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The research that has been done so far on the connection between epigenetics, metabolism, and nutrition encompasses a variety of information but it is also very scattered. From reviewing these sources, an overall connection has been established between epigenetics, metabolism, and nutrition; however, further research needs to be performed in order to find an exact relation at the molecular level. Through this additional research, we can determine how to use this information to help combat the issue of obesity in America. Ultimately, the primary step in combating obesity is educating the public.

First and foremost, before discussing the genetic aspects, the importance of daily exercise and a good diet should be emphasized. As stated earlier, the major causes of obesity in America are poor diet and a largely sedentary lifestyle. Lack of motivation and hectic lifestyles stop people from exercising or eating properly. They do not have time to get their daily exercise or make a healthy meal.

The number of fast food restaurants in America contributes to this problem. There are also people who are successful in accomplishing the difficult goal of losing weight but they are unable to maintain their weight.

Food that shapes you: how diet can change your epigenome |

There are many factors that attribute to the skyrocketing levels of obesity in America, including genetics, lifestyle, inactivity, unhealthy diets, medical problems, and socioeconomic factors. Most people have issues stemming from more than one of these subjects, which is why trying to solve the problem of obesity is so difficult. There are factors that have yet to even be discovered that are related to obesity.

For example, many Americans are vitamin-D deficient but do not realize it. Recent studies have shown that low vitamin D levels can trigger the winter response, which includes accumulation of fat and lower metabolic rates Foss, Another aspect many people do not think about is how their lifestyle affects others.

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The public should be educated on the epigenetic effects of their actions. Many people might be unaware that their actions now can affect their children or future children through the DNA they pass on. The public should also be informed on all the diseases that could affect them or future generations due to their obesity.

Everyone can learn about this important information through organizations like the Department of Health. We can spread the word through the media: magazines, newspapers, TV, radio advertisements, public service announcements, etc. The reality of epigenetics might make people see their diets in a new light, because they would realize that they are not only putting themselves in danger, but future generations as well.

As stated earlier, after determining which nutrients modify these epigenetic modifiers, it would be possible to isolate the nutrients that have a metabolic-related impact.

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Those nutrients with a beneficial metabolic-related effect would be the recommended nutrients and foods for a better diet. A program could be developed that would take the metabolic rate of a person, compare it to the normal rate for gender and age group, and come up with a dietary plan.

This is just a handful of the known foods that increase metabolic rates. Individuals have different needs based on their metabolic processes and should have individualized dietary plans. Based on their metabolic rates and nutrient deficiencies, the program would tell them which nutrients they need to increase to normalize their metabolic rate and the best way to get their recommended value.

Although this sounds like another useless weight loss program, it would be different because the results can be backed up by precise laboratory research. The last step would be to tackle the issue at an epigenetic level. The process by which nutrients help increase metabolic rates can be studied, isolated, and then manipulated through the use of pharmaceutical drugs. If the exact reaction that occurs on a molecular level when nutrients increase metabolism through epigenetic modifications is determined, synthetic drugs could be developed that would tweak certain metabolic enzymes related to histones and methyl groups.

This would help us alter any genetic predispositions people have toward developing various types of diseases or speed up a slow metabolism. Looking at the impact on histones and methyl groups, research should be done on a molecular level to see how these nutrients brought about this beneficial change. Using research found on how these nutrients increase metabolism, pharmaceutical companies could create a synthetic drug that would mimic these properties and bring about these same beneficial effects in an amplified manner.

On a molecular level, there has to be a specific process by which these nutrients manipulate histones and methyl groups, and whether the process involves an enzyme or some other molecule still needs to be determined. The amplification method would depend on what type of process is uncovered, but if it is enzyme induced, a substrate could be added to make the reaction go faster.

Ideally, we hope to find the nutrients that boost metabolism and mimic the process with the creation of a new synthetic drug to help normalize metabolism for those with slower than normal rates. The biggest problem that needs to be tackled is researching the exact hormones, enzymes, or molecules that connect epigenetics, metabolism, and nutrition. With this research, drugs that could help people maximize their metabolism can be created, which would benefit many people who feel that they cannot lose weight no matter how much they control their diet and exercise. This research could potentially revolutionize the way people see nutrition.

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This could help reinforce the idea that a good diet and exercise is beneficial because people will see that a bad diet with no exercise not only affects them but it also affects their children and future generations through epigenetic principles. Diseases caused by obesity, like type 2 diabetes, coronary heart disease, hypertension, arthritis, and cancer depend on where fat is deposited, but they are also affected by genetics Kirchner, Based on this information, many people struggling with obesity might think that changing their lifestyle would do nothing.

They might extrapolate that if obesity is written in their genes, they cannot change. Many people feel hopeless because they have tried everything, from a good diet to exercise, but nothing has worked. However, many times, slow metabolic reactions are the reason for weight gain and this research aims to solve that problem at the roots.

Not only will epigenetics determine which nutrients will help boost metabolism in the long run, but it will also determine the process behind increasing metabolic rates. This information will help to make synthetic drugs that maximize metabolic rates in people who have less than satisfactory rates. People feel helpless in their bodies because of their genes, but with this research, the problem can be solved. If these steps are taken to educate the public and to start this special type of weight loss program based on epigenetic research, we can combat obesity. Overall, this would decrease the amount of obesity that currently exists in the United States, which in turn would also help decrease the likelihood of developing obesity-related diseases.

Everyone can benefit from this research because epigenetic modifications happen at all stages in life.

Nutrients and Epigenetics

With epigenetics, it is never too late to make a change. Present Knowledge in Nutrition. Bowman and R. I: Epigenetics: are there implications for personalized nutrition? Clinical Nutrition and Metabolic Care. BMC Genetics. These growth-retarded rats were found to be highly similar to human fetuses, as they both display symptoms such as lowered glucose and insulin levels.

Gestational diabetes may also be studied through chemical induction using streptozotocin treatment of the pregnant rats. The predominant means of investigating nutriepigenetics involves varying the nutritional conditions to which a subject is exposed to and monitoring the effects thereafter. Restricting caloric and protein intake are the two most common methods. Micronutrients, such as zinc and iron, may also be restricted to investigate the effects on offspring.

Additionally, rats fed diets lacking or including methyl donors are often used to study the effects of diet on epigenomics, as variations within the methylation of DNA are common means of silencing or expressing genes. Diets containing higher carbohydrate and fat content attempt to mimic typical Western-style diets may also be used in nutriepigenetic studies. The possibilities of utilizing nutriepigenomics for intervention are quite expansive. This can include preventative therapies, such as providing an optimal regime for nutrition during pregnancy and lactation.

A highly specific diet, termed an "EpiG diet," may be employed for an individual believed to be at higher risk of developing a metabolic disorder. There also exists potential for therapeutic treatments that may correct metabolic disorders, such as type II diabetes.

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Elucidation of disease pathways is another future direction for nutriepigenomic studies. For example, choline-deficient diets and alcohol metabolism during pregnancy may have very similar metabolic pathways. When compared to studies of maternal transmission, investigations into the role of paternal diets are lacking. A review demonstrated the nutrition of both parents do in fact play a role in determining the health of their offspring.

Assessing the role of epigenetic mechanisms may be easier using paternal inheritance, as sperm transmits epigenetic and genetic information, whereas the female cells also transmit mitochondrial DNA.

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From Wikipedia, the free encyclopedia. Main article: Transgenerational epigenetics. Nutri-epigenomics: Lifelong remodelling of our epigenomes by nutritional and metabolic factors and beyond. Clin Chem Lab Med. Aberrant epigenetic landscape in cancer: How cellular identity goes awry. Dev Cell. Epigenetics in women's health care. Mt Sinai J Med. Placental gene expression responses to maternal protein restriction in the mouse.

Feeding pregnant rats a protein-restricted diet persistently alters the methylation of specific cytosines in the hepatic PPAR alpha promoter of the offspring. Br J Nutr. Induction of altered epigenetic regulation of the hepatic glucocorticoid receptor in the offspring of rats fed a protein-restricted diet during pregnancy suggests that reduced DNA methyltransferase-1 expression is involved in impaired DNA methylation and changes in histone modifications.

Nutrition, epigenetics, and developmental plasticity: Implications for understanding human disease.


Annu Rev Nutr. Perinatal environment and its influences on metabolic programming of offspring. Physiol Behav. Metabolic imprinting, programming and epigenetics - a review of present priorities and future opportunities. Epigenetics and maternal nutrition: Nature v. Proc Nutr Soc. Early differential defects of insulin secretion and action in year-old caucasian men who had low birth weight.

Development of type 2 diabetes following intrauterine growth retardation in rats is associated with progressive epigenetic silencing of Pdx1. J Clin Invest. Individuality and epigenetics in obesity. Obes Rev. Integrity of the methylation cycle is essential for mammalian neural tube closure. Folate protection from congenital heart defects linked with canonical wnt signaling and epigenetics. Curr Opin Pediatr. Molecular Psychiatry. What are VitalSource eBooks? For Instructors Request Inspection Copy. Nutrition and Epigenetics presents new information on the action of diet and nutritional determinants in regulating the epigenetic control of gene expression in health and disease.

Each chapter gives a unique perspective on a different nutritional or dietary component or group of components, and reveals novel mechanisms by which dietary factors modulate the epigenome and affect development processes, chronic disease, and the aging process. This pivotal text:. Nutrition and Epigenetics highlights the interactions among nutrients, epigenetics, and health, providing an essential resource for scientists and clinical researchers interested in nutrition, aging, and metabolic diseases.

Marchlewicz, Olivia S. Anderson, and Dana C. Carter, Kellie L. Tamashiro, and Kevin J. Sabet, Eric D. Ciappio, and Jimmy W. Singh and Moray J. Claycombe, Huawei Zeng, and Gerald F. Combs, Jr.

Epigenetics, Nutrition, and Our Health: How What We Eat Could Affect Tags on Our DNA

Romagnolo and Ornella I. Pham and Ji-Young Lee. She joined the Oregon State University faculty in after receiving her Ph. During the course of her career, Dr. Ho has published 97 peer-reviewed articles and abstracts and four book chapters.