There is much evidence to show that maternal nutrition has specific developmental effects of neurological and physiological development of a fetus. These effects are evident sometimes in utero, immediately or shortly after birth, or sometime in the childhood and adolescent stages of life. However, more and more studies are being done to determine whether or not maternal nutrition during pregnancy will have long-term effects associated with the development of diseases, such as Type 2 diabetes mellitus, osteoporosis, obesity, hypertension and cardiovascular disease, due to genetic fetal adaptations. This type of adaptation to environmental stressors is generally referred to as gene programming and is still hotly debated; however, many studies are now providing evidence of this genetical-environmental interaction.
Type 2 diabetes mellitus (T2DM), alongside the growing obesity epidemic, is an increasingly prevalent chronic condition and a widely discussed topic among health professionals and political leaders. Out of this concern, questions have been raised about developing preventative measures and discovering factors that predispose someone to developing T2DM. Predisposition to the development of T2DM can be decreased as early as the womb. One study on the idea that ?fetal malnutrition may predispose to type 2 diabetes through gene programming and developmental changes1? was done to analyze the effects of famine on gene variants linked to increased T2DM risk. The hypothesis is that ?fetal adaptation to a low-caloric intrauterine environment may involve programming to optimize the use of restricted nutrient sup?ply1?.This adaptation may become permanent and continue to cause optimization of energy later in life, thus storing fat more readily and metabolizing less. This is what leads to disease in later adult years. In the study, DNA is retrieved from participants that were born around the time of the Dutch Famine. Genotypes were determined, correlations between those who were affected in-utero by the famine and exhibited the variants of the gene associated with T2DM risk were observed. Interestingly, there was ?nominally significant interaction1? between the variant associated with T2DM and fetal malnutrition. ?In conclusion, genetic variants involved in fetal development? may influence the response to fetal malnutrition and its consequences in the adult hypercaloric environment1?.
Another major concern among women in America is the development of osteoporosis. Although diet, physical activity, and avoidance of other risk factors for developing osteoporosis are key contributors to prevention, a look at the affects of maternal malnutrition may allow for the opportunity to determine whether an individual is predisposed to developing this disease and to make recommendations for mothers in order to decrease the likelihood that their child will develop osteoporosis later in life. Some studies have produced evidence that a vitamin D deficiency can lead to rickets, a childhood disease characterized by the softening of the bones, However, new studies are being done to show ?direct evidence that the trajectory of bone growth might be modified in-utero2?. A genetic polymorphism in the gene for the vitamin D receptor is an example of a genetic predisposition for the development of osteoporosis2. What about the effects of maternal diet on predisposition toward osteoporosis through gene programming? ?The data [found in the studies conducted by Antoniades et al] are compatible with the hypothesis that environmental stressors during intrauterine or early postnatal life alter the sensitivity of the growth plate to [growth hormone] and cortisol2.? Maternal smoking, diet, and physical activity all potentially contribute to predisposition to rapid bone loss later in life and lower bone mineral densities as ?basal levels of circulating [growth hormone]? are established due to genetic and environmental interactions2. Though benefit of adaptation or alteration of gene expression to the fetus may not be immediate, these adaptations may provide benefits later in life if the predicted environment based on intrauterine stressors is a match to the actual adult environment. These adaptations take place during certain times in utero when development is said to be plastic, meaning that genes are sensitive to environment and can change the way they are expressed in order to comply with the given circumstances to optimize nutrition. This is the idea behind gene programming as ?[d]evelopmental plasticity set the template on which continued postnatal homeostatic and homeorhetic (maintaining a time-dependent process, e.g. growth trajectory) adaptation can occur2?.
Suggesting that the development of obesity is related to genetic predisposition in the state of epidemic could possibly have negative effects on the health status of the United States if people interpret that to mean obesity is not a direct outcome of the positive energy balance over an extended period of time. Studies do show, however, that ?poor pre-natal nutrition followed by improved or even excess post-natal nutrition can render [infants] susceptible to develop obesity later in life3?. When placed under environmental stress, fetal genes will adapt expression in order to optimize energy, and these adaptations, after a certain time period become irreversible. Then, if exposed to a ?constant availability of highly nutritious diet in the post-natal3?, the infant will experience catch-up growth that can possible lead to overweight and obesity. This predisposition and connection between maternal malnutrition and low-birth weight, catch-up growth and then obesity ?suggests that the fetus/infant is unprepared to meet the metabolic demands of a high-fat and nutritious diet3?. Genetic reasons for the predisposition toward obesity and the other chronic illnesses that surround this particular disease can be attributed to ?changes in the glucose metabolism through structural alterations and changes in glucokinase expression in the live3? brought about by maternal protein restriction. Metabolism is not the only aspect of obesity that can be explained by genetic factors. Appetite and satiety are influenced by neurotransmitters. Prenatal exposure to cytokines can have an affect on regulation of neurotransmitters. ?If prenatal diet also has such an [a]ffect on the concentrations of the various neurotransmitters and the cytokines in the brain, this may also influence the development of obesity? later in life? as appetite and satiety signals are flawed3.
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Yet again, another disease associated with obesity and may have ?both inherited and environmental causes? is hypertension, or chronic high blood pressure4. A study was conducted in 1998 and published in the British Medical Journal ?to examine the possibility that low birth weight is a feature of inherited predisposition to high blood pressure4. Since many chronic illnesses are related to low-birth weight and high blood pressure is prevalent among the population of the United States, evidence that maternal high blood pressure decreases birth weight, and thus, predisposing the offspring to hypertension later in life could give an idea of a vicious cycle of maternal illness, low-birth weight, and adult offspring disease that need to be corrected immediately. Although low-birth weight alone is a risk factor for the development of hypertension later in life, maternal high blood pressure increases the likelihood that the offspring will also develop hypertension in the adult years, and information from the study suggests that ?maternal smoking, socioeconomical group, and an[a]emia did not explain the observed relations between low birth weight and subsequent high blood pressure4?. This shows that other suboptimal nutritional factors, such as smoking, do not show a significant correlation between low-birth weight and adult hypertension. The study involved participants who were born to mothers that had high blood pressure. Their blood pressures were measured and factors such as age, weight, and gender were taken into accounts and adjustments were made for these variables. The results showed that the higher maternal or paternal systolic blood pressure was, the higher the systolic blood pressure of the offspring, however, the maternal blood pressure had more influence on the offspring?s development of high blood pressure than the paternal blood pressure, as the maternal health status was more greatly ?associated with lower birth weight and high blood pressure in the offspring4? which ?confirms a relation between low birth weight and high blood pressure in young adults4?. The results of this study also suggest that ?as much as 24%? of the development of the hypertension of the offspring is due to ?inherited factors4?. All of this research supports the idea that fetal adaptations are made in the intrauterine environment program ?permanent changes in factors that influence blood pressure later in life, including cortisol, growth factors, and insulin4?.
Maternal malnutrition oftentimes leads to adult development of obesity and diabetes in the offspring, but what are the effects of the effects of these diseases on long-term disease development? In addition to under-nutrition, over-nutrition intrauterine can also increase the risk and predisposition toward adult obesity, hypertension and cardiovascular disease. Since over-nutrition is a newer problem characteristic to the more developed areas of the world, not as many long-term studies have yet been conducted to show the effect of this type of malnutrition. It is, however, a rapidly growing concern and ?understanding the mechanisms by which obese and diabetic maternal intrauterine environment elicits permanent metabolic and cardiovascular disease in the fetus will provide a basis for future interventional studies in human5?. Some research has been done to show that maternal insulin resistance, as seen in T2DM, is ?associated with increased fetal fat mass5?. Fat is adipose tissue that, in excess can cause inflammation, increased blood pressure, and risk factors related to cardiovascular disease. It is hypothesized that maternal obesity affects the expression of fetal genes, but the ?mechanisms by which maternal obesity increases the risk of metabolic and cardiovascular disease in the offspring [had] not been established as recently as 20055?. Studies are being conducted to research the effects of over-nutrition on the long-term development of disease in offspring. Topics such as the correlation between maternal obesity and fetal gene programming, the effect of adipose tissue on genes, effect of food intake regulation and development of cardiovascular disease are being researched and of much value to society as obesity rates sky-rocket.
The human body in an intricate, wonderful machine that operates and adapts in order to increase efficiency. Fetal genes are sensitive to the environment that the fetus is in and will adjust in order to achieve optimal health and prepare for the predicted post-natal environment. ?Where there is a match between predicted and actual mature environment, these responses are appropriate and assist in survival5?. However, when the intrauterine environment is not consistent with the adult environment, gene expression may clash with actual circumstances such as a mother who experiences under-nutrition during pregnancy, but the offspring is exposed to optimal nutrition post-natal. This can lead to disease later in life. On the other hand, over-nutrition in utero can put a fetus in an inflamed state which can be further exacerbates if a high-fat and over-nutritious environment continues after birth and into adult years. All is not lost if genetic adaptations were made in utero to adjust to the environment because predisposed persons also have the ability to regulate their own environment in their adult years to counter the genetic tendencies by proper energy balance, adequate nutrition, and physical activity.
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