Dietary Choices and Their Contribution to Chronic Diseases

Dietary Choices and Their Contribution to Chronic Diseases

Dietary Choices and Their Contribution to Chronic Diseases

What we eat can have an impact on our health and the development of chronic disease. Making poor choices can negatively impact our health and contribute to disease, while making good choices can often help us from developing health complications. From what you have read in Chapter 11: Nutrition and Chronic Diseases in our textbook Nutrition Concepts and Controversies, 15th ed., please describe how dietary choices can specifically contribute to cardiovascular disease, type 2 diabetes, and cancer. In addition, describe what dietary interventions can be used to help prevent these chronic diseases and control their complications. Use only the information from the textbook to support your statements and be sure to cite the source properly using APA formatting.

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5/18/2021 Print Preview Chapter 11: Nutrition and Chronic Diseases: 11-6e Conclusion Book Title: Nutrition: Concepts & Controversies Printed By: Alvard Tsaturyan (alla.tsaturyan1@gmail.com) © 2020 Cengage Learning, Cengage Learning 11-6e Conclusion No doubt the future of nutrition science will be inextricably linked with the science of genomics, and potential benefits may be enormous. Still, if the authors of this book tried to predict the future, based on libraries full of past evidence, most scenarios might go something like this: “Based on our genomics study, Mr. X needs greater amounts of vitamin C from tomato sauces and pink grapefruit, but not from supplements. He needs the fiber, lycopene, carbohydrates, and other bioactive components of a variety of fruit and vegetables, along with less saturated fat, sufficient protein, and a nutritious balanced diet to ward off future problems.” Experience shows that fiber supplements cannot take the place of whole grains for digestive tract health nor can calcium pills fully replace food sources of calcium for bone health. Besides, supplements come with risks. Many other examples exist to make the case for following a well-planned eating pattern of whole foods, as recommended by the Dietary Guidelines for Americans (see Chapter 2), to help modify the risks to health that a genetic predisposition may pose. Stay alert for updates in the rapidly advancing science of nutritional genomics. Registered dietitian nutritionists will be key providers of precision nutrition care as more becomes known about its potential to minimize disease risks and maximize the health of people everywhere. Critical Thinking 1. Describe the status of nutritional genomics research. Provide two examples of where this type of research is leading us. Dietary Choices and Their Contribution to Chronic Diseases
2. Explain how SNPs may cause disease. What Did You Decide? https://ng.cengage.com/static/nb/ui/evo/index.html?eISBN=9781337907088&id=1052297977&nbId=2184131&snapshotId=2184131&dockAppUid=101& 1/2 5/18/2021 Print Preview Maskot/Getty Images Are your own food choices damaging your heart? Is diabetes caused by eating sugar? Can certain herbs improve your health? Do “natural” foods without additives reduce cancer risks? Chapter 11: Nutrition and Chronic Diseases: 11-6e Conclusion Book Title: Nutrition: Concepts & Controversies Printed By: Alvard Tsaturyan (alla.tsaturyan1@gmail.com) © 2020 Cengage Learning, Cengage Learning © 2021 Cengage Learning Inc. All rights reserved. No part of this work may by reproduced or used in any form or by any means graphic, electronic, or mechanical, or in any other manner – without the written permission of the copyright holder. https://ng.cengage.com/static/nb/ui/evo/index.html?eISBN=9781337907088&id=1052297977&nbId=2184131&snapshotId=2184131&dockAppUid=101& 2/2 5/18/2021 Print Preview Chapter 11: Nutrition and Chronic Diseases: 11-6d Direct-to-Consumer Tests Book Title: Nutrition: Concepts & Controversies Printed By: Alvard Tsaturyan (alla.tsaturyan1@gmail.com) © 2020 Cengage Learning, Cengage Learning 11-6d Direct-to-Consumer Tests For a few hundred dollars, consumers can easily order DNA tests for themselves over the Internet. However, due to gaps in regulation, test quality and validity and the proper use of results are not ensured. Such gaps have made it possible for unscrupulous companies to sell fake tests or mislead consumers into buying expensive supplements and other products based on unfounded assessments of their DNA samples. Even when DNA tests are legitimate, interpreting the results is complex, and a consumer acting without a medical professional’s opinion could easily be misled into taking ill-advised medication or avoiding a necessary one—or even undergoing an unneeded surgery. To help remedy this situation, the FDA sent letters to companies that sell such tests to consumers, warning them to stop marketing their tests and assessments for medical purposes. Are people who purchase and take a personal genetic test also willing to make needed lifestyle changes in response to the findings? In one study, about a third of the participants reported that they were exercising more and eating better diets, regardless of their test results. Countering this positive finding, almost as many people in the same study did the opposite—they exercised less and ate lower-quality diets. Most studies report no significant changes in health behaviors after testing. Without the will to improve health behaviors, it is unlikely that personal genetic testing alone can improve the health of the population in the future. Chapter 11: Nutrition and Chronic Diseases: 11-6d Direct-to-Consumer Tests Book Title: Nutrition: Concepts & Controversies Printed By: Alvard Tsaturyan (alla.tsaturyan1@gmail.com) © 2020 Cengage Learning, Cengage Learning © 2021 Cengage Learning Inc. All rights reserved. No part of this work may by reproduced or used in any form or by any means graphic, electronic, or mechanical, or in any other manner – without the written permission of the copyright holder. https://ng.cengage.com/static/nb/ui/evo/index.html? Dietary Choices and Their Contribution to Chronic Diseases
eISBN=9781337907088&id=1052297977&nbId=2184131&snapshotId=2184131&dockAppUid=101& 1/1 5/18/2021 Print Preview Chapter 11: Nutrition and Chronic Diseases: 11-6c Arguments Surrounding Genetic Testing Book Title: Nutrition: Concepts & Controversies Printed By: Alvard Tsaturyan (alla.tsaturyan1@gmail.com) © 2020 Cengage Learning, Cengage Learning 11-6c Arguments Surrounding Genetic Testing For nutritional genomics to be of practical value, people must undergo genetic testing to detect gene variations that affect nutrition or nutrition-related diseases. Critics of testing, however, question whether identifying a genetic marker for disease by way of expensive testing would translate into better health for the nation or simply waste limited health-care dollars. Consumers voice fears that DNA results, once known, could be misused. A few companies have policies against sharing collected data, but others sell it to scientists who use it in experiments and who may, in turn, release it to someone else. This data sharing helps to advance science; large banks of data from many individuals, both healthy and diseased, are needed to establish links among genes and diseases with certainty. For DNA donors, however, a problem could ensue if test results revealing a disease tendency ended up in the wrong hands. For example, such information could influence a decision maker regarding a person’s acceptance to school, promotion at work, or other critical issues. The law forbids this kind of discrimination, but enforcement is rare and testing companies cannot promise absolute confidentiality. Chapter 11: Nutrition and Chronic Diseases: 11-6c Arguments Surrounding Genetic Testing Book Title: Nutrition: Concepts & Controversies Printed By: Alvard Tsaturyan (alla.tsaturyan1@gmail.com) © 2020 Cengage Learning, Cengage Learning © 2021 Cengage Learning Inc. All rights reserved. No part of this work may by reproduced or used in any form or by any means graphic, electronic, or mechanical, or in any other manner – without the written permission of the copyright holder. https://ng.cengage.com/static/nb/ui/evo/index.html?eISBN=9781337907088&id=1052297977&nbId=2184131&snapshotId=2184131&dockAppUid=101& 1/1 5/18/2021 Print Preview Chapter 11: Nutrition and Chronic Diseases: 11-6b Nutrients Influence the Genes: Epigenetics Book Title: Nutrition: Concepts & Controversies Printed By: Alvard Tsaturyan (alla.tsaturyan1@gmail.com) © 2020 Cengage Learning, Cengage Learning 11-6b Nutrients Influence the Genes: Epigenetics People often think of chromosomes as simple strands of DNA, but chromosomes exist as complex, three-dimensional combinations of DNA, proteins, and other molecules. DNA strands are the primary carriers of inherited information, true, but the epigenome constitutes another parallel bank of inheritable information. The epigenome’s proteins and other molecules associate with DNA and interact with it in ways that regulate genetic activity for example, turning genes on or off. Like DNA itself, the epigenome is inherited from generation to generation, but unlike DNA, it is responsive to environmental influences, including diet, particularly during early development. The genome and the epigenome have been likened to nature’s pen-and-pencil set. The genome, made of DNA, is written in indelible ink, so to speak; its sequence is mostly permanent. Dietary Choices and Their Contribution to Chronic Diseases
The epigenome is written in pencil in the margins and allows for erasures and changes. The Epigenome’s Role in Differentiation Given that every cell of the body contains the same genes, scientists have long wondered how they give rise to distinct body parts. How do the cells of an eye decide to make an eye while the cells of the kidney make a kidney? The epigenome manages this extraordinary process of differentiation by turning different genes on or off in different locations. A cone cell of a person’s eye and a blood-producing cell of that person’s bone marrow contain identical DNA strands, but luckily for the person, the epigenome activates and silences genes on the DNA strands so that each cell type reliably makes only the correct proteins that will perform its own specialized functions. How Epigenetic Regulation Works Mechanisms for epigenetic gene regulation include, among others, the workings of large globular proteins known as histones ((HISS-tones) proteins that lend structural support to the chromosome structure and that help activate or silence gene expression.) and small molecular fragments called methyl groups (molecular fragments consisting of one carbon and three hydrogen atoms that, among their many roles, can alter gene expression when attached by enzymes to strands of DNA.) . The actions of these regulators can be modified by way of diet and other environmental influences. Histones in Gene Expression Millions of histones reside within the chromosomes (shown in Figure C11–2). Like a thread wound around a spool, sections of a DNA “thread” are tightly wrapped around these https://ng.cengage.com/static/nb/ui/evo/index.html?eISBN=9781337907088&id=1052297977&nbId=2184131&snapshotId=2184131&dockAppUid=101& 1/5 5/18/2021 Print Preview histones, giving shape to the chromosome and allowing for efficient storage of DNA molecules within a cell’s nucleus. Figure C11–2 Two Epigenetic Factors and Gene Activity This figure depicts histones, large globular protein “spools” that wrap lengths of DNA. Other epigenetic factors also exist, such as the methyl groups in this illustration, tiny one-carbon structures that attach directly to a DNA strand, modifying its activity. Another is a form of RNA (not shown). The histones also regulate genetic activity. When a DNA segment is wrapped around a histone, its genes are silent—they physically lack the space to perform the tasks required for protein synthesis. Histones, though, can change this arrangement in response to changing needs. https://ng.cengage.com/static/nb/ui/evo/index.html?eISBN=9781337907088&id=1052297977&nbId=2184131&snapshotId=2184131&dockAppUid=101& 2/5 5/18/2021 Print Preview Histones sport protein “tails” that stick out from their DNA wrappings. These tails serve as landing sites for many molecules from the environment that reflect cellular conditions. When a histone receives chemical signals indicating a need for a particular protein, it loosens its grip on its wraps of DNA, allowing the portion of the strand with genes for making that protein to stretch out. Genes on these stretched-out segments can then express their encoded proteins—they are activated. Here’s where nutrition comes in: many of the molecular signals to which histones respond arise from the diet—they consist of nutrients and phytochemicals or of compounds generated during their metabolism. A Broccoli Phytochemical Example One phytochemical, sulforaphane (sull-foh-RAFF-ane) found in broccoli, broccoli sprouts, and other cabbage-family vegetables, may affect cancer processes by way of histone changes in cancer cells. One characteristic of cancerous tissue is uncontrolled cell division. In cancer cells, histones may inappropriately silence genes that would otherwise stop cells from multiplying out of control. In test tubes, sulforaphane reverses those cancer-promoting histone changes and reinstates control of cell division. In mice, sulforaphane inhibits certain cancers. In people, ingestion of one cup of broccoli sprouts alters histone activities in blood cells. Does consumption of broccoli or other cabbage-family food actually prevent cancer in people? People who consume these foods regularly have lower rates of some cancers, but no one knows whether the foods themselves are protective. Researchers are still investigating that question. Many other phytochemicals, including tea flavonoids, curcumin (derived from the spice turmeric), and sulfur compounds from the onion family, along with nutrients such as folate, vitamin , vitamin C, vitamin D, selenium, and zinc add to a growing list of food constituents that affect epigenetic activities in ways that may prevent cancer. Scientists can duplicate some of these activities with synthetic drugs, but the drugs, unlike foods, are highly toxic to living tissues. Dietary Choices and Their Contribution to Chronic Diseases
Methyl Groups and Gene Regulation Genes are also regulated by a number of molecules that adhere to the DNA strand itself. Methyl groups, mentioned earlier, attach directly onto DNA (look again at Figure C11–2), altering gene expression. Typically, when a methyl group attaches to the beginning of a gene sequence on a DNA strand (methylation), the gene is silenced. Removal of that methyl group allows gene expression to commence and protein replication to occur. B Vitamins Transfer Methyl Groups A powerful example of how nutrients affect the genes involves the influence of the B vitamin folate on DNA methylation. Folate (along with other B vitamins) is essential for transferring https://ng.cengage.com/static/nb/ui/evo/index.html?eISBN=9781337907088&id=1052297977&nbId=2184131&snapshotId=2184131&dockAppUid=101& 3/5 5/18/2021 Print Preview methyl groups from molecule to molecule, including to DNA molecules. With too little folate, genes may be insufficiently methylated to suppress the production of unneeded proteins. This effect is illustrated in the accompanying photo of two mice. Despite their strikingly different appearance, these mice have identical DNA. Both possess a gene that tends to produce fat, yellow pups, but their mothers were fed different diets during pregnancy. The mother of the lean, brown mouse received doses of the B vitamins folate and vitamin . By way of methyl group transfer activity, these vitamins silenced the gene for “yellow and fat,” resulting in brown, lean pups. Note that the extra vitamins did not change the DNA sequence. Still, such epigenomic changes established during pregnancy can be inherited along with the DNA and thus persist through several generations. Importantly, pregnant women should tend to their nutrition needs carefully (see Chapter 13). No one should attempt to alter their children’s and grandchildren’s risks of obesity or other diseases by loading up on B vitamins or other substances. The effects of imbalances are unpredictable and can be severe. These two mice share an identical gene that tends to produce fat, yellow mice. The mother of the lean, brown mouse received supplemental B vitamins that silenced the gene. © Jirtie and Waterland Can Adults Modify Their Epigenome? The greatest epigenomic changes from environmental influences occur early during embryonic development (Figure C11–3 demonstrates this concept). Some change can still occur into adolescence and even adulthood, however, and they can affect health outcomes. The findings on sulforaphane of broccoli, described earlier, provide evidence that certain epigenetic factors in adult cells can indeed be changed, at least temporarily, by bioactive constituents of foods. Another example in adults is the development of liver cancer after ingestion of a mold toxin that can form on corn and other grain (aflatoxin.) The toxin is suspected of causing removal of important methyl groups from both histones and the DNA strand, triggering the development of the cancer. Figure C11–3 https://ng.cengage.com/static/nb/ui/evo/index.html?eISBN=9781337907088&id=1052297977&nbId=2184131&snapshotId=2184131&dockAppUid=101& 4/5 5/18/2021 Print Preview An Epigenome Timeline Environmental influences, including diet, most profoundly alter the epigenome during the earliest stages of development, but some changes are probably still possible later in life. Now a theory emerges to suggest at least a partial solution to the mystery of how identical twins can develop different diseases. Although the twins have identical DNA, they acquire differences in their epigenomes. They encounter different environmental influences at various times of life that change their genetic expression. On learning of these revelations in nutritional genomics, many people want to apply the new science to themselves. The next sections explore issues that arise with genetic testing for nutrition. Chapter 11: Nutrition and Chronic Diseases: 11-6b Nutrients Influence the Genes: Dietary Choices and Their Contribution to Chronic Diseases
Epigenetics Book Title: Nutrition: Concepts & Controversies Printed By: Alvard Tsaturyan (alla.tsaturyan1@gmail.com) © 2020 Cengage Learning, Cengage Learning © 2021 Cengage Learning Inc. All rights reserved. No part of this work may by reproduced or used in any form or by any means graphic, electronic, or mechanical, or in any other manner – without the written permission of the copyright holder. https://ng.cengage.com/static/nb/ui/evo/index.html?eISBN=9781337907088&id=1052297977&nbId=2184131&snapshotId=2184131&dockAppUid=101& 5/5 5/18/2021 Print Preview Chapter 11: Nutrition and Chronic Diseases: 11-6a Genes Influence Nutrition and Disease Book Title: Nutrition: Concepts & Controversies Printed By: Alvard Tsaturyan (alla.tsaturyan1@gmail.com) © 2020 Cengage Learning, Cengage Learning 11-6a Genes Influence Nutrition and Disease Small variations in DNA sequences, called mutations (a permanent, heritable change in an organism’s DNA.) , dictate many of the differences among human beings, including differences in nutrient metabolism. The most common mutations are SNPs ((snip) a type of genetic variation involving a single changed nucleotide. The letters SNP stand for single nucleotide polymorphism.) (pronounced “snips”), involving the variation of a single molecule (a nucleotide ((NU-klee-oh-tied) one of the subunits of DNA and RNA are composed.) ) in a strand of DNA. About 10 million possible SNPs are known to exist in human DNA. SNPs and Diseases Most individuals carry tens of thousands of SNPs, and most seem to exert no functional effect at all. Rarely, however, a single SNP in a high-powered gene can produce a severe disease immediately from birth, such as PKU, as described in Chapter 3. More commonly, SNPs do not cause a disease directly but may subtly work with other gene variants and with environmental factors such as diet to raise the risks of developing heart disease or other maladies in later life. A SNP typically sets the stage for a chronic disease; then the person’s own choices contribute to the development of the disease. As an example, a common SNP in a fat metabolism gene changes the body’s response to dietary fats. People with this SNP maintain normal blood LDL cholesterol concentrations when they eat diets rich in polyunsaturated fatty acids (PUFA), and they develop higher than normal LDL concentrations when they consume less PUFA. A gene (in this case, a fat metabolism gene with a SNP) interacts with a nutrient from the diet (in this case, PUFA) to influence a risk factor for a disease (LDL cholesterol con … Dietary Choices and Their Contribution to Chronic Diseases
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