Factors That Affect Overweight And Obesity

(Why People Become Overweight) Different diseases can be passed down through parents or family members that have hereditary diseases. There are ways that the parents can affect the lifestyle of their child also. Research shows that the offspring of mothers who smoked during pregnancy have a higher risk of becoming overweight as they mature. The same outcome goes for mothers who are pregnant and have diabetes. The theory to this condition is the metabolism of the offspring is affected in a negative way. It has been proven that children with mothers who breastfeed longer than three months are less likely to become obese as children. (Why People Become Overweight)

A person is more likely to develop obesity if one or both parents are overweight. Numerous people are obese because of their family history. The reason why genetics can contribute to the obesity issue is because they can change and affect hormones that control the fat cells. “For example, one genetic cause of obesity is Leptin deficiency. Leptin is a hormone produced in fat cells and also in the placenta. Leptin controls weight by signaling the brain to eat less when body fat stores are too high. If, for some reason, the body cannot produce enough leptin or leptin cannot signal the brain to eat less, this control is lost, and obesity occurs” (R.

It is clear that obesity often tracks in families. Having obese relatives increases one's risk for obesity, even if the family members do not live together or shares the same patterns of exercise and food intake. Family studies and twin studies yield estimates of the fraction of the variation in the population that can be attributed to inherited variation or the heritability. Estimates of heritability range from 30 to 70%, with the typical estimate at 50%, meaning about one-half of the variation in body mass within a population is a result of inherited factors. A common

• Genetic factors; Obesity tend to be lowered, so that the genetic cause of the alleged to have. But family members not only share genes, but also food and lifestyle habits, which could push the onset of obesity. It is often difficult to separate the lifestyle factors with genetic factors. The latest research shows that the average genetic factors giving influence of 33% against a person’s body weight.

A problem that continues to exacerbate each year is the rising amount of overweight and obese Americans. This does not come to a surprise considering American’s love for fast food and a living in a society which promotes physical inactivity. According to an article written by Jan Simmonds, “If you are more than a few pounds above your ideal weight, you are overweight. But if you are more than twenty percent above your ideal weight, you are obese.” This means that a person’s weight endangers their health which leads to other complications. The causes of obesity range from genetics, to combinations of hormonal, metabolic, behavioral factors, and changes in society.

Noted by the Research Chair in Obesity from Université Laval (n.d.), “obesity risk is two to eight times higher for a person with a family history as opposed to a person with no family history of obesity, and an even higher risk is observed in cases of severe obesity.” (Université Laval, n.d., n.p.) It is not only genetics though as you can see in the previous paragraphs. If someone is brought up eating unhealthy and exercising less, this chain pattern will continue and the main cause to this would be our parents. The way that you and your family eat now is more than likely the way the generation before ate because it's what they grew up eating and continued to eat when they became an

Genetics is another factor in the rise of obesity. According to the Centers for Disease Control and Prevention (CDC), multiple genes found in some individuals can increase one's susceptibility for obesity (overweight and obesity). Many of these genes require outside factors; like an abundant food supply or little physical activity to cause obesity. The CDC is trying to promote the awareness that genes and behavior are both needed

The world is oversaturated with factors that are detrimental to an individual’s health, but it seems as though the things that are the worst for a person are some of the easiest items to get hold of. The nation is currently undergoing a health crisis with the opioid epidemic, very similarly to how the black community was ravaged by crack a few decades ago. The nation is plagued by factors such as obesity, high sexually transmitted disease rates, tobacco and alcohol use, hard drugs such as cocaine and crystal meth, and prescription drug abuse, such as the ongoing opioid crisis. Factors such as the previously mentioned affect society by affecting large numbers of individuals in society.

Genetics play certain roles in obesity, the role will either be big or little. Genetics will take a big role if the person has been overweight for most of their life, anyone in the family are overweight or obesity, and if the weight cannot be lost even if there is physical activity and a low-calorie diet. Genetics will take a small role if the person is somewhat overweight, but the weight can be lost with a diet and exercise stagey. The individuals with genetics that play a small role should take advantage of this to avoid heart disease, high blood pressure, breathing problems, etc. Harvard School of Public Health stated that “the genetic factors linked to obesity comprise on a small part of overall risk”, so obesity is rarely caused by our

One of the most common diseases today is called obesity or overweight. The definition of obesity is having too much body fat. The most commonly used measure of weight status today is the body mass index, or BMI. This is a simple calculation based on the ratio between height and weight. Scientist of Harvard said “ Genes are no destiny”; for example, If someone ask to an obese person “What is the cause of your obesity?”, they will probably answer the question automatically “Heredity”, but heredity probably plays a big role, but we can counteract them with a healthy lifestyle. There are the causes of obesity today.

Many people struggling with morbid obesity have been fighting their weight since they were kids. Many people assume that obesity in children is the result of parents not knowing taking control of their child’s eating habits, but this is seldom the sole cause. Many research studies have shown that children typically will grow up to have a similar BMI to their parents, and siblings will have similar BMI’s to one another. Researchers use this data to show that there is a heavy genetic influence on a person’s weight and simply eating too much or not exercising enough is not the sole determinant of someone’s BMI.

Polymorphisms in various genes controlling appetite and metabolism predispose to obesity when adequate food energy is present. Studies that have focused on inheritance patterns rather than on specific genes have found that the children of two obese parents were more than likely to become obese, compared to the children of two parents who are of normal weight. Different people exposed to the same environment have diverse risks of obesity due to their underlying genetics. The environment we live in has certainly played major permissive roles in the increasing amount of fat mass people receive. Like some disorders, obesity can be treated, managed, and controlled. Obesity is said to not have a cure because it is a life-long treatment. Almost 10% of morbidly obese people have defects in genes that regulate weight, food intake, and metabolism.

Obesity has become an epidemic health problem. It is not only about genetics but also the environmental factors involved in obesity. According to Kaushik Prashant and James T. Anderson Epigenetic it is the study of heritable but the dynamic changes to genomic function that regulate gene expression independently of DNA sequence. The study have shown that the maternal nutrition is controlled during pregnancy that can alter the metabolic phenotype of the offspring by means of epigenetic regulation of specific genes, and this can be passed to the next generation. Obesity is associated with extensive gene expression changes throughout the body. It is a simple disease with multiple risk factors.

During adiposity, around 5 to 6 years of age, a child’s body fatness declines to a minimum before increasing into adulthood. A study conducted at Group Health Cooperative of Puget Sound found evidence of normal weight children with at least one overweight parent at the time of adiposity rebound, is nearly 5 times as likely to be obese as an adult. However, if both parents are obese before the child reaches adiposity rebound, there is 13 times the risk of the child becoming an obese adult. Generally recognized as genetic predispositions, the causes of excess adiopsity may affect a variety of possible physiological processes, including basal metabolic rates. Individuals with “fat phenotypes” are likely to develop adult obesity but genetic inheritance does not cause obesity alone (Whitiker).

Obesity is known to produce a number of stress and inflammation responses in the body that lead to the activation of the inflammatory signalling molecules, Jun NH2-terminal kinase (JNK) and inhibitory kB kinase (IKK). Activation of these pathways plays a key part in the development of insulin resistance followed by progression to diabetes as they greatly affect inflammatory responses, insulin signalling, and lipid and glucose homeostatis (Nakamura et al. 2014). For example, activating the JNK pathway leads to serine phosphorylation of insulin receptor substrate (IRS) proteins which results in inhibited insulin signalling and thus insulin resistance. Double-stranded RNA-dependent protein kinase (PKR) has recently been shown to control the JNK and other major inflammatory pathways, to directly inhibit insulin signalling, to be activated by fatty acids as well as endoplasmic reticulum (ER) stress, and to be necessary for the activity of inflammasomes (Nakamura et al. 2010; Komiya et al. 2010; Lu et al. 2012). Moreover, PKR has been found to be highly activated in obese people as well as mice with genetically and diet-induced obesity, especially in adipose and hepatic tissues (Boden et al. 2008; Nakamura et al. 2010; Carvalho-Filho et al. 2012). Finally, recent studies have found that PKR knockout obese mice were protected against both IR and obesity-triggered inflammation and that administration of PKR inhibitors reduced JNK activation, reduced inflammation in adipose