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Antidepressants?

George-ananda

Advaita Vedanta, Theosophy, Spiritualism
Premium Member
Prozac worked great for me, but after I built a tolerance I think I got up to 60 or 80 mg. 20 mg worked great for me. But everyone is different so we have to experiment. What is 'AD'?
 

Saint Frankenstein

Here for the ride
Premium Member
I've been on 200mg of Zoloft for over a year and it seems to have helped me. My lows aren't quite as low as before and I seem to snap out of them quicker. I was on Celexa before that. It would work for a while and then not, so the dosage kept having to be increased until I maxed out on it. Tried Wellbutrin. Didn't do anything. I was prescribed Paxil as a teenager, but I never really took it because I was all anti-psych meds at that time, so I can't comment on its effects.
 

1137

Here until I storm off again
Premium Member
I'm on 10mg of Lexapro a day. It should be at least 20, but they made me too tired. I just get it from my PCP and could probably benefit from a more "real" medication that also covers anxiety, but I do so much better as is that the difference is negligible. Anything else I tried ****ed me up. Interestingly I have GI problems, and my doc was saying that the gut is really important to serotonin??? Idk, but SSRIs help both my stomach and depression.
 

beenherebeforeagain

Rogue Animist
Premium Member
Prozac worked for me last summer, but they took me off it because it was making me have to take naps in the afternoon...this was when I wasn't sleeping well at night anyway...So, after a series of other drugs (including a sleeping pill that actually puts me to sleep, so now I get about 8 hours a night of fairly good sleep)...they put me on 40 mg a day...but I started to have constant headache and other symptoms...that's when they realized I have a slow liver, and the drug (and the serotonin) was building up to toxic levels.

They've dropped me back to 20mg every second day, and it's been a month, but the headaches, etc., still haven't stopped, and I'm actually less able to concentrate, think, etc., than I was six months ago...

Other tests start in May...
 

The Hammer

Skald
Premium Member
I'm currently taking 20mg of Paxil (Paroxetine), but it is for Anxiety, not depression. I figured I would chime in anyways since it is still an SSRI. I'm not sure if it is working yet, as I just started it this week. We will see a few weeks from now how it works. Only difference I have noticed is I feel a lot more sluggish.
 

Mackerni

Libertarian Unitarian
My first medication was Lexapro 10mg, for social anxiety disorder, that threw me into a manic phase after finding out that I had dormant bi-polar for most of my life. I hate SSRIs, they're emotionally addicting. I see them as literal "happy pills" that threw my mental chemistry out of wack.
 

Shadow Wolf

Certified People sTabber & Business Owner
Anyone have any luck with SSRI
None. The most recent is Lexapro, but it ended up making me very tired and feeling I needed at least one nap a day. But, I forgot to take it a few times, and by the time I did notice my energy had returned, I realized I wasn't napping throughout the day, and I'm just not willing to take something that's going to sap the energy out of me like that, especially since depression isn't my main issue.
 

Nous

Well-Known Member
Premium Member
The experiences noted here seem to reflect and partly explain why the great majority of people do not take antidepressants very long. Almost half of those who begin taking an antidepressant discontinue it within a month, and within 3 months more than 70% of people have discontinued it: http://www.davidhjacobsphd.com/wp-c...idepressants-debates-in-neuroscience-2006.pdf

Anyone considering taking an antidepressant drug should familiarize oneself with the findings of the NIMH-funded STAR*D study, completed in 2005, which are truly astounding (regardless of the spin by NIMH):

The 35-million-dollar Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study is the largest antidepressant effectiveness study ever conducted. STAR*D enrolled 4,041 depressed patients and provided them with exemplary free acute and continuing antidepressant care to maximize their likelihood of achieving and maintaining remission. Patients who failed to get adequate relief from their first antidepressant were provided with up to three additional trials of pharmacologically distinct treatments. This article identifies numerous instances of apparent bias in the conduct and reporting of outcomes from this study. In contrast to STAR*D’s report of positive findings supporting antidepressants’ effectiveness, only 108 of its 4,041 patients (2.7%) had an acute-care remission, and during the 12 months of continuing care, these patients neither relapsed nor dropped out.​

http://psychrights.org/research/Digest/AntiDepressants/STARDTaleandTrailofBiasPiggot2011.pdf

The protocol for this study was somewhat complicated, and as many reviewers have pointed out, the pre-specified criterion for “remittance” and the criteria for inclusion/exclusion in the various steps of the study were changed after the data were collected. You can’t get much more anti-scientific than changing the criterion for effectiveness after discovering that your drug failed to show effectiveness.

As Pigott explains in the above review, the study consisted of 4 steps in which all subjects were started out on Celexa. The subjects were assessed weekly, and those who did not “remit” (by showing a few points difference on questionnaires) and did not drop out were put into Step 2, which had two possible branches, either trying another one of three possible drugs (Zoloft, Effexor or Wellbutrin), or an “augmentation” study where subjects were given either Buspar or Wellbutrin in addition to Celexa. Those who didn’t drop out and didn’t remit in Step 2 were put into Step 3, again with two branches, either trying one of two tricyclic antidepressants, or an“augmentation” study in which subjects were given lithium and/or thyroid, in addition to their Step 2 drugs. Those who did not remit and did not drop out in this step were put into Step 4, which consisted of trying subjects on either an MAOI or both an SSRI (Effexor) and SNRI (Remeron).

This study was intended to more closely reflect “real world” conditions than the short, small industry-funded efficacy trials that use subjects with atypical characteristics. And obviously the “trial and error” methods of the STAR*D study do reflect the “real world” unscientific methods by which mental disorders are diagnosed and psychiatric drugs are prescribed. Doctors do not need to go through this “trial and error” process for drugs that have been shown to correct actual biochemical imbalances, such as insulin corrects the biochemical imbalance of diabetes Type 1.

But the STAR*D study obviously didn’t resemble the “real world” in most of its methods. Subjects were assessed weekly; had access to free acute care at all times; were given telephone calls prior to appointments and sent letters if no response; and were paid for their participation.

Yet despite all this attention, exemplary care, and cash payments:

. . . Pigott et al.’s analysis found that of the 4,041 patients initially started on citalopram (Celexa), only 1,518 patients (37.6%) obtained remission after up to four medication trials and entered STAR*D’s free continuing care. In every drug trial, more patients dropped out than were remitted and this dropout rate increased throughout the study. Of these 1,518 remitted patients, only 108 (7.1%) survived continuing care without relapsing and/or dropping out. Moreover, it is not known how many of these few patients were one of the 607 patients whose baseline 14 HRSD signified at most only mild symptoms when first started on citalopram (Celexa) and therefore had to score worse during continuing care than when they first entered the study to be counted as relapsed, nor how many actually remained “in remission” during continuing care. This reality directly counters NIMH leaderhip’s false claim that “about 70 percent of those who did not withdraw from the study became symptom-free.”

[. . .]

. . . STAR*D found that 8.6% of step-1 patients reported increased suicidal ideation while taking citalopram (Celexa) during acute phase treatment (Perlis et al., 2007). Furthermore, in another article STAR*D reported that 71.3% of those who had a remission during acute-care treatment reported increased weight gain while taking citalopram (Celexa) and 71.7% reported residual symptoms of sleep disturbance despite having achieved “remission” status (Nierenberg et al., 2010). The increased weight gain during acute-care SSRI drug treatment is of particular significance because a recent study of 165,958 depressed patients found that long-term treatment with SSRIs doubled their risk of developing diabetes (Andersohn, Schade, Suissa, & Garbe, 2009).​

http://psychrights.org/research/Digest/AntiDepressants/STARDTaleandTrailofBiasPiggot2011.pdf

The issue of weight gain and diabetes associated with antidepressant use seems to be rarely mentioned in popular and manufacturer-sponsored articles. I recently noticed that the website WebMD has an article discussing the problem of weight gain (not mentioning diabetes), but claims a far lower percentage of people reporting weight gain than the STAR*D findings of 71%.
 

Jainarayan

ॐ नमो भगवते वासुदेवाय
Staff member
Premium Member
My depression is bipolar hypomanic. I'm on bupropion (Welbutrin) 450 mg. I can't say if it works or not except to say I am still here. Actually between that and lamotrigine (Lamictal, mood stabilizer), my swings are not as frequent. However, they can be rapid and intense. I was on Lexapro but it made the junior Viking not want to go on raids, if you know what I mean. Different meds work differently for different people. My cat is completely different on Prozac (srsly).
 

Shadow Wolf

Certified People sTabber & Business Owner
I was on Lexapro but it made the junior Viking not want to go on raids, if you know what I mean. Different meds work differently for different people.
That's actually a pretty common side effect of Lexapro - Men have a harder time having and maintaning an erection and women have a harder time having an orgasm. But, generally, different meds do tend to work differently for different people.
I'm really not looking forward to telling my therapist that I went off Lexapro. But, she doesn't want me to take naps throughout the day and that was really hard for me to do (sometimes I'd wake up, eat breakfast, and be ready for a nap). If I had the money, I'd try a CBD oil in my vaporizer. It's legal, it doesn't have the psychoactive properties, but it does offer the health benefits of CBD (which is what gives pot a number of it's medicinal properties). If I can take a few puffs to get rid of the edge of anxiety or perk me up when I'm down, I'd much rather do that than keep on playing this game of chemical Russian roulette and popping pills.
 

Nous

Well-Known Member
Premium Member
If I can take a few puffs to get rid of the edge of anxiety or perk me up when I'm down, I'd much rather do that than keep on playing this game of chemical Russian roulette and popping pills.
Me, too. And actually it hardly ever fails to provide me with a few minutes-to-hours of everything being just wonderful.
 

dawny0826

Mother Heathen
I have PMDD and have taken Zoloft off and on for years. It's been more effective than comparable drugs that I've taken. It's not a fix-all, but, does make me feel pretty grounded without draining me of "me".

It's also fairly safe for pregnant and nursing Moms, which is an added plus for me.

Best of luck!
 

Nous

Well-Known Member
Premium Member

atanu

Member
Premium Member
It is surprising to see a lot of people on antidepressants here. Never imagined it to be so widespread.

Risking ridicule and/or ignore, I am suggesting that some of you may wish to try a combination pill containing two herbs called 'Brahmi' and 'Aswagandha'. It may or may not benefit, but will not harm, if tried at minimum dosage for 15 days to a month as a supplement. I am pasting links that may be helpful. With this combination drug there will be no addiction or tapering off of effect. These two work best in combination. One may also wish to study the Ayurvedic perspectives on these two herbs.

https://examine.com/supplements/ashwagandha/
http://v6.examinecdn.com/erd/bengreenfield-ashwagandha.pdf

https://examine.com/supplements/bacopa-monnieri/
http://www.nature.com/npp/journal/v27/n2/full/1395862a.html
http://www.ncbi.nlm.nih.gov/pubmed/21619924
http://www.ncbi.nlm.nih.gov/pubmed/18755259
.........

The following easy meditation can help to soothe troubled minds.

https://itunes.apple.com/us/itunes-u/deep-relaxation-guided-meditation/id434139276?mt=10
 
Last edited:

Nous

Well-Known Member
Premium Member
. . . Zoloft . . .

It's also fairly safe for pregnant and nursing Moms, which is an added plus for me.
There is more thorough information than what I quoted above. I just had not looked at it--since I am not currently planning to become pregnant or nursing an infant:

Sertraline Pregnancy Warnings

Animal studies have failed to reveal evidence of teratogenicity; however, there was evidence of delayed ossification and effects on reproduction attributed to maternal toxicity. Decreased neonatal survival following maternal administration at exposures similar to or slightly greater than the maximum recommended human dose of 200 mg was also observed; the clinical significance is unknown. There are no controlled data in human pregnancy. The results of several studies suggest that the use of SSRIs in the first trimester of pregnancy may be associated with an increased risk of cardiovascular and/or other congenital malformations; however, this association has not been clearly established. The association appears to be strongest for another SSRI, paroxetine. Use of sertraline during pregnancy has been reported to cause symptoms compatible with withdrawal reactions in neonates whose mothers had taken sertraline. Neonates exposed to SSRIs and SNRIs late in the third trimester have uncommonly reported clinical findings including respiratory distress, cyanosis, apnea, seizures, temperature instability, feeding difficulty, vomiting, hypoglycemia, hypotonia, hyperreflexia, tremor, jitteriness, irritability, and constant crying. These effects have mostly occurred either at birth or within a few days of birth. These features are consistent with either a direct toxic effect of SSRIs and SNRIs, or possibly a drug discontinuation syndrome; in some cases, the clinical picture is consistent with serotonin syndrome. The results of a cohort study indicate that 30% of neonates who had prolonged exposure to SSRIs in utero experience symptoms, in a dose-response manner, of a neonatal abstinence syndrome after birth. The authors suggest that infants exposed to SSRIs should be closely monitored for a minimum of 48 hours after birth. Epidemiological data have suggested that the use of SSRIs, particularly in late pregnancy, may increase the risk of persistent pulmonary hypertension in the newborn. Data are not available for SNRIs. One study compared 267 women exposed to an SSRI - either fluvoxamine, paroxetine, or sertraline, to 267 controls. Exposure to SSRIs was not associated with either increased risk for major malformations, higher rates of miscarriage, stillbirth, or prematurity. Mean birth weights among SSRI users were similar to controls as were the gestational ages. The study concluded that the SSRIs fluvoxamine, paroxetine, and sertraline did not appear to increase teratogenic risk when used in their recommended doses. Animal data with sertraline have not shown an effect on fertility. Human case reports from some SSRIs have shown an effect on sperm quality that is reversible. As yet, the impact of this on human fertility has not been observed. AU TGA pregnancy category C: Drugs which, owing to their pharmacological effects, have caused or may be suspected of causing, harmful effects on the human fetus or neonate without causing malformations. These effects may be reversible. Accompanying texts should be consulted for further details. US FDA pregnancy category C: Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks.

This drug should be used during pregnancy only if the potential benefit outweighs the potential risk to the fetus, taking into account the risks of untreated depression. AU TGA pregnancy category: C US FDA pregnancy category: C Comments: Newborns should be monitored if the maternal use of this drug continues into the later stages of pregnancy, particularly, the third trimester.

See references

Sertraline Breastfeeding Warnings

Benefit should outweigh risk; use is not generally recommended. Excreted into human milk: Yes Comments: -This drug has been considered one of the preferred antidepressants during breastfeeding -Accumulation of the drug may occur in preterm infants with impaired metabolic activity; effects similar to neonatal abstinence may rarely present in these infants. -Mothers taking an SSRI during pregnancy and postpartum may have difficulty breastfeeding and may require additional breastfeeding support.

Benign neonatal sleep myoclonus in a 4-month-old infant and agitation in that spontaneously resolved in another infant was reported to the Australian Adverse Drug Reaction Advisory Committee and may be related to the presence of sertraline in breastmilk. Levels of sertraline in breastmilk are reported to be low; the weakly active metabolite desmethylsertraline may be detectable in low levels. In a study of 26 breastfeeding women who were, on average, 15.8 weeks postpartum and receiving an average of 124 mg sertraline daily for at least 14 days for severe depression, complete sets of milk sample data were available for 15 mothers. Analysis of these samples led the study authors to estimate that an exclusively breastfed infant would receive an average of 0.54% of the maternal weight-adjusted dosage. Pumping and discarding milk 8 to 9 hours after the mother's dose would decrease the infant's daily dosage by 17%. Amounts of sertraline ingested by breastfed infants are reported to be small. There was an analysis of 30 breastfed infants aged 6 to 13 weeks, of which 19 were exclusively breastfed and 11 breastfed at least half the time. Serum sertraline levels were below 1 mcg/L in 22 infants. The other 8 infants had an average serum sertraline level of 7.9 mcg/L; their mothers were taking a average of 109 mg sertraline daily, with an average serum level of 52.8 mcg/L. The data from one study on three breast-fed infants suggested that sertraline and/or its almost inactive metabolite norsertraline may be present at very low concentrations in the plasma of breast-fed infants. No adverse effects were noted in the infants. A pooled analysis of 53 mother-infant pairs from published and unpublished cases found that infants had an average of 2% of the sertraline plasma levels of the mothers'; three of the infants had a plasma level greater than 10% of the mothers'. A study of fourteen mother-infant pairs reported that while mothers receiving clinical doses of sertraline experienced substantial blockade of the platelet 5-HT transporter, platelet 5-HT uptake in nursing infants of treated mothers was unaltered. Another study of twelve breast-feeding mothers reported that both sertraline and desmethylsertraline were present in all breast milk samples. Detectable levels of sertraline were reported in three nursing infants and detectable levels of desmethylsertraline were reported in six infants. A case study of a mother breast-feeding while receiving sertraline therapy has also been reported. The drug was found to be present in the mother's milk. However, no sertraline was detected in the infant's serum and no abnormal occurrences were noted in the development of this infant either.

See references​

http://www.drugs.com/pregnancy/sertraline.html

It’s unfortunate that they provide such important information in these unparagraphed walls of writing.
 

dawny0826

Mother Heathen
There is more thorough information than what I quoted above. I just had not looked at it--since I am not currently planning to become pregnant or nursing an infant:

Sertraline Pregnancy Warnings

Animal studies have failed to reveal evidence of teratogenicity; however, there was evidence of delayed ossification and effects on reproduction attributed to maternal toxicity. Decreased neonatal survival following maternal administration at exposures similar to or slightly greater than the maximum recommended human dose of 200 mg was also observed; the clinical significance is unknown. There are no controlled data in human pregnancy. The results of several studies suggest that the use of SSRIs in the first trimester of pregnancy may be associated with an increased risk of cardiovascular and/or other congenital malformations; however, this association has not been clearly established. The association appears to be strongest for another SSRI, paroxetine. Use of sertraline during pregnancy has been reported to cause symptoms compatible with withdrawal reactions in neonates whose mothers had taken sertraline. Neonates exposed to SSRIs and SNRIs late in the third trimester have uncommonly reported clinical findings including respiratory distress, cyanosis, apnea, seizures, temperature instability, feeding difficulty, vomiting, hypoglycemia, hypotonia, hyperreflexia, tremor, jitteriness, irritability, and constant crying. These effects have mostly occurred either at birth or within a few days of birth. These features are consistent with either a direct toxic effect of SSRIs and SNRIs, or possibly a drug discontinuation syndrome; in some cases, the clinical picture is consistent with serotonin syndrome. The results of a cohort study indicate that 30% of neonates who had prolonged exposure to SSRIs in utero experience symptoms, in a dose-response manner, of a neonatal abstinence syndrome after birth. The authors suggest that infants exposed to SSRIs should be closely monitored for a minimum of 48 hours after birth. Epidemiological data have suggested that the use of SSRIs, particularly in late pregnancy, may increase the risk of persistent pulmonary hypertension in the newborn. Data are not available for SNRIs. One study compared 267 women exposed to an SSRI - either fluvoxamine, paroxetine, or sertraline, to 267 controls. Exposure to SSRIs was not associated with either increased risk for major malformations, higher rates of miscarriage, stillbirth, or prematurity. Mean birth weights among SSRI users were similar to controls as were the gestational ages. The study concluded that the SSRIs fluvoxamine, paroxetine, and sertraline did not appear to increase teratogenic risk when used in their recommended doses. Animal data with sertraline have not shown an effect on fertility. Human case reports from some SSRIs have shown an effect on sperm quality that is reversible. As yet, the impact of this on human fertility has not been observed. AU TGA pregnancy category C: Drugs which, owing to their pharmacological effects, have caused or may be suspected of causing, harmful effects on the human fetus or neonate without causing malformations. These effects may be reversible. Accompanying texts should be consulted for further details. US FDA pregnancy category C: Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks.

This drug should be used during pregnancy only if the potential benefit outweighs the potential risk to the fetus, taking into account the risks of untreated depression. AU TGA pregnancy category: C US FDA pregnancy category: C Comments: Newborns should be monitored if the maternal use of this drug continues into the later stages of pregnancy, particularly, the third trimester.

See references

Sertraline Breastfeeding Warnings

Benefit should outweigh risk; use is not generally recommended. Excreted into human milk: Yes Comments: -This drug has been considered one of the preferred antidepressants during breastfeeding -Accumulation of the drug may occur in preterm infants with impaired metabolic activity; effects similar to neonatal abstinence may rarely present in these infants. -Mothers taking an SSRI during pregnancy and postpartum may have difficulty breastfeeding and may require additional breastfeeding support.

Benign neonatal sleep myoclonus in a 4-month-old infant and agitation in that spontaneously resolved in another infant was reported to the Australian Adverse Drug Reaction Advisory Committee and may be related to the presence of sertraline in breastmilk. Levels of sertraline in breastmilk are reported to be low; the weakly active metabolite desmethylsertraline may be detectable in low levels. In a study of 26 breastfeeding women who were, on average, 15.8 weeks postpartum and receiving an average of 124 mg sertraline daily for at least 14 days for severe depression, complete sets of milk sample data were available for 15 mothers. Analysis of these samples led the study authors to estimate that an exclusively breastfed infant would receive an average of 0.54% of the maternal weight-adjusted dosage. Pumping and discarding milk 8 to 9 hours after the mother's dose would decrease the infant's daily dosage by 17%. Amounts of sertraline ingested by breastfed infants are reported to be small. There was an analysis of 30 breastfed infants aged 6 to 13 weeks, of which 19 were exclusively breastfed and 11 breastfed at least half the time. Serum sertraline levels were below 1 mcg/L in 22 infants. The other 8 infants had an average serum sertraline level of 7.9 mcg/L; their mothers were taking a average of 109 mg sertraline daily, with an average serum level of 52.8 mcg/L. The data from one study on three breast-fed infants suggested that sertraline and/or its almost inactive metabolite norsertraline may be present at very low concentrations in the plasma of breast-fed infants. No adverse effects were noted in the infants. A pooled analysis of 53 mother-infant pairs from published and unpublished cases found that infants had an average of 2% of the sertraline plasma levels of the mothers'; three of the infants had a plasma level greater than 10% of the mothers'. A study of fourteen mother-infant pairs reported that while mothers receiving clinical doses of sertraline experienced substantial blockade of the platelet 5-HT transporter, platelet 5-HT uptake in nursing infants of treated mothers was unaltered. Another study of twelve breast-feeding mothers reported that both sertraline and desmethylsertraline were present in all breast milk samples. Detectable levels of sertraline were reported in three nursing infants and detectable levels of desmethylsertraline were reported in six infants. A case study of a mother breast-feeding while receiving sertraline therapy has also been reported. The drug was found to be present in the mother's milk. However, no sertraline was detected in the infant's serum and no abnormal occurrences were noted in the development of this infant either.

See references​

http://www.drugs.com/pregnancy/sertraline.html

It’s unfortunate that they provide such important information in these unparagraphed walls of writing.

I'm well educated as to the potential risks of all medications that I'm taking. Further, I trust the advisement and decisions that I make with my physician over that which is offered by a stranger on the internet.
 

Nous

Well-Known Member
Premium Member
I'm well educated as to the potential risks of all medications that I'm taking. Further, I trust the advisement and decisions that I make with my physician over that which is offered by a stranger on the internet.
I didn’t give any advice; I merely quoted the summary of the evidence cited in the PDR. If you know of any evidence contradicting it, be sure to provide it.
 
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