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ACE Defect and ACE Inhibitor for Blood Pressure?

Discussion in 'General Treatment' started by steelfan95, Apr 13, 2013.

  1. steelfan95

    steelfan95

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    If I have the ACE defect, would it be an issue to take an ACE inhibitor for my blood pressure.

    Just a wild question, but would like something to go by for when I see my doctor this Tuesday.


    Thanky you!
  2. MeSci

    MeSci ME/CFS since 1995; activity level 6

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    Hi,

    I have hypertension, which developed while I had ME (it was sky-high) and started taking an ACE inhibitor years ago when attempts to reduce bp naturally failed. I have been fine with it (perindopril) apart from slight dizziness when I started, which is common and is why my gp had me take it at bedtime at first, then as the dizziness stopped (within days, I think) I switched to taking it in the morning.

    I have the ACE deletion, which I refer to here.

    I'm looking into bp again as today I started feeling dizzy (I was sitting down after my usual light lunch) and found that my pulse pressure was insanely high - bp 153/69 at first, then systolic increased and diastolic decreased until it was 155/67!

    Other people here report having very low pulse pressure. I hope I'm not the only one with the opposite!

    I noticed that my lower abdomen felt tight (similar to trapped wind) so have been looking into whether the weird blood pressure could be caused by the vagus nerve. It seems very possible.

    I hate resorting to a drug without any investigations as to the cause of something. I'd rather get to the root of the problem!

    Good luck anyway.
  3. catly

    catly Senior Member

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    I developed severe hypertension with the onset of my ME. Been through pretty much all the different classes of anti-hypertensives the only one that works and I can tolerate is lisinopril, which is an ACE.

    I've never heard of an ACE defect however, so can't comment on that.
  4. Helen

    Helen Senior Member

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    From your 23andme data ( I suppose your SNP´s aren´t from Yasko´s gene test? ) you can see if you have ACE mutations or a deletion. Just click "browse your data" and then fill in ACE in the left box.

    Yasko excluded the analyze of ACE in her test as almost everyone with ME/CFS had that deletion. She excluded the ACE so that she could have another SNP tested instead. I think the ACE should have been in the panel from GeneticGenie (@kday ).
  5. Valentijn

    Valentijn Activity Level: 3

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    I think rs4343 is what is being referred to here. It isn't a deletion/insertion allele location itself, but rather it reflects whether ACE Del16 (not tested directly by 23andMe) is present. The "G" allele at rs4343 means a likely deletion at ACE Del16. The prevalence of the homozygous deletion (as reflected by rs4343) in the general population is calculated as 14.6%, though actual rates are up to 20-40% in most ethnic populations.

    For the 12 ME patients I have full data for, only 1 is homozygous for the deletion with GG (8.3%), versus 3 of 12 controls (25%). 6 ME patients are heterozygous with AG, versus 7 controls. 5 ME patients are homozygous for AA, versus 2 controls.

    Based on our limited data, I'd say Yasko is quite wrong about the prevelance of the deletion in ME/CFS patients. We actually seem to have unusually low rates of the ACE Del16 deletion - which might itself be of interest.
  6. Helen

    Helen Senior Member

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    @Valentijn, one questions to try to understand this better. I´m AG (rs 4343 from 23andme data) and according to Yasko´s panel I have an ACE deletion (del 16). Do I get you right that you think Yasko is wrong about the deletion?
  7. MeSci

    MeSci ME/CFS since 1995; activity level 6

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    This document (pdf, over 1 Mb) has interesting info about this deletion (and other SNPs). I don't know how authoritative it is but it seems credible.
    Helen likes this.
  8. Valentijn

    Valentijn Activity Level: 3

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    Well, she's wrong about the deletion being common among ME patient :p I don't know what else she's claiming about it, but she usually overstates the significance of very common alleles rather massively.

    The research I'm looking at indicates a lot of variation in which version is protective based on ethnicity or arbitrary sub-grouping after the data was collected. I'm not seeing strong results in either direction, just null, small, or non-significant variations in small patient groups, and nothing significant when directly measuring ACE enzyme levels resulting from the different genotypes. One cached article I couldn't directly access claimed a bigger difference, but I couldn't see any citations or basis for the claims. And the ones directly measuring ACE levels, such an http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2776311/ , show no variation in ACE enzyme activity.

    One study did mention haplotypes being significant, in the context of bigger problems occurring when two highly linked SNPs aren't linked for someone (such as being homozygous for one SNP, and heterozygous or the opposite homozygous for the other SNP). But the 12 ME patients I have data for are completely linked in both SNPs.

    So based on the research that I've looked at, rs4343 probably has little or no impact on anything, but might be interacting with other factors in some situations to create a problem. But there's not much indication what those other factor might be, aside from one or two haplotypes. Also, even when a common homozygous mutation does have a significant effect, the effect of a heterozygous mutation is usually small or non-existent, with a few exceptions.

    If anyone can find a real research paper with better data about ACE del16, I'd love to see it, especially if it's looking directly at ACE activity rather than disease risk.
    Last edited: Jul 26, 2014
  9. catly

    catly Senior Member

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    So I looked up rs4343 on my 23 and me and I am GG.

    So I guess that means I have the defect?

    But as I indicated above, Lisinopril, which is an ACE Inhibitor, has been the only antihypertensive med that I've taken that works and doesn't seem to aggrevate my ME/CFS or cause other side effects.
  10. Valentijn

    Valentijn Activity Level: 3

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    It's an extremely common variation, not a defect.
    catly likes this.
  11. Helen

    Helen Senior Member

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  12. MeSci

    MeSci ME/CFS since 1995; activity level 6

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    Valentijn likes this.
  13. Helen

    Helen Senior Member

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    More confused , but on a higher level :confused:. Thanks for the paper @MeSci . It is 30 degrees C in Sweden and we usually don´t have AC´s so have to wait for cooler temperature to be able to read it :).
  14. MeSci

    MeSci ME/CFS since 1995; activity level 6

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    It's horribly hot here too - not quite 30 though. :eek: I have a shady area in the garden though. :)

    Aircon is also a rarity in the UK.
    Helen likes this.
  15. Valentijn

    Valentijn Activity Level: 3

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  16. xks201

    xks201 Senior Member

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    First Google result of angiotensin converting enzyme chronic fatigue search .... http://www.ncbi.nlm.nih.gov/m/pubmed/8213873/
  17. Valentijn

    Valentijn Activity Level: 3

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    There's no mention there of any specific SNP ... and they seem to be saying that the elevation of ACE was only sensitive and specific enough to be useful in the early cases? So a rather interesting avenue to pursue, but not directly relevant to ACE del16.
  18. xks201

    xks201 Senior Member

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    You asked for levels of patients with CFS. Did not realize you were asking for levels of patience with CFS with that ACE mutation. Good luck finding that study. Unfortunately there isn't enough genetic research going on in regards to CFS.
  19. Valentijn

    Valentijn Activity Level: 3

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    Actually I don't care if it involves CFS. If ACE del16 causes elevated levels, it would show up in any group with that mutation. But I haven't seen any research which can attribute elevations to ACE del16 at all.
  20. MeSci

    MeSci ME/CFS since 1995; activity level 6

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    Just want to alert people to some info about dangers of ACE inhibitors that I heard on the radio last week and which I had started to become aware of shortly before, thanks to info posted by @zzz in another thread.

    I was wrong when I said I had been fine with my ACE inhibitor. I just hadn't made the connection.

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