The effects of phytonutrients/phytochemicals present in food, on gene expression by transcription of DNAÂ into mRNAÂ and then toÂ proteinsÂ and provides a basis for understanding theÂ biologicalÂ activity of phytonutrients or by the influence of genetic variation onÂ nutritionÂ by correlatingÂ geneÂ expression orÂ single-nucleotide polymorphismsÂ with a nutrient's absorption,Â metabolism, elimination or biological effects and to develop rational means to optimizeÂ nutrition, with respect to subject'sÂ genotype is nutrigenomics. It is the application of high-throughput genomic tools in nutrition research to provide methods and tools for disease preventing and health promoting phytonutrients that match their lifestyles, cultures and genetics which is determined by the specific demands of genetic signature and perfectly balances the micro- and macro-nutrient needs. Most scientists thought that food was metabolized to provide energy for the cell but some don't get metabolized to give ligands, the molecules that bind to proteins involved in "turning on" certain genes to one degree or another. For example, genestein, a chemical in soy which attaches to oestrogen receptors and regulates genes and the individuals may have oestrogen receptors that react to genestein differently, helping to explain why two people eating the same diet can respond very differently - one maintaining weight, for example, and the other get fatty. Recent research on nutrigenomics provide answer of why some people can eat a high fat diet and have no problem with their cholesterol levels while others experience the exact opposite response and how nutrients and bioactive components in food turn on or off certain genes which impact important metabolic and physiologic processes in the body. The main goal of nutrigenomics is to elucidate the interaction between diet and genes and optimize health through the personalization of diet, provide powerful approaches to unravel the complex relationship between nutritional molecules, genetic polymorphisms, and the biological system. Nutrigenomics is the emerging face of nutrition and phytonutrients that provide the necessary stepping stones to achieve the ambitious goal of optimizing an individual's health via nutritional intervention.
Definitions and terms
20.1.2. Nutrigenomics: Health from nutrition
20.1.3 Benefits of nutrigenomics
20.1.4 Persons involved in nutrigenomics
20.1.5 Limitations of nutrigenomics
20.2 Technologies involved in nutrigenomics
20.3 Nutrients modulating genome expression
20.4 Nutrition gene and diseases
20.4.1 Metabolic hereditary diseases
20.4.2 Multifactorial diseases
20.1.3 Monogenic and multigenic diseases
20.5 Nutrigenomics and communication
20.6 Nutrigenomics and bioactive nutrients
20.7 Ethical consideration in nutrigenomics
20.8 Market implication of nutrigenomics
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Genomics: Genomics is a discipline in genetics concerned with the study of the genomes of organisms including efforts to determine the entire DNA sequence of organisms and fine-scale genetic mapping (Balammal, G., 2012) while the genome is the set of all genes, regulatory sequences, and other information contained within the noncoding regions of DNA of an organism (Frederick, P. Roth et al., 1998).
Nutritional genomics: The science of relationship between human genome, nutrition and health (Ordovas, J.M., 2004) or the genetic manipulation of plants to create vitamins and minerals that will improve human's diet and analysis of an organism's set of genes so it is an area of science that looks at how environmental factors, such as diet, influence the genetic make-up (Ordovas, J.M., 2004).
Nutrigenetics: It is the interplay between nutrition and genetics of an individual, branch of science concerned with the effect of heredity on diet and nutrition (Simopoulos, A.P., 2010). The term "Nutrigenetics" refers to the research on the impact of changes in inherited traits of nuclear DNA, on the response to specific metabolic dysfunctions outcomes getting health chronic damages and disorders (Paolo Manzelli, 2012, Simopoulos, A.P., 2010).
According to WHO reports diet factors influence occurrence of more than two third of diseases and most of these factors belong to the categories of nutrigenetics. In other words, nutrigenetics concerns individual differences in the reaction to food based on the genetic factors. Nutrigenomics analyses direct influences of nutrients on gene expression (Svacina, S., 2007).
Proteomics: Proteomics is the large-scale study of proteins, particularly their structures and functions and the term proteomics was first coined in 1997 to make an analogy with genomics, the study of the genes. The word proteome is a blend of protein and genome, and was coined by Marc Wilkins in 1994 and proteome is the entire complement of proteins, including the modifications made to a particular set of proteins, produced by an organism or system (James, P., 1997, Marc, R. Wilkins et al., 1996).
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Metabolomics: Metabolomics is the systematic study of the unique chemical fingerprints that specific cellular processes leave behind and the study of their small-moleculeÂ metaboliteÂ profiles is increasingly being used in a variety of health applications including pharmacology, pre-clinical drug trials, toxicology, transplant monitoring, newborn screening and clinical chemistry (Nanda T., 2011). The metabolomeÂ represents the collection of all metabolites in a biological cell, tissue, organ or organism, which are the end products of cellular processes (Daviss, Bennett, 2005).
Gene expression: It is the process by which information from a gene is used in the synthesis of a functional gene product like proteins, but in non-protein coding genes such as ribosomal RNA (rRNA), transfer RNA (tRNA) or small nuclear RNA (snRNA) genes, the product is a functional RNA. The process of gene expression is used by all known life i.e. eukaryotes, prokaryotes and viruses, to generate the macromolecular machinery for life Gene expression occurs in two major stages, first is transcription in which the gene is copied to produce an RNA molecule with essentially the same sequence as the gene and second stage is protein synthesis known as translation (Oliver Brandenberg et al., 2011, Richard Twyman, 2003).
Genotype: The genotype is the genetic makeup of a cell, an organism, or an individual usually with reference to a specific character under consideration which is the internally coded, inheritable information, carried by all living organisms. This stored information is used as a blueprint or set of instructions for building and maintaining a living creature (Oliver Brandenberg et al., 2011).
Phenotype: It is the composite of an organism's observable characteristics or traits such as its morphology, development, biochemical or physiological properties, phenology, behavior, and products of behavior. These are the physical parts, the sum of the atoms, molecules, macromolecules, cells, structures, metabolism, energy utilization, tissues, organs, reflexes and behaviors of a living organism (Oliver Brandenberg et al., 2011).
Polymorphism: Polymorphism in biology occurs when two or more clearly different phenotypes exist in the same population of a species, the occurrence of more than one form or morph. (Oliver Brandenberg et al., 2011).
Allele: An allele is one of two or more forms of a gene or a genetic locus and form allel is also used for an abbreviation of allelomorph and different alleles can result in different observable phenotypic traits, such as different pigmentation. (Oliver Brandenberg et al., 2011).
Epigenetic: A modification of gene expression that is independent of the DNA sequence of the gene (Egger, G., Liang G., et al., 2004). The current definition of epigenetics is the study of heritable changes in gene expression that occur independent of changes in the primary DNA sequence and these heritable changes are established during differentiation and are stably maintained through multiple cycles of cell division, enabling cells to have distinct identities while containing the same genetic information. This heritability of gene expression patterns is mediated by epigenetic modifications, which include methylation of cytosine bases in DNA, posttranslational modifications of histone proteins as well as the positioning of nucleosomes along the DNA (Sharma, Shikhar, 2010).
Nutrigenomics: Health from nutrition
Nutrigenomics is the study of how naturally occurring chemicals in foods alter molecular expression of genetic information in each individual. The term nutrigenomics refers the effect of diet on gene expression or to the impact of inherited on the response to a specific dietary pattern, functional food or supplement on a specific health outcome (Fenech, M., 2005) so called as the "next frontier in the post genomic era" (David Castle, 2007). It can be described as the study of the relationship between genes, diet lifestyle and health that is nutrition regulate gene function like transcription, translation and metabolism i.e. diet gene interaction (Ordovas, J.M., 2004).
Nutrigenomics focuses on understanding that nutrition influences metabolism and maintenance of the internal equilibrium in the body and this regulation affects the diet related diseases (Ordovas J.M., 2004) and offers a powerful and exiting approach to unravel the effect of diet on health. In the past the nutrition research concentrated on nutrient deficiency and impairment of health but nutrigenomics creates a junction between health diet and genomics and it will promotes an increased understanding of how nutrition influences metabolic pathway and homeostasis control.
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Biomedical researcher, private sector firm, public (Timothy Caulfield, 2008) and food industry recognizes the need for nutrigenomics research as a basis for developing the concept of "personalized diet" for identifying molecular biomarkers. Over the past few years, there has been rapid increase in the interest in nutrigenomics as a research topic because it is an area that has been viewed as worthy public funding, both as a topic of basic scientific inquiry and as a field with health care and commercialization possibilities (Ordovas, J. M., 2004). The new scientific understanding of nutrigenomics has led to the increase of commercial development of nutraceutical and functional foods that can be modify negative health effect of individual genetic profiles (Francesco, Marotta et al., 2012).
The main aim of the nutrigenomics is that to improve dilatory advice, development of health promoting supplements, preventive strategies and the reduction of healthcare cost (Ordovas, J.M., 2004). The coming years will likely require patience, realistic expectations and strong advocacy for the needed research funding. A major focus of nutrition research is on prevention of chronic disease such as cardiovascular disease, metabolic disorder and cancer (Afman, L. et al., 2006)
More than simply managing or treating disease or the symptoms associated with disease, the nutrigenomics will be used to identify susceptibilities to disease and implement pro active measures to help individuals avoid contracting said disease in the first place and we can say that nutrigenomics research will lead to development of evidence based healthful food and lifestyle advice and dietary intervention for contemporary humans (Ordovas, J.M., 2004). The advent of modern science led to the realization that not only are certain nutrition essential but also that specific quantity of each were necessary for optimal health thereby leading to such notions as dilatory recommendations, nutritional epidemiology, and the realization that food can directly contribute to disease onset. In this regard human development to disease onset is clearly defined by both environmental influences like diet, smoking education, physical activity etc. and heredity indicating that both aspects must be considered if one aims to optimize health (Ordovas, J.M., 2004).
The excitement about nutrigenomics comes from a growing awareness of the potential for modifications of food or diet to support health and reduce the risk of diet related diseases thus by identifying individual genetic predispositions for chronic diseases and the potential for individuals response to dietary intervention, these diseases may be effectively prevented by properly dietary intake. Nutrigenomics brings together the science of bioinformatics nutrition, molecular biology genomics, epidemiology and molecular medicine (Neeha, V.S., 2012).
Nutrigenomics is the application of high-throughput genomics tools to the study of diet-gene interactions in order to identify dietetic components having beneficial or detrimental health effects (Miggiano, G.A., 2006). Traditionally biomarkers related to onset of disease or organ damage were used to quantify the effects but now it becomes necessary to quantify phenotype changes which are very close or within the range of health state (Ben Van Omen, 2008) and has primarily focused on nutrient deficiencies and the relation between nutrition and health. The advent of genomics has created unprecedented opportunities for increasing understanding of nutrients modulating gene and protein expression and ultimately influence cellular and organizational metabolism (Maria, C. Busstra et al., 2007).
Normally nutrigenomics embodies three normative concepts; first, food is exclusively interpreted in terms of disease prevention. Second, striving for health is interpreted as the quantification of risks and prevention of diseases through positive food-gene interactions and third, normative idea is that disease prevention by the minimization of risks is an individual's task (Korthals, M., 2011).Â
Nutritional factors are thought to be the cause of 30-60% of cancer; diabetes, cardiovascular diseases, and obesity are expensing rapidly (Zeisel, S.H., 2010). The conceptual basis for this new branch of genomic research can best be summarized by the following five tenets of nutrigenomics (Debusk, R., 2005):
Under certain circumstances and in some individuals, diet can be a serious risk factor for a number of diseases.
Common dietary chemicals can act on the human genome, either directly or indirectly to alter gene expression or structure.
The degree to which diet influences the balance between healthy and disease states may depend on individual's genetic makeup.
Some diet regulated genes are likely to play a role in the onset, incidence, progression and severity of chronic disease
Dietary intervention based on knowledge of nutritional requirement, nutritional status and genotype can be used to prevent, mitigate or cure chronic diseases.
Nutrigenomics is therefore significant not only as a matter of improving public health but becomes it can have wide spread. Implicates on the way to understand and practice nutrition.
20.1.3 Benefits of nutrigenomics
Scientific studies show that nutrients in food can cause changes in the behavior of genes and the finding suggest that nutrients play peoples risk for cancer and other disease and through it, researchers hope to find ways to use food to prevent, cure and reduce the risk of diet related disease and benefits include a growth in concern on one's health and the chance to have a personalized nutrition optimized for good health, discovering genetic vulnerabilities which can be a strong motivating factor to encourage people to make the necessary dietary and lifestyle changes, and the high chances of heeding the advice that they have paid for. Profiling and Analyzing one's DNA may cost between $300 and $3,000 and large-scale food corporations are spending fortunes on nutrigenomics, and on development of enhanced or fortified products to deliver personalized diets and multi-national corporations specializing in skin care, aging and beauty products are using nutrigenomics for (David Castle, 2007). The main aims of nutrigenomics are:
Obtaining a personalized dietary regimen may encourage people to become more health conscious.
People are more likely to heed advice that they pay for.
Discovering genetic susceptibilities can be a strong motivator for making dietary and lifestyle changes.
The safe upper and lower limits for essential macro-nutrients like proteins, carbohydrates, fats and micronutrients such as vitamins and minerals will be better defined and understood.
Diseases may be avoided or ameliorated.
Unnecessary vitamins and other dietary supplements can be avoided.
People whose health is relatively unaffected by diet can continue to eat foods that they enjoy.
Lifespan may be extended.
Following commercial interests are responding to established market segments of early adopters seeking new tools to enhance health.
Nutrigenomics: The genes can tells that to eat
The ability of cells to adapt to environmental change by regulation of gene expression is essential for organism survival and organisms vary their gene expression in the absence or presence of nutrients by increasing and decreasing production of cellular proteins necessary for life sustaining function. A perfect example of this evolutionary process is the development of a gene mutation that alters the ability to tolerate lactose and adult mammals typically are unable to digest lactose. Ultimately, the science of nutrigenomics promises to offer the health practitioner greater knowledge, enabling them to predict potential genetic responses to nutritional intake and to target and modify associated behavior (Zeisel, S.H. et al., 2005).
Nutrigenomics explains omega-3's immune health benefits
Omega-3 fatty acids not only lower LDL cholesterol, but also help raise good HDL cholesterolÂ and protection against certain cancers to prevention of heart disease, arthritis, degenerative eye disease, and high blood pressure, are found in walnuts, canola oil, and flax seeds but the best source is cold water fish. A specific omega-3 fatty acid called eicosapentaenoic acid (EPA) was shown to reduce expression of inflammatory genes in arthritic canine cells. (Bouwens, M., 2009, Bahadori, B., et al., 2010, Balk, E.M., et a.l, 2006)
Omega-3 fatty acids are highly concentrated in the brain and appear to be important for brain memory and performance, behavioral function. In fact, infants who do not get enough omega-3 fatty acids from their mothers during pregnancy are at risk for developing vision and nerve problems and symptoms of omega-3 fatty acid deficiency include fatigue, poor memory, dry skin, heart problems, mood swings or depression, and poor circulation.
It is important to have the proper ratio of omega-3 and omega-6 in the diet because omega-3 fatty acids help reduce inflammation, and most omega-6 fatty acids tend to promote inflammation. (Aben, A., 2010, Angerer, P., 2000, Aronson, W.J. et al., 2001)
Nutrigenomics shows blood pressure benefits of cocoa
A new nutrigenomics study shows that potential of polyphenol compounds in cocoa to reduce blood pressure is related to genotype. Activity of the antiotensin-converting enzyme (ACE), a target for blood pressure medication which was significantly inhibited by dark chocolate containing 72 percent cocoa, with the degree of inhibition dependent upon the genotype of the human subjects. ACE inhibitors work by inhibiting the conversion of angiotensin I to the potent vasoconstrictor, angiotensin II, thereby improving blood flow and blood pressure. (Stephen, Daniels, 2011)
Nutrigenomics Shows Benefit of Magnesium's metabolic actions
Magnesium may up and down-regulate a number of genes linked to metabolism and shows favorable effects on certain metabolic pathways are associated with changes in gene expression (Chacko, S.A., 2011) and magnesium supplementation was associated with a decrease in levels of C-peptide, a marker of improved insulin sensitivity. The mineral was also linked to down-regulation of certain genes related to metabolic and inflammatory pathways, the report also says that in terms of gene expression, 24 genes were up-regulated, and 36 genes were down-regulated in response to magnesium supplementation and some findings are also indicated a systemic effect of magnesium supplementation give measurable physiologic changes in the urinary proteome after treatment with magnesium for four weeks, which warrants further investigation into these changes and identification of the proteins involved (Chacko, S.A., 2011).
Nutrigenomics Supports Evidence for Health Benefits of Anthocyanins
Anthocyanins, a large subgroup of flavonoids present in many vegetables and fruits, are safe and potent antioxidants. They exhibit diverse potential health benefits including cardioprotection, anti-atherosclerotic activity, anti-cancer, anti-diabetic, and anti-inflammation properties. Anthocyanins can cross the blood-brain barrier and distribute in the CNS. Recent studies indicate that anthocyanins representÂ novelÂ neuroprotective agents and may be beneficial in ameliorating ethanol neurotoxicity (Gang, Chen and Jia, Luo, 2010). Recently, it is demonstrated thatÂ anthocyanins, which are pigments widespread in the plant kingdom, have the potency of anti-obesity in mice and the enhancement adipocytokine secretion and adipocyteÂ gene expressionÂ in adipocytes (Tsuda, T. et al., 2005).
Nutrigenomics could provide nutrition-relevant biomarkers
Changes to messenger RNA and the corresponding proteins control the transport of certain nutrients and metabolites in the biochemical pathway. Nutrigenomics could also provide a new set of biomarkers with relevance to nutrition. (Van Der Werf, M.J., 2006)
Benefits of nutrigenomics diet for skin
Many skin problems such as acne, eczema, psoriasis, dry skin and premature aging of the skin is associated with diet and inadequate nutrition substantially contribute to the deterioration of such skin conditions and vice versa, with a proper diet the appearance and health of the skin can be significantly improved. The most advisable is beneficial for the blood type and genotype are minimally processed fruits, vegetables, legumes, nuts and seeds, and fermented products from unpasteurized and not homogenized milk. These foods contain nutrients necessary for healthy skin like vitamins B and E and minerals such as calcium, magnesium, potassium, iron, copper and manganese and to all blood groups are friendly flax seed, almonds and walnuts. In the fruits a great choice for all blood types are pineapple, blueberries, raspberries and cranberries. Turkey is the only generally available meat that is suitable for all blood types and genotypes. The leading way to beauty and health healthy diet, lifestyle and products that are tailored to your nutrigenomics diet profile (Ravi Subbiah, M.T., 2010).
Health economics of nutrigenomics in weight management
There is a theoretical modeling study where they sought to evaluate the health economics implications of a nutrigenomic product for weight loss for which constructed a nutrigenomic economic model by linking the published study data related to the efficacy of a product and/or ingredients and validated clinical assessments that have already been tied to health economics data with data involving condition prevalence and overall cost of illness. In this theoretical model, the demonstration is that LG839 variant positively reduces the cost of illness at the macroeconomic and microeconomic level based upon a cost-effectiveness and cost-benefit analysis, have forecasted the prognostic health economic implications of a nutrigenomic intervention to demonstrate a theoretical model of nutrigenomic economics. This study is hypothesis-generating and should be used in the definition of protocols to prospectively test the health economic benefits of nutrigenomics (Brian, Meshkin, 2008).
Nutrigenetic association of the 5-lipoxygenase gene with myocardial infarction
5-Lipoxygenase (5-LO) catalyzes the rate-limiting step of the biosynthesis of proinflammatory leukotrienes from arachidonic acid (AA) and has been associated with atherosclerosis in animal models and humans and previously reports says that variants of a 5-LO promoter repeat polymorphism were associated with carotid atherosclerosis in humans, an effect that was exacerbated by high dietary amino acids but mitigated by high dietary Nâˆ’3 fatty acids. The 5-LO polymorphism was genotyped by Costa Rican case-control pairs and tested for association with myocardial infarction and today, scientists are working with powerful databases to identify variations among genes in individuals and are working to establish correlations for susceptibility to various health conditions, as well as to understand the influence of such genetic variations on responses to dietary components (Allayee, H., 2006).
Persons involved in nutrigenomics (Afman, L., 2006, De Busk, R., 2012, Debusk, R.M., 2005, German, J.B., 2005, Trujillo, E., 2006)
The nutrigenomics practitioner will develop gene-directed nutrition approaches and coach people in how to use food, dietary supplements and lifestyle choices in general in ways that are most appropriate for their genetic makeup. Disease management is expected to become increasingly effective as nutritional genomics is integrated into practice and even more eagerly anticipated is the opening up of new horizons for health care professionals in terms of expertise in health promotion while The ability to identify disease susceptibilities for an individual provides a solid foundation for effective health promotion efforts in ways never before possible (Ruth, M., 2012).Â Two men of the same age eat a diet low in fruits and vegetables and high in sodium and saturated fat. One develops hypertension, hypercholesterolemia, and eventually atherosclerosis, while the other lives a long life without such chronic disease. In another case, two postmenopausal women consume similar diets low in choline. One develops liver dysfunction due to the choline deficiency, but the other does not. However, because there are several genes involved in the development of these and other polygenic illnesses, dietitians and other healthcare professionals don't fully understand the relationship between diet and disease risk, which stifles our ability to make personalized dietary recommendations as a preventive measure (Megan, D. Baumler, 2012).
Epidemiological studies have been helpful in identifying environmental factors associated with incidence or severity of certain diseases.Â However, these are statistical associations and as such, do not indicated the exact cause of the disease.Â Indeed, as the number of environmental variables increase, there is a corresponding need for larger population sizes in order to discriminate between statistically significant and insignificant factors (Malats, N., 2003). Meta-analyses may be helpful in this regard if studies record similar data elements and use similar environmental survey instruments for their populations.Â Alternatively, well-designed laboratory animal studies and comparativeÂ genomicsÂ will be helpful in confirming and extending associations between dietÂ and disease. (Megan, D. Baumler, 2012)
The diverse tissue and organ-specific effects of bioactive dietary components include gene expression patterns organization of the chromatin, protein expression patterns including post-translational modifications as well as metabolite profiles (Corthesy-Theulaz, I., 2005).
The physician with help of nutrigenomics can see the blueprints and better understand the raw materials required by body. Incomplete or bad food causes toxic by-products which accelerate the aging and disease process and free radicals produced by non-specific foods and supplements wreak havoc on our body and in the past two decades, physicians, geneticists, and nutritionists have begun to study the effects of genetic variation and gene-nutrient interactions in the management of chronic diseases, such as coronary heart disease, hypertension, cancer, diabetes and obesity; and the role of nutrients in gene expression. (Artemis, P.S., 2002)
Advances in molecular and recombinant DNA technology have led to exquisite studies in the field of genetics and the recognition in a much more specific way, through DNA sequencing and the extent to which genetic variation occurs. The importance of the effects of genetic variation has been extensively studied and applied by pharmacologists in drug development and evaluation of drug metabolism and adverse reactions to drugs. (Artemis, P.S., 2002)
The role of bioinformatics in nutrigenomics is multifold i.e. to create nutrigenomic databases, to setup special ontologies in using available resources, setup and track laboratory samples being tested and their results, pattern recognition, classification, and data mining, and simulation of complex interactions between genomes, nutrition, and health disparities (David Schaffer, J. et al., 2006)
The current rise in diet-related diseases is compromising health and devaluing many aspects of modern agriculture and steps to increase the nutritional quality of individual foods will assist in personalizing health and in guiding individuals to achieve superior health, the food scientists may use nutrigenomics to provide balanced and healthy diet for a person, and also apply the concept of personalized diet (German, J.B., 2011).
Limitations of nutrigenomics
Nutrigenomics risks includes the knowledge of disease susceptibility may cause high levels of anxiety and stress, genetic testing raises privacy concerns and some companies already sell the results of their genetic profiling to other companies while those with known genetic susceptibilities may be discriminated against in employment or health insurance. Physicians may not be qualified to interpret nutrigenomic reports and make appropriate decisions based on them and the demand for nutrigenomic evaluations may eventually overtax the healthcare system. The high cost of the screening and genotype diagnosis of developing novel and functional foods and the poor availability of functional health systems make even the possibility of tailored diets an impossible dream for most populations relying on poorly functioning and poorly resourced health systems. (Zeisel, S.H., 2005)
20.2. Technologies involved in nutrigenomics
Studies the effect of genetic variations on the interaction between diet and health with implications to susceptible subgroups, more specifically, nutrigenomics studies how individual differences in genes influence the body's response to diet and nutrition, for example, people with an enzyme deficiency caused by mutations in the enzyme phenylalanine hydroxylase cannot metabolize foods containing the amino acid phenylalanine and must modify their diets to minimize consumption (Ordovas, J.M., 2004). This process has several phases that have grown into corresponding new fields within nutrigenomics are transcriptomics, proteinomics and metabolomics. Considers all metabolites in a human cell or organ, is capable of generating large amounts of data at low cost that detects subtle differences in metabolism that contribute to obesity as well as fluctuations in weight (David, M. Mutch, 2005).
Transcriptome is the study of complete set of RNA transcripts produced by the genome at any one time andÂ transcriptomeÂ is the set of all RNA molecules, includingÂ mRNA,Â rRNA,Â tRNA, and otherÂ non-coding RNAÂ produced in one or a population ofÂ cells (Hocquette, J.F., 2009). The term can be applied to the total set of transcripts in a givenÂ organism, or to the specific subset of transcripts present in a particular cell type, unlike theÂ genome, which is roughly fixed for a given cell line, the transcriptome can vary with external environmental conditions because it includes allÂ mRNAÂ transcripts in the cell, the transcriptome reflects theÂ genesÂ that are being activelyÂ expressedÂ at any given time, with the exception of mRNA degradation phenomena such asÂ transcriptional attenuation (Wang, Z., 2009). The study ofÂ transcriptomics, also referred to asÂ expression profiling, examines the expression level of mRNAs in a given cell population, often using high-throughput techniques based onÂ DNA microarrayÂ technology and the use ofÂ next-generation sequencingÂ technology to study the transcriptome at the nucleotide level is known asÂ RNA-Seq (Gupta, Krishna Sen, 2011).
There are two methods of creating transcriptomes, first, maps sequence reads onto a reference genome, either of the organism itself or of a closely related species and second,Â de novo transcriptome assembly, utilizes algorithms built into assembly software to generate transcripts from short sequence reads. DNA microarraysÂ can provide a method for comparing on a genome-wide basis the abundance ofÂ DNAsÂ in the same samples and DNA in spots can only beÂ PCRÂ products that are specific for individual genes. A DNA copy of RNA is made using the enzyme reverse transcriptase and sequencing is now being used instead of gene arrays to quantify DNA levels, at least semi quantitatively (Katayama, S., 2005)
Analysis of the transcriptomes of humanÂ oocytesÂ andÂ embryosÂ is used to understand the molecular mechanisms and signaling pathways controlling early embryonic development, and could theoretically be a powerful tool in making properÂ embryo selectionÂ in vitro fertilisation. (Subramanium, A., 2005)
The transcriptome can be seen as a precursor for theÂ proteome, that is, the entire set of proteins expressed by a genome. However, the analysis of relative mRNA expression levels can be complicated by the fact that relatively small changes in mRNA expression can produce large changes in the total amount of the corresponding protein present in the cell. One analysis method, known as Gene Set Enrichment Analysis, identifies coregulated gene networks rather than individual genes that are up- or down-regulated in different cell populations. (Katayama, S., 2005)
Although microarray studies can reveal the relative amounts of different mRNAs in the cell, levels of mRNA are not directly proportional to the expression level of theÂ proteinsÂ they code for. The number of protein molecules synthesized using a given mRNA molecule as a template is highly dependent on translation-initiation features of the mRNA sequence; in particular, the ability of theÂ translation initiation sequenceÂ is a key determinant in the recruiting ofÂ ribosomesÂ for proteinÂ translation. The complete protein complement of a cell or organism is known as theÂ proteome (Velculescu, V.E., 1997).px
Metabonomics is defined as the quantitative measurement of the dynamic multiparametric metabolic response of living systems to pathophysiological stimuli or genetic modification. The word origin is from the GreekÂ metaÂ meaning change andÂ nomosÂ meaning a rule set or set of laws (Nicholson, J.K., 2006) and itÂ is the scientific study of chemical processes involvingÂ metabolites specifically, metabolomics is the systematic study of the unique chemical fingerprints that specific cellular processes leave behind, the study of their small-moleculeÂ metaboliteÂ profiles (Daviss, 2005) whileÂ metabolomeÂ represents the collection of all metabolites in a biological cell, tissue, organ or organism, which are the end products of cellular processes (Jordan, 2009).
Metabolites are the intermediates and products ofÂ metabolism. Within the context of metabolomics, a metabolite is usually defined as any molecule less than 1 kDa in size (Samuelsson, 2008). However, there are exceptions to this depending on the sample and detection method. For example, macromolecules such asÂ lipoproteinsÂ andÂ albuminÂ are reliably detected in NMR-based metabolomics studies of blood plasma (Nicooholson, J.K., 1995). Human-based metabolomics, it is more common to describe metabolites as being eitherÂ endogenous orÂ exogenous.Â (Nordstrom, A., 2006)Metabolites of foreign substances such as drugs are termed xenometabolites (Crockford, D.J., 2008). TheÂ metabolomeÂ forms a large network ofÂ metabolicÂ reactions, where outputs from oneÂ enzymaticÂ chemical reactionÂ are inputs to other chemical reactions. Such systems have been described asÂ hypercycles. By this technique the toxicityÂ assessment/toxicology (Robertson, 2005), metabolic profiling can be used to detect the physiological changes caused by toxic insult of a chemical and in many cases, the observed changes can be related to specific syndromes, e.g. a specific lesion in liver or kidney. This is of particular relevance to pharmaceutical companies wanting to test the toxicity of potentialÂ drugÂ candidates: if a compound can be eliminated before it reachesÂ clinical trialsÂ on the grounds of adverse toxicity, it saves the enormous expense of the trials (Saghatelian, A., 2004, Chiang, K.P., 2006) so it can be an excellent tool for determining theÂ phenotypeÂ caused by a genetic manipulation, such as gene deletion or insertion (Gibney, M.J., 2005).
It is the large-scale study ofÂ proteins, particularly theirÂ structuresÂ andÂ functions.Â The word proteome is aÂ blendÂ of protein and genome, the entire complement of proteins including the modifications made to a particular set of proteins, produced by an organism or system. This will vary with time and distinct requirements, or stresses, that a cell or organism undergoes and often specifically used for protein purification and mass spectrometry (Anderson, N.L., 1998, Blackstock, W.P., 1999).
Proteomics typically gives us a better understanding of an organism than genomics; first, the level of transcription of a gene gives only a rough estimate of itsÂ level of expression into a protein (Steven, P. Gygi, 1999).Â AnÂ mRNAÂ produced in abundance may be degraded rapidly or translated inefficiently, resulting in a small amount of protein and second, as mentioned above many proteins experienceÂ post-translational modificationsÂ that profoundly affect their activities; for example some proteins are not active until they become phosphorylated. Methods such asÂ phosphoproteomicsÂ andÂ glycoproteomicsÂ are used to study post-translational modifications. Third, many transcripts give rise to more than one protein, throughÂ alternative splicingÂ or alternative post-translational modifications and fourth, many proteins form complexes with other proteins or RNA molecules, and only function in the presence of these other molecules. Finally, protein degradation rate plays an important role in protein content (Belle, Archana, 2006).
Practical applications of proteomics are the identification of potential new drugs for the treatment of disease. This relies on genome and proteome information to identify proteins associated with a disease, which computer software can then use as targets for new drugs. For example, if a certain protein is implicated in a disease, its 3D structure provides the information to design drugs to interfere with the action of the protein (Sreedhar, A., 2011). A molecule that fits the active site of an enzyme, but cannot be released by the enzyme, will inactivate the enzyme. This is the basis of new drug-discovery tools, which aim to find new drugs to inactivate proteins involved in disease. An interesting use of proteomics is using specific protein biomarkers to diagnose disease. A number of techniques allow testing for proteins produced during a particular disease, which helps to diagnose the disease quickly. Techniques includeÂ western blot,Â immunohistochemical staining,Â enzyme linked immunosorbent assayÂ (ELISA) orÂ mass spectrometry (Klopfleisc, R., 2010).Â
Secretomics, a subfield of proteomics that studiesÂ secreted proteinsÂ and secretion pathways using proteomic approaches, has recently emerged as an important tool for the discovery of biomarkers of disease (Hathout, Yetrib, 2007). Proteomic technologies such asÂ mass spectrometryÂ are used for improving gene annotations and play an important role in drug discovery, diagnostics and molecular medicine because is the link between genes, proteins and disease. Advances in proteomics may help scientists eventually create medications that are "personalized" for different individuals to be more effective and have fewer side effects. Clinical pharmacologists, biostatisticians, and clinicians need to give thoughtful consideration to the type and quantity of evidence to support dosing changes in clinical practice or approved labels intended to improve either the efficacy or safety of a medical treatment (Lesko, L.J. 2007).
12.3. Nutrients modulating genome expression
Numerous dietary components can alter genetic events, and thereby influence health. In addition to the essential nutrients, such as carbohydrates, amino acids, fatty acids, calcium, zinc, selenium, folate, and vitamin A, C and E, there is a variety of nonessential bioactive components that seem to significantly influence health (Corthesy-Theulaz et al., 2005, Trujillo et al., 2006)
12.3.1. Effect of carbohydrate on gene expression
Glucose, the most abundant monosaccharide in nature, provides a very good example of how organisms have developed regulatory mechanisms to cope with a fluctuating level of nutrient supply (Sophie, Vaulont, 2000). In mammals the response to dietary glucose is complex because it combines effects related to glucose metabolism itself and effects secondary to glucose-dependent hormonal modifications, mainly pancreatic stimulation of insulin secretion and inhibition of glucagon secretion (Sophie, Vaulont, 2000). In the pancreatic cells, glucose is the primary physiological stimulus for the regulation of insulin In the liver, glucose, in the presence of insulin, induces expression of genes encoding glucose transporters and glycolytic and lipogenic enzymes, e.g. L-type pyruvate kinase (L-PK), acetyl-CoA carboxylase (ACC), and fatty acid synthase, and represses genes of the gluconeogenic pathway, such as the phosphoenolpyruvate carboxykinase gene (Michael, W. King, 2012). Although insulin and glucagon were long known as critical in regulating gene expression, it is only recently that glucose also has been shown to play a key role in transcriptional regulation synthesis and secretion (Sophie, Vaulont, 2000).
Feeding high-energy diet to rats leads to early development of obesity and metabolic syndrome, apparently through an inability to cope with energy density of the diet. Obesity is associated with decrease in mRNA levels for the oxygenic neuropeptides, NPY (neuropeptides Y), Ag RP (Agouti Related Peptide) etc and the effect of hyperglycemia on liver angiotensinogen (AGT) gene expression and found that hyperglycemia activated AGT gene expression in liver increased approximately 3 fold (Gabriely, I., 2001).
12.3.2. Regulation of gene expression by dietary fat
In addition to its role as an energy source and its effects on membrane lipid composition, dietary fat has profound effects on gene expression, leading to changes in metabolism, growth, and cell differentiation. The effects of dietary fat on gene expression reflect an adaptive response to changes in the quantity and type of fat ingested (Jump, D.B., 1999). In mammals, fatty acid regulated transcription factors include peroxisome proliferator-activated receptors (PPARÎ±, -Î², and -Î³), HNF4Î±, NFÎºB, and SREBP1c (Koji, Nagao, 2008). These factors are regulated by direct binding of fatty acids, fatty acyl coenzyme A, or oxidized fatty acids oxidized fatty acid regulation of G-protein-linked cell surface receptors and activation of signaling cascades targeting the nucleus oxidized fatty acid regulation of intracellular calcium levels, which affect cell signaling cascades targeting the nucleus (Jump, D.B., 1999).
12.3.3. Role of PUFA on Gene expression
Lipogenic enzymes in liver decreased as result of feeding a diet containing 60 % linoleic acid. Fatty acids stimulated the expression of adipocyte fatty acid binding protein (ap2) mRNA. In the 3T3-L1 adipocyte cell line, arachidonic acid (n-6) decreased SCD1 m RNA stability in a dose dependent manner (80% maximum repression), as did linoleic and eicosapentanoic acids (Tandon, Mayank, 2012).
12.3.4. Effect of protein on gene expression
Protein is very essential for growth, to develop immunity, normal maintenance of body function and structure apart from reproduction and production and in many developing countries protein insufficiency is still remains a major and serious problem (Tandon, Mayank, 2012). The function of protein in body is not only at macro level but it also functions at gene level and a variety or number of genes responds to dietary protein both protein quantity as well as quality influences gene expression. Insulin secretion was reduced in rats, which are fed with low protein diet due to reduction in pancreatic b-cell mass lower response of remaining b-cells to nutrients and lowered protein kinase activity (PKA) (Fabiano, Ferreira, 2004) which is involved in potentiating of glucose induced insulin secretion by gastrointestinal hormones such as GIP and GLP-1(Sarah Melissa, P., 2009). Low protein diet feeding to rats altered the many gene expression, which are responsible for proteins related to insulin biosynthesis, secretion and cellular remodeling. Normal insulin secretion is influenced by level of Protein Kinase C (PKC), K+ channel protein, calcium ion (Ca 2+) and PKAa and increased ATP to ADP ratio achieved through glucose metabolism, close the K+ ATP channel, which leads to depolarization of b-cells results in opening of voltage dependent Ca 2+ channels which results in influx of calcium leads to exocytosis of insulin granules while feeding low protein diet also increased expression of PFK in islets results in defective glucose metabolism and it further leads to deceased glucose induced insulin secretion and also decreases insulin level, it also acts through decreased movement of intracellular calcium (Tandon, Mayank, 2012).
12.3.5. Influence of Amino Acids on gene expression
The first step of protein translation is the formation of the 43s pre-initiation complex containing methionyl tRNA, eIF2, GTP, followed by the assocoiation of methionyl tRNA and eIF2-GTP that bind to the 40s ribosomal sub unit then GTP is hydrolyzed late in the initiation process, and eIF2 is released from the ribosome as an inactive eIF2-GTP complexresults in formation of eIF2-GTP is mediated by the guanine nucleotide exchange factor eIF2B. The mechanism to regulate eIF2B activity may be at the level of the ribosomal protein S6 and eukaroyotic elongation factor 2 (eEF-2) which is phosphorylated in response to many agents, including growth factors and hormones initiation process and amino acids regulate protein translation through modulation of eIF2B activity, 4 E-BP phosphorylation and protein S6 phosphorylation (Tandon, Mayank, 2012).
12.3.6. Effect of minerals on gene expression
Zinc (Zn) is an essential trace element with cofactor functions in a large number of proteins of intermediary metabolism, hormone secretion pathways and immune defense mechanism, involved in regulation of small intestinal, thymus and hepatocytes gene expression (Kindermann, B., 2004). MTF-I (Metal Responsive element Factor- I) is a Zn dependent transcriptional activator regulates mettalothionin I and II through MRE. Zn depedent KLF4 transcription factor is involved in protein preparation of HT-29 cells. The other protein have Zn in it as constituents are ATP synathase, cytochrome c, a, NADP dehydrogenase I and II. Deficiency of one or more mineral in diet lead to impaired body functions Geographical differences in mineral level of Soil/Plants (diet) have effects up to gene level such as Iron, Iodine, Selenium deficiency or excess of heavy metal ions like Anaemia (Vallee, B.L., 1990, Wu, F.Y., 1987).
12.3.7. Effect of vitamins on gene expression
Vitamins are micronutrients needed in very small quantity and are involved in gene expression. Vitamin A is involved in gene expression of Phospho Enol Pyruvate Kinase (PEPCK) is vitamin, insulin like growth factor (IGF 9) (Tandon, Mayank, 2012). Vitamin C is involved in hepatic gene expression. PEPCK is involved in conversion of oxaloacetate to phospho enol pyruvate, one of the important steps in gluconeogenesis. Vitamin A deficiency condition leads to changes in chromosomal structure of Retinoic Acid Responsive Element (RARE), which further leads to change in co regulator binding and activity. PEPCK -RARE and pre initiation complex interaction leads to RNA polymerase II association with PEPCK promoter is reduced, finally all results in insufficient PEPCK or no PEPCK leads to improvement of gluconeogenesis. In vitamin A sufficient mice PEPCK gene expression is highly induced in the food deprived state, when blood glucose levels are reduced (Tandon, Mayank, 2012).
Biotin is involved in various essential proteins (enzymes) synthesis at gene level (Dakshinamurti, K., 2005). Vitamins B12, B6, and folic acid converge at the homocysteine metabolic junction where they support the activities of two key enzymes involved in intracellular homocysteine management, methionine synthase (MS) and cystathionine beta-synthase. B12 supplementation does not alter mRNA or protein turnover rates but induces translational up-regulation of MS by shifting the mRNA from the ribonucleoprotein to the polysome pool. The B12-responsive element has been localized by deletion analysis using a reporter gene assay to a 70-bp region located at the 3' end of the 5'-untranslated region of the MS mRNA. The cellular consequence of the B12 response is a 2- and 3.5-fold increase in the flux of homocysteine through the MS-dependent transmethylation pathway in HepG2 and 293 cells, respectively (Oltean, S., 2003).
20.4. Nutrition gene and diseases
20.4.1 Metabolic hereditary diseases
Some hereditary disorders of metabolism can be diagnosed in the fetus by using amniocentesis or chorionic villus sampling and blood test or examination of a tissue sample to determine whether a specific enzyme is deficient or missing (Lee, M. Sanders, 2009).
In most inherited metabolic disorders, a single enzyme is either not produced by the body at all, or is produced in a non-working form. Depending on the function of that enzyme, toxic chemicals may build up, or an essential product may not be produced. The code or blueprint to produce an enzyme is usually contained on a pair of genes and most people with inherited metabolic disorders inherit two defective copies of the gene one from each parent. Both parents are carriers of the bad gene, meaning they carry one defective copy and one normal copy. Inherited metabolic disorders may affect about 1 in 1,000 to 2,500 newborns. In certain ethnic populations, such as Ashkenazi Jews (Jews of central and eastern European ancestry), the rate of inherited metabolic disorders is higher. (Fleisher, G, 2006) The symptoms of genetic metabolic disorders vary widely depending on the metabolism problem present, includes Lethargy, Poor appetite, Abdominal pain, Vomiting, WeightÂ loss, Jaundice, Failure toÂ gain weightÂ or grow, Developmental delay, Seizures, Coma, Abnormal odor of urine, breath, sweat, or saliva. Symptoms may be brought on by foods,Â medications,Â dehydration, minor illnesses, or other factors. Hundreds of inherited metabolic disorders have been identified, and new ones continue to be discovered. Some of the more common and important genetic metabolic disorders include (Scriver, C., 2001):
Lysosomal storage disorders like Hurler syndrome, Niemann-Pick disease, Tay-Sachs disease, Gaucher diseaseÂ , Fabry disease, Krabbe disease, Galactosemia, Maple syrup urine disease in which deficiency of an enzyme called branched-chain alpha-keto acid dehydrogenase (BCKD) causes buildup of amino acids in the body and the urine smells like syrup (Muranjan, M., 2010), Phenylketonuria (PKU), deficiency of the enzyme PAH results in high levels of phenylalanine in the blood (Mitchell, J.J., 2010), Glycogen storage diseases, Friedreich ataxia i.e. problems related to a protein called frataxin cause nerve damage and often heart problems (Hasan, Ozen, 2007).
Peroxisomal disorders include Zellweger syndromeÂ (abnormal facial features, enlarged liver, and nerve damage in infants) and AdrenoleukodystrophyÂ , Metal metabolism disorders like Wilson disease (toxic copper levels accumulate in the liver, brain, and other organs) and Hemochromatosis (the intestines absorb excessive iron, which builds up in the liver, pancreas, joints, and heart, causing damage), Organic acidemias, Urea cycle disorders including ornithine transcarbamylase deficiencyÂ and citrullinemia are the few examples of metabolic hereditary disorders (Hasan, Ozen, 2007). Inborn errors of metabolism (IEM) are sometimes referred to as "silent killers" because they can strike healthy-appearing full-term infants without warning.Â The signs, when present, can be subtle, difficult to detect, or easy to mistake for other, more common neonatal pathologies, requires a high index of suspicion to include an IEM in the differential diagnosis of an initially healthy full-term baby who begins to display hypoglycemia or poor feeding (Conway-Orgel, M., 2007, Enns, G.M., 2005).
Failures of energy production or utilization result from defects in the liver, myocardium, muscle, or brain and disrupt cytoplasmic or mitochondrial energy production, including the fatty acid oxidation disorders and the congenital lactic acidemias, present with a variety of findings, but a consistent symptom is hypoglycemia with clinical features are lactic acidosis, hypotonia, and cardiac involvement (Saudubray, J.M., 2002) while hypoglycemia related to fasting can signal a fatty acid oxidation disorder, while hypoglycemia following eating is characteristic of hereditary fructose intolerance (Garganta, C.L., 2005).
A multifactorialÂ diseaseÂ has a combination of distinctive characteristics that can be differentiated from clear-cut Mendelian or sex-limited conditions including theÂ diseaseÂ can occur in isolation and affected children born to unaffected parents. Although familial aggregation is also common, there is no clearÂ Mendelian pattern of inheritance, Environmental influencesÂ can increase or decrease the risk of theÂ disease, theÂ diseaseÂ occurs more frequently in one gender than in the other, but it is not aÂ sex-limitedÂ trait. In addition, first-degree relatives of individuals belonging to the more rarely affected gender have a higher risk of bearing theÂ disease. TheÂ concordanceÂ rates, is a measure of the rate at which both twins bear a specificÂ disease. TheÂ diseaseÂ occurs more frequently in a specific ethnic group (i.e., Caucasians, Africans, Asians, Hispanics, etc.) (Lobo, Ingrid, 2008) in monozygotic andÂ dizygotic twinsÂ contradict Mendelian proportions. On a pedigree, polygenic diseases do tend to run in families, but the inheritance does not fit simple patterns as withÂ MendelianÂ diseases (Burmeister, Margit, 1999).
Table No. 20.4: Multifactorial diseases
Inflammatory bowel disease
Inflammatory bowel disease
20.4.3 Monogenic and multigenic diseases
Monogenic diseases result from modifications in a single gene occurring in all cells of the body and they affect millions of people worldwide as scientists currently estimate that over 10,000 of human diseases (Ikonen, E. 2006). According to WHO, single-gene or monogenic diseases can be classified into three main categories like Dominant, Recessive and X-linke and the global prevalence of all single gene diseases at birth is approximately 10/1000 (WHO, 2012). Thalassaemia is a blood related genetic disorder which involves the absence of or errors in genes responsible for production of haemoglobin, a protein present in the red blood cells while sickle-cell anemia is a blood related disorder that affects the haemoglobin molecule, and causes the entire blood cell to change shape under stressed conditions (Weatherall, D. J., 2000). Haemophilia is a hereditary bleeding disorder, in which there is a partial or total lack of an essential blood clotting factor, lifelong disorder, that results in excessive bleeding, and many times spontaneous bleeding. Haemophilia A is the most common form, referred to as classical haemophilia. It is the result of a deficiency in clotting factor 8, while haemophilia B is a deficiency in clotting factor 9, a sex-linked recessive disorder (WHO, 2012).
Cystic Fibrosis is a genetic disorder that affects the respiratory, digestive and reproductive systems involving the production of abnormally thick mucus linings in the lungs and can lead to fatal lung infections. The disease can also result in various obstructions of the pancreas, hindering digestion (WHO, 2012). Tay-Sachs disease is a fatal genetic disorder in which harmful quantities of a fatty substance called ganglioside GM2 accumulate in the nerve cells in the brain (WHO, 2012). This is caused by a decrease in the functioning of the hexosaminidase A enzyme. The Fragile X syndrome is caused by a "fragile" site at the end of the long arm of the X-chromosome. It is a genetic disorder that manifests itself through a complex range of behavioral and cognitive phenotypes (McMillan, J., 2006).
20.5. Nutrigenomics and communication
Nutrient-gene interactions are responsible for maintaining health and preventing or delaying disease. Unbalanced diets for a given genotype lead to chronic diseases such as obesity, diabetes, cardiovascular, and are likely to contribute to increased severity and/or early-onset of many age-related diseases. Many nutrition and many genetic studies still fail to properly include both variables in the design, execution, and analyses of human, laboratory animal, or cell culture experiments (Kaput, J., 2006). The complexity of nutrient-gene interaction has led to the realization that strategic international alliances are needed to improve the completeness of nutrigenomic studies, a task beyond the capabilities of a single laboratory team. Eighty-eight researchers from twenty two countries recently outlined the issues and challenges for harnessing the nutritional genomics for public and personal health. The next step in the process of forming productive international alliances is the development of a virtual center for organizing collaborations and communications that foster resources sharing, best practices improvements, and creation of databases. There is a requirement of nutrigenomics information portal, a web-based resource for the international nutrigenomics society. This portal aims at becoming the prime source of information and interaction for nutrigenomics scientists through a collaborative effort (Kaput, J., 2006).
20.6. Nutrigenomics and bioactive nutrients
20.6.1 Elk Antler Velvet
Elk Antler Velvet (EAV) is the fast -growing, soft cartilaginous tissue that develops out of the frontal bone of the Cervus species (which includes elk, deer, caribou, wapiti and reindeer) that rises from skin covered pedicles before it calicifies and hardens. Antlers are unique in nature and different from horns because they are naturally re-grown and cut off each year. Elk antler velvet, pumped tight with blood and pulsing with hormones, is the most regenerative mammal tissue known, capable of growing over half an inch in one day.
The increased energy, improved movement, enhanced resistance to disease, increased blood flow, promotion of rapid healing in tissues and bones, relief of symptoms in arthritis and gout, and pain reduction associated with disease or injury to muscles and joints. Active ingredients have been found to include a variety of minerals, proteins, collagens, fatty acids, and glycosaminoglycans (GAG) in varying concentrations.
EAV is an excellent, renewable source of chondronitin sulfate (CSA), glucosamine sulfate, type II collagen and prostaglandins. The research shows the benefits for joint maintenance and specifically arthritis. They have exhibited the ability to restore the integrity to the joints, prevent and repair damage to and breakdown of cartilage and collagenous tissues, reduce inflammation and pain and protect and maintain the synovial membranes and fluids. One study showed type II collagen to significantly reduce pain and swelling 80 percent of participants with juvenile rheumatoid arthritis. Another study from China demonstrated accelerated bone fracture healing by stimulating chondrocytes (cartilage producing cells) and osteoblasts (bone synthesizing cells). Other studies show these and other components have a variety of healing contributions.
Polymeric-N-acetyl-glucosamine accelerates wound healing by as much as 42 percent by stimulating epidermal growth factor (EGF). In a double-blind study, Pantrocrine, a specific extract of EAV, significantly aided recovery from cervical injuries while use in animal studies enabled quick recovery from whiplash-like injuries. In addition, Dr. James Suttie, a New Zealand researcher, discovered neutrotrophin , a powerful nerve growth factor, in EAV.
A variety of cardiovascular benefits have been confirmed, including CSA is reversing arteriosclerosis and dramatically improving circulation. Dr. Lester Morrison reports that for some, CSA may reduce incidence of fatal heart attacks and strokes by over 400 percent. Increasing the formation and oxygen carrying capacity of red blood cells, strengthening the pulse, reducing blood clotting, and lowering of cholesterol have all been evidenced by research on EAV.
20.6.2 Vegan Chyawanprash
This formula has a basis in one of India's most famous anti-aging recipes - Chyawanprash. According to Ayurveda, Chyawanprash comes under the category of 'Rasayana' which aims at maintaining youthfulness, vigor, vitality of the body and keeping away aging process, senility and debility. It maintains the proper functioning of the cells and rejuvenates the cells and also keeps away diseases. The Rasayanas are mean to impart long, healthy, disease free life, intelligence, power of memory, youth and luster. It is the most popular rejuvenating Ayurvedic tonic in India having a consistency of Jam and consisting of about 35 natural herbs including Amla (Embellica Officinalis) the richest natural source of vitamin C, works on the immune system of the body protecting body against everyday infections like cough cold and fever and thus it is very useful in children, old persons, tubercular patients and debilitated persons.
Mangosteen is carefully cultivated from an organic farm in Thailand under the most stringent conditions for