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Psychiatrists wake-up to biological causes, tests and more targeted treatments?

Discussion in 'Other Health News and Research' started by Firestormm, Feb 28, 2013.

  1. Firestormm

    Firestormm

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    Featured on BBC Radio 4 Today this morning. The talk was of genetic causation, use of scanning technology etc. A more biological approach.

    This is not about ME but perhaps indicates an increasing acknowledgement that is it possible now to move beyond complete reliance on 'listening' and 'interpretation' and even of form-filling:

    One of the 5 disorders was I believe (can't get full paper yet) Autism.
     
  2. Simon

    Simon

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    Thanks. I agree this move to put the biological back into psychiatry appeart to bepart of a growing trend.

    This quote from the abstract:
    The study had 33,000 cases, plus controls - a good size, even by the standards of Genome Wide Association Studies (which are prone to throw up false positives if underpowered).

    Will be posting a blog v soon aboutMady Hornig (works with Ian Lipkin) on work to uncover biological roots of neuropsychiatric illnesses. It's really fascinating stuff, and not a questionnaire in sight.
    .
     
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  3. Desdinova

    Desdinova Senior Member

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    They want to put the biological science back in psychiatry to prop up their industry. Rest assure that they'll still try to treat and cure via their current bag of tricks. Just imagine one day everyone having to be tested at various intervals. And if found to have the genes mandatory psych evaluation to determine if they need treatment for one or more of the associated conditions.
     
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  4. Firestormm

    Firestormm

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    Dr Shepherd Facebook:

    Will try to dig out that research. I did not know of it before now (or can't recall), and I'll try to transcribe the short interview that appeared on the Radio - tomorrow perhaps...

    Look forward to your blog, Simon.
     
  5. Firestormm

    Firestormm

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  6. natasa778

    natasa778 Senior Member

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    Re calcium channelopathy in ME, that is nothing new actually a few researchers have suggested looking into more deeply, there are several published papers including one or two case studies treating post-viral ME with calcium antagonists.

    I wrote years ago about various aspects of calcium channel dysufnction in autism (years before postmortem findings + chemokine receptor polymorphism findings confirmed much of my hypotesis :))

    If bookies were taking bets on this I would have been rich by now LOL. Still waiting for the science to catch up with a couple more pieces of the oracle so if anyone out there willing to take bets do let me know ;-)
     
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  7. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    it seems that the serotonin theory of depression for which ad's supposed increase and thus treat depression is slowly being taken over by the neurogenesis theory of ad's.

    Basically ad's do increase neurotransmitters but its this increase that supposedly works on growth and repair of neurons but alledgedly takes several weeks for this to occurr.

    Im unsure of who exactly is doing this research but research coming from big pharma doesnt increase my confidence. Maybe a team of neurologists not sponsored by big pharma would give this theory more credit, but whats the likely hood of that. The idea of neurogenesis is an attractive theory in neurological illnesses like cfs/me etc
     
  8. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    Just posting for interest sake, not sure if its psychobabble trying to come across as science or not?? The problem is we have been burnt by babblers before??



    Do antidepressants really cause neurogenesis? World Jl Biological Psych, Sept 12

    27.09.2012
    Psychological stress can increase cortisol and this could suppress BDNF synthesis.This can lead to neuronal damage . Antidepressants are now thought to induce BDNF expression and neurogenesis.
    There are many lines sof evidence to support neurogenesis in adult brain . 1.Stress-induced suppression of neurogenesis in certain strains of rats 2. Elevated blood cortisol levels in submissive primates.3. Delayed onset of antidepressant action which could be explained by the time taken for neurogenesis to occur.4. All major classes of antidepressant drugs as well as ECT, induced neurogenesis in rodents 5. Potent reversal of corticosteroid-induced suppression of cell proliferation by paroxetine (Lau et al. 2007; Qiu et al. 2007) and other antidepressants. 6. sertraline increases neurogenesis in a hippocampal progenitor cell line etc.
    There are increasing number of reports of neurogenesis in adult human brain.It is thought that it occurs in a small scale only.The relationship of such genesis to age is also unclear.
    Clinical benefits of antidepressants is difficult to be explained by neurogenesis ( mainly in hippocampus) alone. In rodents, hippocampal neurogenesis is associated with learning, memory and spatial orientation than with mood. All symptoms in major depression cannot be explained by defective hippocampal function alone .If neurogenesis is limited in older people, that process cannot explain the antidepressant effect in that group.
    Mood stabilizers (lithium) and atypical antipsychotics also induce neurogenesis ie the effect is not specific to antidepressants.
    It is interesting to note that non medication interventions like exercise is also associated with neuronogenesis in rodents. Some studies have suggested a link between increased cognitive performance after exercise, but not all.
    Neuronogenesis alone cannot explain all depressive symptoms or the reversal of symptoms after antidepressant treatment. New neurones , in rodents, are thought to be contributing to learning and memory and the link to emotional status/regulation is unclear.
    Authors caution against considering brain volume changes to necessarily mean neuronogenesis. Haloperidol causes acute (within 1–2 h), reversible (by 24 h) striatal gray matter volume reduction in human brain (Tost et al. 2010). This effect is likely to be at the synaptic level ie unlikely to be related to changes in cell number since the effects were both rapid and reversible .So synaptogenesis may be an important factor in brain area volume changes other than neurogenesis in certain circumstances.
    Antidepressant drug treatment, though capable of inducing hippocampal neurogenesis, cannot treat the primary pathology of other disorders such as schizophrenia and dementia, where neuronal loss also occurs. The authors argue that reversal of suppressed neurogenesis is not specific and also too simplistic a model to explain the therapeutic action of antidepressant drugs.
    Pro inflammatory cytokines are elevated in blood and CSF of depressed individuals suggesting that depression is an inflammatory response. Pro-inflammatory cytokines play an active role in synaptic plasticity and will be an important area of further research. Another area of interest is the role neuroglial cells play in all these.Astrocytes are particularly important in the mainte- nance of neuronal homeostasis and are likely to play protective or damaging role depending on concentration or activation status. According to this view, the therapeutic efficacy of antidepressants can be attributable to the repair to neuronal circuits, damaged by chronic, low-grade inflammation, in the prefrontal cortex and limbic regions by indirectly increasing synaptogenesis.
    Authors suggest that we would need to integrate neurogenesis, synaptogenesis, inflammation and other non-neurogenesis factors in to a new model to explain the role of neurogenesis and neurodegeneration in depression and the therapeutic action of antidepressant drugs.

    http://psychiatristupdate.wordpress...urogenesis-world-jl-biological-psych-sept-12/
     

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