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Re: Actually, that's not what the study found. linkadge

Posted by Larry Hoover on December 30, 2008, at 22:10:53

In reply to Re: Actually, that's not what the study found., posted by linkadge on December 30, 2008, at 20:58:26

> Yes, but in spite of the initial state of the partipants, the TCA group still deteriorated faster in terms of white matter. Yes, I suppose that this could be a result of worsening depression. It could also simply be that the TCA was infact producing white matter atrophy.

Those two explanations are equally valid, IMHO, which is all I was suggesting. There may be other explanations, not yet considered.

> For a while, enhanced cardiac mortality on TCA's was also blamed on depression. It is now strongly believed that TCA's perpetuate cardiac disease.

It can be very difficult to discriminate with respect to causation when both disease and treatment are potential explanations for a single phenomenon. It takes a lot of work to sort it out, once the question has been raised.

> I understand that the study may not be conclusive proof of anything, but it is still worth considering the possability. I mean there are a few potential mechanisms by which such such an effect could occur.

I think it deserves consideration, absolutely.

> I know certain anticonvulsants (ie tegretol) is linked to white/grey matter atrophy as well as cytotoxicity. Many of the SSRI's are cytotoxic as well many increase oxidative stress. The TCA's can definately enhance cortical excitability and glutamatergic output. Some antidepressants, like elavil and fluoxetine directly decrease glutamate reuptake. There was a study which demonstrated how fluvoxamine enhanced glutamate neurotoxicity associated with MSG. Anyhow.
>
>
> Linkadge

It all gets so complicated.

When I first saw the following paper (full-text link at bottom), I had a moment of personal epiphany. Treatments for depression are all incomplete. None addresses all of the adverse biochemical effects of the underlying disease, depression itself. Even when treatment is considered to be successful, functional brain pathologies persist. During treatment, the brain continues to endure unremediated effects of the underlying illness. I wonder if it is even possible to isolate the possible adverse effects of treatment from those of the natural progression of the disease, so I don't even try to do so. I address whatever challenges I face with CBT techniques, mindfulness, exercise, nutritional approaches, and so on, because I'd rather face the future than try to label the past.

Didn't mean to sound preachy. I hope I didn't.

Lar

Here's the abstract:

Eur Neuropsychopharmacol. 2002 Dec;12(6):527-44.
Functional anatomical correlates of antidepressant drug treatment assessed using PET measures of regional glucose metabolism.
Drevets WC, Bogers W, Raichle ME.
Neuroimaging in Mood and Anxiety Disorders Section, National Institutes of Health, NIMH/MIB, Bethesda, MD 20892, USA. drevetsw@intra.nih.gov

Neurophysiological studies of major depression performed using PET imaging have shown abnormalities of regional cerebral blood flow (CBF) and glucose metabolism in multiple prefrontal cortical and limbic structures that have been more generally implicated in emotional processing. The current study investigated the effects of antidepressant drug treatment in these regions using PET measures of glucose metabolism. Subjects with primary MDD (n=27) were imaged while unmedicated and depressed, and, of these, 20 were rescanned following chronic antidepressant drug treatment. Regional metabolism was compared between unmedicated depressives and controls and between the pre- and post-treatment conditions in regions-of-interest (ROI) where metabolism or flow had previously been shown to be abnormal in unmedicated depressives. At baseline, the mean metabolism was increased in the left and right lateral orbital cortex/ventrolateral prefrontal cortex (PFC), left amygdala, and posterior cingulate cortex, and decreased in the subgenual ACC and dorsal medial/dorsal anterolateral PFC in the unmedicated depressives relative to controls, consistent with the results of previous studies. Following treatment, metabolism significantly decreased in the left amygdala and left subgenual ACC, and corresponding changes in the orbital and posterior cingulate cortices approached significance. The metabolic reduction in the amygdala and right subgenual ACC appeared largely limited to those subjects who both responded to treatment and remained well at 6 months follow-up, in whom the reduction in amygdala metabolism tightly correlated with the reduction in HDRS scores. The magnitude of the treatment-associated, metabolic change in the amygdala also correlated positively with the change in the stressed plasma cortisol levels measured during scanning. These data converge with those from other PET studies to indicate that primary MDD is associated with abnormal metabolism in limbic and paralimbic structures of the mesiotemporal and prefrontal cortices. Chronic antidepressant drug treatment reduces metabolism in the amygdala and ventral ACC in subjects showing a persistent, positive treatment response. In contrast, the persistence of the abnormal metabolic deficits in the dorsomedial/dorsal anterolateral PFC in MDD during treatment may conceivably relate to the histopathological changes reported in these regions in post mortem studies of MDD.

Full text:
http://www.nil.wustl.edu/labs/raichle/MER_papers/168_Functional%20anatomical%20correlates%20of%20antidepressant%20%20drug%20treatment.pdf

 

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poster:Larry Hoover thread:871107
URL: http://www.dr-bob.org/babble/20081223/msgs/871532.html