Hello,
I am seeing that in the detox section many risk alleles are different compared to Genetic Genie and Snpedia. For example, in your report the G allele is the risk one for this SNP:
BMP2 C282Y G GG +/+
Additional Information
rsID: rs235756
SNPedia: http://snpedia.com/index.php/rs235756
But when I go to the snpedia link, it looks like T is the risk allele and the C allele (or G I assume) is normal.
This is one of many examples.
Please advise.
Haramandeep Singh
Hi Haramandeep,
The risk allele for rs235756 is G. The information in this link from 23andMe explains why sometimes you will see different alleles and risk alleles from different resources. https://customercare.23andme.com/hc/en-us/articles/202907660-Which-DNA-strand-does-23andMe-report-for-SNP-genotypes- The information used for Sterling’s App V2.1 Variant report correlates with the alleles used by 23andMe.
Lea
Hi Haramandeep,
The risk allele for rs235756 is G. The information in this link from 23andMe explains why sometimes you will see different alleles and risk alleles from different resources. https://customercare.23andme.com/hc/en-us/articles/202907660-Which-DNA-strand-does-23andMe-report-for-SNP-genotypes- The information used for Sterling’s App V2.1 Variant report correlates with the alleles used by 23andMe.
Lea
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?
Hello Vcarterjohnson,
Could you please provide details of the SNPs you are concerned about.
Feel free to ask all the questions at once.
Lea
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?
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
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.
Hi,
I’m adding my 2 cents.
Much research is looking at the resulting amino acids selected (e.g., COMT V158M), and not the actual nucleotide that was swapped.
The other thing to note, is that “risk” associated with a risk allele, may be a risk for some things, but confer a benefit for other things. So, there is research on on both the wild type (normal) and the “risk” allele.
The reality is that you have to look at SNPs in groupings. So, for example a VDR SNP may not be ideal wrt Vit D absorption, buts it’s a benefit to those who have COMT ++ for V158M and H62H.
Cynthia
Hi, I have a question that I am looking for advice/confirmation on.
I have been damaged by a fluoroquinolone antibiotic. I am very confused on if this antibiotic is capable or deleting or altering my dna, specifically mitochondrial dna. My mom passed away a long time ago and I have been told that the mother passes the mitochondrial dna to her child. The next best thing is her sister as I would assume they have the same mitochondrial dna since they share same mother & father.
So i had my aunt tested along with myself and we do not share the same mutations along with one marker that my Aunt has, but I do not seem to have at all.
So my questions are as follows:
Am I just confusing myself or shouldn’t we match up including mutations?
Do fluoroquinolones have the power to cause mutations? And if so what should I be checking?
Do fluoroquinolones have the power to delete segments/snps/genes?
Is there a specific gene that I can verify damage on or is that just impossible?
Regards,
Traci
Hi Traci,
Your questions have been forwarded for reply. Our practitioners answer questions here on a voluntary unpaid basis so may not always be able to reply immediately due to work/life commitments but do their best. Your patience in awaiting a response is appreciated.
Lea
Hi Traci,
When you do your 23andMe and then run results through Sterlings App, you are looking at NUCLEAR DNA. There is one copy per cell, and its highly protected in the nucleus. Its the DNA that drives biochemistry of your body.
Different from that is MITOCHONDRIAL DNA that what we inherit from our Mom’s mostly, It lives in the mitochondria (not the nucleus). There are multiple copies. AS we age, it becomes damaged from free radicals and things like Fluoroquinolones. Some cells have one or two mitochondria, and other cells have hundreds of mitochondria (e.g., heart muscle, parietal cells that make stomach acid, etc.). Red blood cells have no mitochondria. Mitochondria is where our ATP/cellular energy is produced.
So, like you, my Mother passed away young. Thats part of the reason I do what I do and researched relentlessly for years. Like you, I was damaged by Cipro. At the time, I didn’t understand why I had tears in my leg’s connective tissues as I had been working out at gym for years. Suddenly a jog tore my connective tissue and weird bruising patterns that reached from my calf and wrapped around my foot. I was unable to walk. It happened twice, 6 months apart in different legs. Thanks to Sterling and my friendship with her, I dug into the research, along with Julie H. What we discovered wrt Fluoroquinolone damage that is very complicated. Yes, mitochondrial DNA is damaged as it looks much like bacterial DNA; what the Fluoroquinolones are designed to disrupt in the bacterial infections. But, some folks take them and are unscathed; others are damaged wrt their energy levels and cells affected and cell’s “housekeeping” ability and doing their job. If the cell is crippled, so too are the tissues that are built by them.
So, SNPS include SOD2, electron transport chain SNPs, collagen SNPs (folks with EDS), and estrogen clearing are in play to increase susceptibility. G6PD SNPs and heme modulation are part of the picture as well. There are likely more that Im not aware of.
So, what to do….Support cell membrane health with phospholipids but go low and slow as many folks that have been damaged by Fluoroquinolones have autoimmune antibodies to phospholipids. Make sure that CoQ10 levels are in the normal range. Make sure that glutathione levels are in the normal range. Personally, I take Bullet Proof glutathione daily. Exercise and lift weights as thats the way to build mitochondria. If you have COMT V158M homozygous, make sure that you clear estrogen well via sulfation, glucaronidation and proper methylation support. You may want to work with someone who is familiar with this as the pathways need to be addressed in a particular order, individualized to you. Sterling has a list of Practitioners on her website. Cynthia
Greetings,
Forgive me if I overlooked the answer to this question somewhere but the APOE 3 and 4 are not showing on my MTHFR report. I did find that I was supposed to unlock the 19th chromosome on 23andme to make that information available. I have done that, now my question is do I need to resubmit the 23andme data again or is there something someone can do to add that information to my MTHFR report that was already generated.
Thanks!
Ginger
Hi Ginger,
As a goodwill gesture MTHFR Support would be happy to provide you with a promo code so that you can re-run your raw data through Sterling’s App V2.1.
You will need to download your raw data from 23andMe again and upload the new file to the App.
I will email the code to you shortly.
Lea
What genetics are linked with fibrous tissues, muscles and tendons?
Spreading rapidly in my calves, ankles, thighs
I want to know what I can do for this, tissues are hard as a rock in
places in mucles, lumpy places for many years.
Thank you
Thea here is a genetic database. go into the search bar and put some of your terms up in there. Hopefully you can find some genes related to your condition. http://www.hmdb.ca/metabolites/HMDB01659
I’m confused.
I understand that it is expected that I will find a practitioner to interpret these results and I plan on contacting one for a Skype consultation just as soon as I can get my Skype up and running again (I’m in Northern Ireland and no one else is concerned with or tuned into methylation and related issues).
At any rate, I’ve been doing a lot of research on my own and thought I might familiarise myself with the various processes / figures before a Skype appointment so I can best make use of my time.
It’s my understanding that the figures are based on my particular SNPs. Beyond the first one, I just don’t see it. What should I be looking for on the figures that is particular to my snps / situation?
Thanks for the help.
Hi Lovelifeback,
Your question has been forwarded on for a response from Cynthia Smith who designed the diagrams.
Due to work/life commitments our practitioners who answer here voluntarily are not always able to respond immediately but do there best.
Your patience in awaiting a reply is appreciated.
Hi,
The drawings depict the enzymatic biochemical pathways that we all share. The enzymes are noted in the ovals. The Variant Report is looking at the DNA that codes for the enzymes. So, for example, if you are assessing your ability to generate MTHF from folate, you would look at SNPs in DHFR, MTHFD1 and MTHFR. Cynthia
Thanks… must be brain fog… I thought the figures would be DNA specific and I was just too fogged to figure it out (i.e., showing genes/enzymes effected). Will chart my own.