"I don't think anti-depressants re-thicken a cortex"

I don't know...if lithium can do it, why not antidepressants?

Depression and alcoholism run together in family histories, alcoholism causes brain damage. Too many conflating factors for me to get excited about this. Also, if reasoning and social cues are in the same place, why are so may people with severe depression people who are both very intelligent and very sensitive (perhaps over-sensitive) to social cues? Lots of famous folks I could list you all probably know, lots of folks we all know who are very bright, very sensitive to others and go through a lot of depression.

it is the same old directionality issue. Simlpy because physiological researchers believe that physiology is the cause, these cross-sectional results are interpreted as supporting a causal direction from some physiological brain deficit to depression.

my opinion is that the directionality can very well be in the other direction. there is evidence for this. other brain imaging studies have shown brain volume and activity changes following successful cognitive therapy with people treated for depression.

There is a great deal of evidence supporting the theory that, along with physiological predispositions (genetics, teratogenic effects, congenital, etc.), life experiences shape a person's perception of the world leading to depression, differences in quantity of rumination on emotionally laden experiences, that cogntive therapy can revael these and can help people to change these cognitive patterns, that there is physiologically measurable evidence of these brain-activity-related problems, and that cognitive therapy success can be measured with brain imaging, such as fMRI in a pre/post design.

I am posting one reference, with a bit of the abstract, to support the view that the causal direction has been documented to go from psychotherapy TO physiologically measured brain outcome. This shows that any person CLAIMING that brain differences (volume, structure, or activity) provide PROOF that depression ALWAYS follows physiology, justifying physiological treatments such as SSRI, needs to address this expansive, coherent body of evidence. It also shows that the beenfits of SSRI may be through some effect on the brain affected by experiences and cognitive styles characterisitc of depression, since cog therapy and SSRI were conducted side-by-side.

This is my opinion, backed up by evidence. Fellow readers, please do not attack me, my humanity, my profesisonalism, etc. personally for this evidence-backed opinion. If you have a conflicting opinion, just state your case as best as you can with no name-calling.

Brody AL, Saxena S, Stoessel P, Gillies LA, Fairbanks LA, Alborzian S, Phelps ME, Huang SC, Wu HM, Ho ML, Ho MK, Au SC, Maidment K, Baxter LR Jr. Regional brain metabolic changes in patients with major depression treated with either paroxetine or interpersonal therapy: preliminary findings. Arch Gen Psychiatry. 2001 Jul;58(7):631-40.

METHODS: Twenty-four subjects with unipolar MDD and 16 normal control subjects underwent resting F 18 ((18)F) fluorodeoxyglucose positron emission tomography scanning before and after 12 weeks. Between scans, subjects with MDD were treated with either paroxetine or interpersonal psychotherapy…
CONCLUSIONS: Subjects with MDD had regional brain metabolic abnormalities at baseline that tended to normalize with treatment. Regional metabolic changes appeared similar with the 2 forms of treatment. These results should be interpreted with caution because of study limitations (small sample size, lack of random assignment to treatment groups, and differential treatment response between treatment subgroups).

SSRI's have been shown to release neurotrophic factors leading to generation of brain matter. Since this process is slow, this may be why it takes 4-6 weeks for them to have an effect (even though their effect on seretonin happens in hours). It is possible that the thickening of these thin cerebral regions by SSRI's is how depression is lifted. But I wonder if this thickening is permanent or would it go away when the medicine is stopped.

"The cerebral cortex is the region of the brain centrally involved in reasoning, planning and mood, and thinning of the cortex may affect an individual’s ability to pay attention to and interpret social and emotional cues, scientists suggested."

1) Involved doing what?
I would also like to know how this 131 people who were predisposed to depression who were chosen for the test can be considered "high-risk". A 6-years-old can be considered high-risk because...

blah blah blah... this is all not scientific enough for me.
Please! Stop the scientific mockery.
You are guessing too much with little data!

I believe that Bioscience is the only branch of science that don't use "might".
They are sure that that is the way it happens and strangely enough they are all at the same page.
There are no other theories at the table and worse:
nobody has to explain their theories to their peers.

Dr. Weissman is also the senior author on a paper Philip reviewed in his September 2008 post titled “Study: If Depressed Moms Don't Take Their Meds Then Their Kids Will Go Crazy.” The aim of the STAR-D Child Study is explained in a March 2003 study newsletter (page 4):
http://www.edc.gsph.pitt.edu/stard/public/newsletter/Vol.2-Test21.pdf

In the paper reviewed by Philip (Am J Psychiatry 2008; 165:9), Dr. Weissman disclosed that she “has received investigator-initiated grant support from Eli Lilly and GlaxoSmithKline, and she has served as a scientific advisor to Eli Lilly; she has received investigator-initiated research funds from GlaxoSmithKline and Eli Lilly and research funding from NIMH, the National Alliance for Research on Schizophrenia and Depression, the Josiah Macy Foundation, and the Sackler Foundation; she has received royalties from Oxford University Press, Perseus Press, American Psychiatric Publishing, and MultiHealth Systems; and she has attended scientific advisory meetings for Eli Lilly.”

Dr. Weissman coauthored a commentary on conflict of interest in the March 2009 issue of the American Journal of Psychiatry, which Philip discussed in his post on March 4, 2009.

My first question is: Was the "high risk group" medicated? I always have a problem with these brain scan studies because they rarely specify whether someone has been or is being treated. Unless we know that it's pretty useless. I have no doubt that mood problems and, as MedsvsTherapy suggests, therapy itself can have physiological effects on the brain, but I am also darn sure psych drugs do too in ways we ill understand.

With as much medication as I was given my cerebral cortex must be gigantic. It's a wonder it still fits inside my skull.

Have gone without those little "green 'n whites" for years....wonder if that's why I feel a little soft spot on my head???

Weissman and COI. Staggering to consider the magnitude of sponsorship she has received over the past 20 years. If we could only look at the correlation between her bank deposits and her publications for the past 20 years. Wow.