Interpreting results for recovery

[sleepy]

Hey everyone…I am making some progress with my mitochondrial function from 25% to 65% in 18 months with supplements for mitochondrial support and methylation. I feel that the methylation has definitely been key to my improvement.

I am really keen to learn how my genes will limit my recovery and tailoring treatment. Last year I had a Detoxigenomics test done but I haven’t found anyone who can interpret the results for me in terms of what I need to do, what I shouldn’t do and what I can’t change. For example my oestrogen and testosterone are high and SHBG is high, is this because I can’t metabolise estrogen. Is it ok to take high dose SAMe etc. Can anyone shed any light on this?

I would really like to get full gene testing like Amy Yasko’s Nutrigenomic test – but don’t want to duplicate any tests because of the costs. Can anyone recommend what tests would be useful to give a fuller picture?

I have also attached my metabolic Analysis results plus Rich’s interpretation of these in case they shed light on the detoxigenomics results.

Thanks heaps peeps

Sleepy
x

 

[heapsreal]

Male or female??
if male estrogen can be high as testosterone can aromatise into estrogen, you need to get free testosterone levels measured, at a guess if u have high estrogen u probably have low free testosterone, the stuff that actualy is active, high SHBG could also be a sign that your free T levels are low. Causes of increased estrogen and SHBG can be high body fat levels so if there is a way to lose some weight this can help improve hormone profiles, but it is hard to lose with high estrogen. Look into a drug called arimidex, it can help lower high estrogen levels and help increase freeT and also help u to lose weight better with good diet and exercise if u can. Once weight is down then one can stop arimidex, dosing of arimidex for men is very different to women, most using .5mg arimidex twice a week or maybe abit lower dose. Also improving insulin resistance can help in this area.

Good to see your mito function improving, maybe in time this improved function can help correct these hormone issues too.

 

[sleepy]

hey thanks for your message
I'm female, BMI 20 so not really any need to lose weight! My estrogen has always been high and my genetic report suggests that I have issues metabolising estrogen - I wondered if this could be the cause of high levels.
At this stage I'm really looking at causes of problems rather trying to fix symptoms but thanks for the advice re arimidex, doc has suggested possible pituitary gland damage but I haven't tested for that.

 

[heapsreal]

hey thanks for your message
I'm female, BMI 20 so not really any need to lose weight! My estrogen has always been high and my genetic report suggests that I have issues metabolising estrogen - I wondered if this could be the cause of high levels.
At this stage I'm really looking at causes of problems rather trying to fix symptoms but thanks for the advice re arimidex, doc has suggested possible pituitary gland damage but I haven't tested for that.

Ignore my advice its for the guys. I think if women have problems it could be the balance between estrogen and progesterone. A high dhea could also cause this in women??

cheers!!!

 

[richvank]

Hi, Sleepy.

You have inherited the combination of SNPs in CYP1B1, COMT, and a GST enzyme that I have suggested is the reason why ME/CFS is more prevalent in women than in men. You can find the paper I wrote on that in my documents near the beginning of the detox/methylation forum.

The idea is that when a woman has the CYP1B1 SNP, this enzyme is speeded up, and that diverts more of the estrogens down that pathway for metabolizing them. The homozygous SNP in COMT slows that enzyme down. The result is that when the estrogens get to that point, they are cycled back and forth between quinones and semiquinones, and each cycle produces an oxidizing free radical. The GST SNP slows that enzyme, so the redox cycling persists. This causes the woman's body to be biased toward oxidative stress moreso, and that contributes to a greater load on glutathione, tending to oxidize it and deplete the reduced form of glutathione. Depletion of reduced glutathione is the "trip wire" for onset of ME/CFS, at least according the the GD-MCB hypothesis.

Note that men can also inherit this set of SNPs, but it doesn't matter as much in them, because they don't have to break down a lot of estrogens every month.

Emotional stress is also more of a problem for a person who has the COMT homozygous SNP, because epinephrine, which is elevated under emotional stress, also depends on COMT to metabolize it, and when this is slow, adrenochrome can form, which is also a quinone, and it also cycles back and forth with a semiquinone, also producing oxidative stress.

Improvement in methylation, and with it, a rise in glutathione, are the best things I know of to do in this situation. The methylation will help to metabolize estrogens by another pathway, and the glutathione will counter the redox cycling by disposing of the quinones.

Best regards,

Rich

 

[Star-Anise]

Rich do you think a diet low in estrogens would help in the case of homozygous SNP in COMT? I find I crave foods high in phytoestrogens like chickpeas, but then feel all foggy headed & heavy fatigue afterwards

 

[brenda]

Star-Anise

Rich passed away unexpectedly last October with a heart attack. Maybe start a new thread?

 

[Star-Anise]

Oh my, thank-you for letting me know Brenda! I'm new to the forum. That is such a tragedy as I have been benefiting greatly from the information he has shared on this forum. Star