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Most Helpful Snri Or Ssri You Have Tried


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Effexor. I tried Zoloft, and it burned a whole in my tummy -- awful nausea, vomiting, jitters, felt like I was on fire. Ended up in the ER it freaked me out so much. BUT, Effexor did the same thing when I first started it for about 4-5 days -- in addition to insomnia. Docs really felt like I needed it so we just pushed through w/ some tummy meds to protect my tummy and Klonopin for sleep for the first few weeks. And, when I was on the right dose it made all the difference in the world - felt 100% normal, no bp issues / syncope at all.

Currently upping my dose from 75 to 112.5 (and getting the jitters!!), because ever since we reduced my dose from 112.5 to 75 in the fall I've been having pre-syncope / syncope issues and been having real difficulty reducing my florinef.

I do best on Effexor and nothing else -- another reason we are upping the dose, so that I can eventually discontinue the florinef.

I figure Effexor gives me a "three fer" in my control of my NMH -- (1) increased serotonin = help with vessels not being so "vagally"; (2) increased norepinephrine = increased sympathetic activity = increased vasoconstriction; and (3) increased serotonin makes your body naturally produce more aldosterone = more volume (and less florinef to accomplish that).

All that being said, I have tried once to get off of Effexor and it was absolutely horrible, no matter how slow we tried to go. So, I'm a lifer (which I am ok with if it makes me feel good)!

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I figure Effexor gives me a "three fer" in my control of my NMH -- (1) increased serotonin = help with vessels not being so "vagally"; (2) increased norepinephrine = increased sympathetic activity = increased vasoconstriction; and (3) increased serotonin makes your body naturally produce more aldosterone = more volume (and less florinef to accomplish that).

Really? Increased serotonin upregulates aldosterone? Is that true?

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This was 2 years ago, but my cardiologist started me on Paxil and it was super helpful at first for a lot of symptoms. Eventually it was too strong so I switched to a low dose lexapro which was helpful for a while too. The side effects can sometimes be annoying though (it was restless leg for me and feeling jittery) so make sure you have the right dose.

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I've tried Zoloft and Lexapro neither of which worked for me. In fact they both made me have some awful suicidal thoughts. Zoloft gave me severe dry mouth and lexapro made me clench my jaw so bad I had migraines. I gave Zoloft all of four days. I couldn't take the depression it was causing. The first three weeks of lexapro seemed okay, then the start of the fourth week within an hour of taking the lexapro I would be vomiting and my chest and hands would burn. It was awful!! I stopped the lexapro after six weeks cold turkey (which I do not recommend).

I am now trying more natural alternatives. Fluid and Salt loading, exercise, and slowly weaning off of klonopin. My scenario isn't the same as many others here, I am not a severe case. Very mild.

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Tried Prozac, celexa and lexapro... all made me feel worse where before the meds I would have pre-fainting episodes that I could work to get through, but with the meds felt that I would actually pass out (where my teeth would start tingling).

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I figure Effexor gives me a "three fer" in my control of my NMH -- (1) increased serotonin = help with vessels not being so "vagally"; (2) increased norepinephrine = increased sympathetic activity = increased vasoconstriction; and (3) increased serotonin makes your body naturally produce more aldosterone = more volume (and less florinef to accomplish that).

Really? Increased serotonin upregulates aldosterone? Is that true?

It does. I found several studies while I was researching over the weekend. Apparently the more available serotonin stimulates your body to produce aldosterone. And sometimes folks who are on SSRIs or SNRIs can get false negatives for things like Addison's because it in essence covers it up. I'll see if I can find the studies I was looking at and post them.

Forgot to mention that I tried Prozac too, but it made me really dizzy.

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Here you go:

Horm Metab Res. 1998 Jun-Jul;30(6-7):398-403.

Serotonergic regulation of adrenocortical function.

Lefebvre H, Contesse V, Delarue C, Vaudry H, Kuhn JM.

Source

European Institute for Peptide Research, Group for Hormone Research, CHU of Rouen, France.

Abstract

Serotonin (5-HT) plays a pivotal role in the regulation of the hypothalamo-pituitary-adrenal axis. In particular, 5-HT is involved in the stimulation of ACTH secretion during stress. Recent data indicate that, at the adrenal level, 5-HT acts as a local regulator of corticosteroid secretion. The presence of 5-HT in the adrenal gland has been demonstrated immunohistochemically and biochemically in various species including frog, mouse, rat and human. In the mouse, 5-HT has been detected in nerve fibers while, in the frog and rat, 5-HT appears to be sequestered in chromaffin cells. In man, 5-HT is stored in perivascular mast cells. In vivo and in vitro studies have shown that 5-HT stimulates mineralo- and glucocorticoid secretion from adrenal cells. In rat, the type of receptor involved in the corticotropic effect of 5-HT is still controversial. In the frog and the human, the effect of 5-HT on the adrenal cortex is mediated through a 5-HT4 receptor subtype positively coupled to adenylyl cyclase and calcium influx. Clinical studies indicate that 5-HT4 receptor agonists stimulate aldosterone secretion in healthy volunteers and in patients with aldosterone disorders. The 5-HT4 receptor agonist cisapride and angiotensin II exert additive effects on aldosterone secretion. In contrast, cisapride has no influence on ACTH-induced aldosterone release. Collectively, these findings suggest that intra-adrenal 5-HT stimulates the secretory activity of adrenocortical cells through a paracrine mode of communication involving a 5-HT4 receptor type. Serotonergic control of corticosteroid production may be involved in the physiological control of the activity of the adrenal cortex, in particular during inflammatory stress. 5-HT may also be implicated in the pathophysiology of aldosterone disorders.

PMID:

9694569

[PubMed - indexed for MEDLINE]

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It does. I found several studies while I was researching over the weekend. Apparently the more available serotonin stimulates your body to produce aldosterone. And sometimes folks who are on SSRIs or SNRIs can get false negatives for things like Addison's because it in essence covers it up. I'll see if I can find the studies I was looking at and post them.

Thanks...really good info. Perhaps that explains why I had wicked dry skin when I tapered off Lexapro. I could go running for 50min and barely break a sweat. Trialing prozac...it does make me dizzy if I don't take a 1/8 tablet of Florinef...hopefully that will go away in time (at least my stomach is okay and I can sleep).

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Tried citalopram at the lowest therapeutic dose 10 mg - horrible side effects: jittery, tachy, BP swings, insomnia (even though I used to take it early in the morning) panic attacks, shakiness.

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thanks all - first interesting observation is that many have taken and tolerated SNRIs well despite there being some literature suggesting that NET inhibition might make POTS worse. I know of two people with Hyper type presentations and bad anxiety that did wonderfully on an SNRI.

Ive never tried either. I did try Rhodiola rosea which is a MAO-I and that definately improves mood subtely as well as seeming to calm down the ANS.

For those where its not clear - can you please clarify whether you have POTS or not? Thanks.

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When i was relatively well I once spoke to a psyciatrist at a party who was interested in POTS and really seemed convinced it was the result of abnormal serotonin levels - hypersensitive receptors from reduced SE levels.

She thinks that what would happen if took an SSRI is that I would be in for at least two weeks of **** before the receptors would down regulate to normal and id feel good as new.

Im not sure my work would like me freaking out for two weeks.

I also seem to sometimes crave caffeine and feel great for about twenty minutes while the dopamine kicks in then less so when it subsides leaving the upped ANS.

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I also seem to sometimes crave caffeine and feel great for about twenty minutes while the dopamine kicks in then less so when it subsides leaving the upped ANS.

Hello my fellow coca cola addict. :)

Wellbutrin effects dopamine and norepinephrine so it's not technically a SNRI. It's the only AD-type drug I could tolerate. I've tried most of the others. I could sort of tolerate a very small (baby) dose of zoloft but didn't feel like it did much for me. However my neuro at Mayo is wondering if the wellbutrin is causing some of the "hyper-POTS" presentation and exaggerating the problem caused by the neuropathic form of POTS he thinks is my primary issue.

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Rama, I don't have POTS, I have NMH.

She is probably right about the two weeks of yuck -- in my experience every time I up a dose on an SNRI, it gives awful side effects for about a week, then settles a bit and then the side effects go away by the end of the 2nd week (if they are going to go away). I'm in my first week of yuck right now and it is not fun. :( But, in the scheme of things, two weeks of yuck is worth months (or years) of health -- that's why I took some time off from work to do this!

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