Some nutrients may also act to protect the genome from damage. DNA is constantly replicating itself, and thousands of mistakes are made each day as a result. If the mistakes were not fixed, the genome eventually would be irreparably damaged, and we would develop diseases or die. Genes, nutrients, and lifestyle (exercise, smoking, environmental pollutants) determine how well repair takes place and how much damage occurs. Nutrigenomic scientists suspect that cell damage that is not effectively repaired is the cause of many diseases, such as cancer.

For example, in a 2007 experiment, special mice with genes that predisposed them to skin cancer were exposed to UVB radiation, similar to radiation from the sun. Half the mice were given a component of B vitamins called inositol in their drinking water. These mice developed far fewer skin tumors than those who received no inositol—23% versus 51%. The researcher, A.M. Shamsuddin, suggested that this result could have meaning for people who are airline pilots or frequent fliers. They might need more inositol in their diets to protect them from skin cancer. The experiment seemed to demonstrate one way  that nutrients can protect DNA when the environment is harmful.

Nutrigenomics says…

Studies such as Shamsuddin’s, however, never yield results of 100% certainty. All the mice receiving inositol did not avoid tumors. All the mice eating a regular diet did not develop cancer. Whether with mice or human cells or people, scientists do not discover “magic bullets” or simple answers that explain how to prevent disease. Part of the reason is that individuals respond differently to the same diet. The trick for scientists is identifying both the specific genes and the nutrients that determine health and disease. For the most part, Dr. Kaput explains, nutrigenomic principles of disease prevention are most easily applied to groups of people who share similar metabolic genetic profiles and lifestyles. These similar profiles may be due to having the same ancestry or belonging to the same ethnic group. Some gene variants occur more frequently in one ethnic group than another. However, there are no genes exclusive to one race or ethnic group. All groups of humans are susceptible to the same gene variations.

Similar Ancestry, Similar Genetic Problems

One well-established gene variant, for example, occurs on the angiotensin gene, called ANG. One variation in ANG increases a person’s risk for high blood pressure. This gene variant occurs most commonly in African Americans. People with this gene variant can control high blood pressure with a low-salt diet. About 73% of African Americans are salt sensitive and will be helped by such a diet. Many people of European ancestry have the same variation in the same gene. Those people, too, will be helped by a low-salt diet. But the same diet will not help people with high blood pressure due to another cause. Some people, for instance, need a diet rich in calcium to lower blood pressure. If a physician knows a person has the ANG variant, he or she can better treat high blood pressure.

The thrifty genes that may lead to metabolic syndrome, obesity, diabetes, and heart disease also seem to vary among populations. Although these gene variations affect many people of European ancestry, they are even more common among certain indigenous populations, such as Native Americans, Polynesians, and aboriginal peoples in Australia and Canada. Among many of these peoples, the high-fat, high-sugar diets of wealthy Europeans have had devastating health effects. For example, the Pima Indians of Arizona have the highest incidence of type 2 diabetes of any group of people in the world. Out of 11,000 Pima Indians living along the Gila River, half have diabetes and 95% are overweight. Nutrigenomics researchers are trying to identify the genes that cause this reaction to specific diets. If they succeed, they will be able to warn vulnerable people and recommend appropriate diets to prevent the chronic diseases caused by the interaction of thrifty genes and diet. This would help to reduce some of the health disparities between ethnic groups.

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About The Author

Dr. Leroy Rebello is a well established and internationally qualified anti-aging consultant and cosmetologist from Mumbai and a director in Eternesse – the best hair removal clinics in Mumbai. He lectures in reputed Institutions such as AIIMS, JIPMER and other Medical Colleges around India. With over 10 Research Papers published in Indexed Journals, Dr. Rebello is continuously researching and developing new treatments and cures.

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Nutrition Gene Relation

People with metabolic disorders or inherited diseases are not the only ones who have variations and mutations in their genes: Everyone does! Vulnerability to disease and how our metabolisms work depends partly upon the gene variations we have inherited. How much of a nutrient we need to prevent disease and achieve optimum health may be as unique to each person as appearance and personality.

Our particular set of genes and all of our DNA is called our genome. Each individual’s genome is unique, although we share many similarities with others. An emerging science named nutrigenomics focuses on the interaction between nutrition and our genes. Its ultimate goal is to someday tailor each person’s diet to his or her specifi c genetic needs. With personalized nutritional advice, each person could live a longer life and have fewer diseases.

Nutrients and Gene Interactions

The idea that we should eat what is best for our genes is a logical one and based on a good deal of evidence. No one can genetically tailor people’s diets today, but nutrigenomics scientists are working toward a future when they will know enough about nutrients and genes to make the idea a reality. In a 2008 interview with Whole Foods magazine, nutrigenomics expert Dr. Jim Kaput explained what he said are “the five guiding precepts” of nutrigenomics research. They are:

● Common dietary chemicals act on the human genome, either directly or indirectly, to alter gene expression (the translation or interpretation of information coded in the gene’s DNA) or structure.

● Under certain circumstances and in some individuals, diet can be a serious risk factor for a number of diseases.

● Some diet-regulated genes (and their normal, common variants) are likely to play a role in the onset, incidence, progression and/or severity of chronic diseases. 

● The degree to which diet influences the balance between healthy and disease states may depend on an individual’s genetic makeup.

● Dietary intervention based on knowledge of nutritional requirement, nutritional status, and genotype (each individual’s articular set of genes; i.e., “individualized nutrition”) can be used to prevent, mitigate or cure chronic disease.

Nutrients as Gene Switches

In 2000, scientists Randy Jirtle and Robert Waterland experimented with the effect of nutrients on gene expression and disease with some specially bred laboratory mice. The mice carried a gene known as the agouti gene. The gene made them yellow instead of brown, caused them to be ravenously hungry and become obese, and made them susceptible to diseases such as diabetes and cancer. The scientists mated the agouti mice and, when the mothers were pregnant, Jirtle and Waterland fed them food supplements rich in methyl donors. Methyl donors are nutrient chemicals found in some B vitamins and common in foods such as garlic, beets, and onions. The nutrient chemicals attached to the agouti genes in the developing baby agouti mice and acted like a chemical switch for the genes. The genes and DNA coding were still there, but gene expression was turned off. The baby mice were born brown, had normal appetites, and lived long, disease-free lives.

Writing about this experiment in a 2006 Discover magazine article, journalist Ethan Watters notes, “More and more,  researchers are finding that an extra bit of a vitamin, a brief exposure to a toxin, even an added dose of mothering…[can] alter the software of our genes.” In the case of the baby agouti mice, it was a nutrient that changed the phenotype (the looks,  behaviors, and traits) of the mice, even though the genotype was not changed. Mice are not people, and people do not have agouti genes, but nutrigenomics experts believe that different nutrients can act as switches that turn genes on and off in humans, too. Scientists now know that not all nutrients are metabolized for energy or maintaining cell functions.

Some chemicals from nutrients, such as the methyl donors, may actually prevent gene variations from causing harm or leading to disease. Jirtle and Waterland’s experiment is a good example of how a nutrient might affect cell activity and gene expression, whether that nutrient is a macronutrient, a micronutrient, or another nutrient chemical. In Watter’s Discover article, Jirtle is quoted as saying “Now everything we do—everything we eat or smoke—can effect our gene expression and that of future generations.”  And that is a fact!

Note: Feel free to republish this article on your own blog or website but please copy paste the below ‘Author Credits’ and include it at the bottom of your post or page. Thank you. 

About The Author

Dr. Leroy Rebello is a well established and internationally qualified anti-aging consultant and cosmetologist from Mumbai and a director in Eternesse – the best liposuction clinics in Mumbai. He lectures in reputed Institutions such as AIIMS, JIPMER and other Medical Colleges around India. With over 10 Research Papers published in Indexed Journals, Dr. Rebello is continuously researching and developing new treatments and cures.

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