Prenatal Nutritional Physiological Phenomena: Nutrition of FEMALE during PREGNANCY.Sports Nutritional Physiological Phenomena: Nutritional physiology related to EXERCISE or ATHLETIC PERFORMANCE.Elder Nutritional Physiological Phenomena: Nutritional physiology of adults aged 65 years of age and older.Dental Physiological Phenomena: Physiological processes and properties of the DENTITION.Digestive System and Oral Physiological Phenomena: Properties and processes of the DIGESTIVE SYSTEM and DENTITION as a whole or of any of its parts.Reproductive and Urinary Physiological Phenomena: Physiology of the human and animal body, male or female, in the processes and characteristics of REPRODUCTION and the URINARY TRACT.Musculoskeletal and Neural Physiological Phenomena: Properties, and processes of the MUSCULOSKELETAL SYSTEM and the NERVOUS SYSTEM or their parts.Circulatory and Respiratory Physiological Phenomena: Functional processes and properties characteristic of the BLOOD; CARDIOVASCULAR SYSTEM; and RESPIRATORY SYSTEM.Integumentary System Physiological Phenomena: The properties and relationships and biological processes that characterize the nature and function of the SKIN and its appendages.Reproductive Physiological Phenomena: Physiological processes, factors, properties and characteristics pertaining to REPRODUCTION.Physiological Phenomena: The functions and properties of living organisms, including both the physical and chemical factors and processes, supporting life in single- or multi-cell organisms from their origin through the progression of life.Adolescent Nutritional Physiological Phenomena: Nutritional physiology of children aged 13-18 years.Urinary Tract Physiological Phenomena: Properties, functions, and processes of the URINARY TRACT as a whole or of any of its parts.Prenatal Exposure Delayed Effects: The consequences of exposing the FETUS in utero to certain factors, such as NUTRITION PHYSIOLOGICAL PHENOMENA; PHYSIOLOGICAL STRESS; DRUGS; RADIATION; and other physical or chemical factors. These consequences are observed later in the offspring after BIRTH.Prenatal Diagnosis: Determination of the nature of a pathological condition or disease in the postimplantation EMBRYO; FETUS; or pregnant female before birth.Maternal Nutritional Physiological Phenomena: Nutrition of a mother which affects the health of the FETUS and INFANT as well as herself.Prenatal Care: Care provided the pregnant woman in order to prevent complications, and decrease the incidence of maternal and prenatal mortality.Child Nutritional Physiological Phenomena: Nutritional physiology of children aged 2-12 years.Nutritional Physiological Phenomena: The processes and properties of living organisms by which they take in and balance the use of nutritive materials for energy, heat production, or building material for the growth, maintenance, or repair of tissues and the nutritive properties of FOOD.Infant Nutritional Physiological Phenomena: Nutritional physiology of children from birth to 2 years of age.Musculoskeletal Physiological Phenomena: Processes and properties of the MUSCULOSKELETAL SYSTEM.Virus Physiological Phenomena: Biological properties, processes, and activities of VIRUSES.Pregnancy: The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.Animal Nutritional Physiological Phenomena: Nutritional physiology of animals.Digestive System Physiological Phenomena: Properties and processes of the DIGESTIVE SYSTEM as a whole or of any of its parts.Ultrasonography, Prenatal: The visualization of tissues during pregnancy through recording of the echoes of ultrasonic waves directed into the body. The procedure may be applied with reference to the mother or the fetus and with reference to organs or the detection of maternal or fetal disease.Blood Physiological Phenomena: Physiological processes and properties of the BLOOD.Ocular Physiological Phenomena: Processes and properties of the EYE as a whole or of any of its parts.Fetal Diseases: Pathophysiological conditions of the FETUS in the UTERUS. Some fetal diseases may be treated with FETAL THERAPIES.Nervous System Physiological Phenomena: Characteristic properties and processes of the NERVOUS SYSTEM as a whole or with reference to the peripheral or the CENTRAL NERVOUS SYSTEM.Cell Physiological Phenomena: Cellular processes, properties, and characteristics.Respiratory Physiological Phenomena: Physiological processes and properties of the RESPIRATORY SYSTEM as a whole or of any of its parts.Skin Physiological Phenomena: The functions of the skin in the human and animal body. It includes the pigmentation of the skin.Plant Physiological Phenomena: The physiological processes, properties, and states characteristic of plants.Bacterial Physiological Phenomena: Physiological processes and properties of BACTERIA.Cardiovascular Physiological Phenomena: Processes and properties of the CARDIOVASCULAR SYSTEM as a whole or of any of its parts.Infant, Newborn: An infant during the first month after birth.Maternal Exposure: Exposure of the female parent, human or animal, to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals that may affect offspring. It includes pre-conception maternal exposure.Gestational Age: The age of the conceptus, beginning from the time of FERTILIZATION. In clinical obstetrics, the gestational age is often estimated as the time from the last day of the last MENSTRUATION which is about 2 weeks before OVULATION and fertilization.Amniocentesis: Percutaneous transabdominal puncture of the uterus during pregnancy to obtain amniotic fluid. It is commonly used for fetal karyotype determination in order to diagnose abnormal fetal conditions.
Environment (biophysical): Environment}}Prenatal diagnosis: Prenatal diagnosis or prenatal screening (note that prenatal diagnosis and prenatal screening refer to two different types of tests) is testing for diseases or conditions in a fetus or embryo before it is born. The aim is to detect birth defects such as neural tube defects, Down syndrome, chromosome abnormalities, genetic disorders and other conditions, such as spina bifida, cleft palate, Tay Sachs disease, sickle cell anemia, thalassemia, cystic fibrosis, Muscular dystrophy, and fragile X syndrome.Prenatal nutrition: Nutrition and weight management before and during :pregnancy has a profound effect on the development of infants. This is a rather critical time for healthy fetal development as infants rely heavily on maternal stores and nutrient for optimal growth and health outcome later in life.Gastrointestinal physiology: Gastrointestinal physiology is a branch of human physiology addressing the physical function of the gastrointestinal (GI) system. The major processes occurring in the GI system are that of motility, secretion, regulation, digestion and circulation.Gestational age: Gestational age (or menstrual age) is a measure of the age of a pregnancy where the origin is the woman's last normal menstrual period (LMP), or the corresponding age as estimated by other methods. Such methods include adding 14 days to a known duration since fertilization (as is possible in in vitro fertilization), or by obstetric ultrasonography.
(1/328) Abuse history and nonoptimal prenatal weight gain.
OBJECTIVE: The purpose of this study was to examine the differences between women who reported current and past physical or sexual abuse and those who did not in terms of mean total prenatal weight change, the odds for inadequate prenatal gain, and the odds for excessive prenatal gain. METHODS: This study used a matched retrospective cohort design. Data were from the charts of 578 clients of an urban prenatal care clinic. Multiple regression analyses, stratified by maternal age, were conducted to examine the association of past and current abuse with total prenatal weight change and with adequacy of prenatal weight gain for Body Mass Index category. RESULTS: For teens, abuse was not associated with prenatal weight change. For adults, mean total gains were 6.9 pounds greater for those who reported current abuse than for those who reported no abuse. Compared to women who reported no abuse, adults who reported only a history of physical abuse had 3.1 times the odds, and those who reported a history of sexual abuse (with or without physical abuse) had 3.0 times the odds for inadequate prenatal weight gains. Adults who reported a history of sexual abuse were 2.4 times as likely to have excessive prenatal weight gains as adults who reported no abuse. CONCLUSIONS: The relationship of abuse and prenatal weight gain was different in adults and teens. This study may be the first to report an association between abuse and excessive prenatal gains, suggesting that addressing the psychosocial needs of women may help optimize prenatal weight gain. (+info)
(2/328) Prenatal programming of postnatal endocrine responses by glucocorticoids.
Epidemiological studies have led to the hypothesis that a major component of the risk of diseases such as hypertension, coronary heart disease and non-insulin-dependent diabetes (the 'metabolic syndrome') is established before birth. Although the underlying mechanisms of this 'programming' of disease have not yet been conclusively determined, a reduced fetal nutrient supply as a consequence of poor placental function or unbalanced maternal nutrition is strongly implicated. It has been proposed that one outcome of suboptimal nutrition is exposure of the fetus to excess glucocorticoids, which restrict fetal growth and programme permanent alterations in its cardiovascular, endocrine and metabolic systems. This review focuses on the effects of endogenous and exogenous glucocorticoid exposure in utero on postnatal hypothalamo-pituitary-adrenal (HPA) axis activity, both in humans and experimental animals. The physiological consequences and proposed underlying molecular and cellular mechanisms are discussed. Current data indicate that key targets for programming may include not only the HPA axis but also glucocorticoid receptor gene and 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) gene expression in a range of tissues. (+info)
(3/328) Leptin levels in rat offspring are modified by the ratio of linoleic to alpha-linolenic acid in the maternal diet.
The supply of polyunsaturated fatty acids (PUFA) is important for optimal fetal and postnatal development. We have previously shown that leptin levels in suckling rats are reduced by maternal PUFA deficiency. In the present study, we evaluated the effect of maternal dietary intake of (n-3) and (n-6) PUFA on the leptin content in rat milk and serum leptin levels in suckling pups. For the last 10 days of gestation and throughout lactation, the rats were fed an isocaloric diet containing 7% linseed oil (n-3 diet), sunflower oil (n-6 diet), or soybean oil (n-6/n-3 diet). Body weight, body length, inguinal fat pad weight, and adipocyte size of the pups receiving the n-3 diet were significantly lower during the whole suckling period compared with n-6/n-3 fed pups. Body and fat pad weights of the n-6 fed pups were in between the other two groups at week one, but not different from the n-6/n-3 group at week 3. Feeding dams the n-3 diet resulted in decreased serum leptin levels in the suckling pups compared with pups in the n-6/n-3 group. The mean serum leptin levels of the n-6 pups were between the other two groups but not different from either group. There were no differences in the milk leptin content between the groups. These results show that the balance between the n-6 and n-3 PUFA in the maternal diet rather than amount of n-6 or n-3 PUFA per se could be important for adipose tissue growth and for maintaining adequate serum leptin levels in the offspring. (+info)
(4/328) Effect of maternal feed restriction on blood pressure in the adult guinea pig.
Small size at birth has been associated with increased blood pressure in adult men and women. In rats, isocaloric protein restriction reduces fetal growth and increases systolic blood pressure in adult offspring. Balanced maternal undernutrition in the rat also increases adult blood pressure, but not consistently. The aim of this study was to determine the effect of moderate balanced maternal undernutrition (85% of ad libitum intake from 4 weeks before, and throughout pregnancy) on blood pressure of adult offspring in the guinea pig, a species that is relatively mature at birth. Blood pressure was measured in chronically catheterised offspring of ad libitum fed or feed-restricted mothers, at 3 months of age (young adult). Maternal feed restriction reduced birth weight (-17%) and increased systolic blood pressure (+9%, P < 0.03) in young adult male offspring. In offspring of ad libitum fed and feed-restricted mothers, combined data showed that systolic blood pressure and mean arterial pressure correlated negatively with head width at birth (P = 0.02 and P = 0.04, respectively, n = 28). Systolic blood pressure also correlated negatively with birth weight and the ratio birth weight/birth length, but only in offspring of ad libitum fed mothers (P = 0.04 and P = 0.03, respectively, n = 22). The effect of maternal feed restriction on systolic blood pressure in male offspring was not significant when adjusted for these measures of size at birth. Thus, moderate balanced undernutrition in the guinea pig increases systolic blood pressure in young adult male offspring; however, these effects may be mediated, at least in part, through effects on fetal growth. (+info)
(5/328) Increased systolic blood pressure in rats induced by a maternal low-protein diet is reversed by dietary supplementation with glycine.
When rat dams consume a diet low in protein during pregnancy, their offspring develop high blood pressure. On a low-protein diet, the endogenous formation of the amino acid glycine is thought to become constrained. Glycine may become conditionally essential, as its rate of endogenous formation is inadequate to meet metabolic needs, and may be limiting for the normal development of the fetus. In the present study, five groups of Wistar rats were provided during pregnancy with one of five diets: a control diet containing 18% (w/w) casein (CON), a low-protein diet containing 9% casein (MLP), or the low-protein diet supplemented with 3% glycine (MLPG), alanine (MLPA) or urea (MLPU). The offspring were weaned on to standard laboratory chow, and blood pressure was measured at 4 weeks of age. Blood pressure was significantly increased in the MLP, MLPA and MLPU groups compared with the CON group, but for the MLPG group blood pressure was not significantly different from CON. Compared with the CON group, body weight was significantly reduced for the MLP, MLPA and MLPG groups, but for the MLPU group body weight was not different from CON. These data show that different forms of non-essential dietary nitrogen, when consumed during pregnancy, exert different effects upon the growth and function of the offspring. The availability of glycine appears to be of critical importance for normal cardiovascular development. (+info)
(6/328) Will feeding mothers prevent the Asian metabolic syndrome epidemic?
Evolutionary pressures have probably amplified the mechanisms for minimizing the impact of environmental factors through compensatory maternal mechanisms. Nevertheless, experimentally there are clear long-term programming effects of manipulations to the maternal diet on the likelihood of neural-tube defects associated with folate deficiency The fat/lean ratios of the newborn, and subsequent development, seem to be linked to amino acid or folate supply. An altered balance in the hypothalamic-pituitary-adrenal axis, which experimentally has profound effects on brain development, is induced by low-protein maternal diets. Such diets are linked to a reduced pancreatic capacity for insulin production and to an altered hepatic architecture, with a change in the control of glucose metabolism. Human studies suggest that what happens in pregnancy is modified by the child's diet in the first months of life. Low birthweight is linked to early stunting, and predisposes to abdominal obesity and metabolic syndrome in later life. Metabolic syndrome amplifies the risks of diabetes, hypertension, coronary heart disease and probably some cancers. Mothers with gestational diabetes are themselves prone to early type 2 diabetes and produce heavier babies prone to childhood obesity and adolescent type 2 diabetes. There is increasing evidence of an intergenerational effect, with big babies being prone to excess weight gain, which then, in girls, predisposes them to diabetes in pregnancy, which, in turn, promotes an accelerating cycle of early diabetes in subsequent generations. Essential fatty acids and fat soluble vitamins are important, but we need early interventions and monitoring systems to justify coherent policies. (+info)
(7/328) Nutrition before birth, programming and the perpetuation of social inequalities in health.
The need to explain social inequalities in health has led to the theory that chronic disease is due, in part, to a legacy of adverse experiences in early life. Epidemiological studies show consistently that individuals who are small at birth have an increased risk of cardiovascular disease in adulthood. There is growing consensus that this association reflects a causal relationship and is not simply the product of bias or confounding. The concept of programming is invoked as the biological mechanism; birth size is thus a proxy for fetal programming. Recent findings suggest that fetal programming interacts with the post-birth environment. The adverse exposures that are thought to underlie and potentiate programming cluster in socially patterned ways, thus creating substantial inequalities in health. Experiments in animals demonstrate that nutritional interventions before or during pregnancy can produce programming phenomena in the offspring, sometimes without an impact on birth size. However, the extent to which maternal nutrition contributes to programming in contemporary developed countries is uncertain. (+info)
(8/328) Nutrition and the early origins of adult disease.
There is now overwhelming evidence that much of our predisposition to adult illness is determined by the time of birth. These diseases appear to result from interactions between our genes, our intrauterine environment and our postnatal lifestyle. Those at greatest risk are individuals in communities making a rapid transition from lives of 'thrift' to a lives of 'plenty'. From a global perspective, such origins of diabetes, coronary heart disease and stroke, should render research in these fields as one of the highest priorities in human health care. Prevention will be enhanced by elucidation of the mechanisms by which the fetus is programmed by the mother for the life she expects it to live. At the present time, there is evidence that fetal nutrition and premature exposure to cortisol are effective intrauterine triggers, but a multitude of alternative pathways require investigation. It is also likely that programming extends across generations, and may involve the embryo and perhaps the oocyte. An oocyte that becomes an adult human develops in the uterus of its grandmother, so further research is required to describe the role of environments of grandmothers and mothers in predisposing offspring to health or illness in adult life. (+info)