Jump to content

Nutritional genomics: Difference between revisions

From Wikipedia, the free encyclopedia
Content deleted Content added
rm advertising
Emwallac (talk | contribs)
mNo edit summary
 
(28 intermediate revisions by 17 users not shown)
Line 1: Line 1:
{{Short description|Science of the Effects of Nutrition on Genes}}
'''Nutritional genomics''', also known as '''nutrigenomics''', is a science studying the relationship between [[human genome]], [[human nutrition]] and health. People in the field work toward developing an understanding of how the whole body responds to a food via [[systems biology]], as well as single gene/single food compound relationships.<ref name=Neeha2013>{{cite journal | last1 = Neeha | first1 = V. S. | last2 = Kinth | first2 = P. | year = 2013 | title = Nutrigenomics research: a review | journal = Journal of Food Science and Technology | volume = 50 | issue = 3| pages = 415–428 | doi=10.1007/s13197-012-0775-z| pmc = 3602567 | pmid=24425937}}</ref><ref name="FenechEl-Sohemy2011">{{cite journal|last1=Fenech|first1=Michael|last2=El-Sohemy|first2=Ahmed|last3=Cahill|first3=Leah|last4=Ferguson|first4=Lynnette R.|last5=French|first5=Tapaeru-Ariki C.|last6=Tai|first6=E. Shyong|last7=Milner|first7=John|last8=Koh|first8=Woon-Puay|last9=Xie|first9=Lin|last10=Zucker|first10=Michelle|last11=Buckley|first11=Michael|last12=Cosgrove|first12=Leah|last13=Lockett|first13=Trevor|last14=Fung|first14=Kim Y.C.|last15=Head|first15=Richard|title=Nutrigenetics and Nutrigenomics: Viewpoints on the Current Status and Applications in Nutrition Research and Practice|journal=Journal of Nutrigenetics and Nutrigenomics|volume=4|issue=2|year=2011|pages=69–89|issn=1661-6758|doi=10.1159/000327772|pmc=3121546|pmid=21625170}}</ref> Nutritional genomics or Nutrigenomics is the relation between food and inherited genes, it was first expressed in 2001.
'''Nutritional genomics''', also known as '''nutrigenomics''', is a science studying the relationship between [[human genome]], [[human nutrition]] and health. People in the field work toward developing an understanding of how the whole body responds to a food via [[systems biology]], as well as single gene/single food compound relationships.<ref name=Neeha2013>{{cite journal | last1 = Neeha | first1 = V. S. | last2 = Kinth | first2 = P. | year = 2013 | title = Nutrigenomics research: a review | journal = Journal of Food Science and Technology | volume = 50 | issue = 3| pages = 415–428 | doi=10.1007/s13197-012-0775-z| pmc = 3602567 | pmid=24425937}}</ref><ref name="FenechEl-Sohemy2011">{{cite journal|last1=Fenech|first1=Michael|last2=El-Sohemy|first2=Ahmed|last3=Cahill|first3=Leah|last4=Ferguson|first4=Lynnette R.|last5=French|first5=Tapaeru-Ariki C.|last6=Tai|first6=E. Shyong|last7=Milner|first7=John|last8=Koh|first8=Woon-Puay|last9=Xie|first9=Lin|last10=Zucker|first10=Michelle|last11=Buckley|first11=Michael|last12=Cosgrove|first12=Leah|last13=Lockett|first13=Trevor|last14=Fung|first14=Kim Y.C.|last15=Head|first15=Richard|title=Nutrigenetics and Nutrigenomics: Viewpoints on the Current Status and Applications in Nutrition Research and Practice|journal=Journal of Nutrigenetics and Nutrigenomics|volume=4|issue=2|year=2011|pages=69–89|issn=1661-6758|doi=10.1159/000327772|pmc=3121546|pmid=21625170}}</ref> Nutritional genomics or Nutrigenomics is the relation between food and inherited genes, it was first expressed in 2001.<ref>{{Cite journal|last=Peregrin|first=Tony|date=2001|title=The new frontier of nutrition science: Nutrigenomics|journal=Journal of the American Dietetic Association|url=https://www.proquest.com/openview/a9c2b504123a00a9ea4f66236489116e/1?pq-origsite=gscholar&cbl=49142|volume=101|issue=11|page=1306|doi=10.1016/S0002-8223(01)00309-1|pmid=11716306}}</ref><ref>{{Cite web |date=2023-09-05 |title=PHBI – Pharmagreen Starts Sales of MaxGenomicTM Supplement on Amazon.com and Develops Its Next Pre-Workout Formulation |url=https://finance.yahoo.com/news/phbi-pharmagreen-starts-sales-maxgenomictm-110000863.html |access-date=2024-02-16 |website=Yahoo Finance |language=en-US}}</ref>

<ref>{{Cite journal|last=Peregrin|first=Tony|date=2001|title=The new frontier of nutrition science: Nutrigenomics|journal=Journal of the American Dietetic Association|url=https://search.proquest.com/openview/a9c2b504123a00a9ea4f66236489116e/1?pq-origsite=gscholar&cbl=49142|volume=101|issue=11|page=1306|doi=10.1016/S0002-8223(01)00309-1|pmid=11716306}}</ref>


== Introduction ==
== Introduction ==
The term "nutritional genomics" is an umbrella term including several subcategories, such as nutrigenetics, nutrigenomics, and nutritional epigenetics. Each of these subcategories explain some aspect of how genes react to nutrients and express specific phenotypes, like disease risk.<ref name=":0">{{Cite journal|last1=Camp|first1=Kathryn M.|last2=Trujillo|first2=Elaine|date=February 2014|title=Position of the Academy of Nutrition and Dietetics: Nutritional Genomics|journal=Journal of the Academy of Nutrition and Dietetics|volume=114|issue=2|pages=299–312|doi=10.1016/j.jand.2013.12.001|pmid=24439821|issn=2212-2672}}</ref> There are several applications for nutritional genomics, for example how much nutritional intervention and therapy can the successfully used for disease prevention and treatment.<ref name=":0" />
The term "nutritional genomics" is an umbrella term including several subcategories, such as nutrigenetics, nutrigenomics, and [[nutritional epigenetics]]. Each of these subcategories explain some aspect of how genes react to nutrients and express specific phenotypes, like disease risk.<ref name=":0">{{Cite journal|last1=Camp|first1=Kathryn M.|last2=Trujillo|first2=Elaine|date=February 2014|title=Position of the Academy of Nutrition and Dietetics: Nutritional Genomics|journal=Journal of the Academy of Nutrition and Dietetics|volume=114|issue=2|pages=299–312|doi=10.1016/j.jand.2013.12.001|pmid=24439821|issn=2212-2672|doi-access=free}}</ref> There are several applications for nutritional genomics, for example how much nutritional intervention and therapy can successfully be used for disease prevention and treatment.<ref name=":0" />


==Background and preventive health==
==Background and Preventive Health==
Nutritional science originally emerged as a field that studied individuals lacking certain nutrients and the subsequent effects,<ref name=Neeha2013/> such as the disease [[scurvy]] which results from a lack of vitamin C. As other diseases closely related to diet (but not deficiency), such as obesity, became more prevalent, nutritional science expanded to cover these topics as well.<ref name=Neeha2013/> Nutritional research typically focuses on preventative measure, trying to identify what nutrients or foods will raise or lower risks of diseases and damage to the human body.
Nutritional science originally emerged as a field that studied individuals lacking certain nutrients and the subsequent effects,<ref name=Neeha2013/> such as the disease [[scurvy]] which results from a lack of vitamin C. As other diseases closely related to diet (but not deficiency), such as obesity, became more prevalent, nutritional science expanded to cover these topics as well.<ref name=Neeha2013/> Nutritional research typically focuses on preventative measure, trying to identify what nutrients or foods will raise or lower risks of diseases and damage to the human body.<ref>{{Cite web |last=Alvaro |date=2022-12-15 |title=Efficient use of phosphorus in production animals |url=https://nutrinews.com/en/efficient-use-of-phosphorus-in-production-animals/ |access-date=2024-02-16 |website=nutriNews, la revista de nutrición animal |language=en}}</ref><ref>{{Cite web |last=nutraingredients-asia.com |date=2023-08-15 |title=Growth Asia 2023: Nestle to share exclusive insights on precision nutrition from a product perspective |url=https://www.nutraingredients-asia.com/Article/2023/08/15/nestle-to-share-exclusive-insights-on-precision-nutrition-at-growth-asia-summit-2023 |access-date=2024-02-16 |website=nutraingredients-asia.com |language=en-GB}}</ref>


For example, [[Prader–Willi syndrome]], a disease whose most distinguishing factor is insatiable appetite, has been specifically linked to an epigenetic pattern in which the paternal copy in the chromosomal region is erroneously deleted, and the maternal loci is inactivated by over methylation.<ref>{{cite journal | pmc = 3717174|doi= 10.1111/nyas.12020 | pmid=23360386 | volume=1281 | title=The genetics of human obesity | year=2013 | journal=Ann N Y Acad Sci | pages=178–90 | last1 = Xia | first1 = Q | last2 = Grant | first2 = SF}}</ref>&nbsp;Yet, although certain disorders may be linked to certain [[single-nucleotide polymorphism]]s (SNPs) or other localized patterns, variation within a population may yield many more polymorphisms.<ref name=":6">Bisen, Prakash A.; Debnath, Mousumi; Prasad, Godavarthi B.K.S. (2010).&nbsp;''Molecular Dianostics: Promises and Possibilities''. Springer Science & Business Media. p.&nbsp;26.{{ISBN|9048132614}}.</ref>
For example, [[Prader–Willi syndrome]], a disease whose most distinguishing factor is insatiable appetite, has been specifically linked to an epigenetic pattern in which the paternal copy in the chromosomal region is erroneously deleted, and the maternal loci is inactivated by over [[methylation]].<ref>{{cite journal | pmc = 3717174|doi= 10.1111/nyas.12020 | pmid=23360386 | volume=1281 | title=The genetics of human obesity | year=2013 | journal=Ann N Y Acad Sci | pages=178–90 | last1 = Xia | first1 = Q | last2 = Grant | first2 = SF}}</ref>&nbsp;Yet, although certain disorders may be linked to certain [[single-nucleotide polymorphism]]s (SNPs) or other localized patterns, variation within a population may yield many more polymorphisms.<ref name=":6">Bisen, Prakash A.; Debnath, Mousumi; Prasad, Godavarthi B.K.S. (2010).&nbsp;''Molecular Dianostics: Promises and Possibilities''. Springer Science & Business Media. p.&nbsp;26.{{ISBN|9048132614}}.</ref>
== Mediterranean diet ==
The [[Mediterranean diet]] refers to naturally occurring foods native to Greece, Italy and Spain before globalization of food products in the 20th century. The diet includes relatively high consumption of fruit, vegetables, olive oil, legumes, whole grains and moderate amounts of red wine.<ref>Shannon, O. M., Ashor, A. W., Scialo, F., Saretzki, G., Martin-Ruiz, C., Lara, J., Matu, J., Griffiths, A., Robinson, N., Lillà, L., Stevenson, E., Stephan, B. C. M., Minihane, A. M., Siervo, M., & Mathers, J. C. (2021). Mediterranean diet and the hallmarks of ageing.&nbsp;European journal of clinical nutrition,&nbsp;75(8), 1176–1192. https://doi.org/10.1038/s41430-020-00841-x
</ref> Foods with increased fat and dairy are minimally consumed. Some nutritional genomics studies have pointed towards the Mediterranean diet to be most nutritionally beneficial. It has been positively linked towards decreased mortality by providing protective agents against metabolic diseases, cardiovascular disease and several types of cancer. These benefits have been attributed to the abundance of dietary compounds present in Mediterranean staples. Examples of this include ''[[Curcuma longa]]'' (turmeric), [[resveratrol]], [[lycopene]], [[capsaicin]], [[quercetin]], and [[polyphenol]]s in extra virgin olive oil. It has been suggested that each of these allegedly bioactive compounds, along with several others, interacts with the body's cellular and molecular function, gene expression and epigenome to prevent [[angiogenesis]] and the development of [[neurodegenerative disease]].<ref>Divella R, Daniele A, Savino E, Paradiso A. Anticancer Effects of Nutraceuticals in the Mediterranean Diet: An Epigenetic Diet Model. Cancer Genomics Proteomics. 2020 Jul-Aug;17(4):335-350. doi: 10.21873/cgp.20193. </ref>


== Applications ==
== Applications ==
The applications of nutritional genomics are multiple. With personalized assessment some disorders ([[diabetes]], metabolic syndrome) can be identified. Nutrigenomics can help with personalized health and nutrition intake by assessing individuals and make specific nutritional requirements.<ref>{{Cite web|last=Cameron|first=Louise|date=9 November 2016|title=Nutrigenomics - looking at the individual within their nutritional environment|url=https://www.phgfoundation.org/blog/nutrigenomics-looking-at-the-individual}}</ref> The focus is in the prevention and the correction of specific genetic disorders. Examples of genetic related disorders that improve with nutritional correction are obesity, [[Coronary artery disease|coronary heart disease]] (CHD), hypertension and diabetes mellitus type 1.<ref>{{Cite book|last=Information (US)|first=National Center for Biotechnology|url=https://www.ncbi.nlm.nih.gov/books/NBK22259/|title=Nutritional and Metabolic Diseases|date=1998|publisher=National Center for Biotechnology Information (US)|language=en}}</ref> Genetic disorders that can often be prevented by proper nutritional intake of parents include [[spina bifida]], alcoholism and [[Phenylketonuria|phenylketouria]].
The applications of nutritional genomics are multiple. With personalized assessment some disorders ([[diabetes]], metabolic syndrome) can be identified. Nutrigenomics can help with personalized health and nutrition intake by assessing individuals and make specific nutritional requirements.<ref>{{Cite web|last=Cameron|first=Louise|date=9 November 2016|title=Nutrigenomics - looking at the individual within their nutritional environment|url=https://www.phgfoundation.org/blog/nutrigenomics-looking-at-the-individual}}</ref> The focus is in the prevention and the correction of specific genetic disorders. Examples of genetic related disorders that improve with nutritional correction are obesity, [[Coronary artery disease|coronary heart disease]] (CHD), hypertension and diabetes mellitus type 1.<ref>{{Cite book|last=Information (US)|first=National Center for Biotechnology|url=https://www.ncbi.nlm.nih.gov/books/NBK22259/|title=Nutritional and Metabolic Diseases|date=1998|publisher=National Center for Biotechnology Information (US)|language=en}}</ref> Genetic disorders that can often be prevented by proper nutritional intake of parents include [[spina bifida]], alcoholism and [[Phenylketonuria|phenylketouria]].


'''Coronary heart disease'''
===Coronary heart disease===


Genes tied to nutrition manifest themselves through the body's sensitivity to food. In studies about CHD, there is a relationship between the disease and the presence of two alleles found at E and B apolipoprotein loci.<ref>{{Cite book|last=Health|first=National Research Council (US) Committee on Diet and|url=https://www.ncbi.nlm.nih.gov/books/NBK218767/|title=Genetics and Nutrition|date=1989|publisher=National Academies Press (US)|language=en}}</ref> These loci differences result in individualized reactions to the consumption of lipids. Some people experience increased weight gain and greater risk of CHD whereas others with different loci do not. Research has shown a direct correlation between the decrease risk of CHD and the decrease consumption of lipids across all populations.<ref>{{Cite book|last=DeBruyne, Linda K.|title=Nutrition & diet therapy|others=Pinna, Kathryn,, Whitney, Ellie|date=8 January 2015|isbn=978-1-305-11040-3|edition=Ninth|location=Australia|oclc=910704712}}</ref>
Genes tied to nutrition manifest themselves through the body's sensitivity to food. In studies about CHD, there is a relationship between the disease and the presence of two alleles found at E and B [[apolipoprotein]] loci.<ref>{{Cite book|last=Health|first=National Research Council (US) Committee on Diet and|url=https://www.ncbi.nlm.nih.gov/books/NBK218767/|title=Genetics and Nutrition|date=1989|publisher=National Academies Press (US)|language=en}}</ref> These loci differences result in individualized reactions to the consumption of lipids. Some people experience increased weight gain and greater risk of CHD whereas others with different loci do not. Research has shown a direct correlation between the decrease risk of CHD and the decrease consumption of lipids across all populations.<ref>{{Cite book|last=DeBruyne, Linda K.|title=Nutrition & diet therapy|others=Pinna, Kathryn,, Whitney, Ellie|date=8 January 2015|isbn=978-1-305-11040-3|edition=Ninth|location=Australia|oclc=910704712}}</ref>


=== Obesity ===
=== Obesity ===
Obesity is one of the most widely studied topics in nutritional genomics. Due to genetic variations among individuals, each person could respond to diet differently. By exploring the interaction between dietary pattern and genetic factors, the field aims to suggest dietary changes that could prevent or reduce obesity.<ref name=Doo2015>{{Cite journal|title = Obesity: interactions of genome and nutrients intake|journal = Preventive Nutrition and Food Science|date = 2015-03-01|issn = 2287-1098|pmc = 4391534|pmid = 25866743|pages = 1–7|volume = 20|issue = 1|doi = 10.3746/pnf.2015.20.1.1|first1 = Miae|last1 = Doo|first2 = Yangha|last2 = Kim}}</ref>
Obesity is one of the most widely studied topics in nutritional genomics. Due to genetic variations among individuals, each person could respond to diet differently. By exploring the interaction between dietary pattern and genetic factors, the field aims to suggest dietary changes that could prevent or reduce obesity.<ref name=Doo2015>{{Cite journal|title = Obesity: interactions of genome and nutrients intake|journal = Preventive Nutrition and Food Science|date = 2015-03-01|issn = 2287-1098|pmc = 4391534|pmid = 25866743|pages = 1–7|volume = 20|issue = 1|doi = 10.3746/pnf.2015.20.1.1|first1 = Miae|last1 = Doo|first2 = Yangha|last2 = Kim}}</ref>


There appear to be some [[Single-nucleotide polymorphism|SNPs]] that make it more likely that a person will gain weight from a high fat diet; for people with AA genotype in the [[FTO gene]] showed a higher BMI compared those with TT genotype when having high fat or low carbohydrate dietary intake.<ref name=Doo2015/> The [[Apolipoprotein B|APO B]] SNP rs512535 is another diet-related variation; the A/G heterozygous genotype was found to have association with obesity (in terms of BMI and waist circumference) and for individuals with habitual high fat diet (>35% of energy intake), while individuals with GG homozygous genotype are likely to have a higher BMI compared to AA allele carriers. However, this difference is not found in low fat consuming group (<35% of energy intake).<ref name=Doo2015/>
There appear to be some SNPs that make it more likely that a person will gain weight from a high fat diet; for people with AA genotype in the [[FTO gene]] showed a higher BMI compared those with TT genotype when having high fat or low carbohydrate dietary intake.<ref name=Doo2015/> The [[Apolipoprotein B|APO B]] SNP rs512535 is another diet-related variation; the A/G heterozygous genotype was found to have association with obesity (in terms of BMI and waist circumference) and for individuals with habitual high fat diet (>35% of energy intake), while individuals with GG homozygous genotype are likely to have a higher BMI compared to AA allele carriers. However, this difference is not found in low fat consuming group (<35% of energy intake).<ref name=Doo2015/>


=== Phenylketonuria ===
=== Phenylketonuria ===
Phenylketonuria, otherwise known as PKU, is a uncommon autosomal recessive metabolic disorder that takes effect postpartum but the debilitating symptoms can be reversed with nutritional intervention.<ref name=":0" />
Phenylketonuria, otherwise known as PKU, is an uncommon autosomal recessive metabolic disorder that takes effect postpartum but the debilitating symptoms can be reversed with nutritional intervention.<ref name=":0" />


==See also==
==See also==
Line 31: Line 33:
* [[Foodomics]]
* [[Foodomics]]
* [[Genomics]]
* [[Genomics]]
* [[Global Health Share Initiative]]
* [[Nutriepigenomics]]
* [[Nutriepigenomics]]
* [[Nutriomics]]
* [[Nutriomics]]
Line 45: Line 48:
{{DEFAULTSORT:Nutritional Genomics}}
{{DEFAULTSORT:Nutritional Genomics}}
[[Category:Nutritional science]]
[[Category:Nutritional science]]
[[Category:Food science]]
[[Category:Genetic mapping]]
[[Category:Genetic mapping]]
[[Category:Genomics]]
[[Category:Genomics]]

Latest revision as of 00:53, 14 April 2024

Nutritional genomics, also known as nutrigenomics, is a science studying the relationship between human genome, human nutrition and health. People in the field work toward developing an understanding of how the whole body responds to a food via systems biology, as well as single gene/single food compound relationships.[1][2] Nutritional genomics or Nutrigenomics is the relation between food and inherited genes, it was first expressed in 2001.[3][4]

Introduction

[edit]

The term "nutritional genomics" is an umbrella term including several subcategories, such as nutrigenetics, nutrigenomics, and nutritional epigenetics. Each of these subcategories explain some aspect of how genes react to nutrients and express specific phenotypes, like disease risk.[5] There are several applications for nutritional genomics, for example how much nutritional intervention and therapy can successfully be used for disease prevention and treatment.[5]

Background and Preventive Health

[edit]

Nutritional science originally emerged as a field that studied individuals lacking certain nutrients and the subsequent effects,[1] such as the disease scurvy which results from a lack of vitamin C. As other diseases closely related to diet (but not deficiency), such as obesity, became more prevalent, nutritional science expanded to cover these topics as well.[1] Nutritional research typically focuses on preventative measure, trying to identify what nutrients or foods will raise or lower risks of diseases and damage to the human body.[6][7]

For example, Prader–Willi syndrome, a disease whose most distinguishing factor is insatiable appetite, has been specifically linked to an epigenetic pattern in which the paternal copy in the chromosomal region is erroneously deleted, and the maternal loci is inactivated by over methylation.[8] Yet, although certain disorders may be linked to certain single-nucleotide polymorphisms (SNPs) or other localized patterns, variation within a population may yield many more polymorphisms.[9]

Mediterranean diet

[edit]

The Mediterranean diet refers to naturally occurring foods native to Greece, Italy and Spain before globalization of food products in the 20th century. The diet includes relatively high consumption of fruit, vegetables, olive oil, legumes, whole grains and moderate amounts of red wine.[10] Foods with increased fat and dairy are minimally consumed. Some nutritional genomics studies have pointed towards the Mediterranean diet to be most nutritionally beneficial. It has been positively linked towards decreased mortality by providing protective agents against metabolic diseases, cardiovascular disease and several types of cancer. These benefits have been attributed to the abundance of dietary compounds present in Mediterranean staples. Examples of this include Curcuma longa (turmeric), resveratrol, lycopene, capsaicin, quercetin, and polyphenols in extra virgin olive oil. It has been suggested that each of these allegedly bioactive compounds, along with several others, interacts with the body's cellular and molecular function, gene expression and epigenome to prevent angiogenesis and the development of neurodegenerative disease.[11]

Applications

[edit]

The applications of nutritional genomics are multiple. With personalized assessment some disorders (diabetes, metabolic syndrome) can be identified. Nutrigenomics can help with personalized health and nutrition intake by assessing individuals and make specific nutritional requirements.[12] The focus is in the prevention and the correction of specific genetic disorders. Examples of genetic related disorders that improve with nutritional correction are obesity, coronary heart disease (CHD), hypertension and diabetes mellitus type 1.[13] Genetic disorders that can often be prevented by proper nutritional intake of parents include spina bifida, alcoholism and phenylketouria.

Coronary heart disease

[edit]

Genes tied to nutrition manifest themselves through the body's sensitivity to food. In studies about CHD, there is a relationship between the disease and the presence of two alleles found at E and B apolipoprotein loci.[14] These loci differences result in individualized reactions to the consumption of lipids. Some people experience increased weight gain and greater risk of CHD whereas others with different loci do not. Research has shown a direct correlation between the decrease risk of CHD and the decrease consumption of lipids across all populations.[15]

Obesity

[edit]

Obesity is one of the most widely studied topics in nutritional genomics. Due to genetic variations among individuals, each person could respond to diet differently. By exploring the interaction between dietary pattern and genetic factors, the field aims to suggest dietary changes that could prevent or reduce obesity.[16]

There appear to be some SNPs that make it more likely that a person will gain weight from a high fat diet; for people with AA genotype in the FTO gene showed a higher BMI compared those with TT genotype when having high fat or low carbohydrate dietary intake.[16] The APO B SNP rs512535 is another diet-related variation; the A/G heterozygous genotype was found to have association with obesity (in terms of BMI and waist circumference) and for individuals with habitual high fat diet (>35% of energy intake), while individuals with GG homozygous genotype are likely to have a higher BMI compared to AA allele carriers. However, this difference is not found in low fat consuming group (<35% of energy intake).[16]

Phenylketonuria

[edit]

Phenylketonuria, otherwise known as PKU, is an uncommon autosomal recessive metabolic disorder that takes effect postpartum but the debilitating symptoms can be reversed with nutritional intervention.[5]

See also

[edit]

References

[edit]
  1. ^ a b c Neeha, V. S.; Kinth, P. (2013). "Nutrigenomics research: a review". Journal of Food Science and Technology. 50 (3): 415–428. doi:10.1007/s13197-012-0775-z. PMC 3602567. PMID 24425937.
  2. ^ Fenech, Michael; El-Sohemy, Ahmed; Cahill, Leah; Ferguson, Lynnette R.; French, Tapaeru-Ariki C.; Tai, E. Shyong; Milner, John; Koh, Woon-Puay; Xie, Lin; Zucker, Michelle; Buckley, Michael; Cosgrove, Leah; Lockett, Trevor; Fung, Kim Y.C.; Head, Richard (2011). "Nutrigenetics and Nutrigenomics: Viewpoints on the Current Status and Applications in Nutrition Research and Practice". Journal of Nutrigenetics and Nutrigenomics. 4 (2): 69–89. doi:10.1159/000327772. ISSN 1661-6758. PMC 3121546. PMID 21625170.
  3. ^ Peregrin, Tony (2001). "The new frontier of nutrition science: Nutrigenomics". Journal of the American Dietetic Association. 101 (11): 1306. doi:10.1016/S0002-8223(01)00309-1. PMID 11716306.
  4. ^ "PHBI – Pharmagreen Starts Sales of MaxGenomicTM Supplement on Amazon.com and Develops Its Next Pre-Workout Formulation". Yahoo Finance. 2023-09-05. Retrieved 2024-02-16.
  5. ^ a b c Camp, Kathryn M.; Trujillo, Elaine (February 2014). "Position of the Academy of Nutrition and Dietetics: Nutritional Genomics". Journal of the Academy of Nutrition and Dietetics. 114 (2): 299–312. doi:10.1016/j.jand.2013.12.001. ISSN 2212-2672. PMID 24439821.
  6. ^ Alvaro (2022-12-15). "Efficient use of phosphorus in production animals". nutriNews, la revista de nutrición animal. Retrieved 2024-02-16.
  7. ^ nutraingredients-asia.com (2023-08-15). "Growth Asia 2023: Nestle to share exclusive insights on precision nutrition from a product perspective". nutraingredients-asia.com. Retrieved 2024-02-16.
  8. ^ Xia, Q; Grant, SF (2013). "The genetics of human obesity". Ann N Y Acad Sci. 1281: 178–90. doi:10.1111/nyas.12020. PMC 3717174. PMID 23360386.
  9. ^ Bisen, Prakash A.; Debnath, Mousumi; Prasad, Godavarthi B.K.S. (2010). Molecular Dianostics: Promises and Possibilities. Springer Science & Business Media. p. 26.ISBN 9048132614.
  10. ^ Shannon, O. M., Ashor, A. W., Scialo, F., Saretzki, G., Martin-Ruiz, C., Lara, J., Matu, J., Griffiths, A., Robinson, N., Lillà, L., Stevenson, E., Stephan, B. C. M., Minihane, A. M., Siervo, M., & Mathers, J. C. (2021). Mediterranean diet and the hallmarks of ageing. European journal of clinical nutrition, 75(8), 1176–1192. https://doi.org/10.1038/s41430-020-00841-x
  11. ^ Divella R, Daniele A, Savino E, Paradiso A. Anticancer Effects of Nutraceuticals in the Mediterranean Diet: An Epigenetic Diet Model. Cancer Genomics Proteomics. 2020 Jul-Aug;17(4):335-350. doi: 10.21873/cgp.20193.
  12. ^ Cameron, Louise (9 November 2016). "Nutrigenomics - looking at the individual within their nutritional environment".
  13. ^ Information (US), National Center for Biotechnology (1998). Nutritional and Metabolic Diseases. National Center for Biotechnology Information (US).
  14. ^ Health, National Research Council (US) Committee on Diet and (1989). Genetics and Nutrition. National Academies Press (US).
  15. ^ DeBruyne, Linda K. (8 January 2015). Nutrition & diet therapy. Pinna, Kathryn,, Whitney, Ellie (Ninth ed.). Australia. ISBN 978-1-305-11040-3. OCLC 910704712.{{cite book}}: CS1 maint: location missing publisher (link)
  16. ^ a b c Doo, Miae; Kim, Yangha (2015-03-01). "Obesity: interactions of genome and nutrients intake". Preventive Nutrition and Food Science. 20 (1): 1–7. doi:10.3746/pnf.2015.20.1.1. ISSN 2287-1098. PMC 4391534. PMID 25866743.