Poll Were You Ever Prescribed Antidepressants for ME/CFS or Fibromyalgia?

[IrisRV]

I am not saying they are the same disease. I said they might share a common root.

Ah, I see. This is the part that confused me:

When you stop looking at these as separate diseases it will all start to make sense.

[my bolding]
I'm still not convinced that the root is the same. There's a great deal more to ME than a serotonin issue. Serotonin has some effects on some body systems, but it doesn't explain many of the common features of ME. I can't see it as the root of ME.

That isn't to say that there may not be serotonin issues with some PWME, just that we don't know where the cause/effect relationships are. If I understand correctly, you are suggesting that serotonin/glutamate/dopamine problems are at the root of ME. I suggest that it is even more likely that neurological issues related to ME cause serotonin/glutamate/dopamine problems in some PWME. That is, the cause/effect could be the other way around.

If you are saying that depression-only patients and some cases of ME have some neurochemical problems in common, I will agree that that could be possible, but is unproven. Depression-only patients may have some features in common with many other diseases.

If we're looking for commonalities, we need better quality research than Michael Sharpe (a psychologist, not a biomedical scientist) using Oxford definition patients. A BPS bias combined with lack of biomedical training, and a very poor patient cohort does not produce reliable biomedical evidence on ME. His data could easily reflect the inclusion of depression-only patients in his research on what he calls cfs using the crap Oxford definition.

I think we agree that there may be some commonalities in neurochemical abnormalities between depression-only patients and some PWME.

Where we may need to agree to disagree is in causality, universality, and the quality of the currently available research on neurochemical dysfunction in ME.

That's just fine. We can interpret the available evidence differently and we can have different opinions as a result. The world would be a terrible place if we all agreed on everything.

 

[weyland]

If we're looking for commonalities, we need better quality research than Michael Sharpe (a psychologist, not a biomedical scientist) using Oxford definition patients.

Agreed, but the interesting part was that Sharpe's study reproduced a previous study done by Behan using a different serotonin provocation agent. Behan's study was on very well characterized enteroviral ME patients and actually showed a difference between the ME patients and depressed patients. What Behan thought it showed was increased serotonin receptor sensitivity in the ME patients. With my very limited understanding of neuroscience, I think there is a chance this could be due to serotonin depletion caused by this mechanism:

Inflammation has been shown to affect serotonin through activation of the kynurenine pathway. Pro-inflammatory cytokines activate the enzyme indoleamine 2,3-dioxygenase (IDO). IDO shuttles tryptophan, the precursor to 5-hydroxytryptophan (5-HTP), down the kynurenine pathway rather than down the pathway that would result in the synthesis of serotonin (Figure 2). Activation of the kynurenine pathway can result in depletion of tryptophan and consequently, depletion of serotonin. Furthermore, 5-HTP and serotonin itself can be substrates for IDO leading to further depletions4.

Source

Lipkin and Hornig pointed out this possibility in their plasma cytokine study as well.

 

[IrisRV]

I think there is a chance this could be due to serotonin depletion caused by this mechanism:

That mechanism makes more sense to me.

 

[Croatoan]

Ah, I see. This is the part that confused me:
[my bolding]
I'm still not convinced that the root is the same. There's a great deal more to ME than a serotonin issue. Serotonin has some effects on some body systems, but it doesn't explain many of the common features of ME. I can't see it as the root of ME.

That isn't to say that there may not be serotonin issues with some PWME, just that we don't know where the cause/effect relationships are. If I understand correctly, you are suggesting that serotonin/glutamate/dopamine problems are at the root of ME. I suggest that it is even more likely that neurological issues related to ME cause serotonin/glutamate/dopamine problems in some PWME. That is, the cause/effect could be the other way around.

If you are saying that depression-only patients and some cases of ME have some neurochemical problems in common, I will agree that that could be possible, but is unproven. Depression-only patients may have some features in common with many other diseases.

If we're looking for commonalities, we need better quality research than Michael Sharpe (a psychologist, not a biomedical scientist) using Oxford definition patients. A BPS bias combined with lack of biomedical training, and a very poor patient cohort does not produce reliable biomedical evidence on ME. His data could easily reflect the inclusion of depression-only patients in his research on what he calls cfs using the crap Oxford definition.

I think we agree that there may be some commonalities in neurochemical abnormalities between depression-only patients and some PWME.

Where we may need to agree to disagree is in causality, universality, and the quality of the currently available research on neurochemical dysfunction in ME.

That's just fine. We can interpret the available evidence differently and we can have different opinions as a result. The world would be a terrible place if we all agreed on everything.

The root of all late onset diseases is the inability to handle reactive oxygen species. Cancer, depression, anxiety, colds, all of them. The severity of each leads back to higher or lower levels of oxidative stress. Give me a disease and I will show you the oxidative stress.

So to heal, the trick is to find where you create oxidative stress, both endogenously and exogenous, and what you need to reduce oxidative stress. I have found a way to do this by looking at people's genetics and by using specific cofactors to increase enzyme activity to get the pathways flowing again.

For example, when MAOA breaks down serotonin it uses an oxygen and creates hydrogen peroxide.

Serotoinin + H2O + O2 -->[MAOA]--> ammonia + 5-HDA + H2O2.

If MAOA is slow because of your genetics, there will be a build up of oxygen in the neuron and in the synaptic space. When electrons hit the oxygen molecules they create superoxides. These are bad and they lead to neurological damage and inflammation.

Now if your MAOA are fast because of genetics your body will make too much H2O2. Having too much H2O2 will cause inflammation and can do things like stimulate the Thyroid peroxidase giving you hyperthyroidsim and give your inflammation.

Now everytime your MAOA enzyme goes to work it uses a little bit of riboflavin. The more the enzyme works, the more riboflavin it needs, if you do not eat riboflavin eventually you will become deficient and the enzyme will not work, hence you create more and more oxidative stress as you become more and more deficient.

The MAOA enzyme is in so many tissues of the body so it will create these superoxides every where it is.
http://www.proteinatlas.org/ENSG00000189221-MAOA/tissue

 

[Croatoan]

Agreed, but the interesting part was that Sharpe's study reproduced a previous study done by Behan using a different serotonin provocation agent. Behan's study was on very well characterized enteroviral ME patients and actually showed a difference between the ME patients and depressed patients. What Behan thought it showed was increased serotonin receptor sensitivity in the ME patients. With my very limited understanding of neuroscience, I think there is a chance this could be due to serotonin depletion caused by this mechanism:


Source

Lipkin and Hornig pointed out this possibility in their plasma cytokine study as well.

I want to show you the pathway map I created so you can see the flow this research is talking about. The variation in symptoms we find in ME patients is based on the many different was these genes express themselves in the body.

Here is a direct link to the image:

https://goo.gl/photos/ZZ1LFhhiHfLdP1St7

You can see how taking B6 will increase serotonin and dopamine and taking B2 will decrease serotonin and dopamine. To me those two supplements are the key to balancing neurotransmitters.

 

[weyland]

Antidepressants and other means of raising serotonin help cfsers feel better about feeling like shit. But then there are alot of cfsers that cant tolerate any measures towards serotonin. Does seem to be the root cause.

In the study I mentioned above, the serotonin agonist made the ME patients feel sick.

The buspirone caused excessive fatigue, lightheadedness, and nausea in patients but not in controls.

 

[IrisRV]

Does seem to be the root cause.

Do you mean doesn't seem to be the root cause?

 

[loki]

yes, and they made me want to slit my wrists

 

[Croatoan]

Whoa! Nice chart!

Does having high dopamine always then mean one would also have high serotonin, and same for both would be low?

No, not necessarily. Plus the EFFECT of each will depend on their corresponding receptors and transporters.

 

[Croatoan]

Yes, I understand a little bit about the receptor issues, well, a very little, but I never heard of the transporters.

With respect to the receptors, you can have adequate neurotransmitter but if the receptors are blocked the neurotransmitter won't do you much good.

Yes, and the transporters, if they are fast, they will remove too much of the neurotransmitter from the synaptic space, also lowering the power of the neurotransmitter.

 

[IrisRV]

Again, can we stay on-topic please? This is a poll thread is about whether you were prescribed ADs for ME or FM.

Please take OT discussions to an existing thread on the topic, or start a new thread if there isn't an existing one. You can always put in a pointer on this thread for anyone interested in pursuing the OT topic.

The OT information here can be very interesting, but it's not going to be easily found by people looking for it. It also detracts from the topic at hand. People come here to see the results of the poll and information about being prescribed ADs. An interrupting discussion on side topics makes it hard for others to read the information they came here for.

 

[ShyestofFlies]

I've been prescribed ADs for my fibro and mental health issues (mdd, gad, ptsd, ocd, others)

Effexor is well documented as an aid for nerve pain in peripheal neuropathy... It did not help my fibro, my pn, or my mental health issues. It gave me bad side effects.

Cymbalta was prescribed dor depression and fibro. For me it helped neither. I had few side effects.

I have also taken Viibryd an AD and 5-htp and it helped nothing.

I have taken Zoloft and it helped my mental health issues a lot, but did not have a single effect on my pain, fibro, or "cfs/me undiagnosed miscellanious disorder of complete body shut down." It gave me some side effects.

I have taken Wellbutrin to help my energy levels, mental health, and reverse the Zoloft side effects. It was very effective in everything stated but my energy levels, which did not improve in any noticeable way. It gave no side effects except weight loss which was desired.

All of these except Viibryd were generics... Today I was reading about how taking a generic can sometimes be like taking an entirely different medication depending on several factors. Your milage may vary.

 

[loki]

nonono i wanted to go to bed but i stay awake for this last post:
generics don't significantly differ when it comes to the action the ingredient is performing.
for example, Wellbutrin has some neuroprotective activities but also, and that is the great minus in nearly all NDRI, it increases the imbalance and makes the cycle of inflammation more aggressive what counteracts the positive features of Wellbutrin. this is such hard matter when you research alone all the time... at least this board supports the research

 

[Snow Leopard]

Low dose Amytriptyline for better sleep. At higher doses (50-75mg) I had severe side effects - severe orthostatic hypotension such that I couldn't stand up the next day. I also suspect it led to a mild worsening of orthostatic hypotension that cleared up some time after I stopped taking it.

It had no effect on my mood.

MAOIs have shown effectiveness for depression in CFS patients, but because of their broader effect, doctors are generally reluctant to prescribe them.
The evidence base suggests that SSRIs are NOT EFFECTIVE for depression in ME/CFS patients. Studies also show (in both healthy and CFS patients) that taking SSRIs leads to reductions in receptor expression that persist after ceasing the drug - so once you take such drugs, there can be consequences if you try to come off them - withdrawal symptoms.

 

[Remy]

MAOIs have shown effectiveness for depression in CFS patients, but because of their broader effect, doctors are generally reluctant to prescribe them.

Aren't there some more selective MAOIs that are easier to take? I'm thinking of moclobemide in particular.

Studies also show (in both healthy and CFS patients) that taking SSRIs leads to reductions in receptor expression that persist after ceasing the drug - so once you take such drugs, there can be consequences if you try to come off them - withdrawal symptoms.

I would highly recommend anyone thinking of taking SSRIs read Kelly Brogan's new book first. More and more people are doubting serotonin's impact on depression and looking to inflammatory models instead.

And Google the drug plus withdrawal to see if you are prepared to deal with the worst case scenario.

I think I remember studies showing autoantibodies against serotonin receptors in our population too...that may be a reason our serotonin is low, among others.

 

[Snow Leopard]

Aren't there some more selective MAOIs that are easier to take? I'm thinking of moclobemide in particular.

Yes. I don't know why most doctors don't consider it. I guess they seem to believe all the hype about SSRIs, so that they don't consider alternatives.

I think I remember studies showing autoantibodies against serotonin receptors in our population too...that may be a reason our serotonin is low, among others.

Autoantibodies against small molecules like serotonin doesn't make much sense... I've seen the Maes study which made the claim and I don't think much of it.

 

[Forebearance]

I was offered them back in the mid-90s, which were like the dark ages compared to now. The only tools the CFS specialist I saw had to offer were gentle exercise and low dose antidepressants. I said No thanks.

But years later I experimented with tiny amounts of 5-HTP, a serotonin precursor, to help me sleep.
It did help for a while. Maybe 3-4 months.
But then my brain said it didn't want any more.

You can tell when you are getting too much serotonin because it causes horrible nightmares that go on forever. Serotonin nightmares.
Once you've had a couple of those, you get the message.
I think serotonin supplements are like a jump start for your brain. You don't need them forever, unless you have clinical depression.

 

[loki]

SSRI / NDRI wanted me to slit my wrists, i got switched to Attentin (Dextroamphetamine) and everything's fine now
what i hate was the fact that it took me about half a year to convince my doc of the fact that it's the only CNS medication that helps without nearly any side effects.
for the brain, this is pure energy. and there's a sharp border between too less(where it doesn't do a thing) and too much (where you crash deeply)... needs time to find the right dose, but then it does really help



i know that inflammation issues mess with dopamine precursors cns wide. inflammation produces cytokines like ifn-gamma. ifn-gamma destroys the precursor chemicals, that the brain needs to form the dopamine derivatives. Adderall and other amphetamines do 2 things. they provide Dopamine and inhibit the reuptake where other meds just inhibit reuptake which is, in my eyes, senseless when the brain struggles to produce dopamine on it's own. when there's no dopamine, why should the inhibition of the reuptake does anything good? it's like money. when you don't have money on your bank account even 100% taxes won't make you rich.
so, when you struggle with inflammation issues and want CNS stimulants, always ask for amphetamine based meds.

 

[Mary Hamilton]

ME/CFS and Fibromyalgia are often mistaken for depression and antidepressants are often a doctors first option. The situation is complicated by the fact that depression is not uncommon in either disease, and antidepressants can relieve pain in people with FM and ME/CFS who are not depressed. Some antidepressants may also affect immune functioning; antidepressants are not just for depression anymore.

Studies suggest, however, that antidepressants are not particularly helpful for most people.

The question is "Were you ever prescribed antidepressants and if so, how did it go?

Provide more complete reviews in our review section

• Cymbalta (Duloxetine)
• Elavil (Amytriptyline)
• Prozac (Fluoxetine)
• Paxil (Paroxetine)

The only thing that has ever helped me is Viibryd. I've been on almost every other kind of anti-depressant.

 

[Ladyliegh]

After my Mom died, I tried Cymbalta, it helped for a few days, but I started having weird very vivid dreams & I started feeling worse than before I took it.
Dr. took me off it immediately & said the side effects can get worse where dreams become too real. I am not a fan of antidepressants, I know some people need them & that is fine. But I feel they are overperscribed & under monitored. Because ME/CFS is in the brain, experimenting with meds can be tricky. They really don't understand how some of these meds work, but they use them anyway. Why would I take something that can make my depression worse? Playing with my serotonin is a bad idea, I would rather smoke to adjust my mood. Hell, I already have a bad memory & no energy, at least I feel better & depression is alleviated... I forget some other my suffering