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Personalized Nutrition

personalized nutrition personalized medicine nutrigenomics nutrigenetics

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#151 albedo

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Posted 06 May 2017 - 09:57 PM

Harkijn, thank you for sharing. I think to keep up with the promise of nutrigenomics we would need to consider the integration of all possible "omics", in that sense nutrigenomics might be a misguiding name us as genetics represents only a part. Between the "omics" the epigenome is fundamental and similarly to a genotypes which might differ from cell to cell the epigenome is known to be tissue dependent. Probably our body ages differently from region to region, organ to organ, cell to cell and it is said you are "as old as your oldest organ". To try an answer to your question one strategy could be to integrate the knowledge about the organs most likely to age quicker than the others in a particular individual and personalize nutrition (as a part of the so call "exposome") starting from there.


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#152 albedo

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Posted 09 May 2017 - 07:51 PM

 

This is nutrigenomics. It's exciting and the future, but we have a long way to go.

 

For anyone with a chronic condition being disappointed from the outcomes with standard medicine, and therefore already exploring nutrient-epigenetic options, the future is already here.

 

 

Abstract 309: Twelve Year Followup for Managing Coronary Artery Diease Using a Nutrigenomics Based Diet and Supplement Program With Quarterly Assessment of Biomarkers
  1. Steven R Gundry

+ Author Affiliations

  1. The Cntr for Restorative Medicine, Intl Heart & Lung Institute, Palm Springs, CA
Abstract

Introduction: Coronary Artery Disease (CAD) is thought to be progressive; standard protocols call for a low fat/low cholesterol diet, exercise, and lipid lowering agents in an effort to slow the onset of recurrent MI’s, stents, CABG’s, stroke, or death. This results in an approximate 30-40% new event rate in 5 yrs.

Methods: Based upon our experience using a Nutrigenomic-based, Lectin-limited diet to prevent/reverse Metabolic Syndrome and CAD, we have enrolled and followed 978 pts (aged 42-89 yrs) with known CAD, defined as previous MI, stent, CABG, or positive stress test/angiogram, positive Corus score greater than 30, into a diet and supplement based, physician coached program, which emphasizes large amts of leafy green vegetables, olive oil, radical reduction of grain, legumes, nightshades, and fruits; and 4 oz amts of animal proteins, emphasizing shellfish, wild fish, and grass fed meats, while avoiding commercial poultry (Matrix Protocol). All Apo E 4 genotypes ate large amts of shellfish and avoided animal fats and cheeses. All pts were instructed to take 2-4,000 mg of high DHA fish oil, 200mg of Grape Seed Extract, and 50 mg of Pycnogenol per day. Supplements were individualized based on results of Advanced Cardiovascular Risk Markers, which were sent to three core labs, (Berkeley Heart Labs, and Singulex, Alameda, CA, Health Diagnostics Labs, Richmond,VA) q 3 months and followed to measure compliance and to change supplement/eating regimens.

Results: Pts have been followed for 1.5 to 12 years (mean 9 yrs). While enrolled, 13/978 pts (1.3%) have received a new stent, two that were predicted by a rising Lp-PLA2, two required CABG, based on a rising Corus score, despite HDL’s of 110-120 mg/dl. There have been no MI’s, unstable angina. One pt underwent carotid endarterectomy ; one pt suffered a CVA and died, while in atrial fibrillation, A second pt expired from a ruptured cerebral berry aneurysm. Total CV events over 12 years is 16/978 (1.6%).

Conclusions: We conclude that simple Nutrigenomic-based dietary interventions, emphasizing lectin avoidance, with compliance and supplement choices based upon q 3 month assessment of biomarkers, represents a quantum leap forward in preventing/modifying Cardiovascular events in known CAD patients.

Key Words:
  • Author Disclosures: S.R. Gundry: Consultant/Advisory Board; Modest; SINGULEX.

  • © 2015 by American Heart Association, Inc.

 

 

With standard protocols (low fat/low cholesterol diet, exercise, and lipid lowering agents) 1 in 3 patients experiences a new adverse event within 5 years.

 

With Nutrigenomic-based dietary interventions (reduction of grains, real food, individualized supplementation) only about 1 in 60 patients experiences a new adverse event within 9 years.

 

 

There is new book from Steven Guntry (The Plant Paradox). I was at a webimar today (hosted by Peter Diamantis) https://livestream.c.../events/7266303 which was pretty interesting. I hope the recording will be available soon which I plan to post here.
 



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#153 albedo

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Posted 10 May 2017 - 04:57 PM

 

 

There is new book from Steven Guntry (The Plant Paradox). I was at a webimar today (hosted by Peter Diamantis) https://livestream.c.../events/7266303 which was pretty interesting. I hope the recording will be available soon which I plan to post here.
 

 

 

And here it is:
 



#154 albedo

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Posted 15 May 2017 - 08:46 PM

Here is an interesting personalized nutrition company (Habit) delivering personalized foods to determine what they refer to as phenotyping flexibility as a biomarker of health. They base their recommendations also on a challenge response of individuals, e.g. think about glucose challenge.

 

Do you have any experience with them?

 

https://habit.com/

 

"Habit looks at over 60 indicators, including ones from your blood and your DNA, as well as other body metrics. Blood indicators include glucose, triglycerides, LDL cholesterol, and more.  DNA is analyzed for variants within the FTO, FADS1, IL6, and PPARG genes, and self-reported body metrics include body weight, and height and waist circumference.  

Head to our science page for a more detailed overview of the testing process and our recommendations."

 

https://habitsupport...ed-at-by-Habit-

 

(edit: spelling)


Edited by albedo, 15 May 2017 - 08:59 PM.


#155 albedo

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Posted 24 May 2017 - 11:41 AM

AI seems poised to blur the border between personalized medicine and personalized nutrition.

In-Depth: AI in Healthcare- Where we are now and what's next

 



#156 albedo

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Posted 11 June 2017 - 04:08 PM

Attached File  personalized medecine.PNG   194.46KB   2 downloads

 

https://www.pathway....-interest-list/


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#157 albedo

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Posted 07 July 2017 - 10:01 AM

The following article on Medscape is from 2008 but I found it a good introduction also today and well referenced.

 

What I particularly liked in the Exec Summary is the focus on the integrative approach which I think is a key step forward as mentioned elsewhere (e.g. see my post here on integrated Personalized Omics Profiling or iPOP), emphasizes epigenetics and intersects with the precision medicine trend:

 

"...the genomics sciences have delivered proof of the principle that humans are different with respect to optimal diets. As nutrigenomics and nutrigenetics build the scientific foundation for this, and as genotyping technologies become readily accessible, consumers may gain value through information on their personal genetic code. However, only those genetic variations should be assessed that can be adequately addressed by appropriate diets. However, humans are not only genetically different. This highlights the necessary synergies between the genotyping and the holistic investigations of the metabolism deploying transcriptomics, proteomics and metabolomics, the latter three providing insights into how diet and health alter the expression or 'manifestation' of our genomes..."

 

http://www.medscape....rticle/583041_1



#158 albedo

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Posted 21 July 2017 - 09:25 AM

"...Nutrition science needs to actively seek and embrace the addition of new, innovative concepts to adequately study the effects of nutrition on health maintenance and disease prevention in real life,
in collaboration with other relevant disciplines..."

 

Capable and credible? Challenging nutrition science

https://link.springe...0394-017-1507-y


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#159 albedo

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Posted 23 July 2017 - 12:15 PM

Nutrino and IBM Introduce Watson-Powered Nutrition Recommendations for Expectant Moms-to-Be

http://www.prweb.com...web13117207.htm

 

"Nutrino’s FoodPrint App Integrates with the LibreLink Mobile App, Designed for Abbott’s FreeStyle Libre System"

 

http://www.businessw...Link-Mobile-App

https://nutrino.co/#/

 



#160 albedo

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Posted 23 July 2017 - 12:38 PM

The future of food? Technology that prepares meals based on our DNA

http://www.sbs.com.a...s-based-our-dna



#161 Benko

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Posted 24 July 2017 - 01:26 AM

The future of food? Technology that prepares meals based on our DNA

http://www.sbs.com.a...s-based-our-dna

 

" meals based on our DNA"

 

People are not their DNA, they have become what they are because of DNA to be sure, but also their environment.  A good practitioner (think it was CHris KResser) today does not treat people based on their DNA (23 and me) profile of e.g. methylation, but on functional tests that tell him whether a persons methylation is currently functioning well or inadequate.

 

 

 

In theory, there is no difference between theory and practice, in practice, their is.


Edited by Benko, 24 July 2017 - 01:28 AM.


#162 aribadabar

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Posted 24 July 2017 - 02:24 AM

 not treat people based on their DNA (23 and me) profile of e.g. methylation, but on functional tests that tell him whether a persons methylation is currently functioning well or inadequate.

 

 

In theory, there is no difference between theory and practice, in practice, there is.

 

How can one overcome the methylation SNPs they have been born with besides targeted supplementation based precisely on the DNA information?



#163 albedo

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Posted 24 July 2017 - 07:42 AM

Benko, I also think there is much more to personalized nutrition than genetics which underlies basically the difference between nutigenetics and nutrigenomics. I posted the link to show how the business is developing, there are many companies already in the area, now including also CSIRO which is a highly reputed Australian scientific organization. While I do agree on the necessity to go beyond genetics, methylation and folate status is probably one of the most well researched areas where competent dietary advise might be a guide for reducing risks of chronic diseases.


Edited by albedo, 24 July 2017 - 07:53 AM.


#164 Benko

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Posted 24 July 2017 - 12:14 PM

"do agree on the necessity to go beyond genetics"

 

I have not been following this thread closely, and that was my only point.  Because to many people theory=reality.



#165 Benko

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Posted 24 July 2017 - 12:22 PM

 

 

How can one overcome the methylation SNPs they have been born with besides targeted supplementation based precisely on the DNA information?

 

 

Your assumption is that 100% of people with those snps when tested will be functionally not methylating adequately.  That may or may not be correct and as I said I ran across one practitioner I have a high regard for (again I think it was Chris Kresser) who goes only by functional status.  



#166 albedo

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Posted 26 July 2017 - 04:30 PM

Though I do not carry the risk allele A on the FTO gene (rs9939609), hence I am not studying all this in detail, I thought you might be interested to these key studies on strong association to risk of obesity in child’s and adults and the importance of a Mediterranean style diet recommendation known to be beneficial from many other population studies. Note that the study (1) also mentions rs1121980 but do not report it due to the high linkage disequilibrium between the two.  SNPedia reports that at least four other SPNs are also highly correlated to the two (rs9939973, rs7193144, rs9940128 and rs8050136)

  1. Fat mass- and obesity-associated genotype, dietary intakes and anthropometric measures in European adults: the Food4Me study

http://www.ncbi.nlm....pubmed/26620191

  1. A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity.

http://www.ncbi.nlm....pubmed/17434869

  1. A 3-year intervention with a Mediterranean diet modified the association between the rs9939609 gene variant in FTO and body weight changes.

http://www.ncbi.nlm....pubmed/19918250

 

This recent paper unfortunately paywalled is much more complete in reviewing the genetic associated to obesity. It looks in detail to FTO as well as MTHFR, PPAR, APO-A, APO-E, LIPC, INSIG2 and MC4R.

 

Piñero (2017) The future of Nutrition: Nutrigenomics and Nutrigenetics in Obesity and Cardiovascular Diseases, Critical Reviews in Food Science and Nutrition, DOI:10.1080/10408398.2017.1349731

http://www.tandfonli...98.2017.1349731


Edited by albedo, 26 July 2017 - 04:31 PM.


#167 albedo

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Posted 28 July 2017 - 08:33 AM

The future of food? Technology that prepares meals based on our DNA

http://www.sbs.com.a...s-based-our-dna

 

https://research.csi...soft-materials/
Attached File  CRIRO.PNG   108.98KB   1 downloads



#168 albedo

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Posted 06 August 2017 - 09:54 AM

A very interesting workshop report on the highly overlooked area of drug-nutrition interactions, particularly for the elderly, with focus on many important nutrients such as Vit D, K, Folate, Omega 3 fatty acids etc .. and impact on microbiota. The nutrition personalisation to the patient takes here a particular relevance.

 

Péter S, Navis G, De borst MH, et al. Public health relevance of drug-nutrition interactions. Eur J Nutr. 2017

https://www.ncbi.nlm...pubmed/28748481

 

"The public health relevance of drug-nutrition interactions is currently highly undervalued and overlooked. This is particularly the case for elderly persons where multi-morbidity and consequently polypharmacy is very common. Vitamins and other micronutrients have central functions in metabolism, and their interactions with drugs may result in clinically relevant physiological impairments but possibly also in positive effects. On 12 April 2016, the University Medical Center Groningen (The Netherlands), as part of its Healthy Ageing program, organized a workshop on the public health relevance of drug-nutrient interactions. In this meeting, experts in the field presented results from recent studies on interactions between pharmaceuticals and nutrients, and discussed the role of nutrition for elderly, focusing on those persons receiving pharmaceutical treatment. This paper summarizes the proceedings of the symposium and provides an outlook for future research needs and public health measures. Since food, pharma and health are closely interconnected domains, awareness is needed in the medical community about the potential relevance of drug-nutrition interactions. Experts and stakeholders should advocate for the integration of drug-nutrition evaluations in the drug development process. Strategies for the individual patients should be developed, by installing drug review protocols, screening for malnutrition and integrating this topic into the general medical advice."



#169 albedo

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Posted 11 August 2017 - 10:29 AM

This paper reviews the evidence on how our genetic make up makes some of us benefiting more or less from plant based bioactive compounds and to me the need to have more than genetics. I found the section on the "Impact of genetic polymorphism on the effects of plant-food bioactive compounds" for cardiovascular and metabolic diseases particularly interesting.

 

Milenkovic D, Morand C, Cassidy A, et al. Interindividual Variability in Biomarkers of Cardiometabolic Health after Consumption of Major Plant-Food Bioactive Compounds and the Determinants Involved. Adv Nutr. 2017;8(4):558-570.

http://advances.nutr...nt/8/4/558.long

 

"...Nevertheless, the limited evidence suggest that genetic factors may be important for the interindividual variability, in particular, genetic polymorphisms of genes involved in phase I and phase II metabolism, such as COMT or CYP7A1, and others, such as the APOE genotype or cholesterol transporters. The gut microbiota is an emerging key player explaining variability, as evidenced by the differences in biological response observed between equol and non–equol producers, but also in the differential effects observed in relation to ellagitannin metabolism. Finally, health and metabolic status seem to be other factors playing a role, with some evidence suggesting that “at-risk” participants or patients may be more likely to gain benefits from increased plant bioactive compound intake than healthy individuals may be. Although some variability according to age and sex has been shown, the current evidence is not strong enough to make any conclusion..."

Attached File  CVD & metabolic factors.PNG   621.56KB   0 downloads

 



#170 albedo

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Posted 10 September 2017 - 12:15 PM

Interesting: NUTRIOMI

 

http://nutriomi.com/



#171 albedo

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Posted 14 September 2017 - 11:36 AM

Very complete state of the art guide on genetic and very importantly epigenetic biomarkers to predict the risk of chronic diseases and possible nutritional interventions (see tables 1-6):

  • Nutrigenetic examples of SNPs-diet interactions involved in disease risk
  • Certain nutrigenetic trials analyzing SNPs-diet interactions involved in the differential responses to nutritional interventions
  • Nutrigenomic examples of interactions between dietary intakes and gene expression profiles involved in disease risk
  • Certain nutrigenomic studies assessing gene expression profiles associated with nutritional interventions
  • Nutriepigenetic examples of interactions between dietary intakes and epigenetic modifications involved in disease risk
  • Certain nutriepigenetic studies evaluating epigenetic modifications related to diverse nutritional interventions

Ramos-lopez O, Milagro FI, Allayee H, et al. Guide for Current Nutrigenetic, Nutrigenomic, and Nutriepigenetic Approaches for Precision Nutrition Involving the Prevention and Management of Chronic Diseases Associated with Obesity. J Nutrigenet Nutrigenomics. 2017;10(1-2):43-62.

 


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#172 albedo

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Posted 21 September 2017 - 01:05 PM

Will see what will come out of this but understand BASF has positioned strongly in this area:

 

BASF and InsideTracker Take Leading Steps to Advance Personalized Nutrition

https://www.basf.com...9/p-17-309.html

 

 



#173 albedo

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Posted 13 October 2017 - 11:49 AM

Hjorth MF, Roager HM, Larsen TM, et al. Pre-treatment microbial Prevotella-to-Bacteroides ratio, determines body fat loss success during a 6-month randomized controlled diet intervention. Int J Obes (Lond). 2017

 

"On the basis of the abundance of specific bacterial genera, the human gut microbiota can be divided into two relatively stable groups that might have a role in personalized nutrition. We studied these simplified enterotypes as prognostic markers for successful body fat loss on two different diets. A total of 62 participants with increased waist circumference were randomly assigned to receive an ad libitum New Nordic Diet (NND) high in fiber/whole grain or an Average Danish Diet for 26 weeks. Participants were grouped into two discrete enterotypes by their relative abundance of Prevotella spp. divided by Bacteroides spp. (P/B ratio) obtained by quantitative PCR analysis. Modifications of dietary effects of pre-treatment P/B group were examined by linear mixed models. Among individuals with high P/B the NND resulted in a 3.15kg (95% confidence interval (CI): 1.55; 4.76, P<0.001) larger body fat loss compared with ADD, whereas no differences was observed among individuals with low P/B (0.88kg (95% CI: −0.61; 2.37, P=0.25)). Consequently, a 2.27kg (95% CI: 0.09; 4.45, P=0.041) difference in responsiveness to the diets were found between the two groups. In summary, subjects with high P/B ratio appeared more susceptible to lose body fat on diets high in fiber and whole grain than subjects with a low P/B ratio."


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#174 albedo

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Posted 15 October 2017 - 01:27 PM

We touched the choline individual requirements previously in this thread. Here is a recent paper which next to the unmodifiable genetic factors (such as SNPs in one-carbon metabolism enzymes) focus on looking at individual gut microbiomes.

 

"...This work suggests that interpersonal differences in microbial metabolism should be considered when determining optimal nutrient intake requirements..." (from the abstract)

 

"...Our results suggest that choline consuming,TMA-producing gut microbes can significantly impact health not only through TMAO accumulation, but also by competing with the host for this essential nutrient, eliciting a quasi-choline-deficient state. This previously ignored aspect of microbial choline metabolism could have major implications for health and development, especially during pregnancy. Epigenetic mechanisms provide a direct link between the environment (e.g., diet) and regulation of gene expression. While DNA methylation is in part regulated by non-modifiable genetic risk factors (e.g., SNPs in one-carbon metabolism enzymes), it is profoundly affected by modifiable dietary factors. Methylation reactions depend heavily on a steady input of methyl-donor precursors, including choline, folate, and betaine, which are obtained through our daily diet (Pogribny and Beland, 2009). We found that microbial choline utilization affected DNA methylation patterns across multiple tissues in adult mice while simultaneously increasing adiposity (Figures 5A, 5D, and S3)..."

 

Romano KA, Martinez-del campo A, Kasahara K, et al. Metabolic, Epigenetic, and Transgenerational Effects of Gut Bacterial Choline Consumption. Cell Host Microbe. 2017;22(3):279-290.e7.



#175 albedo

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Posted 04 November 2017 - 12:36 PM

An interesting genetic part follow-on research by the FoodforMe.org EU project on the interaction between Mediterranean Diet and genetic risk factors:

 

San-cristobal R, Navas-carretero S, Livingstone KM, et al. Mediterranean Diet Adherence and Genetic Background Roles within a Web-Based Nutritional Intervention: The Food4Me Study. Nutrients. 2017;9(10)

http://www.mdpi.com/...-6643/9/10/1107

 

"...All SNPs were analysed for the following genes: ADRB2 (rs1042713 and rs1042714); AGT (rs5051 and rs699); APOE (rs429358 and rs7412); FTO (rs1121980 and 9939609); GC (rs2282679, rs7041, and rs4588); and CETP (rs3764261 and 708272), which all presented p-values less than 0.005 for LD, except for VDR (rs1544410 and rs2228570), where the p-value was 0.984 for LD. For the SNPs within the same gene that were shown to be in high LD, those with the strongest association with relevant traits, based on published evidence (Genome-wide association studies -GWAS- or meta-analysis) were selected, i.e., rs1042714 [58], rs699 [59], rs7412 [60], rs9939609 [61,62,63], rs2282679 [64,65], and rs3764261 [60,66]...."

 

"...Interestingly, this study demonstrated the beneficial effects of greater adherence to the MedDiet on anthropometric and biochemical markers, even in the presence of an elevated genetic risk. Environmental factors, together with a higher GRS, have been found to interact with nutritional status [69]..."

 

"...These results demonstrate that considering the genotype in personalised dietary advice may improve the effect on dietary interventions and may help to achieve an adequate status in nutritional biochemical markers [96]..."


Edited by albedo, 04 November 2017 - 12:37 PM.


#176 albedo

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Posted 17 November 2017 - 05:50 PM

A case for a targeted nutrition supplementation:

 

Nock TG, Chouinard-watkins R, Plourde M. Carriers of an apolipoprotein E epsilon 4 allele are more vulnerable to a dietary deficiency in omega-3 fatty acids and cognitive decline. Biochim Biophys Acta. 2017;1862(10 Pt A):1068-1078.

 

" Carriers of an epsilon 4 allele (E4) of apolipoprotein E (APOE) develop Alzheimer's disease (AD) earlier than carriers of other APOE alleles. The metabolism of plasma docosahexaenoic acid (DHA, 22:6n-3), an omega-3 fatty acid (n-3 FA), taken up by the brain and concentrated in neurons, is disrupted in E4 carriers, resulting in lower levels of brain DHA. Behavioural and cognitive impairments have been observed in animals with lower brain DHA levels, with emphasis on loss of spatial memory and increased anxiety. E4 mice provided a diet deficient in n-3 FA had a greater depletion of n-3 FA levels in organs and tissues than mice carrying other APOE alleles. However, providing n-3 FA can restore levels of brain DHA in E4 animals and in other models of n-3 FA deficiency. In E4 carriers, supplementation with DHA as early as possible might help to prevent the onset of AD and could halt the progression of, and reverse some of the neurological and behavioural consequences of their higher vulnerability to n-3 FA deficiency. "


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#177 albedo

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Posted 15 December 2017 - 03:04 PM

I have been always looking at genetics of prostate cancer and diet. This study is an additional confirmation of genetics for the initiation of the processes taking to PCa and the role environment (e.g. diet) plays in progression and aggressiveness. It confirms to me the care we must have with a pro-inflammatory diet "...we propose that the inflammatory pathway is one of the most important pathways responsible for initiating the disease, and crucial roles in driving non-aggressive PCa to the aggressive stage..." I looked into SNPs of putative oncogene (MYEOV - Myeloma Overexpressed) and particularly rs10896438, rs11228565, rs7931342 statistically highly significant for aggressiveness.  

 

Vaidyanathan V, Naidu V, Karunasinghe N, et al. Effect of ageing and single nucleotide polymorphisms associated with the risk of aggressive prostate cancer in a New Zealand population. Mol Biosyst. 2017;13(10):1967-1980. (on ResearchGate)

http://pubs.rsc.org/...th#!divAbstract

 

 


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#178 albedo

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Posted 18 December 2017 - 05:28 PM

Excellent review, by leading scientists in the field, on the caution we must exercise in jumping too fast to conclusions for personalized nutrition recommendation. The paper does not analyze clinical evidence (which to me is crucial) but frames how scientific evidence should be assessed.

 

Proposed guidelines to evaluate scientific validity and evidence for genotype-based dietary advice

https://ueaeprints.uea.ac.uk/65167/

(on ResearchGate)

 

I found the example of TCF7L2 (rs7903146) for the risk of diabetes 2 a very good exemplification of the point (btw, I am CT on that)

 

" Primary prevention in high-risk groups. Genetics × diet × T2DM (type 2 diabetes mellitus)––The T allele of the TCF7L2 rs7903146 SNP has been associated repeatedly with an increased risk of T2DM (2-fold in homozygotes [85]). Compared with non-risk allele carriers, individuals who carry the risk allele and who are at high risk phenotypically (glucose intolerance, pre-diabetes diagnosis) require a longer lasting and a more intense dietary and lifestyle recommendation to divert the trajectory from disease over a period of 12 months and to maintain health gains over a 4-year period [86]. Although useful, these findings have been obtained in clinical trials of unhealthy people, who typically were older. Thus, to be precise, it does not demonstrate, and cannot be used to claim, that specific dietary modifications in younger, healthier people will prevent the development of glucose intolerance or T2D in those carrying the risk allele. However, this evidence of gene × diet interactions in pre-diabetics is consistent with the evidence from other types of studies in healthy subjects (epidemiological, cohort, effects on biomarkers) and can provide supporting evidence, but not conclusive evidence, that specific dietary guidelines would be appropriate for healthy carriers of this TCF7L2 risk allele. This example shows how difficult it is to validate a gene-diet interaction but suggests that adjusting the environment will improve the individuals’ health. The same TCF7L2 genetic variant was assessed in the recently published study from the PREDIMED project [14], a large randomised trial in 7018 highcardiovascular- risk individuals comparing two Mediterranean (Med) diets and a control diet. TCF7L2 TT homozygotes at SNP rs7903146 had higher blood glucose levels, total cholesterol, LDL cholesterol and triglycerides but only when adherence to the Med diet was low. Furthermore, incidence of stroke was almost three times higher in TT homozygotes as in the control group, but this increased risk was completely dissolved in the Med diet group (Hazard Ratio, HR = 0.96). Thus, compared to the control diet, both Med diets were effective at reducing both risk biomarkers and disease incidence itself in a genotype specific manner. While this is a strong endorsement of the Mediterranean diet, it is also relevant that the age range was 55 to 80 years. This RCT supports the epidemiological evidence for health benefits of the Med diets for older persons, and those at increased risk of CVD, and can only suggest such benefits for other age groups who carry the TCF7L2 TT genotype at rs7903146." (bold mine)

edit: link correction

 


Edited by albedo, 18 December 2017 - 05:51 PM.

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#179 albedo

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Posted 10 January 2018 - 02:44 PM

Interesting for the folks out there TT homozygotes for APOE rs1064725:

 

Shatwan IM, Weech M, Jackson KG, Lovegrove JA, Vimaleswaran KS. Apolipoprotein E gene polymorphism modifies fasting total cholesterol concentrations in response to replacement of dietary saturated with monounsaturated fatty acids in adults at moderate cardiovascular disease risk. Lipids Health Dis. 2017;16(1):222.

 

"...In summary, our findings have demonstrated a greater sensitivity of the APOE SNP rs1064725 to dietary fat composition, with a total cholesterol lowering effect observed following substitution of SFA with MUFA but not n-6 PUFA. Further large intervention studies incorporating prospective genotyping are required to confirm or refute our findings..."



#180 ceridwen

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Posted 10 January 2018 - 04:28 PM

I have just started doing Dr Axe's course on leaky gut where he looks at various causes of leaky gut and posts different dietary modifications for each. I don't think I should pass the information on as I had to pay for it and think I might get into trouble if I do





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