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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 12 to 36 of 36. Go back in thread:
Posted by Quintal on August 21, 2007, at 17:01:46
In reply to Re: SSRIs and bone loss » Quintal, posted by Larry Hoover on August 21, 2007, at 16:34:56
Well I've taken multivitamins containing vitamin D for years, long before I started taking psych meds, so I hope that confers some protection. I suspect you're going to tell me I'm not taking enough though?
>Maybe SSRIs do inhibit the blasts....but vitamin D activates them.
I trust you know better than me on that Lar, though we'd need controlled trials to demonstrate that vitamin D was actually effective in reversing/preventing SSRI-induced bone loss. It seems exposure to TCAs may also be a risk factor. I wonder what the powers that be are going to do about this?
>Vitamin D intake recommendations are being constantly increased. Last I saw, there were doctors lobbying for an RDA of about 4000 IU/day.
My multivitamin supplement falls well short of that at 5 micrograms/day. 4000IU seems to be well above the current U.S. Dietary Reference Intake Tolerable Upper Intake Level:
__________________________________________________The exact long-term safe dose of vitamin D is not entirely known, but dosages up to 60 micrograms (2,400 IU) /day in healthy adults are believed to be safe.[8] The U.S. Dietary Reference Intake Tolerable Upper Intake Level (UL) of vitamin D for children and adults is 50 micrograms/day (2000 IU/day).
http://en.wikipedia.org/wiki/Calciferol#Overdose
__________________________________________________Q
Posted by linkadge on August 21, 2007, at 17:17:17
In reply to Re: SSRIs and bone loss » Larry Hoover, posted by Quintal on August 21, 2007, at 17:01:46
Could the differential effects of the two classes on HPA axis function have anything to do with it?
Amitryptaline and other TCA's fairly potently supresses the release of certain steroid hormones (ie cortisol) wherase the SSRI's can increase.
Linkadge
Posted by Quintal on August 21, 2007, at 17:23:13
In reply to Re: SSRIs and bone loss » Quintal, posted by Larry Hoover on August 21, 2007, at 16:30:48
>I'd have speculated on the orthostatic hypotension and heart rhythm disturbances associated with tricyclics....
Well I suggested another two there to add to your list.
>On reading the abstract, I don't see anything about mechanism.
True, such a statement would not stand in a court of law, but I hoped it would suffice to convey my meaning on a message board. Please forgive my vagueness, I am a little impaired at present.
From what I gather the secondary-amine TCAs nortriptyline and desipramine have less affinity for the serotonin transporter than tertiary-amine TCAs, yet in this study they correlate with a higher incidence of hip fracture than the tertiary-amine TCAs, unless I read the results backwards. So this would imply some other causal factor besides the serotonin transporter?
Q
Posted by Larry Hoover on August 21, 2007, at 17:38:26
In reply to Re: SSRIs and bone loss » Larry Hoover, posted by Quintal on August 21, 2007, at 17:01:46
> Well I've taken multivitamins containing vitamin D for years, long before I started taking psych meds, so I hope that confers some protection. I suspect you're going to tell me I'm not taking enough though?
It depends on many variables....however, it is my belief that >90% do not obtain an optimal intake of this vitamin.
> >Maybe SSRIs do inhibit the blasts....but vitamin D activates them.
>
> I trust you know better than me on that Lar, though we'd need controlled trials to demonstrate that vitamin D was actually effective in reversing/preventing SSRI-induced bone loss. It seems exposure to TCAs may also be a risk factor. I wonder what the powers that be are going to do about this?If vitamin D is not the solution, then I really don't know what might work in its place....apart from drugs such as Fosamax. Yes, the whole thing needs more study.
> >Vitamin D intake recommendations are being constantly increased. Last I saw, there were doctors lobbying for an RDA of about 4000 IU/day.
>
> My multivitamin supplement falls well short of that at 5 micrograms/day.I believe the conversion is 5 mcg = 200 IU. That's modest, in current thinking.
> 4000IU seems to be well above the current U.S. Dietary Reference Intake Tolerable Upper Intake Level:
> __________________________________________________
>
> The exact long-term safe dose of vitamin D is not entirely known, but dosages up to 60 micrograms (2,400 IU) /day in healthy adults are believed to be safe.[8] The U.S. Dietary Reference Intake Tolerable Upper Intake Level (UL) of vitamin D for children and adults is 50 micrograms/day (2000 IU/day).
> http://en.wikipedia.org/wiki/Calciferol#Overdose
> __________________________________________________
>
> QIndeed, but as mentioned in this one example of the debate I alluded to, that level was set in 1997, based on data obtained much earlier than that.
Am J Clin Nutr. 2007 Jan;85(1):6-18.
Risk assessment for vitamin D.Hathcock JN, Shao A, Vieth R, Heaney R.
Council for Responsible Nutrition, Washington, DC 20036-5114, USA. jhathcock@crnusa.orgThe objective of this review was to apply the risk assessment methodology used by the Food and Nutrition Board (FNB) to derive a revised safe Tolerable Upper Intake Level (UL) for vitamin D. New data continue to emerge regarding the health benefits of vitamin D beyond its role in bone. The intakes associated with those benefits suggest a need for levels of supplementation, food fortification, or both that are higher than current levels. A prevailing concern exists, however, regarding the potential for toxicity related to excessive vitamin D intakes. The UL established by the FNB for vitamin D (50 microg, or 2000 IU) is not based on current evidence and is viewed by many as being too restrictive, thus curtailing research, commercial development, and optimization of nutritional policy. Human clinical trial data published subsequent to the establishment of the FNB vitamin D UL published in 1997 support a significantly higher UL. We present a risk assessment based on relevant, well-designed human clinical trials of vitamin D. Collectively, the absence of toxicity in trials conducted in healthy adults that used vitamin D dose > or = 250 microg/d (10,000 IU vitamin D3) supports the confident selection of this value as the UL.
I have seen literature that supports 4,000 IU as the a physiological median requirement for normalization of blood chemistry. That's not to say that more might not yet be superior, but that less *is* deficient.
Lar
Posted by Larry Hoover on August 21, 2007, at 17:42:33
In reply to Re: SSRIs and bone loss » Larry Hoover, posted by Quintal on August 21, 2007, at 17:23:13
> >I'd have speculated on the orthostatic hypotension and heart rhythm disturbances associated with tricyclics....
>
> Well I suggested another two there to add to your list.Lots of reasons to wobble.
> >On reading the abstract, I don't see anything about mechanism.
>
> True, such a statement would not stand in a court of law, but I hoped it would suffice to convey my meaning on a message board. Please forgive my vagueness, I am a little impaired at present.Sorry. I wasn't meaning to sound picky. I just didn't see what you meant.
> From what I gather the secondary-amine TCAs nortriptyline and desipramine have less affinity for the serotonin transporter than tertiary-amine TCAs, yet in this study they correlate with a higher incidence of hip fracture than the tertiary-amine TCAs, unless I read the results backwards. So this would imply some other causal factor besides the serotonin transporter?
>
> QI don't know. And I've spent my frail capacity for today. I can no longer think clearly. Let's see what others can add to this understanding.
Lar
Posted by Quintal on August 21, 2007, at 18:23:24
In reply to Re: SSRIs and bone loss » Quintal, posted by Larry Hoover on August 21, 2007, at 17:42:33
>Sorry. I wasn't meaning to sound picky. I just didn't see what you meant.
It seemed to me that the authors expected to find a lower incidence of hip fracture among SSRI users because of this passage: "Selective serotonin-reuptake inhibitors (SSRIs) are reported to be better tolerated than TCAs.". TCAs are usually deemed less tolerable due to their common side effects; sedation, cognitive impairment, and yes certainly orthostatic hypotension and cardiac problems. These side effects are a common cause of falls in the elderly, and falls are the main cause of hip fractures in the elderly. Therefore it would be logical to hypothesize that SSRIs would be associated with lower incidence of hip fractures than TCAs; because they are associated with a lower incidence of these fall-inducing side effects than TCAs. I thought this was the most likely explanation the inclusion of this passage in their report: "Selective serotonin-reuptake inhibitors (SSRIs) are reported to be better tolerated than TCAs.". They found results to the contrary (of what I'm assuming was their hypothesis); that SSRIs were associated with a higher incidence of hip fractures than TCAs, yet still found that treatment with TCAs increased the risk of hip fracture. So that's what I meant.
Q
Posted by Quintal on August 21, 2007, at 18:38:09
In reply to Re: SSRIs and bone loss, posted by linkadge on August 21, 2007, at 17:17:17
I remember you saying that SSRIs could cause adrenal fatigue or something like that a while ago, because they increase cortisol release/production? And the HPA axis controls cortisol release/production? I've read that serotonin is the neurotransmitter that modulates stress response, by activating the HPA axis and increasing cortisol. So that is an interesting link. How to explain the differential effects of the secondary-amine TCAs/tertiary-amine TCAs on serotonin though? Secondary-amine TCAs have less affinity for the serotonin transporter don't they? Yet in that study they were associated with a higher incidence of hip fractures than tertiary-amine TCAs, which have greater affinity for the serotonin transporter, if my source is correct.
So what to make of it? Do they have different effects on the HPA axis independent of the serotonin transporter? Or is some other mechanism at play, or more likely a combination of mechanisms.
Q
Posted by linkadge on August 21, 2007, at 19:37:22
In reply to Re: SSRIs and bone loss » linkadge, posted by Quintal on August 21, 2007, at 18:38:09
>I remember you saying that SSRIs could cause >adrenal fatigue or something like that a while >ago, because they increase cortisol >release/production? And the HPA axis controls >cortisol release/production? I've read that >serotonin is the neurotransmitter that modulates >stress response, by activating the HPA axis and >increasing cortisol. So that is an interesting >link. How to explain the differential effects of >the secondary-amine TCAs/tertiary-amine TCAs on >serotonin though? Secondary-amine TCAs have less >affinity for the serotonin transporter don't >they?
But the HPA regulating effects of the TCA's are probably unrelated to their effects on monamine uptake. The TCA trimipramine shares with other TCA's the ability to regulate genes responsable for HPA axis regulation, wherase the SSRI's don't have any class effect on the HPA axis.
>Yet in that study they were associated with a >higher incidence of hip fractures than tertiary->amine TCAs, which have greater affinity for the >serotonin transporter, if my source is correct.
Not exactly sure. Old data may be less direct or comprehensive. One wouldn't expect the less anticholinergic tertiary TCA's to produce more falls. I would tend to think that the correlation is not directly related to affinity for the serotonin uptake pump.
Perhaps, because the tertiary amines are better tollerated, they can be used in higher doses?
>So what to make of it? Do they have different >effects on the HPA axis independent of the >serotonin transporter? Or is some other >mechanism at play, or more likely a combination >of mechanisms.
Not sure. Did they comapre those treated with AD's to age matched depression sevarity matched drug free controls? (I didn't read all of above data). Ie to exclude the possability that depression itself isn't the cause of the bone loss?
Linkadge
Posted by Larry Hoover on August 21, 2007, at 19:47:03
In reply to Re: SSRIs and bone loss, posted by linkadge on August 21, 2007, at 19:37:22
> Did they comapre those treated with AD's to age matched depression sevarity matched drug free controls? (I didn't read all of above data). Ie to exclude the possability that depression itself isn't the cause of the bone loss?
>
>
> LinkadgeThe study of older females did use factor analysis to control for confounders, including and excluding depression. It didn't seem to make a difference.
"After adjustment for potential confounders, including the Geriatric Depression Scale score, mean total hip BMD decreased 0.47% per year in nonusers compared with 0.82% in SSRI users (P<.001) and 0.47% in TCA users (P=.99). Higher rates of bone loss were also observed at the 2 hip subregions for SSRI users. Results were not substantially altered when women who scored at least 6 on the Geriatric Depression Scale were excluded from the analysis."
The data for males were not corrected for depression. Yes, depression may be a true confound, notwithstanding the lack of significant effect of depression in the female cohort.
Lar
Posted by linkadge on August 21, 2007, at 19:50:02
In reply to Re: SSRIs and bone loss, posted by linkadge on August 21, 2007, at 19:37:22
Does anyone have any idea what percentage of tranporter occupancy a TCA would produce at theraputic concentrations?
I am not of the belief that a certain SERT binding is necessary to produce and AD effect.
NRi's are better REM supressors than SSRI's, and multiplicity of action probably means less of each target is necessary to produce an effect.
Linkadge
Posted by linkadge on August 21, 2007, at 19:52:38
In reply to Re: SSRIs and bone loss » linkadge, posted by Larry Hoover on August 21, 2007, at 19:47:03
Who knows, perhaps SSRI's users are in general more hypokinetic?
I did a lot more veging out on SSRI's than off.
Any animal studies?
Linkadge
Posted by Larry Hoover on August 21, 2007, at 20:00:59
In reply to Re: SSRIs and bone loss, posted by linkadge on August 21, 2007, at 19:37:22
Doh! Didn't take a second to find that the link with depression is quite well established.
Lar
Full text: http://www.pnas.org/cgi/content/full/103/45/16876
Abstract:
Proc Natl Acad Sci U S A. 2006 Nov 7;103(45):16876-81. Epub 2006 Oct 30.
Depression induces bone loss through stimulation of the sympathetic nervous system.
Yirmiya R, Goshen I, Bajayo A, Kreisel T, Feldman S, Tam J, Trembovler V, Csernus V, Shohami E, Bab I.
Department of Psychology, Faculty of Social Sciences, Hebrew University of Jerusalem, Mount Scopus, Jerusalem 91905, Israel. razyirmiya@huji.ac.ilMajor depression is associated with low bone mass and increased incidence of osteoporotic fractures. However, causality between depression and bone loss has not been established. Here, we show that mice subjected to chronic mild stress (CMS), an established model of depression in rodents, display behavioral depression accompanied by impaired bone mass and structure, as portrayed by decreases in trabecular bone volume density, trabecular number, and trabecular connectivity density assessed in the distal femoral metaphysis and L3 vertebral body. Bone remodeling analysis revealed that the CMS-induced skeletal deficiency is accompanied by restrained bone formation resulting from reduced osteoblast number. Antidepressant therapy, which prevents the behavioral responses to CMS, completely inhibits the decrease in bone formation and markedly attenuates the CMS-induced bone loss. The depression-triggered bone loss is associated with a substantial increase in bone norepinephrine levels and can be blocked by the beta-adrenergic antagonist propranolol, suggesting that the sympathetic nervous system mediates the skeletal effects of stress-induced depression. These results define a linkage among depression, excessive adrenergic activity, and reduced bone formation, thus demonstrating an interaction among behavioral responses, the brain, and the skeleton, which leads to impaired bone structure. Together with the common occurrence of depression and bone loss in the aging population, the present data implicate depression as a potential major risk factor for osteoporosis and the associated increase in fracture incidence.
Posted by Quintal on August 21, 2007, at 20:06:51
In reply to Re: SSRIs and bone loss, posted by linkadge on August 21, 2007, at 19:37:22
>But the HPA regulating effects of the TCA's are probably unrelated to their effects on monamine uptake. The TCA trimipramine shares with other TCA's the ability to regulate genes responsable for HPA axis regulation, wherase the SSRI's don't have any class effect on the HPA axis.
How do SSRIs raise cortisol levels?
>One wouldn't expect the less anticholinergic tertiary TCA's to produce more falls. I would tend to think that the correlation is not directly related to affinity for the serotonin uptake pump.
The tertiary-amine TCAs are associated with more anticholinergic side effects than the secondary-amine TCAs.
>Perhaps, because the tertiary amines are better tollerated, they can be used in higher doses?
The tertiary-amine TCAs amitriptyline, imipramine etc. are the lest well tolerated out of the three antidepressant groups.
Q
Posted by linkadge on August 21, 2007, at 20:10:27
In reply to Re: depression and bone loss » linkadge, posted by Larry Hoover on August 21, 2007, at 20:00:59
Interesting that they link this to an effect of of the stress responce system.
I wonder what AD's were used in this study, or if differential effects among AD's on HPA axis function is relavant?
I know, for instance, in a study of women, cortisol levels remained elevated even after months of sertraline treatment. I wonder if this normalizes over time.
Linkadge
Posted by Quintal on August 21, 2007, at 20:16:00
In reply to Re: depression and bone loss » linkadge, posted by Larry Hoover on August 21, 2007, at 20:00:59
__________________________________________________
1: J Am Geriatr Soc. 2007 Jun;55(6):824-31.Click here to read Links
Depressive symptoms and rates of bone loss at the hip in older women.
Diem SJ, Blackwell TL, Stone KL, Yaffe K, Cauley JA, Whooley MA, Ensrud KE; Study of Osteoporotic Fractures.Department of Medicine, Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN 55415, USA. sdiem@umn.edu
OBJECTIVES: To ascertain whether depressive symptoms are associated with increased rates of bone loss at the hip. DESIGN: Population-based prospective cohort study. SETTING: Four clinical centers in the United States. PARTICIPANTS: Four thousand one hundred seventy-seven community-dwelling women, aged 69 and older, enrolled in the Study of Osteoporotic Fractures. MEASUREMENTS: Depressive symptoms were assessed using the Geriatric Depression Scale (GDS). Subjects were categorized as depressed if their GDS score was 6 or greater at the fourth examination. Bone mineral density (BMD) at the hip was measured using dual-energy x-ray absorptiometry at the fourth and sixth examinations (average 4.4 years between examinations). Use of antidepressant medications was assessed by interview and verified from medication containers at the fourth and sixth examinations of the Study of Osteoporotic Fractures. A computerized dictionary was used to categorize type of medication. RESULTS: In age-adjusted models, mean total hip BMD decreased 0.69%/year in 3,977 women with a GDS score of less than 6, compared with 0.96%/year in 200 women with a GDS score of 6 or greater (P<.01). Results were not substantially altered when adjusted for potential confounders and when users of antidepressants were excluded from the analysis. CONCLUSION: Depression, as defined by a GDS score of 6 or greater, was associated with an increased rate of bone loss at the hip in this cohort of older women. Clinicians should be aware of a possible increased rate of bone loss in older, depressed women.
PMID: 17537081 [PubMed - indexed for MEDLINE]
__________________________________________________Q
Posted by Quintal on August 21, 2007, at 20:20:21
In reply to Re: depression and bone loss, posted by Quintal on August 21, 2007, at 20:16:00
__________________________________________________
1: Med Hypotheses. 2001 Oct;57(4):469-71.Click here to read Links
Selective serotonin-reuptake inhibitor antidepressants increase the risk of falls and hip fractures in elderly people by inhibiting cardiovascular ion channels.
Pacher P, Ungvari Z.Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. ppacher@hotmail.com
Surprising results from recently published retrospective studies show that the use of new selective serotonin-reuptake inhibitor antidepressants (SSRIs), similarly to the older tricyclic antidepressants (TCAs), increases the risk of falls and hip fractures among elderly people.The mechanism whereby antidepressants increase this risk is complex and may include orthostatic hypotension, arrhythmias, sedation and confusion. The increased risk of falls and hip fractures with the use of TCAs is not surprising considering their well-known cardiovascular, anticholinergic and antihistaminergic side-effects. But the increased risk of falls with SSRIs is highly unexpected since these drugs are believed to be free from the disadvantages of TCAs.We hypothesized that the new SSRI antidepressants may also have cardiovascular effects similarly to the older TCA compounds, which may be an explanation for the increased rate of falls and hip fractures. The experimental and clinical evidence in support of this hypothesis are discussed. Copyright 2001 Harcourt Publishers Ltd.
PMID: 11601871 [PubMed - indexed for MEDLINE]
--------------------------------------------------: Am J Epidemiol. 2003 Jul 1;158(1):77-84.Click here to read Links
Exposure to tricyclic and selective serotonin reuptake inhibitor antidepressants and the risk of hip fracture.
Hubbard R, Farrington P, Smith C, Smeeth L, Tattersfield A.Division of Respiratory Medicine, University of Nottingham, Nottingham City Hospital, Nottingham, England. Richard.hubbard@nottingham.ac.uk
The use of tricyclic antidepressants is associated with an increased risk of hip fracture. Despite a better side effect profile, this adverse effect has also been reported for selective serotonin reuptake inhibitors. To determine whether these findings result from bias arising from the case-control method, the authors have performed a case-control analysis and a self-controlled case-series analysis using 1987-1999 diagnosis data for 16,341 cases of hip fracture and 29,889 controls drawn from the United Kingdom General Practice Research Database. Both analyses showed an association between hip fracture and antidepressant treatment, and this was most marked during the first 15 days of treatment. The estimates from the case-control study were larger than those from the case-series analysis: The odds ratios for fracture within the first 15 days of a prescription for tricyclic antidepressants and serotonin reuptake inhibitors were 4.76 (95% confidence interval (CI): 3.06, 7.41) and 6.30 (95% CI: 2.65, 14.97), whereas the equivalent incidence ratios were 2.30 (95% CI: 1.82, 2.90) and 1.96 (95% CI: 1.35, 2.83). Tricyclic antidepressants and serotonin reuptake inhibitors are both associated with an independent increase in hip fracture incidence during the first weeks of treatment. The estimates from the case-series analyses were smaller than those from the case-control analyses, suggesting that the case-control method is subject to bias.
PMID: 12835289 [PubMed - indexed for MEDLINE]
__________________________________________________Q
Posted by linkadge on August 21, 2007, at 20:26:09
In reply to Re: SSRIs and bone loss » linkadge, posted by Quintal on August 21, 2007, at 20:06:51
>How do SSRIs raise cortisol levels?
Not sure. Some, but not all, studies link them to long term elevations in cortisol levels.
>The tertiary-amine TCAs are associated with more >anticholinergic side effects than the secondary->amine TCAs.Yeah, pardon me, I confused the two class names. Perhaps, since the secondary amines are better tollerated, they can be used in higer doses. If some, yet undidentified, dose related factor was at work, then a higher dose might mean something.
For instance, if there was a noradrenergic link to bone loss too, then higher doses, or more relative affinity for norepiniehprine reuptake might be important. (The study lary posted, for instance, said that stress induced bone loss could be prevented by beta adrenergic receptor blockade). So beta adrenergic receptor agonism might be a factor.
Linkadge
Posted by linkadge on August 21, 2007, at 20:29:09
In reply to Possible Mechanisms, posted by Quintal on August 21, 2007, at 20:20:21
The SSRI's are still powerful CNS active drugs. I am fairly young but noted increased in "accidencts" on SSRI's. Bumping into walls, falling etc.
Thats why I thought it was necessary to separate the CNS responsable effects on falling, and the effects of the drug on bone demineralziation.
Linkadge
Posted by linkadge on August 21, 2007, at 20:31:58
In reply to Re: Possible Mechanisms, posted by linkadge on August 21, 2007, at 20:29:09
There are other potential hormonal mechanisms too. SSRI's can affect testosterone, growth hormone levels etc.
The effects of hormones on bone density are well documented.
Linkadge
Posted by Quintal on August 21, 2007, at 20:43:11
In reply to Re: SSRIs and bone loss, posted by linkadge on August 21, 2007, at 20:26:09
>For instance, if there was a noradrenergic link to bone loss too, then higher doses, or more relative affinity for norepiniehprine reuptake might be important. (The study lary posted, for instance, said that stress induced bone loss could be prevented by beta adrenergic receptor blockade). So beta adrenergic receptor agonism might be a factor.
Yeah, I saw that too, and when you consider that the secondary-amine TCAs desipramine and nortriptyline are strongly noradrenergic that might explain the higher incidence of hip fracture relative to the tertiary-amine TCA group, but not the SSRI group, unless the SSRIs used were the more strongly noradrenergic ones, like Prozac, and used at high doses. The study says "The proportion of current use in the low-dose range was 22% for SSRIs, 50% for secondary-amine TCAs, and 58% for tertiary-amine TCAs.". So most of the SSRI group were in the moderate-to-high dose range (possibly due to greater tolerability at high doses)? The tertiary-amine group were exposed to the lowest doses out of the three groups. So there may be at least some correlation between dose and risk of hip fracture, and that may be just as important as drug class.
Q
Posted by Quintal on August 21, 2007, at 21:00:18
In reply to Re: Possible Mechanisms, posted by linkadge on August 21, 2007, at 20:31:58
I wish there were studies on the association between reboxetine and atomoxetine and hip fracture, but I can't find any.
Q
Posted by nellie7 on August 22, 2007, at 14:11:30
In reply to Re: Possible Mechanisms, posted by linkadge on August 21, 2007, at 20:31:58
> There are other potential hormonal mechanisms too. SSRI's can affect testosterone, growth hormone levels etc
What do SSRIs do to testosterone and growth hormone levels?
Posted by linkadge on August 22, 2007, at 16:37:01
In reply to Re: Possible Mechanisms » linkadge, posted by nellie7 on August 22, 2007, at 14:11:30
Not sure specifically for testosterone or estrogen, but I do know that SSRI's can reduce growth hormone excretion, esp in the nighttime.
I think they can also decrease testosterone.
Linkadge
Posted by Phillipa on August 23, 2007, at 12:12:16
In reply to Re: Possible Mechanisms, posted by linkadge on August 22, 2007, at 16:37:01
My endo says synthroid or other thyroid meds can cause osteoporosis or penia too especially with cytomel. I do have both now. Don't want to take boniva,actonel, or fosamax. Phillipa
Posted by rskontos on August 25, 2007, at 16:27:34
In reply to Re: Possible Mechanisms, posted by Phillipa on August 23, 2007, at 12:12:16
Something else we aren't being told prior to taking the SSRI. I am new to this thread. How long do you have to be on the SSRI before the loss occurs?
This is the end of the thread.
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