Personalized Nutrition

An interesting paper applying nutrigenetics to health effects of caffeine on blood pressure and cardio vascular disease risks. I quote some of the article's “practical implications”. A good example of going from research to practice:

Moving towards Specific Nutrigenetic Recommendation Algorithms: Caffeine, Genetic Variation and Cardiovascular Risk

http://www.ncbi.nlm....pubmed/27467525

“…Male subjects with the ADORA2A TT (rs5751876) or the ADRA2B II genotypes are more prone to acute surges in BP in response to caffeine-containing beverages. The amount of caffeine used in that study was 3 mg/kg, meaning 210 mg in a 70-kg average subject; for comparison, one small espresso cup yields about 80 mg of caffeine. In practical terms, drinking a double espresso would yield a sufficient amount of caffeine to differentiate the acute SBP increase in ADORA2A TT or ADRA2B II individuals from that of alternative genotypes. Although there are no data to state that these gene variants are associated with an increased cardiovascular risk, it would appear prudent that such individuals, especially if they are hypertensive, refrain from such amounts of acute coffee drinking (grade IIa, LOE B). No statement can be made for females, although prudent recommendations could be similar (grade IIa, LOE C)…”

“…Heavy coffee drinkers (>814 ml) with the low-activity COMT rs4680 AA genotype should be advised to limit their coffee drinking (grade IIb, LOE B)…”

“…Intake of coffee was associated with an increased risk of nonfatal MI only among individuals with slow caffeine metabolism. Findings appear applicable to both male and female, and both to younger and older individuals, perhaps with even greater effects among younger subjects. The risk of nonfatal MI appears to increase selectively in slow caffeine metabolizers already at a level of habitual intake of 2 cups per day. Therefore, slow caffeine metabolizers who are carriers of even one allele with an A>C substitution at position –163 (rs762551) in the CYP1A2 gene should refrain from drinking more than one cup of coffee per day…” (red mine)

An interesting result from the European Food4Me large project (see also my initial post here).

From the conclusion "... Our results provide strong evidence for the effectiveness of a personalized approach, compared with a conventional ‘one size fits all’ approach in achieving dietary change to improve health..."

That is for the good news. For the "bad" news, or at least for what would require more investigation, is that "...we found no evidence that including phenotypic or phenotypic plus genotypic information in the derivation and communication of PN advice enhanced the effectiveness of the intervention compared with personalization of nutrition advice based on evaluation of current individual dietary intake alone..." (bold mine)

I think this tells quite a lot on people and professionals education but also on personal empowerment (made easier by use of AI, as touched previously). Of course this assumes (and we might be still far from clinical validation in every area of investigation) personal nutrition advise based on genotype/phenotype is well grounded scientifically. Also, it tells to me genetics is maybe a small part of the picture which would become much more complete when using the full nutrigenomic approach, including e.g. metabolomics, IMHO.

Effect of personalized nutrition on health-related behaviour change: evidence from the Food4me European randomized controlled trial

http://ije.oxfordjou...ije.dyw186.full

(edit: adding url)

Edited by albedo, 16 August 2016 - 03:05 PM.

I continued to look at the interaction between genetic polymorphisms and isoflavones intake in relation to the risk of prostate cancer.

In my previous post, I looked at the gene estrogen receptor beta, ER-beta (aka ESR2).

Here, I found one of the best and most recent reviews of literature (1) which has a somewhat more critic view quoting, next to the results on ER-beta, also CYP19 (the gene encoding the aromatase enzyme converting testosterone into estrogen) and the SHBG polymorphisms based on the work in ref. 2. You might be interested:

(1) Isoflavones and Prostate Cancer: A Review of Some Critical Issues

http://www.ncbi.nlm....pubmed/26831238

(2) Polymorphisms in the CYP19 Gene May Affect the Positive Correlations between Serum and Urine Phytoestrogen Metabolites and Plasma Androgen Concentrations in Men

http://www.ncbi.nlm....pubmed/16251630

Prophets pointed here to an interesting supplement (Xanthohumol, a metabolite of beer) which might inhibit the cholesteryl ester transfer protein (CETP) rising good cholesterol and thus lowering risks of cardio vascular disease (CVD).

Medical and nutritional interventions should care about the CETP genotype and I wish to log here a couple of papers for the further reading I would like to do, see (1) and (2).

Ref. (1) points to a possible deleterious interaction with statin treatment and ref. (2) gives,  in the Table 1, a complete list of CETP genetic variants with their association to HDL levels.

SNPedia lists in particular 3 SNPs with “reported significance”:

rs708272, also known as Taq1B

rs5882, also known as Ile405Val or I405V

rs2303790, Asp442Gly

and in the summary table gives the respective genotype information in relation to to faster aging, dementia and the possible reduction of CVD risk with moderate alcohol consumption.

A 3^rd paper (3) links nutrigenomics and CVD, despite the cautionary statement: “…Whereas Nutrigenomics cannot be rigorously applied to cardiovascular prevention and treatment at this time, important results are being generated that will serve as the basis to increase the consistency of future research which, in turn, will achieve the necessary level of evidence. At that point, Nutrigenomics will become a reality in dietary personalization, in cardiovascular medicine, and subsequently in optimizing CVD treatment and prevention…” (bold mine)

(1) CETP genotype predicts increased mortality in statin-treated men with proven cardiovascular disease: an adverse pharmacogenetic interaction.

http://www.ncbi.nlm....pubmed/18957472

(2) Genetic-epidemiological evidence on genes associated with HDL cholesterol levels: A systematic in-depth review

https://www.ncbi.nlm...les/PMC2730542/

(3) Nutrigenomics in cardiovascular medicine

http://www.ncbi.nlm....les/PMC2810265/

A nice example of how looking at the Vitamin E status and possibly using a low dose supplementation (e.g. average 300 IU/day) can reduce risks of developing a blood clot which can be life threatening (e.g. after a long flight).

Of course, this is by no means a medical recommendation and you need to discuss with your doctor if you are at risk and mostly if you are already on anticoagulant treatment.

Prothrombin F2 gene “…provides instructions for making a protein called prothrombin (also called coagulation factor II). Coagulation factors are a group of related proteins that are essential for normal blood clotting (hemostasis)…”

The  20210G>A polymorphism (rs1799963) seems to increase prothrombin expression and promote blood clotting (1). The risk is increased for the carriers of the F5 gene 1691A allele SNP (factor V Leiden variant, rs6025) (2).

“…These data suggest that supplementation with vitamin E may reduce the risk of VTE in women, and those with a prior history or genetic predisposition may particularly benefit…” (2)

Efficacy of Vitamin E supplementation can go up to -67% decrease in risk for those with the prothrombin 20210G>A genotype (2)

1. G20210A is a functional mutation in the prothrombin gene; effect on protein levels and 3'-end formation. http://www.ncbi.nlm....pubmed/14717975
2. Effects of random allocation to vitamin E supplementation on the occurrence of venous thromboembolism: report from the Women's Health Study. http://www.ncbi.nlm....pubmed/17846285

An interesting review on the similar molecular pathways between cancer and aging, focusing on telomerase activity, CR, DNA repair, oxidative stress, and the potentially revolutionary role of nutrigenomics:

Nutrigenomics at the Interface of Aging, Lifespan, and Cancer Prevention

https://www.research...ncer_Prevention (ahead of print, Aug 2016)

The percentage of elderly people with associated age-related health deterioration, including cancer, has been increasing for decades. Among age-related diseases, the incidence of cancer has grown substantially, in part because of the overlap of some molecular pathways between cancer and aging. Studies with model organisms suggest that aging and agerelated conditions are manipulable processes that can be modified by both genetic and environmental factors, including dietary habits. Variations in genetic backgrounds likely lead to differential responses to dietary changes and account for some of the inconsistencies found in the literature. The intricacies of the aging process, coupled with the interrelational role of bioactive food components on gene expression, make this review a complex undertaking. Nevertheless, intriguing evidence suggests that dietary habits can manipulate the aging process and/or its consequences and potentially may have unprecedented health benefits. The present review focuses on 4 cellular events: telomerase activity, bioenergetics, DNA repair, and oxidative stress. These processes are linked to both aging and cancer risk, and their alteration in animal models
by selected food components is evident.

Some of the genes we can look at for personalized nutrition recommendations:

 Genes PN.PNG   401.36KB   3 downloads

http://www.nugo.org/...n_Kohlmeier.pdf

A summary of an important meeting by some of the leading scientists in the field:

A systems approach to personalised nutrition: Report on the Keystone Symposium “Human Nutrition, Environment and Health”

https://www.ncbi.nlm...les/PMC5025480/

A possible step toward personalized supplementation. It will be interesting to watch this collaboration developing:

Life Extension™ joins with Insilico Medicine to develop advanced anti-aging technologies utilizing artificial intelligence

http://www.prnewswir...-300280735.html

Advances in computational biology and artificial intelligence used to identify compounds with potential to extend human life

http://www.prnewswir...-300334445.html

(edit: adding links)

Edited by albedo, 08 October 2016 - 02:25 PM.

Maybe to watch if you have children:

Television food advertisement exposure and FTO rs9939609 genotype in relation to excess consumption in children.

https://www.ncbi.nlm...pubmed/27654143

"...Food advertisement exposure was associated with greater caloric consumption of a recently advertised food, and this effect was modified by an FTO genotype..."

The FTO gene and rs9939609 was also studied in this thread, here.

An interesting article on what is going in the commercial space, inclusive a good dose of skepticism:

"Personalized nutrition” isn’t going to solve our diet problems

http://www.vox.com/2...t-nutrition-dna

There are several limitation of this study as also expressed by the authors in the discussion (size, control case, ...) but if concerned I would look anyway at the ZNF259 polymorphism (rs964184 C>G) and proactively check how to limit possible dyslipidemia and metabolic syndrome:

Mirhafez SR, Avan A, Pasdar A, et al. Zinc Finger 259 Gene Polymorphism rs964184 is Associated with Serum Triglyceride Levels and Metabolic Syndrome. International Journal of Molecular and Cellular Medicine. 2016;5(1):8-18.

https://www.ncbi.nlm...les/PMC4916779/

"Metabolic syndrome (MetS) is characterized by a cluster of cardiovascular risk factors that include: abdominal obesity, dyslipidaemia, hypertension, insulin resistance and impaired glucose tolerance. Recent genome wide association studies have identified several susceptibility regions involved in lipid metabolism that are also associated with MetS. We have explored the association of 9 genetic polymorphisms involved in lipid metabolism and hypertension, including: MTHFR C677T, SELE L554F, FGB - 455G>A, GNB3 C825T, ZNF259 C>G, PSRC-1 A>G, CETP I405V, LPL S447X and LPA C>T in 97 subjects with MetS and 96 individuals without MetS who were recruited randomly from Mashhad stroke and heart atherosclerotic disorder (MASHAD) study using a stratified cluster random sampling technique. Anthropometric parameters and biochemical measurements were determined in all the subjects. Genotyping was carried out followed by univariate and multivariate analyses. The subjects with MetS had a higher triglyceride and lower HDL- C. CG+ GG genotypes of ZNF259 polymorphism (rs964184 C>G) and TT+CT genotypes of MTHFR C677T (rs1801133) were associated with MetS, and individuals carrying the G allele for ZNF259 or the T allele for MTHFR polymorphisms were associated with MetS (e.g, odds ratio (OR) for CG+GG genotypes vs. CC wild type: 2.52, CI=1.33-4.77; P=0.005). However, after multiple comparison adjustment, this relationship remained significant only for CG+ GG genotypes of ZNF259 polymorphism. Moreover, the ZNF259 CG+ GG genotypes were associated with increased serum concentrations of triglycerides and LDL-C, compared to the wild type. These data support the necessity for further studies in larger multicenter settings." (bold mine)

Impressive paper (2012) from Prof. Michael Snyder et al. (Stanford) actually analyzing by iPOP (integrative Personal Omics Profiling) his own data set during health and disease periods of time. It gives a good idea where the future of medicine (and possibly nutrition) might be heading. I also report a talk he gave last November in Switzerland on his work. On nutrition he mentioned (about 1:25:25 and on) they are testing lot of supplements on about 100 people but results are not ready yet:

Chen R, Mias GI, Li-pook-than J, et al. Personal omics profiling reveals dynamic molecular and medical phenotypes. Cell. 2012;148(6):1293-307.

https://www.ncbi.nlm...pubmed/22424236

Personal Omics

https://mediaserver....e.ch/play/97787

Impressive paper (2012) from Prof. Michael Snyder et al. (Stanford) actually analyzing by iPOP (integrative Personal Omics Profiling) his own data set during health and disease periods of time. It gives a good idea where the future of medicine (and possibly nutrition) might be heading. I also report a talk he gave last November in Switzerland on his work. On nutrition he mentioned (about 1:25:25 and on) they are testing lot of supplements on about 100 people but results are not ready yet:

 

Chen R, Mias GI, Li-pook-than J, et al. Personal omics profiling reveals dynamic molecular and medical phenotypes. Cell. 2012;148(6):1293-307.

https://www.ncbi.nlm...pubmed/22424236

 

Personal Omics

https://mediaserver....e.ch/play/97787

Thanks for sharing Albedo . Dr. Snyder's talk inspires me to consider doing an (epi)genomic test, which sofar didnot seem useful to me, because I would not know how to interpret most data.

Less motivating, however is that he is dismissive about commercial parties in this field. (See the very last minutes of the video)

You are welcome Harkijn and happy you find the study/talk interesting.

I think he wished to show the rigor and the in depth of the scientific work he carried on his own data to demonstrate the point of what you can possibly do with true personalized medicine and nutrition. He said that the work and analysis were very expensive but I think he could not be possibly dismissive on the industry on one side and at the same time pretend the future of medicine is what he described if industry is not involved, implying decreasing costs and affordability for the people. Rather I imagine he wished to be cautious as interpretation is key, not jumping blindly on wagons which are not yet ready to go.

ISNN (International Society of Nutrigenetics and Nutrigenomics) position paper (Part 1) on the field:

Ferguson LR, De caterina R, Görman U, et al. Guide and Position of the International Society of Nutrigenetics/Nutrigenomics on Personalised Nutrition: Part 1 - Fields of Precision Nutrition. J Nutrigenet Nutrigenomics. 2016;9(1):12-27.

https://www.karger.c...FullText/445350

 ISNN PN status.PNG   37.42KB   3 downloads

Abstract
Diversity in the genetic profile between individuals and specific ethnic groups affects nutrient requirements, metabolism and response to nutritional and dietary interventions. Indeed, individuals respond differently to lifestyle interventions (diet, physical activity, smoking, etc.). The sequencing of the human genome and subsequent increased knowledge regarding human genetic variation is contributing to the emergence of personalized nutrition. These advances in genetic science are raising numerous questions regarding the mode that precision nutrition can contribute solutions to emerging problems in public health, by reducing the risk and prevalence of nutrition-related diseases. Current views on personalized nutrition encompass omics technologies (nutrigenomics, transcriptomics, epigenomics, foodomics, metabolomics, metagenomics, etc.), functional food development and challenges related to legal and ethical aspects, application in clinical practice, and population scope, in terms of guidelines and epidemiological factors. In this context, precision nutrition can be considered as occurring at three levels: (1) conventional nutrition based on general guidelines for population groups by age, gender and social determinants; (2) individualized nutrition that adds phenotypic information about the person’s current nutritional status (e.g. anthropometry, biochemical and metabolic analysis, physical activity, among others), and (3) genotype-directed nutrition based on rare or common gene variation. Research and appropriate translation into medical practice and dietary recommendations must be based on a solid foundation of knowledge derived from studies on nutrigenetics and nutrigenomics. A scientific society, such as the International Society of  Nutrigenetics/Nutrigenomics (ISNN), internationally devoted to the study of nutrigenetics/nutrigenomics, can indeed serve the commendable roles of (1) promoting science and favoring scientific communication and (2) permanently working as a ‘clearing house’ to prevent disqualifying logical jumps, correct or stop unwarranted claims, and prevent the creation of unwarranted expectations in patients and in the general public. In this statement, we are focusing on the scientific aspects of disciplines covering nutrigenetics and nutrigenomics issues. Genetic screening and the ethical, legal, social and economic aspects will be dealt with in subsequent
statements of the Society.

Personalized nutrition importance for Inflammatory Bowel Disease (IBS) and Crohn's disease (CD):

Ferguson LR. Nutritional Modulation of Gene Expression: Might This be of Benefit to Individuals with Crohn's Disease?. Front Immunol. 2015;6:467.

https://www.ncbi.nlm...les/PMC4566049/

The incidence of inflammatory bowel diseases (IBD), including Crohn’s disease (CD), is increasing worldwide, especially in young children and adolescents. Although hospitalized patients are usually provided with enteral or parenteral support, continuing care typically requires a trial-and-error approach to suppressing symptoms and maintaining disease remission. Current nutritional advice does not differ from general population guidelines. International collaborative studies have revealed 163 distinct genetic loci affecting susceptibility to IBD, in some of which host–microbe interactions can be seen to play an important role. The nature of these loci enables a rationale for predicting nutritional requirements that may not be evident through standard therapeutic approaches. Certain recognized nutrients, such as vitamin D and long-chain omega-3 polyunsaturated fatty acids, may be required at higher than anticipated levels. Various phytochemicals, not usually considered in the same class as classic nutrients, could play an important role. Prebiotics and probiotics may also be beneficial. Genomic approaches enable proof of principle of nutrient optimization rather than waiting for disease symptoms to appear and/or progress. We suggest a paradigm shift in diagnostic tools and nutritional therapy for CD, involving a systems biology approach for implementation.

"...The data extracted confirmed a connection between genetics and zinc requirements, although the direction and magnitude of the dietary modification for carriers of specific genotypes could not be defined. This study highlights the need to summarise nutrigenetics studies to enable health professionals to translate scientific evidence into dietary recommendations..."

Day KJ, Adamski MM, Dordevic AL, Murgia C. Genetic Variations as Modifying Factors to Dietary Zinc Requirements-A Systematic Review. Nutrients. 2017;9(2)

Matching your Amino Acid intake to your exome could in future achieve balance between growth and longevity:

Consuming a diet with a relatively low proportion of protein is critical for lifelong health (Le Couteur et al., 2016). However, the costs to early life vigor, reproduction, and low satiety value (Gosby et al., 2011, Solon-Biet et al., 2015, Sørensen et al., 2008) are major detractions. We show that an exome-matched AA composition can reduce voluntary food consumption, and that its enhanced value for growth and reproduction means it can be supplied at low enough levels so as to avoid any cost to lifespan.

http://www.cell.com/...4131(17)30095-5

Interesting find Harkjin. An interesting theoretical template which possibly one day will go into clinical nutrition. I also appreciate the point the authors make of possible kidney disease management by exome matching.

Zipongo Incorporates 23andMe Reports Into Personalized Nutrition Plans

http://finance.yahoo...-130100161.html

Momentum in the market place (I am going to visit Vitafoods Europe 2017 next May):

This time it’s personal: personalised nutrition emerging as next big industry trend

http://www.newfoodma...industry-trend/

Very good review including nutrigenetics approaches to obesity treatments:

Solas M, Milagro FI, Martínez-urbistondo D, Ramirez MJ, Martínez JA. Precision Obesity Treatments Including Pharmacogenetic and Nutrigenetic Approaches. Trends Pharmacol Sci. 2016;37(7):575-93.

http://www.cell.com/...6147(16)30022-0

"...Precision medicine-based pharmacogenetic and nutrigenetic studies concerning the effects of the genetic variation on drug and dietary response are paving the way for personalized treatment of obesity. In this context, health care providers and practitioners could mitigate the obesity epidemic by personalizing these dietary strategies and pharmacotherapies depending on the genotype, accompanying medical manifestations,and drug safety concerns..."

 Obesity nutrigenetics 2.PNG   81.11KB   6 downloads

 Obesity nutrigenetics.PNG   75.58KB   6 downloads

The following paper (2014) argues "...that we are ready for some DNA-based dietary advice in general nutrition and it can be beneficial. Examples of the scientific validity and health utility of gene–diet interactions will be given and the development of guidelines for assessment and validation of benefits will be discussed...".

The Table 1 provides "...Examples of gene–diet interactions that can be considered to be scientifically valid and have potential benefit..."

 GxD scientifically valid.PNG   106.49KB   5 downloads

A large and well conducted study on personalized nutrition using folic acid intervention based on MTHFR genotype (rs1801133 or C677T) for people on high BP treatment (enalapril)

Zhao M, Wang X, He M, et al. Homocysteine and Stroke Risk: Modifying Effect of Methylenetetrahydrofolate Reductase C677T Polymorphism and Folic Acid Intervention. Stroke. 2017

https://www.ncbi.nlm...pubmed/28360116

Studying environmental exposures (nutrition is one element of exposure in the so called exposome) impacting the risk of diabetes 2, I pop into this very interesting study which uses the same statistical methods as in genetic GWAS studies (e.g. Manhattan Plots in Fig 2) to find associations and found a surprising result with Vitamin E (form: gamma-tocopherol) associated with increasing risk of the disease (and beta carotene decreasing the risk):

"...We discovered a vitamin that increased risk for T2D. Surprisingly, γ-tocopherol, a form of vitamin E, was highly significantly and positively associated with T2D (final adjusted OR 1.5; 95% CI 1.3–1.7; p<0.001) in two cohorts (adjusted OR of 1.8 and 1.6; p = 0.02 and 0.01 for 1999–2000 and 2001–2002 cohorts) and nearly significant in the two others (adjusted OR of 1.3 and 1.6; p = 0.06 and 0.04 for 2001–2002 and 2005–2006 cohorts). For the prototypical participant, low levels of the γ-tocopherol equated to a 7% improvement in risk (13% vs. 6%). To our knowledge, this is a novel association between γ-tocopherol and T2D..."

Patel CJ, Bhattacharya J, Butte AJ. An Environment-Wide Association Study (EWAS) on type 2 diabetes mellitus. PLoS ONE. 2010;5(5):e10746.

http://journals.plos...al.pone.0010746

Potentially something to watch out in our blood tests and supplementation.

 EWAS on DMT2.PNG   257.06KB   4 downloads

Edited by albedo, 14 April 2017 - 12:30 PM.

Studying environmental exposures (nutrition is one element of exposure in the so called exposome) impacting the risk of diabetes 2, I pop into this very interesting study which uses the same statistical methods as in genetic GWAS studies (e.g. Manhattan Plots in Fig 2) to find associations and found a surprising result with Vitamin E (form: gamma-tocopherol) associated with increasing risk of the disease (and beta carotene decreasing the risk) .....

While the EWAS exposome study findings above (high statistical relevance) on Vitamin E risks is only associative, I found strange that gamma-tocopherol turns to be included as anti-aging compound in the AI defined LEF formula here (it is included together with NAC, EGCG and Myricetin (similar to Quercetin)) ! See also the discussion on LC here.
 

.. and found a surprising result with Vitamin E (form: gamma-tocopherol) associated with increasing risk of the disease (and beta carotene decreasing the risk):

Like you, I think the gamma-tocopherol is an association that hinds at the higher soy-oil consumption form processed foods, where it is mostly found in our diet. Now processed foods, with their high omega6:3 ratio, HFCS, chemical additives, herbicides etc., wouldn't come that much of a surprise and might have nothing to do with gamma-tocopherol itself.

Just as higher beta-carotene might indicate an increased consumption of leafy greens, unprocessed.

I tend to agree with you Pamojja. However, considering the really high statistical significance, I wish some additional studies be made in particular testing the gene-environmental hypothesis on the gamma-tocopherol impact as the authors also mention that in the text. As far as I understand from the methodology section, the NHANES cohort is not stratified genetically. The authors mention their results confirm the inverse  beta-carotene hypothesis as found in several other studies so to the light of the high statistical significance the same should be warranted for the gamma-tocopherol hypothesis.

"...We have rediscovered factors such as carotenes and PCBs with previously known association with T2D. Unexpectedly, we found higher levels of c-tocopherol were associated with higher likelihood of T2D, independent of dietary intake. Of the components of Vitamin E, c-tocopherol is the most abundant form in the US diet [36], and makes up to 50% of the total vitamin E in human muscle and adipose tissue [37], two known insulin target tissues. As c-tocopherol has been previously suggested as a preventive agent against colon cancer [38], any potential adverse metabolic effects for this vitamin should be studied closely...."

Edited by albedo, 26 April 2017 - 10:16 AM.

 

The following paper (2014) argues "...that we are ready for some DNA-based dietary advice in general nutrition and it can be beneficial. Examples of the scientific validity and health utility of gene–diet interactions will be given and the development of guidelines for assessment and validation of benefits will be discussed...".

 

The Table 1 provides "...Examples of gene–diet interactions that can be considered to be scientifically valid and have potential benefit..."

 

GxD scientifically valid.PNG

 

Nutrigenetics and personalized nutrition: are we ready for DNA-based dietary advice?

Keith A Grimaldi

Personalized Medicine, May 2014 ,Vol. 11, No. 3 , Pages 297-307
(doi: 10.2217/pme.14.2)

http://www.futuremed...0.2217/pme.14.2

 

If the research below is confirmed the question will be: which of your genotypes will you take as starting point for your nutrition? The genome as sequenced from your spittle by 23and me and others may not be as representative as we thought...

https://www.scientif...etically-alike/