A few queries regarding the SNps report

[vcarterjohnsonParticipant November 1, 2015 at 9:52 pm Post count: 2]

#22507

I have a few queries but not sure if its best to ask them all at once or seperately- so let me start with one:
I am a Naturopath and am learning to read and utilise these reports, and looking at the different websites that offer reports . First thing I have noticed with my report that I am using to compare is that there are a few SNPs that show up as -/- on the MTHFR report but if I feed them into other programms (Livewello/ Nutrahacker etc.) it is +/+. What could be the difference for this?

[Lea (Admin)Keymaster November 2, 2015 at 3:57 am Post count: 296]

#22508

Hello Vcarterjohnson,

Could you please provide details of the SNPs you are concerned about.

Feel free to ask all the questions at once.

Lea

[vcarterjohnsonParticipant November 2, 2015 at 4:42 am Post count: 2]

#22509

Hi Lea,

There are a few, but one example would be the following SNP: CYP1B1 L432V

Other queries that seems to have conflicting answer depending where I check:
1) Is it possible to turn these SNPs off/ and on or are there genetically fixed and the information provided gives you information about work arounds? If they do change- then do they change anyway or do specific actions need to be taken- eg. Can you take a sample a few weeks apart and get different results?
2) Does +/- or +/+ always mean that that *pathway/ enzyme (by lack of a better word)/ SNP is not working at optimum function? What about if it’s a SNP that when researching shows increased incidence of testicular cancer in males (obviously) and the report is for a female- would you then suspect to see it turned off or is that irrelevant?
3) When reading the report, and reading so in groups, is there an order in which they should be read and then treated?

[Lea (Admin)Keymaster November 3, 2015 at 5:26 am Post count: 296]

#22566

Hi vcarterjohnson,

Sterling’s App V2.1 correlates with 23andMe and I have checked that particular SNP and the information is correct. If other sources differ you will find this link from 23andMe https://eu.customercare.23andme.com/hc/en-us/articles/204420114-Which-DNA-strand-does-23andMe-report-for-SNP-genotypes- may explain why otherwise or you will need to contact the other report sources for explanation.

Regarding your other questions I am going to forward your post on to one of our practitioners for comment. They reply on a voluntary basis and are not always able to do so immediately due to their professional committments however they do their best. Your patience in awaiting a reponse is appreciated.

Lea

[Cynthia SmithParticipant November 4, 2015 at 10:08 pm Post count: 206]

#22684

The CYPs are confusing. The risk allele is associated with research that connected a nucleotide swap with some sort of statistical health issue.

rs1800440 is associated with an amino acid substitution at codon 453 of Asparagine (sometimes referred to a A in literature) to Serine (sometimes referrred to as G in literature). aka 4390A>G.
Using the amino acid substitution rather the nucleotide would would something that looks like this:

Asn453Ser (A/G) rs1800440
AA 71 (68) 64 (57) 1
AG 29 (27) 42 (37) 0.11 0.6 (0.4-1.1) 0.12 0.6 (0.4-1.1)
GG 5 (5) 6 (6) 0.70 0.9 (0.5-1.6) 0.70 0.9 (0.5-1.6)
AG+GG 34 (32) 48 (43) 0.11 0.6 (0.4-1.1) 0.12 0.7 (0.4-1.1)
Allele
A 171 (82) 170 (76)
G 39 (18) 54 (24) 0.16 0.7 (0.5-1.1)

– “CYP1B1 Asn453Ser (rs1800440) polymorphism, a decreased risk was observed in G allele compared with A allele”

VS
– “Carriers of variant Ser allele in codon 453 of cytochrome P450 1B1 (rs1800440) were at a significantly lower risk of colorectal cancer compared to carriers of the wild-type allele”

VS
– “Overall, the variant genotypes (GG and GA) of the 453 A/G were not associated with CRC risk when compared with the wild-type AA homozygote”

Sterling reports SNPs as nucleotide swaps and research often reports them as he subsequent amino acid replacements.

If you dig into the research, both wild type and amino acids resulting from SNPs yield different risks. Remember, in our evolution, SNPS that survived, conferred a benefit in the time they survived. Due to epigenetic, they manifest in different phenotypes and could be “bad” now, but “god” when they occurred and were passed on. For example, sickle cell anemia SNPs conferred a benefit for those who were exposed to malaria when they were first introduced in genetics in African countrys. Now they do not. Same for HLA SNPs during Neanderthal time. Now they confer autoimmune if paired with IgA and FUT2 SNPs.

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