Any success with long term Minocycline/Doxycycline?

[bayles]

Hi all. My teen daughter has been taking Doxy for about 2 weeks for her cystic acne, and we have definitely noticed an increase in her alertness and general better attitude. Her acne protocol is 2 months, so I'm looking forward to seeing if this continues. What now concerns me, is that after the two months, she will just revert to her regular state. I have seen some studies that show Mino/Doxy has shown to help CFS, but I don't think those studies went anywhere since they were flawed studies (I think 30% stop taking the antibiotics due to intolerance). My daughter also threw up first day, but was determined to keep going as she obviously hates her acne more than the side effects and is tolerating it just fine after that first day. Anyway, just wondering people's experience!

 

[Wishful]

Minocycline didn't do anything for my ME. With ME, some treatments work for some people, but not others, and some treatments work for a short time then stop working and never work again. So, the short answer is that your daughter's response to ME is unpredictable, and you won't know what the results will be for her before she stops taking it or after she stops taking it until those events actually occur.

ME's unpredictability means that not only can't we predict what treatments will work for an individual, we can't predict what will make a treatment more or less successful. One individual might have success with slow ramp-up of dosage of a drug, while that method might cause it to fail for someone else who might have had success by starting with full dosage, or double dosage.

Many PWME probably regret some past decisions, such as doing too much which led to a long-term crash. However, even that is only guessing, since it might have been some other factor causing the crash, and the extra exertion might have had no effect or even prevented the crash from being worse. There's just no way to know. So, whatever decisions regarding ME we make at any time are correct according to what we know at that time.

 

[bayles]

Minocycline didn't do anything for my ME. With ME, some treatments work for some people, but not others, and some treatments work for a short time then stop working and never work again. So, the short answer is that your daughter's response to ME is unpredictable, and you won't know what the results will be for her before she stops taking it or after she stops taking it until those events actually occur.

ME's unpredictability means that not only can't we predict what treatments will work for an individual, we can't predict what will make a treatment more or less successful. One individual might have success with slow ramp-up of dosage of a drug, while that method might cause it to fail for someone else who might have had success by starting with full dosage, or double dosage.

Many PWME probably regret some past decisions, such as doing too much which led to a long-term crash. However, even that is only guessing, since it might have been some other factor causing the crash, and the extra exertion might have had no effect or even prevented the crash from being worse. There's just no way to know. So, whatever decisions regarding ME we make at any time are correct according to what we know at that time.

Thanks for the feedback. Appreciate you taking the time to share your experience.

 

[junkcrap50]

I just stumbled across minocycline myself for use as an neuroinflammation inhibitor by working on the microglia. So perhaps it is working by lowering your daughter's neuroinflammation. Also, the dosages required for the anti-inflammatory effect may be lower than the normal dosagse used for acne & antibiotics. For instance, those taking doxycycline for their collagen & MMP9 inhibition use low doses compared to normal. I haven't looked into it too much, but will link the 3 papers I came across: 1) Could Minocycline Be a “Magic Bullet” for the Treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome?, 2) Would Repurposing Minocycline Alleviate Neurologic Manifestations of COVID-19? 3) Neuroinflammatory alterations in trait anxiety: modulatory effects of minocycline .

I would also urge you to look into "Remission Biome" online. As several patients have found that going on antiobiotics have improved their ME/CFS or even it in remission [EDIT: completely temporarily.] Two patients are leading a open-source expirement. They are most active on twitter where much of the discussion about this occurs. They believe that the remission events are due to alterations in their gut microbiome.

Lastly, if your daughter's mood has been change/improved, then I think neuroinflammation is a likely issue. If you have not heard of or know about PANDAS/PANS, I would encourage you to read about it. The spectrum of neuroinflammatory caused mood, behavior, & psychiatric changes is likely greater than just OCD & text book cases and probably include autoantibodies that are yet to be discovered (see recent WashPost article about locked-in syndrome patient). The point is, neuroinflammation plays a major role and is supported in the literature for many psychiatric diseases.

I myself can tell symptomatically when my neuroinflammation is high because my mood is worse, i'm very irritable, short tempered, and have a brain on fire feeling. I become Mr. Jekyll like. What has helped me for that has been peptides Thymosin Alpha & Thymosin Beta, which dramatically lowered the inflammation in my brain. It was like I got a new personality. I didn't notice much in terms of alertness or cognitive improvement, besides having more patience to do things.

 

[Wishful]

or even it in remission completely.

I just read that article, and it mentioned temporary remission, but not long-term remission. If you're after a few hours of remission, that only occurs once or twice, then antibiotics and probiotics and FMTs might do that, but there might be no benefit past that brief remission.

Temporary remissions do feel really wonderful though. If nothing else, they let you believe that ME can be treated/cured, somehow, someday.

 

[datadragon]

Thanks for sharing your experience. I will mention that both vancomycin and amoxicillin (not others) showed improvement with Autism. https://pubmed.ncbi.nlm.nih.gov/10921511/ Unfortunately the improvements were temporary and waned on later follow up after it was stopped. Briefly, there is a gut dysbiosis with higher levels of propionate and lower butyrate in those with autism and I learned much later that vancomycin eradicated the propionic acid producing bacteria and reduced the propionate level in fecal samples from a child with propionic acidemia. https://adc.bmj.com/content/archdischild/82/2/169.full.pdf ASD features and ASD have been reported also in patients with propionic acidemia caused by propionic acid (PPA) accumulation due to propionyl-CoA carboxylase enzyme deficiency. The temporary reduction in propionic acid gave relief, but did not 'fix' the cause of the ongoing imbalance so it returned upon the antibiotic stoppage.

In the case of ME/CFS, especially in later stages, we are also seeing low butyrate levels https://www.youtube.com/playlist?list=PLA9aaXOpxIE3QBETBfDtz545PrnROUkBo which need restoration so far so there is some overlap as well as the gut dysbiosis caused from the same inflammatory reason. Minocycline, an anti-inflammatory antibiotic also used as a microglial inhibitor, significantly reduced the numbers and activation of microglia in the paraventricular nucleus of hypothalamus (PVN), reduced expression of cytokines such as IL-1β, IL-6, and TNF-α, attenuated lung inflammation, heart hypertrophy and sympathetic drive in monocrotaline-treated rats. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5945302/
Minocycline also has shown regulation of immune cell activation and proliferation. https://pubmed.ncbi.nlm.nih.gov/23085382/ This may help allow the reduction of the inflammation in earlier stages that is leading to the eventual cascade of issues.

 

[heapsreal]

Look up Dr Garth Nicolson mycoplasma infections cfs, gulf war illness.

 

[bayles]

I would also urge you to look into "Remission Biome" online. As several patients have found that going on antiobiotics have improved their ME/CFS or even it in remission [EDIT: completely temporarily.] Two patients are leading a open-source expirement. They are most active on twitter where much of the discussion about this occurs. They believe that the remission events are due to alterations in their gut microbiome.

I've been following this as well, and I just put two and two together that my daughter was taking the same antibiotic that they have in their protocol. Since she hasn't done any of the gut health check firsts, not sure if she would have the same result, but I'm considering buying the biomesight test anyway, as it specifically says if you are taking your antibiotic for acne, it can actually help determine what can make the antibiotics work the best.

As far as PANS/PANDA, I hadn't thought of it, although have had a few extended friends kids on the protocol up at Stanford a while back. What I find most intriguing, is that my daughter definitely has had many of those symptoms, and in particular, a tic that has come and gone since her original EBV, and no physician has ever bought up this possibility (although I have brought it up multiple times). She doesn't have any extreme anger or strep, which is were the main symptoms for both of the kids I know that were treated for it. But she is definitely an odd clean freak, although not OCD in the classic sense and sensitive to light. Thanks for bring it up, I really appreciate the insight and will look further into it.

 

[datadragon]

A different look at Doxycycline and CFS:

doxycycline inhibits LPS priming of NLRP3. doxycycline dose dependently inhibited the production of the cytokines IL-1β, IL-6, TNF-α, and IFN-γ and the chemokines MCP-1, MIP-1α, and MIP-1β by PBMC https://pubmed.ncbi.nlm.nih.gov/34577552/

Serotonin binds to the 5HT2 and 5HT1A receptors in the motoneuron system. 5HT2 receptors are excitatory and appear to be the receptor that allows serotonin to be involved with promoting locomotion. When serotonin levels reach very high levels, a spillover effect will be seen, and serotonin will begin binding to 5HT1A receptors (which are known to be inhibitory) and will prevent motoneuron firing. (and orexin). Overexpression of serotonin 5HT1A receptor in the orexin neurons enhanced serotonergic inhibition and resulted in severe fragmentation of wakefulness, specifically early in the dark (active) period. Normalization of 5HT1A expression in the orexin neurons in the presence of doxycycline (DOX) eliminated this fragmentation. These results suggest that serotonergic inhibition of orexin neurons may function as a negative feedback circuit early in the active period and could thereby contribute to the diurnal rhythms of sleep and wakefulness. Consistent with its likely role in promoting wakefulness, blockade of 5HT neuro-transmission through 5HT2A antagonists reduces wakefulness and enhances SWS. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3738049/ (Consider that under inflammation, many cytokines induce IDO1 and therefore will shunt tryptophan away from serotonin.)

Wei, Glaser, and Deng (2014), through indirect measures with humans, found that serotonin release increases in concentration as the force of muscular contraction increases in exercise (addition of the inhibitory axonal binding site). No studies on humans have directly measured serotonin concentrations in the brain; however, 5HT1A receptors are known to exist in humans, and D’Amico et al. (2015) showed that motoneuron excitability in humans can be reduced via 5HT1A agonist drugs administration. https://simplifaster.com/articles/central-fatigue-role-neurotransmitters-reduced-work-output

 

[bayles]

A different look at Doxycycline and CFS:

doxycycline inhibits LPS priming of NLRP3. doxycycline dose dependently inhibited the production of the cytokines IL-1β, IL-6, TNF-α, and IFN-γ and the chemokines MCP-1, MIP-1α, and MIP-1β by PBMC https://pubmed.ncbi.nlm.nih.gov/34577552/

Serotonin binds to the 5HT2 and 5HT1A receptors in the motoneuron system. 5HT2 receptors are excitatory and appear to be the receptor that allows serotonin to be involved with promoting locomotion. When serotonin levels reach very high levels, a spillover effect will be seen, and serotonin will begin binding to 5HT1A receptors (which are known to be inhibitory) and will prevent motoneuron firing. (and orexin). Overexpression of serotonin 5HT1A receptor in the orexin neurons enhanced serotonergic inhibition and resulted in severe fragmentation of wakefulness, specifically early in the dark (active) period. Normalization of 5HT1A expression in the orexin neurons in the presence of doxycycline (DOX) eliminated this fragmentation. These results suggest that serotonergic inhibition of orexin neurons may function as a negative feedback circuit early in the active period and could thereby contribute to the diurnal rhythms of sleep and wakefulness. Consistent with its likely role in promoting wakefulness, blockade of 5HT neuro-transmission through 5HT2A antagonists reduces wakefulness and enhances SWS. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3738049/ (Consider that under inflammation, many cytokines induce IDO1 and therefore will shunt tryptophan away from serotonin.)

Wei, Glaser, and Deng (2014), through indirect measures with humans, found that serotonin release increases in concentration as the force of muscular contraction increases in exercise (addition of the inhibitory axonal binding site). No studies on humans have directly measured serotonin concentrations in the brain; however, 5HT1A receptors are known to exist in humans, and D’Amico et al. (2015) showed that motoneuron excitability in humans can be reduced via 5HT1A agonist drugs administration. https://simplifaster.com/articles/central-fatigue-role-neurotransmitters-reduced-work-output

Thanks for this information, but I don't really get this. This is way above my intellect level. Is this a good or bad thing? My daughter continues to show improvement, and is it on it for at least another 5 weeks, so I am hoping it sticks after she is done. She had a doc appointment yesterday with her CFS person and we told him that she was on doxy and showing signs of improvement, and he literally laughed in our face and said he didn't know of a correlation. Fun times!

 

[hapl808]

She had a doc appointment yesterday with her CFS person and we told him that she was on doxy and showing signs of improvement, and he literally laughed in our face and said he didn't know of a correlation. Fun times!

Yeah, that's unfortunately and yet typical - despite lots of good reports of Doxy (myself included). My doctor at least was willing to experiment with it, but my short term gains were better than the long term gains. It seems variable - hopeful your daughter will benefit significantly. Seems to be anti-inflammatory, improve collagen, and obviously work against some pathogens. Who knows why it's helpful in ME/CFS, but doctors are pretty useless.

 

[datadragon]

Thanks for this information, but I don't really get this. This is way above my intellect level. Is this a good or bad thing? My daughter continues to show improvement, and is it on it for at least another 5 weeks, so I am hoping it sticks after she is done. She had a doc appointment yesterday with her CFS person and we told him that she was on doxy and showing signs of improvement, and he literally laughed in our face and said he didn't know of a correlation. Fun times!

This is a good thing. doxycycline is anti inflammatory, and over active inflammation leads to all the later problems so stopping it before it can do that is good and may prevent the other issues from worsening. Also overexpression of a serotonin receptor (5HT1A) appears to be capable to cause the fatigue and it mentioned that normalization by doxycycline prevented this from happening so it may have these additional benefits besides the anti inflammatory benefits (and antibiotic).

 

[heapsreal]

Thanks for this information, but I don't really get this. This is way above my intellect level. Is this a good or bad thing? My daughter continues to show improvement, and is it on it for at least another 5 weeks, so I am hoping it sticks after she is done. She had a doc appointment yesterday with her CFS person and we told him that she was on doxy and showing signs of improvement, and he literally laughed in our face and said he didn't know of a correlation. Fun times!

Most cfsers I think are immune suppressed to a certain degree. So it possible we could have a few chronic bacterial infection that would normally be dormant or controlled by our immune system, spark up and cause us issues. Using doxycycline for awhile can help lower this bacterial load and help the immune system get back on top of things🤞
Just follow it up with good probiotics.

 

[JasonPerth]

Hi all. My teen daughter has been taking Doxy for about 2 weeks for her cystic acne, and we have definitely noticed an increase in her alertness and general better attitude. Her acne protocol is 2 months, so I'm looking forward to seeing if this continues. What now concerns me, is that after the two months, she will just revert to her regular state. I have seen some studies that show Mino/Doxy has shown to help CFS, but I don't think those studies went anywhere since they were flawed studies (I think 30% stop taking the antibiotics due to intolerance). My daughter also threw up first day, but was determined to keep going as she obviously hates her acne more than the side effects and is tolerating it just fine after that first day. Anyway, just wondering people's experience!

Might be worth following RemissionBiome on Twitter- they are doing patient-led study/research after the 2 founders had a breif Remission when being on a Antibiotic.
They currently have the first 50 people starting their protocol. I dont think they have released it yet.