Relationship between Poor Fetal Growth and the Subsequent Development of Obesity, Type 2 Diabetes and Metabollic Syndrome

Although the mechanism of obesity development is not fully understood, it is confirmed that obesity occurs when energy intake exceeds energy expenditure. There are multiple etiologies for this imbalance, hence, and the rising prevalence of obesity cannot be addressed by a single etiology (Dehghan et al., 2005, p.

When thinking of public health in regards specifically to obesity, a study into maternal obesity and the long-term health of the offspring, found that ‘maternal obesity has been associated with a number of long-term adverse health outcomes in the offspring, including lifelong risk of obesity and metabolic dysregulation with increased insulin resistance, hypertension and dyslipidaemia, as well as behavioural problems and risk of asthma’ (O’Reilly et al, 2012:1), this highlights to us the implications not just to mother, but the long term effects to her child.

The entire population of the Netherlands suffered severe food restriction while under Nazi occupation during the “Dutch Hunger Winter” in 1944-45. Many women who were pregnant during this time of nutritional stress gave birth to low-birth-weight infants who, surprisingly, had a greater tendency than their siblings to become obese in adulthood. Maternal malnutrition had influenced their fetal metabolism to become extremely efficient and well adapted for a lifetime of nutritional stress. But postwar food abundance promoted rapid growth and weight gain after birth and the development of obesity, diabetes, and heart disease later in adulthood. Their siblings, who were born before or after the famine, were not affected in the same way (Bellisari, 2013, p. 38).

Worldwide over the last twenty years there have been many research studies into the causes of obesity. While many correlational links have been found, it is safe to say that obesity is a complex multi-faceted problem. Researchers have found a relationship between fetal malnutrition and later in life obesity, as well as a relationship between the thrifty genotype and inability to lose weight. Both of these correlations to obesity are thing that an individual has no real control of so they will not be examined in this essay. Relationships have also been found between increased caloric intake, decreased physical activity, and sleep deprivation with obesity, which are all things we can control so they will be discussed in this essay.

acute effects of leptin on synaptic plasticity in the arcuate nucleus of the hypothalamus. The arcuate nucleus is one of the key targets of circulating hormones such as leptin. At least two distinct populations of neurons with opposing actions on food intake residein the arcuate nucleus, " (p.63). Pinto's data is ultimately described as helpful but also created many more questions, probably more than it answered.

Sadly though, obesity in children has doubled over the last thirty years and eighteen percent of children age six to eleven are obese. This percentage rate increase to over twenty percent in children between the age of twelve and nineteen (Anonymous, 2016). With the increase in childhood obesity, experts have been researching why there is a spike among children developing obesity. Some evidence points to genetics as a contributing factor in childhood obesity. Studies show that among parents with weight problems there is a greater chance of their children being overweight or obese (Steele and Steele, 2006). The DNA is passed down from parent to child through the “thrifty” gene. It is believed that this gene is a risk factor because it causes a child to have a lower level of energy (Anonymous, 2010). Next there is the idea that childhood obesity is a nutritional

For now lets discuss how nutrition plays a role in our lives before birth and how our parents nutritional values factor into our lives just as their parents nutrition factor into their lives. Women who start off pregnancy overweight are already predisposing the future adult to obesity and diabetes(1). When a fetus experiences large amounts of glucose and large amounts of insulin, the result will be a higher birth weight, or more fat per child (1). Studies suggest that if a future mother has poor health at a young age it will affect the health of the next generation (4). This idea later became known as the “intergenerational hypothesis”, factors such as the mother's height, health, weight, and environment in which the mother grew up in are all good indicators of the future status of the unborn fetus

1994). Leptin is secreted primarily by adipocytes, proportionally to fat cell mass, and contributes to energy metabolism. Leptin will affect the energy balance by acting on the brain. Leptin can activate, directly or indirectly, specific centers in the hypothalamus to decrease food intake, to increase any energy expenditure, to influence the glucose, lipid metabolism, and alter neuroendocrine function (Campfield, Smith et al. 1995). Leptin resistance, in regards to obesity, was coined due to the increased leptin levels with no impact on regulating energy homeostasis. Leptin resistance causes insulin resistance and the accumulation of lipids is a direct result of the reduction of lipid oxidation in insulin-sensitive organs; shown in preclinical and clinical experiments with obese rodents and humans. However, the mechanisms that may lead to leptin resistance are still being researched (Mori, Hanada et al.

Parents can calculate their children’s percentile to see if the baby is growing well. Percentile is a number that tells parents directly if their baby’s body weight is in the normal by comparing the baby’s weight to other children in the same age group and the baby’s weight history. 50th is the midpoint, 75th indicates overweight while 25th means underweight. However, it is not a big problem if a baby’s percentile keeps being high or low. In other words, if the infant’s body weight fluctuates too much in a certain period of time, parents should be aware that something is wrong. The amount of nutrition that a baby takes in can be one of the causes for the dramatically change on the infant’s body weight. It could be too much, while also could be not enough. The outcomes of nutritional deficiencies could be both short-term and long-term.

The University of Cincinnati (UC), hypothesized that that the body was developing extra leptin to fight the temptations of obesity. This is due to the fact that leptin is the protein that signals the brain to stop eating. The more leptin, the more signals that will tell the body to stop eating (Babcock,2017). They thought this was the case, however, in human preclinical trials, giving obese patients more leptin didn't work. They ate at the same rate, and still remained obese. The results of this study show that scientist need to rethink the ways of using leptin to treat obesity (University of Cincinnati Academic Health Center, 2015). There must be other options out there and it could be that researchers are focusing on the wrong

The author is a physiologist and obesity theorist at the Nutrition and Obesity Research Center, the University of Alabama at Birmingham. Adults with children would be the targeted audience of this web publication. The author, who was once a student working in labs, discusses a study and his observations when working with mice; then decides to begin his own experiments to further his evidence in proving why we can’t blame obesity on our genes. The experiment that Edward Archer conducted was in 2014 and showed when pregnant women are physically active; the increased energy demands redirect nutrients to her muscles and away from the fetus. Therefore, showing the answer was a combination of a mother’s body composition and physical activity

Childhood obesity has been an uprising issue these past several decades. The re-search regarding this issue has grown massively, mainly on how it occurs and its origins. Over eating, the lack of exercise, and poor eating habits have been a problem with today’s youth. With new scientific research, there has been a new discovery. Childhood obesity can be passed through the umbilical cord from the mother if she falls under the obese cat-egory. It is theorized that mothers who have a Body Mass Index (BMI) greater than 30 could be considered obese; which in turn, could pass diabetes and possibly cardiovascular diseases through the umbilical cord during pregnancy. It is also said that those who hit the 30 BMI index, would have bigger babies, when

Obesity and type 2 diabetes are both classified as metabolic syndrome resulted from metabolic dysregulation. Both the obese mothers and the fetuses have shown a higher serum insulin and glucose concentration, which contribute to the high insulin resistance (Catalano et al. 2009 & Boney et al. 2005). However, the high exposure to insulin during utero development encourages fat deposition in the utero to serve as an the energy substrate for the utero, suggests a positive correlation to adiposity, hence, expressing a close association between diabetes and obesity in contributing to the development

Pregnant women who suffer from obesity during pregnancy increase their risk for gestational diabetes, surgical delivery and even maternal fatality. Gestational diabetes is defined as “glucose intolerance first detected in pregnancy” (World Health Organization, 1999) and can lead to serious complications during pregnancy. Pregnant women who are obese (BMI ≥ 30) increase their chances for the need of a caesarean delivery versus a normal vaginal delivery. Developing gestational diabetes during pregnancy is “a failure of insulin secretion to rise in response to the physiological insulin resistance of pregnancy” (Webb, 2013). This failure may lead to the mother later developing Type 2 diabetes well after giving birth.

Leptin, also known as the OB protein/gene, is released from adipose tissue (a connective tissue of fat) (INSERT CITE). The OB protein itself plays a very important role in the control of body fat stores in accordance to eating tendency, metabolism, autonomic nervous system (the nervous system responsible for bodily functions such as a heartbeat) and energy equity in primates, rodents and humans (INSERT CITE). Leptin (OB) is the primary cause for the results in the regulation of body fat, even though the brain is obligated to determine the level at which fat content is supervised (INSERT CITE). There are substantial amounts of genetic evidence that suggests that when the leptin system is disrupted (a mutation), it results in the expansion