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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 25 of 36. This is the beginning of the thread.
Posted by Larry Hoover on August 21, 2007, at 14:56:13
I'm not convinced of the explanation given in these abstracts (other agents have serotonin transporter suppressive action, but are not implicated), but the circumstantial evidence is there: SSRIs are associated with bone density reduction in both genders. Vitamin D, folks. Vitamin D.
Lar
Posted by Quintal on August 21, 2007, at 15:18:45
In reply to SSRIs and bone loss, posted by Larry Hoover on August 21, 2007, at 14:56:13
"The observed difference in BMD for SSRIs is similar to that seen with glucocorticoids."
Bloody Hell...
__________________________________________________CONCLUSIONS: In this population of men, BMD was lower among those reporting current SSRI use, but not among users of other antidepressants. Further research is needed to confirm this finding in light of widespread SSRI use and potentially important clinical implications.
--------------------------------------------------
CONCLUSION: Use of SSRIs but not TCAs is associated with an increased rate of bone loss at the hip in this cohort of older women.
__________________________________________________What inspired you to seek out these studies Lar? I see they're both very recent - June/July this year. Interesting. Of course I knew they were bad all along ;-) I've never checked to see if SSRI use is correlated with cellulitis, but I think I will. Doctors always told me there was no link, but I had this with every SSRI, and it was debilitating. Ruined my education because I had to keep going into hospital every few months. I'll have a look and see.
Q
Posted by sam123 on August 21, 2007, at 15:32:00
In reply to Re: SSRIs and bone loss » Larry Hoover, posted by Quintal on August 21, 2007, at 15:18:45
> "The observed difference in BMD for SSRIs is similar to that seen with glucocorticoids."
>
I had bone loss due to glucocorticoid use; it is easy to reverse. I now have normal done density
for a person my age. Done density is easy to measure.
Posted by Quintal on August 21, 2007, at 15:36:21
In reply to SSRIs and bone loss, posted by Larry Hoover on August 21, 2007, at 14:56:13
So what is the vitamin D link Lar?
I see this older study found increased risk of hip fracture in all groups taking antidepressants, but the SSRI group had the highest incidence. Interesting, because I get the impression the researchers seem to have set out expecting to find a lower incidence of hip fracture among SSRI users because they are 'better tolerated' (I assume they were thinking sedation and cognitive impairment was the cause of falls, and hence higher incidence of hip fractures, but their results seem to suggest a different mechanism).
__________________________________________________1: Lancet. 1998 May 2;351(9112):1303-7.Click here to read Links
Comment in:
Lancet. 1998 Aug 1;352(9125):400-1; author reply 401-2.
Lancet. 1998 Aug 1;352(9125):400; author reply 401-2.
Lancet. 1998 Aug 1;352(9125):401-2.
Lancet. 1998 Aug 1;352(9125):401; author reply 401-2.Use of selective serotonin-reuptake inhibitors of tricyclic antidepressants and risk of hip fractures in elderly people.
Liu B, Anderson G, Mittmann N, To T, Axcell T, Shear N.Kunin-Lunenfeld Clinical Research Unit, Baycrest Centre for Geriatric Care, Toronto, Ontario, Canada.
BACKGROUND: Tricyclic antidepressants (TCAs) are associated with an increased risk of falls and hip fractures in elderly people. Selective serotonin-reuptake inhibitors (SSRIs) are reported to be better tolerated than TCAs. We investigated the risk of hip fractures associated with SSRIs and TCAs. METHODS: This case-control study used administrative healthcare data from the province of Ontario, Canada. 8239 cases-patients aged 66 years or older, treated in hospital between April, 1994, and March, 1995, for hip fracture-were each matched for age and sex to five controls. Logistic regression was used to calculate the odds ratio for hip fracture with adjustment for potential confounding effects produced by concomitant drug use and comorbidity. FINDINGS: With participants who had no exposure to antidepressants as the reference category, the adjusted odds ratio for hip fracture was 2.4 (95% CI 2.0-2.7) for exposure to SSRIs, 2.2 (1.8-2.8) for exposure to secondary-amine TCAs, and 1.5 (1.3-1.7) for exposure to tertiary-amine TCAs. For all types of antidepressants, current use was associated with a higher risk of hip fracture than former use. The odds ratios for hip fracture were higher for new current users than for continuous current users in all three drug classes. 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. INTERPRETATION: Exposure to any of the three classes of antidepressants is associated with a significant increase in the risk of hip fracture. Despite differences in dose distribution, this analysis suggests that SSRIs do not offer an advantage over TCAs in terms of risk of hip fracture.
PMID: 9643791 [PubMed - indexed for MEDLINE]
__________________________________________________Q
Posted by sam123 on August 21, 2007, at 16:01:45
In reply to Re: SSRIs and bone loss, posted by sam123 on August 21, 2007, at 15:32:00
> I had bone loss due to glucocorticoid use; it is easy to reverse. I now have normal done density
> for a person my age. Done density is easy to measure.I forgot to mention how I did it. Vitamin D + calcium + weight bearing exercise.
Vitamin D is a steroid hormone that has an important role in regulating body levels of calcium and phosphorus, and in mineralization of bone.
Posted by Quintal on August 21, 2007, at 16:12:29
In reply to Re: SSRIs and bone loss, posted by sam123 on August 21, 2007, at 16:01:45
>Vitamin D is a steroid hormone that has an important role in regulating body levels of calcium and phosphorus, and in mineralization of bone.
Yeah, I know vitamin D is essential for bone mineralization. I was wondering why Lar suggested vitamin D was important here, since the study itself did not mention vitamin D. Do SSRIs imapair vitamin D absorption?
Q
Posted by Quintal on August 21, 2007, at 16:15:57
In reply to Re: SSRIs and bone loss » Larry Hoover, posted by Quintal on August 21, 2007, at 15:18:45
What's happened to Lar's original post?! I can't access it for some reason. Anyway, does anybody know if the secondary TCAs are more/less serotonergic than the tertiary TCAs? I have a feeling there is a difference in affinity for the serotonin transporter.
Q
Posted by Larry Hoover on August 21, 2007, at 16:25:31
In reply to Re: SSRIs and bone loss » Larry Hoover, posted by Quintal on August 21, 2007, at 15:18:45
> What inspired you to seek out these studies Lar? I see they're both very recent - June/July this year. Interesting.
I am on a number of abstract notification services. Most of it is ho-hum, but once in a while, something stands out.
> Of course I knew they were bad all along ;-)
Of course.
> I've never checked to see if SSRI use is correlated with cellulitis, but I think I will. Doctors always told me there was no link, but I had this with every SSRI, and it was debilitating. Ruined my education because I had to keep going into hospital every few months. I'll have a look and see.
>
> QI got nothing on that, from Pubmed. Not saying it isn't true for you, of course. Perhaps you should try and get published as a case report?
Lar
Posted by Larry Hoover on August 21, 2007, at 16:30:48
In reply to Re: SSRIs and bone loss » Larry Hoover, posted by Quintal on August 21, 2007, at 15:36:21
> So what is the vitamin D link Lar?
Standard therapy for low bone density. It alters the balance between osteoblast and osteoclast activities. Bone is constantly being dissolved (osteoclast) and recrystallized (osteoblast), with bone density being the dynamic equilibrium between the opposing actions. Maybe SSRIs do inhibit the blasts....but vitamin D activates them.
> I see this older study found increased risk of hip fracture in all groups taking antidepressants, but the SSRI group had the highest incidence. Interesting, because I get the impression the researchers seem to have set out expecting to find a lower incidence of hip fracture among SSRI users because they are 'better tolerated' (I assume they were thinking sedation and cognitive impairment was the cause of falls, and hence higher incidence of hip fractures, but their results seem to suggest a different mechanism).
I'd have speculated on the orthostatic hypotension and heart rhythm disturbances associated with tricyclics....On reading the abstract, I don't see anything about mechanism.
Lar
Posted by Larry Hoover on August 21, 2007, at 16:34:56
In reply to Re: SSRIs and bone loss » sam123, posted by Quintal on August 21, 2007, at 16:12:29
> I was wondering why Lar suggested vitamin D was important here, since the study itself did not mention vitamin D. Do SSRIs imapair vitamin D absorption?
>
> QNothing like that. Depressed people are already less likely to get sunshine, and perhaps also to obtain sufficient exercise, to optimize bone deposition. Vitamin D intake recommendations are being constantly increased. Last I saw, there were doctors lobbying for an RDA of about 4000 IU/day.
Vitamin D supps are a good idea for folk like me, prone to sunburn (so I avoid direct sun, and/or use gobs of sunscreen), low vigour (so I don't get the exercise I'd like to have), and now add in "exposed to SSRI".
Lar
Posted by sam123 on August 21, 2007, at 16:40:02
In reply to Re: SSRIs and bone loss » sam123, posted by Quintal on August 21, 2007, at 16:12:29
> Yeah, I know vitamin D is essential for bone mineralization. I was wondering why Lar suggested vitamin D was important here, since the study itself did not mention vitamin D. Do SSRIs imapair vitamin D absorption?
>
> QNot that I know of. He suggested it as it is key to building bone. The risks of skin cancer, at least for me, are significant so it is better to take as a supp. Sunscreen lotions have proven far less protective than they were promoted to be.
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
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