data showed significant negative correlation between LAB, AP, and weight gain and energy efficiency, and significant positive correlation of BAC and AP activity with body fat. These data support the concept that postnatal nutritional experience represents an important factor affecting the ontogeny of intestinal microbial communities and intestinal function. These acquired changes could be a component of regulatory mechanisms involved in adverse and/or positive consequences of HF diet for adiposity, body weight, and energy-balance control in later life.

Early Sprouts: Gardening and Nutrition Experiences for the Young Child

Early Sprouts: Gardening and Nutrition Experiences for the Young Child

Models and mechanisms of energy balance regulation in the young

The proportion of the child and adolescent population that is in appropriate energy balance is declining throughout the developed world, and childhood obesity is a particular problem in the UK relative to other northern European countries. Assessment of the underlying causes of obesity, and the different routes to its development, may assist in the definition of successful intervention strategies. The network of peripheral and central (brain) regulatory systems that underlie energy balance and body weight and composition can, for the most part, only be approached experimentally through the study of appropriate laboratory animal models. This problem is particularly acute when the target is overweight and obesity in the young. Some of the mechanisms underlying the development of energy imbalance and specifically the onset of overweight and obesity in the young, and the metabolic health consequences of obesity, can be addressed by examination of experimental rodent models in which mutation of a single gene causes early-onset extreme obesity, genetic susceptibility to obesity is revealed in an obesogenic environment or early-life nutritional experience programmes susceptibility to obesity or metabolic problems in later life. These studies highlight genes that are essential to normal body-weight regulation in rodents and man, the impact of diet and diet-induced obesity on regulatory systems in the young and the potential sensitivity of developing regulatory systems to nutritional experiences in utero and during early life.

What we know that could influence future treatment of phenylketonuria

Phenylketonuria (PKU), a Mendelian autosomal recessive phenotype (OMIM 261600), is an inborn error of metabolism that can result in impaired postnatal cognitive development. The phenotypic outcome is multifactorial in origin, based both in nature, the mutations in the gene encoding the L-phenylalanine hydroxylase enzyme, and nurture, the nutritional experience introducing L-phenylalanine into the diet. The PKU story contains many messages including a framework to appreciate the complexity of this disease where phenotype reflects both locus-specific and genomic components. This knowledge is now being applied in the development of patient-specific therapies.

Intestinal microflora and obesity in rats

The relationship was evaluated between early nutritional experiences, the intestinal microflora and the small intestinal functions in the mechanism of predisposition to obesity development. Male Sprague-Dawley rats were used in which the quantity of nutrition was manipulated from birth to weaning (day 30) by adjusting the number of pups in the nest to 4 small litters (SL) and 10 normal litters (NL) and fed a standard diet from days 30 to 40 of age. After 40 d, the postnatally overfed SL pups became heavier, displayed significantly enhanced adiposity, body mass gain and food intake as well as a significantly higher jejunal alkaline phosphatase and maltase activity than in rats nursed in NL nests. The effect of different early nutrition was also accompanied by the appearance of significantly decreased Bacteroides and significantly increased enterococci and lactobacilli of obese rats than in lean NL rats. The amounts of Bacteroides were negatively correlated with fat pad mass, body mass, body-mass gain and food intake whereas enterococci and lactobacilli were correlated positively with the same parameters. Our results demonstrate that postnatal nutritional experience may represent a predisposing factor influencing ontogeny of small intestine function and development of intestinal microbial communities. The acquired changes and associated alterations in food digestion could be a component of regulatory mechanisms contributing to the development of obesity and its maintenance in later life.

Compensating for a bad start: catch‐up growth in juvenile lizards (Amphibolurus muricatus, agamidae)

In most natural environments, food availability varies unpredictably through space and time, and growth rates of individual organisms respond accordingly. However, growth rates are not necessarily a simple function of current nutritional conditions: growth rates can be affected by earlier nutritional experience as well as current circumstances. Thus, even a brief period of dietary restriction early in life might influence growth rates later on: either reducing them (if early experience sets subsequent rates, as in the "silver spoon" effect) or increasing them (if underfed individuals can compensate by growing more rapidly to cancel out the early decrement). Alternatively, later growth may be unaffected by earlier rates of growth. We experimentally manipulated food supply (and thus, growth rates) of hatchling lizards (Amphibolurus muricatus) for 1 month post-hatching, then maintained both high-food and low-food animals under identical nutritional conditions in outdoor enclosures for another 6 months. Low food abundance early in life significantly reduced juvenile growth, but these previously underfed animals exploited the subsequent (common garden) conditions to grow much faster than their larger (initially better-fed) siblings. Thus, the two groups were indistinguishable in body size at 6 months of age. Intriguingly, the compensatory growth occurred in winter, a period that is generally unsuitable for rapid growth in ectotherms.

From epidemiology to cancer prevention: implications for the 21st Century

As I move to Washington University School of Medi? cine and the Alvin J. Siteman Cancer Center I con? clude my term as editor-in-chief of the journal. Over the past 8 years the journal has increased in number of issues and pages published per year, number of sub? mission, and the scope of topics covered. The increase in articles reporting prevention interventions, risk communication, and related topics, reflects in part, the growing program of research funded by the US National Cancer Institute. As Dr. Giovannucci takes over as the Editor-in-Chief, bringing his extraordinary wealth of experience in nutrition and cancer to the leadership of the Journal, I will join the growing team of Associate Editors to work with him in the coming years. In the essay that follows, I reflect on the direc? tion our field is taking. I also identify some of the challenges that we must address particularly in cancer epidemiology and cancer prevention more generally. To place this in context, we might consider that the emergence of the "genetic revolution" in medicine and public health provides hope and a distraction from the underlying mission of disease prevention, health pro? motion, and the reduction in the burden of cancer. Doll and Peto noted that uncovering the mechanism for an

Functional changes of the small intestine in over- and undernourished suckling rats support the development of obesity risk on a high-energy diet in later life

To investigate the relationship between early nutritional experience, ontogeny of the small intestinal functions and predisposition to obesity development, the following experimental models of male Sprague-Dawley rats were used: 1) rats in which the quantity of nutrition was manipulated from birth to weaning (day 30) by adjusting the number of pups in the nest to 4 (SL), 10 (NL) and 16 pups (LL) and 2) littermates of SL, NL and LL rats fed either a standard or a hypercaloric diet from days 80 to 135 of age. The overfed SL pups were overweight after day 15 and became permanently obese, whereas the underfed smaller LL pups, due to accelerated growth and enhanced food intake from day 30 to day 35, attained a body fat level that did not differ from normally fed NL rats. Moreover, a significantly increased duodenal and jejunal alkaline phosphatase (AP) activity was found in SL and LL rats and these acquired somatic and intestinal characteristics persisted from weaning throughout life. Eight weeks of high-energy diet feeding elicited a similar pattern of intestinal response in SL and LL rats that was clearly different from NL rats. Despite energy over-consumption in these three groups, both SL and LL rats still displayed enhanced AP activity and showed a significant increase in protein/DNA ratio accompanied with a significant body fat accretion. These results indicate that the postnatally acquired small intestinal changes induced by over- and undernutrition could be involved in the similar predisposition to obesity risk in later life when caloric density of the diet is raised.

ThePAH gene, phenylketonuria, and a paradigm shift

"Inborn errors of metabolism," first recognized 100 years ago by Garrod, were seen as transforming evidence for chemical and biological individuality. Phenylketonuria (PKU), a Mendelian autosomal recessive phenotype, was identified in 1934 by Asbjörn Fölling. It is a disease with impaired postnatal cognitive development resulting from a neurotoxic effect of hyperphenylalaninemia (HPA). Its metabolic phenotype is accountable to multifactorial origins both in nurture, where the normal nutritional experience introduces L-phenylalanine, and in nature, where mutations (>500 alleles) occur in the phenylalanine hydroxylase gene (PAH) on chromosome 12q23.2 encoding the L-phenylalanine hydroxylase enzyme (EC 1.14.16.1). The PAH enzyme converts phenylalanine to tyrosine in the presence of molecular oxygen and catalytic amounts of tetrahydrobiopterin (BH4), its nonprotein cofactor. PKU is among the first of the human genetic diseases to enter, through newborn screening, the domain of public health, and to show a treatment effect. This effect caused a paradigm shift in attitudes about genetic disease. The PKU story contains many messages, including: a framework on which to appreciate the complexity of PKU in which phenotype reflects both locus-specific and genomic components; what the human PAH gene tells us about human population genetics and evolution of modern humans; and how our interest in PKU is served by a locus-specific mutation database (http://www.pahdb.mcgill.ca; last accessed 20 March 2007). The individual Mendelian PKU phenotype has no "simple" or single explanation; every patient has her/his own complex PKU phenotype and will be treated accordingly. Knowledge about PKU reveals genomic components of both disease and health.

Delivering Nutrition Education in a Service-learning Course

For the past six years, students at the University of Connecticut have delivered interactive nutrition education integrated with literacy activities in the waiting rooms of inner-city pediatric clinics in Hartford, Connecticut. This initiative, named Husky Reads for the university’s canine mascot, provides students with real-life, hands-on experiences in community nutrition while the Department of Nutritional Sciences reaches an underserved population. Teams of students visit clinics weekly for two-hour shifts to read aloud and play games with waiting children and to interact with their parents and caregivers (Figure). All program materials, such as children’s books, games and craft activities, feature food and nutrition themes. Hartford provides both economic and ethnic diversity that students could not experience on campus or in nearby communities; it is the second poorest midsize city in the U.S. and Hartford’s children are 92% Black and Hispanic.

Resources for a healthy diet: school meals

School meals have changed during the last decades. The traditional service style with on-site food preparation has shifted towards catering delivery services. Vending machines, school cafeterias and other ways of food distribution are widely used in many schools, particularly in secondary schools. From a health promotion approach, the quality and quantity of food and beverages consumed while in school have an enormous potential impact on the health and well-being of young people. Most children spend a significant part of their lives in school. Additionally, school meals supply 30-35 % of daily energy intake and provide an important contribution to nutrient intake. School life is a critical period in the acquisition and practice of healthy behaviours. Environmental interventions in schools, to increase availability and access to healthy foods such as fruit and vegetables, have proved to be effective. School meals should make high-quality foods available which allow nutrient requirements to be met, consistent with dietary guidelines and offering a positive nutritional experience. School meals should be part of the educational process in the life of the school.

Regulation of leptin synthesis and secretion before birth: implications for the early programming of adult obesity

A series of epidemiological, clinical and experimental studies have shown that there are associations between the fetal and neonatal nutritional environment and the amount and distribution of adipose tissue in adult life. This review considers the evidence for these relationships and discusses the potential impact of the prenatal nutritional experience on the development of the endocrine and neuroendocrine systems that regulate energy balance, with a particular emphasis on the role of the adipocyte-derived hormone, leptin. In the rodent, leptin derived from the mother may exert an important influence on the development of the appetite regulatory neural network and on the subsequent regulation of leptin synthesis and the risk for obesity in the offspring. In species such as the human and sheep, there is also recent evidence that the synthesis and secretion of adipocyte-derived hormones, such as leptin, are regulated in fetal life. Furthermore, the hypothalamic neuropeptides that regulate energy intake and expenditure in adult life are also present within the fetal brain and may be regulated by the prevailing level of maternal and hence fetal nutrient and hormonal signals, including leptin. This work is important in determining those initiating mechanisms within the 'fat-brain' axis in early life that precede the development of adult obesity.