/sci/ - Science & Math

WRONG CASUAL ATTRIBUTION OF NEGATIVITY BIAS

- cognitive theories treat mental illness a self-fulfilling prophecy, which inevitably lead to a chicken-and-egg problem (assuming the premise, that thoughts can have consequences were true!)
- if the symptoms came first, what is their cause, when "cognitive distortions" were not present by that time?
- if "cognitive distortions" came first, what caused them? and why did they persist rather than appear and disappear, when there had not been any symptoms to perpetuate them?
- no explanation for the primordial "negative thought"
- cognitive theories no not actually explain anything (in addition to relying on factually incorrect premises)
- "distorted thoughts"/negativity bias are symptoms of illness, rather than its cause
- defeatist thought content is a consequence of unsuccessful and/or unenjoyable behavioral activity due to deminished motivation and anhedonia
- believing one's ability to successfully complete plans/actions to be impaired, when it actually is, is rational, plaubsible and factually true and in no way "irrational" or "distorted"

SENSITIVITY AND SPECIFITY OF "COGNITIVE DISTORTIONS" IN DEPRESSION

- naive "homo oeconomicus" theories of human behavior have been repeatedly disproven
- "negative thoughts", flawed reasoning and "cognitive distortions" also present in healty individuals: why do they remain healthy, then?
- what is the prevalence of "cognitive distortions" in depression sufferers, anyway? is it significantly larger than in demograpically matched healthy individuals?
- have there been any tests of reasoning ability in regards to sentential and/or predicate logic (e.g. deduction of syllogisms, recognition of non-sequiturs) in depression sufferers and healthy comparisons?
- are there sufferers without "cognitive distortions"? if so, how do they differ? what is the cause of their depression? are they non-responders to CBT? if not, why would CBT still work?
- research shows, the addition or omission of "cognitive restructuring" does not affect outcomes
- are thoughts actually distorted? social psychology: exaggerated perception of self-efficacy is a sign of mental well-being ("depressive realism")
- does CBT actually remediate "cognitive distortions", rather teach clients/patients to dissimulate them due to social desirability (in order to not disappoint/compromise the "therapist")?

LOGICAL FLAWS OF CLINICAL PSYCHOLOGICAL "THEORIES" OF DEPRESSION

- if external stressors + cognitive distortions = symptoms, why are there cases of idiopathic depression, where no external stessors are identifiable?
- if patients present with "cognitive distortions", what is "correct/rational/helpful (sic!) thinking", then?
- if depression is an impairment of causation recognition, causal attribution and logical reasoning, why does it deteriorate mood and decrease motivation, rather than affect it randomly?
- does the client's/patient's consent to cognitivist disease models ("insight", i.e. agreeing to to notion, that his thought contents are wrong and his reasoning is flawed) affect outcomes?
- proposed efficacy for a wide array of distinct conditions: red flag for placebo
- various clinical psychological theories about disease causation are inconsistent and even contradictory, yet the the resulting "treatments" supposedly show no reproducible, significant difference in effect size
- CBASP: if symptoms are attenuated by decreasing disfunctional/"preoperational" interpersonal behavior (inadequate submission, dominance oder hostility), whydo symptoms persist when depression/dysthymia sufferers abstain from human contact for prolonged periods of time?
- according to CBASP premises, solitude should be an effective treatment for chronic depression

DELETERIOUS CONSEQUENCES OF COGNITIVE AND BEHAVIORAL THEORIES

- cognitive psychological theories are thinly disguised verbal abuses targeting the intellectual abilities of suffereres in a pseudo-academic jargon
- cognitive theories are effectively blaming the client/patient: "they are not thinking correctly, therefore they experience symptoms"
- cognitivist reframing is a functionalist approach that does not always align with reality: expedient/opportune beliefs are favored over factually true beliefs
- behavioral treatment are not proved to be effective due to the impossiblity of blinding, yet put unnecessary burden and distress on patients (i.e. graded exercise or CBT for chronic fatigue syndrom)


COGNITIVE "THERAPY" IS ACTUALLY DISSIMULATION, NOT IMPROVEMENT

- CBT instructs clients/patients to act as if they were "healthy": so called "therapy" is actually an "instruction for dissimulation"
- higher symptom severity = inferior ability to dissimulate = study drop-out!
- "therapy" is a selection process between individuals with lower (continuing participants) and higher symptom severity (drop-outs)
- lower symptom severity in study completers is due to disproportionally higher amount of drop-outs among more severely ill initial participants

BEHAVIORAL "THERAPY" IS ACTUALLY SELECTION FOR SPONTANEOUS REMITTERS, NOT IMPROVEMENT

- behavioral theories suggest symptoms are due to a loss of positive reinforcers
- are the biological prerequisites for reinforcement still intact?
- alternative hypothesis: spontaneous remission due to the natural (episodic) course of the disease occurs in a portion of study participants. remission reinstates the susceptibility to classical/operant conditioning and enables them to complete behavioral tasks, whereas non-remitters fail to do so and drop out more frequently

>>9861757
>PSYCHOTHERAPY
not science or math

FLAWS IN CLINICAL STUDIES/TRIALS OF PSYCHOLOGICAL TREATMENTS

- since the drop-out rates in the treatment arms of clincal studies are significantly higher, the whole "intended to treat" group is relevant for the outcome, not just the study completers
- no blinding: trials need to be conducted vs. a control condition that is superfically indistinguishable to psychotherapy-naive probands
- waiting lists show worse outcomes when compared to the natural course of the disease: nocebo effect
- unblinded oder insufficiently blinded trials measure placebo effects of the treatment + nocebo effects of waiting-while-consciously-not receiving-treatment
- how does psychotherapy compare to equally effortful, time demanding conversations with non-psychiatric health professionals, non-medical practioners, attorneys, social workers, etc. when professions are single-blinded?
- how can behavioral approaches be blinded?
- non-pharmacological treatments require a single-blinded experimental set-up (study participants and symptom raters need to be blinded, practioners cannot be blinded for practical reasons)
- general problem of behavioral "treatments" (CBT "homework", physical exercise): requirement of effort/motivation/activity disproportionally burdens probands with higher symptom severity, thus causing considerably more dropouts when compared to less impaired probands. the supposedly beneficial effects are not caused by actual improvements, but rather by withdrawal of more severely ill probands from the treatment arm

FLAWS IN PSYCHOMETRIC TESTING

- psychometric tests are intrinsically flawed
- several insoluble epistemologic problems
- inability to find relations between two psychometric constructs: correlations of two distinct constructs cannot be distinguished from insufficient divergent construct validity (only possible, if one variable is physically measureable)
- inability to detect temporal alterations of psychometric constructs: do changes in test scores reflect changes in the actual construct or deficits in retest reliability?

WHY A SIGNIFICANT PORTION OF PSYCHIATRY LACKS SCIENTIFIC EVIDENCE

SEROTONIN AND DEPRESSION

- serotonin has no effects on mood other than irritability/impulsivity (as seen in sepiapterin reductase defiency) and aggression (related to a certain MAO A allele)
- low serotinin phenotype: sepiapterin reductase deficiency (rare genetic disease) does not decrease mood or mimic depression
- high serotonin phenotype: serotonin syndrome (simultaneous intake of 5-HTP and MAO A inhibitors) does not ameliorate mood or alleviate depression
- SSRIs are supposed to improve symptoms, yet opipramol (low affinity 5-HT2a antagonist) und tianeptine (serotonin reuptake enhancer, the opposite effect of SSRIs!) allegedly show antidepressant effects as well
- mono amine oxidase A inhibitors: effects likely mediated by tyramine (TAAR1 agonist) and/or N-acetyl serotonin (TrKB agonist)
- tryptophan depletion: effects likely due to N-acetyl serotonin defiency and/or products of the kynurenine pathway
- tryptophan: primarily glutamatergic effects (transamination kynurenine -> alpha-ketoglutarate produces glutamate, katabolites kynurenic acid, anthranilic acid, quinolinic acid all show glutamatergic activity)
- possible targets that are actually implicated in depression: ionotropic glutamate receptors (primarily AMPA) and CB1 receptor


"SCHIZOPRENIA" IS NOT A SYNDROME

- schizophrenia is not a distinct disease entity
- a high-impact medical disorder with a worldwide lifetime prevalence of ~1% (which is extremely high, given the grave consequences) with the original description occuring not earlier than 1908 is highly curious
- there is no "schizophrenic syndrome" given the frequent changes of diagnosis criteria
- "schizophrenia" is intermiggling multitudinous, for as yet mostly unknown, actual disease entities (anti-NMDAR-encephalitis, toxoplasmosis, etc.)

DOPAMINERGIC (DRD2) AND SEROTONERIC (5-HTR2a) THEORIES OF SCHIZOPHRENIA ARE WRONG

- DRD2 antagonists were not products of rational drug design, but rather attempts to commercialize methylene blue derivates for medical purposes
- the first "antipsychotic", chlorpromazine, had previously been tried for several other indications (migraine, insomnia, emesis, amoebiocide, etc.)
- DRD2 antagonists cause generalized functional impairments of the nervous system, they do not specifically target symptoms of schizophrenia
- do untreated female schizophrenics experience regular mammary growth and laktation? do they have significantly decreased incidences of breast cancer and osteoporosis? (all of these are prolactostatic effects of high dopamine levels)
- do adamantyl amines (DRD2 agonists: memantine, amantadine) cause transient schizophrenia in healthy individuals?
- DRD2/5-HT2a antagonists likely do not improve mid- and long-term outcomes
- do DRD2/5-HT2a antagonists actually work short-term? given the severe and very common adverse effects, it is likely placebo effects occur disproportionally more often/stronger in the verum group when compared to inert placebos?
- DRD2 or 5-HT2a agonists do not cause a syndrom that resembles schizophrenia, the effects of dopamine or serotonine releasing agents (MDMA, fenfluramine) are clearly different

GLUTAMATERGIC (NMDAR, MGLUR2) THEORIES ARE PROMISING, YET INSUFFICIENTLY RESEARCHED

- animal models for "schizophrenia" use prepulse disinhibition by NMDAR-antagonists phencyclidine or dizoclipine
- some exogenic 5-HT2a agonists (lysergic acid diethylamide, psilocybin, psilocin) exhibit hallucinogenic effects, which are due to allosteric inhibition of mGluR2 receptors forming heterodimers with 5-HTR2a
- yet, orthosteric mGluR2 agonists (pomaglumetad, failure in phase II) do not significantly improve symptoms
- NMDAR are voltage- and ligand-gated, they require slight depolarisation, glutamate and low molecular D-amino acid or glycine
- NMDAR ligands have narrow therapeutic margins: agonists cause glutamatergic excitotoxicity, antagonists cause Olney's lesions
- glycine reuptake inhibitors (bitopertin, GlyT1, failure in phase III; ethanol, GlyT2) do no improve symptoms, which is unsurprising, since there is no glycinergic/D-alanergic/D-serinergic excitotoxicity (glutamate is the limiting factor)


FLAWS IN CLINCAL STUDIES/TRIALS OF PHARMACOLOGICAL TREATMENTS

- pharmacological treatments need to be tested vs. an active placebo, that causes the same adverse effects with a similar incidence
- no control groups with ACTIVE placebos: uneven occurence/effect size of placebo effects in verum and placebo group, improvements caused by placebo effects are falsely attributed to the pharmacodynamic properties of the verum
- hypothesis: non-linear dose-response curve, bends towards a horizontal asymptote when cumulative incidence of adverse effects approximates 100%
- unsolved problem for all kinds of pharmacotherapy: verum x placebo interaction
- pharmacodynamic properities of the the verum cause unblinding by initial relief, therefore exaggerating the effect size of improvements due to disproportional higher placebo effect in the verum group when compared to placebo group

>>9861765
look below for the neurophysiological and pharmaceutical part

>>9861757
Have you ever been diagnosed with a mental illness?

>>9861797
no

i'm just being triggered by bad science and medical scams

>>9861757
>emotions (phylogenetically ancient brain regions) predate thoughts (neocortical regions): defeatist thoughts therefore cannot possibly cause sadness

This seems intuitive, but I imagine it's still wrong somehow.

Oh, you don't know? Depression is caused by inflammation. Stick that in your wall of text somewhere.

>>9861828
the neocortex has synaptic connections to more primitive brain regions and it can override them which is why society can exist and bad thoughts can make you sad

didn't read any other post in this thread btw

>>9861835
i read about interferon-gamma, interleukin 6 and tumor necrosis factor alpha being implicated in a subset of depression, the latter especially in cases of comorbidity with psoriatic arthritis.

if you have any papers/resources on hand, i would be very interested!

>>9861850
Not on hand unfortunately. What do you study/work at?

>>9861846
it's not the actual thoughts that sadden you, but rather the EPSPs/IPSPs (or the lack thereof) that cause both defeatist thoughts and sadness.

>>9861854
i have a background in chemistry and a personal interest in neurobiology, though i usually care more about nootropics rather than medical remedies.

(i got into this stuff because i looked into ways of improving motivation and cognitive ability. after reading dozens of books and a myriad of papers on clinical psychology and psychiatry, the lack of scientific rigor pissed me off big time...)

>>9861757
thoughts cause emotions, try hearing "you'll die alone" from a close family member and then deny it.

>>9861874
So do you have any scientifically backed solutions?

>>9861878
being told that is not actually a thought but rather an external stimulus, which is a physical entity or process with possible consequences

a thought is an emergent property of physical states/process, but not physical itself. how can anything non-physical affect something physical?

>>9861882
i don't do any original research, just collect bits and pieces of already existing information in order to get a more coherent picture.

if you are troubled by depression and conventional approaches do not work (which would not surpise me in the slightest, see above), give minocycline a try. in no way am i claiming this to be a scientifically reliable solution, but there some preliminary evidence on PubMed (minocycline has a relatively benign adverse effect profiles/incidences, so unblindling by side effects is less likely).

>>9861894
What do you mean when you mention blinding and unblinding. You've mentioned it several times but I haven't been able to infer it's meaning from context.

>>9861894
Oh I see you probably meant binding there, but previously you mentioned blinded trials. I'm guessing that has something to do with who knows what information about the trial to reduce the chance of biases?

>>9861757
>thoughts and emotions are not physical entities

stoppedreadingthere.jpeg

>>9861906
i did in fact mean blinding.

blinding in a controlled trial is making sure the probands themselves (the persons being treated), the examiners (the persons gathering data on medical improvements) and - ideally, but impossible with psychological treatments - the practitioners (the persons providing the probands with treatment) cannot tell whether a proband receives the actual treatment (verum) or a placebo by any means other than the remission of symptoms.

if the trial was unblinded (= "removal of blinding", either by lack of initial blinding or by side effects of the verum), placebo and nocebo effects would both affect the verum and the placebo arm of the trial unevenly. more probands receiving the verum would assume they are actually being treated, thus increasing the placebo effect, whereas comparatively more probands in the placebo group would realise they are denied treatment, resulting in a nocebo effect (being conscious about not receiving an available treatment generally leads to worse outcomes than the natural course of the disease) both effects.

both effects together can considerably inflate the effect size of an alleged treatment or even make ineffective treatments appear as if they had significant benefits. drugs with common and/or easily noticeable adverse effects should therefore be tested versus active placebos that cause similar side effects at a similar rate.

>>9861928
care to elaborate?

do you argue that thoughts/emotions are actually physical (do you assume them to equal action potentials?) or do you disagree with the notion that non-physical entities are causal "dead ends"?

all I know is I got the schizophrenia and my psychiatrist and psychotherapist are both complete memes

Psychology is simply a shallow, reductionist, psuedoscientific way of understanding humanity. You can learn much more about human behavior by reading Shakespeare or La Rochefoucauld or any great literature.

>>9862669
Is Lord of the Flies forrealzies?>>9862669

>>9861757
Stopped reading after "epiphenomenons"

>>9862657
what kinds of treatments did/do you receive? has there been any alleviation you attribute to treatment?

>>9862732
by "epiphenomenon" i mean a state or process that has a cause, yet cannot exert consequences of its own, i.e. a "causal dead end".

>>9862758
i take antipsychotics

honestly nothing really helps, my anhedonia and avolition is too pervasive, I told my psychotherapy in so many words that I understand that they can't really do anything for me at this point in time my treatment basically amounts to harm reduction and nothing else, it's all about preventing me from going full blown psychotic and hurting myself or somebody else and pretty much nothing else and she got mad at me

I smoke weed like twice a year, I know i am not supposed to but it's pretty much the only thing that gives me some kind of relief, just smoke some weed and eat a large pie of pizza by myself and even then I barely enjoy it

I basically feel like I'm underwater with concrete in my brain 24/7 with no end in sight

>>9862866
if you feel that a certain treatment does not cause relief of any relevant symptoms, you should really consider quitting and try something different... if things get worse that way, you can still get back on it.

the stance of individuals affected by "mental" health issues themselves is much different from that of a scientic researcher/reviewer.

if i were you, i would try anything that has a) tolerable adverse effects and b) some proof of concept (= a general idea of how/why it could possibly work), regardless of RCTs.

to help with anhedonia/avolition, you might want to consider:

memantine*
https://www.ncbi.nlm.nih.gov/pubmed/28508107

celecoxib
https://www.ncbi.nlm.nih.gov/pubmed/28445800

methyl folate
https://www.ncbi.nlm.nih.gov/pubmed/28289280

minocycline
https://www.ncbi.nlm.nih.gov/pubmed/27919523
https://www.ncbi.nlm.nih.gov/pubmed/24503176

omega 3 polyunsatured fatty acids
https://www.ncbi.nlm.nih.gov/pubmed/26679763

ginkgo biloba extract
https://www.ncbi.nlm.nih.gov/pubmed/25980333

modafinil*
https://www.ncbi.nlm.nih.gov/pubmed/25306261
https://www.ncbi.nlm.nih.gov/pubmed/21947320

sodium benzoate
https://www.ncbi.nlm.nih.gov/pubmed/24089054

riluzole*
https://www.ncbi.nlm.nih.gov/pubmed/24013610

lisdexamfetamine*
https://www.ncbi.nlm.nih.gov/pubmed/23756608

mirtazapine*
https://www.ncbi.nlm.nih.gov/pubmed/23491969

alpha2 antagonists (read paper for details)
https://www.ncbi.nlm.nih.gov/pubmed/22169246

granisetron*
https://www.ncbi.nlm.nih.gov/pubmed/23375406

* = high risk of inflated effect size due to unblinding by side effects

>>9861775

SSRI and other Serotonin-enhancing drugs allegedly show a delayed onset of effect about 1 to 2 weeks after the first intake!

This is incompatible with a Serotonergic mode of action, since Serotonergic effects, such as Nausea, Emesis, Diarrhoe and Vasoconstriction already appears just a few minutes/hours after a single dose, depending on pharmacokinetic properties and pharmacogenetic interaction!

This thread is going to die because of too much information, which is sad

>>9863303
This thread is going to die because it's a thread made by a brainlet for brainlets.

>>9863319
Keep telling yourself that.
I'm sure it makes you feel better than actually challenging your preconceived notions of mental illness

>>9863321
What is this thread even trying to accomplish? It's scientology-tier anti-psychiatry propaganda.

>>9863352
>Thank God Scientology is anti-psych. Without that we wouldn't be able to disregard any actual criticism to the field outright.

>>9863321
Telling yourself that schizophrenia does not exist will not make your schizophrenia go away, Jon.

>>9863358
Likewise telling yourself a mental illness exists doesn't magically make it exist

>>9863361
Your chimp outs on arXiv and in those other threads you made makes me believe otherwise
>hurr durr I'm going to kill your family and watch you suffer
Yeah, sounds sane to me.

>>9863368
Sorry, *viXra

>>9863368
Oh you mean that LORD guy?
Not him. Though it is possible for there to be something off with that guy that is not explainable by psych. Can we at least agree to that?

>>9863370
No, he's fucking nuts and that's exactly how you'll end up if you don't take your meds. The delusions and hallucinations are just perceptive symptoms of the physical breakdown of nervous tissue. As schizophrenia progresses, MRIs show that brain volume decreases and the tissue atrophies.

>>9863376
>he delusions and hallucinations are just perceptive symptoms of the physical breakdown of nervous tissue
Citation needed
Or did you just string that together to appear intelligent?
>As schizophrenia progresses, MRIs show that brain volume decreases and the tissue atrophies.
Then point to a study which relates the percentage of individuals who are pre-diagnosed with schizophrenia to brain scans that later confirm this diagnosis
As far as I can find, that study does not exist
Further if it did exist I would hypothesize that greater than 50% of the people diagnosed wouldn't exhibit neurological signs.

>>9863352
scientology "treatments" are as much of a scam as DRD2-antagonists and SSRIs.

it's not propaganda (feel free to ask for evidence/papers regarding specific claims!) and not even anti-psychiatry, since i generally agree with the biomedical approach.

in fact, i strongly believe that GABAa positive allosteric modulators (benzodiazepines, z-drugs) and μ-opiode agonists (morphine, tramadol) are effective and generally well tolerated short-term treatments for insomnia or pain, respectively.

however, the dopamine theory of schizophrenia and the serotonin, cognitive bias and lack-of-positive-reinforcement theories of depression all belong in the trash bin, unfortunately.

>>9863395
Could you list more examples of positive outcomes of psych?
For example, which psychiatric disorders do you believe are justifiably treated with medication?

>>9861757
psychotherapy is a jewish psyop to undermine the stability of White European civilization

>>9863358
schizophrenia very likely does not exist. otherwise, sensitive and specific biomarkers and SNPs would have been found by now.

there are several genome-wide association studies and most of these found false positive associations with SNPs that could not be reproduced by later studies.

as far as biomarkers are concerned, there are several weak correlations (kynurenic acid, homovanillic acid, dermal conductivity, etc.) that cannot reliably distinguish schizophrenics from health controls, i.e. they are non-specific.

however, symptoms of schizophrenia undeniably DO exist, but their causes are largely undiscovered as of now. some cases currently diagnosed as schizophrenia may actually be a chronic, mild form of anti-NMDAR encephalitis, which supports the glutamate hypothesis: https://www.ncbi.nlm.nih.gov/pubmed/29073246

>>9863376
some but not all forms of schizophrenia (precisely those with certain gene variants of neuregulin-1) are neurodegenerative by ventricular enlargement: https://www.ncbi.nlm.nih.gov/pubmed/28826413

once again, this is non-specific since not all schizophrenics have reduced brain volume.

DRD2 antagonists apparently exert a neurodegenrative effect of their own, which is unsurprising given the neurodegenerative nature of Parkinson's disease (a deficit in striatal dopamine). note that the loss of brain volume is not associated with symptom severity, so an unfavorable course of the diease cannot be a common cause of brain volume loss AND higher DRD2 antagonist dosages: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0101689

>>9863405
as already mentioned above, i think there are several good (= effective, well-tolerated, cost-efficient) medications for anxiety, insomnia, pain and epilepsy. they may be limited to short-term use due to the danger of possible addiction but they work nevertheless.

i don't see anything with proven effectiveness for depression or schizophrenia, however.

the most promising candidate (for both health conditions, ironically) might be minocycline, which has fairly mild and relatively scarce side effects (https://www.ncbi.nlm.nih.gov/pubmed/303498)) and therefore could possibly produce reliable results when tested versus an inert placebo:
https://www.ncbi.nlm.nih.gov/pubmed/?term=minocycline+trial+depression
https://www.ncbi.nlm.nih.gov/pubmed/?term=minocycline+trial+schizophrenia

additionally, the patent protection has expired decades ago, so there are no financial incentives to withhold negative results (publication bias). i'm not claiming it does actually work, but i certainly wouldn't be surprised if it did.

>>9863452
How about ADD/ADHD?
I've heard many say that would it not had been for amphetamines they wouldn't be able to focus enough to make it through college.
Having tried adderall on a couple occasions I could see similar benefits to focus, though I've never been diagnosed nor do I have any of the symptoms associated with the disorder.
So do you believe that their lack of ability to focus should warrant long-term use of these drugs?
In my mind it just seemed more like a performance-enhancing drug, though I'm not sure if the effects are the same for everybody.

>>9863405
as far as psychological treatments are concerned, i honestly cannot see ANY of them working.

there is no "proof of concept" (= a sound proposal of how/why a certain method could possibly cause improvement) and the trials supposed showing effectiveness are methodically flawed.

the tl;dr version of the op:
- cognitivist theory relies on false premises
- cognitivist conclusions are not strigent (cum hoc ergo propter hoc)
- cognitivist models don't explain anything, but defer unsolved questions to the next level
- cognitivist "treatments" teach dissimulation
- behavioral "treatment" does simply sort out more severely ill study participants, evoking the mere appearance of improvement
- trials measure placebo effect of "treatment" + nocebo effect of being denied treatment
- trial use unreliable psychometric testing rather than biomarkers to measure symptoms

>>9863460
to be honest, i haven't looked into that thoroughly enough to answer your question.

one thing i have read about is the unusual dose-response curve of cortical dopamine effects on working memory, which resembles an inverted "u".

dopamine is partially degraded by COMT (catechol-o-methyltransferase), an enzyme with a well researched SNP that exchanges a single methionine in the polypeptide chain for valine.

the valine allele has a higher activity and degrades dopamin faster which in turn leads to less dopamine.

if persons with the val/low-DA allele are given tolcapone (a COMT inhibitor), their working memory increases.

however, study participants with the met/high-DA allele see their working memory impaired upon administration of tolcapone!

i find this fascinating!

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3314969/ (see figure 2!)

>>9862975
thanks anon, I'll look into it, but I won't hold my breath

>>9861757
Very interesting thread. And from a frogposter no less.

>>9863410

Do you have any data on this? A suspiciously high proportion of psychotherapy school founders are jews. Would be interesting to see whether (((they))) are overrepresented among practioners and overrepresented among patients

I don't understand how something so provably non-scientific could be so widely accepted

The depth of the mental agony I have experienced over the course of my depression recently led me to researching the nature of free will (it doesn't exist) and discovering the philosophy of anti-natalism which I see no logical reason to disagree with.

Today I drafted my suicide note and will, although for now I have decided to live until I die of natural causes.

I do not think this is something that a neurotypical person would ever experience over the course of their life.

>>9863536
Ignorance is bliss, anon.
"Neurotipical" is often a synonym for idiot

>>9863529
there is actually quite a large community of psychiatrists and science journalists critical of pharmacotherapy in general. trying googleing david healy, joanna moncrieff or robert whitaker. i read through some of their work, but found it fairly trivial.

e.g., healy claims SSRIs do actually increase rather than decrease suicide risk. medical trials won't help to settle this case because suicide is such a rare event, that even highly elevated risks never reach the significance threshold given the sample size of the average trial is in the low to mid triple-digits.

in my opinion this cannot be examined from an epidemiological stance either, since the condition SSRIs are supposed to treat increases suicide risk as well. so the question whether SSRIs do actually influence suicide risks in either way remains unresolved and healy's notion is as speculative as claims about their effectiveness in depression.

from my perspective, the criticism you can find on the internet barely scratches the surface and should focus much more on proof-of-concept issues:

if the lack of central nervous serotonin due to sepiapterine reductase defiency (a rare genetic condition) does not coincide with depression, why should depression be caused by serotonergic hypoactivity? if excess serotonin as seen in serotonin syndrome does not cause mood elevation, why should SSRIs?

>>9863529
as for psychological treatments:

i have NEVER seen ANY substantiated criticism of psychotherapy ANYWHERE. people seem to just assume it works without ever questioning the theorical premises or the design of the trials.

this is especially astonishing, given the fact that critical examination of psychotropic drugs requires at least some knowledge of neurobiology and biochemistry, whereas basic logical inferences are sufficient to completely destroy the theoretical groundwork of cognitivism.

you can easily show that motivation can exist without or even repugnant to cognition/thought content by simple counterexamples: a person affected by akathisia constantly moves, even though he does not actually want to.

the assertion that negativity bias is the cause of depressive symptoms is both a "petitio principii" (begging the question) and a "cum hoc ergo propter hoc" (correlation implies causation) fallacy.

telling a depressed individual he will recover if he just puts enough effort into doing his CBT "homework" is like telling a deaf person he will eventually hear again if he just tries listening harder. except for the fact that deafness usually does not follow an episodic course, where a spontaneous remission can be erroneously attributed to this kind of "treatment".

>>9863654
>>9863650
I appreciate all of the references
I've seen many anons on here deny psych but not put up any evidence or actual examples of why it's wrong
If more people were this coherent in their arguments against it perhaps it wouldn't be so blindly followed.

>>9863436
Most forms of schizophrenia are due to neuroregulin disorders.
>DRD2 antagonists apparently exert a neurodegenrative effect of their own
That doesn't help your argument that schizophrenia doesn't exist, schizo. Take your meds or become brain damaged.

>>9863739
>Is that what you call an argument?

>>9863739
>Most forms of schizophrenia are due to neuroregulin disorders.
>Most
+ there a several neuroregulin disorders, that do not cause symptoms associated with schizophrenia, but rather anxiety, myelination deficits, cancer or cardiac disease
= neither sensitive, nor specific

which does actually support my notion that schizophrenia is not a single, distinct disease entity, but rather several rare diseases mingled together by non-rigorous, low quality research. (unless you want to argue schizophrenic symptoms are caused by divine afflatus...)

and if i ever experienced any symptoms of schizophrenia on my own, i'd likely abstain from DRD2 antagonists alltogether, since they add to (rather than diminish) the loss of brain volume: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0101689

>Symptom severity, functioning level, and decline in cognition were not associated with brain volume reduction in schizophrenia. The amount of antipsychotic medication (dose years of equivalent to 100 mg daily chlorpromazine) over the follow-up period predicted brain volume loss (p=0.003 adjusted for symptom level, alcohol use and weight gain).
>Symptom severity ... not associated with brain volume reduction in schizophrenia.
symptom severity is NOT a confounder, where neurodegeneration -> more severe symptoms -> higher medication dosage. apparently, neurodegeneration a genuine effect of DRD2 hypoactivity, similar to what is seen in Parkinson's disease.

>>9864666
You're getting desperate anon. It would be better to face facts and try to come up with a way to treat your schizophrenia than to stay in denial about its existence. One gives you a shot at living a normal life, the other makes you feel comfy as your mind melts away.

t. guy going blind

>>9864702
Rather be a schizo than a tripfag

>>9863663
>I've seen many anons on here deny psych but not put up any evidence or actual examples of why it's wrong

i do not actually deny psychiatry or clinical psychology. in fact, i am a fierce proponent of at least the former's approach. i do argue however, that a vast proportion of comtemporary theories und research methods are rubbish and the resulting treatments are likely quackery.

my interest in all of this started to emerge when i looked into ways to stop procrastinating my master's thesis. i found literally no scientifically backed claims of how to boost motivation/concentration in general, so i continued to enquire about health conditions that present with a lack thereof and about how they are treated.

after the initial disappointment, i noticed that most of the stuff i had just read was at odds with the basic neurophysiological and medical knowledge i had (e.g., serotonin syndrome not elevating mood, when SSRI are supposed to) and started to dig deeper...

several dozens of textbooks and hundreds of papers on psychiatry and clinical psychology later i'm fully convinced that most of this is quackery (short-term treatments of anxiety, insomnia, epilepsy, etc. being notable exceptions) and this issue is now finished for me.

i did not want this to be for nought, however, so i decided to write a short version of my new insights down and publish it here. (i even considered writing a paper on his, but it likely would get accepted for being to critical and me not having any formal education in medicine/psychology.)

>>9864702
dude, i do NOT deny the existence of schizophrenic SYMPTOMS. yes, here are people suffering from hallucinations, delusions, cognitive deficits, lack of motivation and so on.

but they do not suffer from "schizophrenia", but rather from an unknown quantity of as of yet mostly undiscovered or unspecified medical conditions, that should be narrowed down and identified asap. example: anti-NMDA receptor encephalitis

>>9863138
Studies showing that SSRI's (in general) are associated with suicidal ideation and violent crime:

>https://www.bmj.com/content/355/bmj.i5504

>http://www.bmj.com/content/352/bmj.i65

>http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1001875

>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5066537/

>>9861757
Psychotherapy will always be valid if for no other reason than it would be a really cool name for a band

>>9864791
>I haven't read the thread and suffer from reverse-confirmation bias
the post

>>9864785
this is very interesting, thanks alot!

the association with violent is very plausible from a proof-of-concept point of view, since aggression regulation is one of the very few behavioral effects serotonine undeniably has!

>>9864749
If schizophrenia is “akshually just” NDMADdR2 ftxbhdwfnhvdeasdf then why are traditional antipsychotics so effective?

>>9864821
Further, this study explores the link between suicidal ideation and violence in "healthy adults" with no signs of mental disorder:

>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5066537/

I'm pointing this out due to the fact that some researchers tend to say that antidepressants, for whatever reason, tend to address executive dysfunction (motivation/energy issues) first, before addressing the depression and suicidal ideation. They claim that this results in people who have been thinking of suicide for awhile, now finally having the gumption to go through with it.
The above posts have been taken from my thread here:
>https://archive.4plebs.org/pol/thread/176376284/

>link between suicidal ideation, violence, and SSRI's in "healthy adults" with no signs of mental disorder:
fixed

>>9864745
That's fair. I just have a hard time supporting a science in which only the fringe exhibit adequate rigor

>>9864823
The studies which state this exclude 80-90% of the patient population and as such should be discarded
A perfectly apt explanation is that the healthiest ~10% of schizophrenics are capable of suppressing symptoms with aid of a placebo.

>>9864823
are they? DRD2 antagonists have very frequent and serious adverse effects, so it is very easy to tell them apart from an inert placebo. in order to reliably measure their effectiveness, they need to be tested against an active agent without DRD2 affinity, that nevertheless causes hyperprolactinemia, extrapyramidal effects, akathisia, dystonia, othostatic dysregulation, amenorrhea in females, etc. at similar rates.

note: i'm not claiming, they do NOT improve some subsets of symptoms. i'm claiming this has not been proven, because all trials versus inert placebos are at a very high risk of unblinding by side effects. therefore you cannot possibly tell whether the improvement shown in past trials is due to pharmacodynamic properties or disproportional occurance of placebo effects.

let's suppose they actually do alleviate hallucinations and delusions: even the contemporary psychiatric research literature, which i've been criticizing alot, agrees that some of the core symptoms (cognitive impairment, anhedonia, avolition) are largely unaffected by DRD2 antagonists.

on the other hand, DRD2 agonists like bromocriptine do very rarely cause hallucinations, and have never been observed to induce cognitive or so called "negative symptoms" of schizophrenia. i.e., DRD2 hyperactivity is associated with a phenotype much different from what is seen in schizophrenia.

additionally, DRD2 agonists do even cause common adverse effects, that do not usually present in schizophrenia. due to the prolactostatic properties of dopamine DRD2 agonists suppress mammary growth and laktation, yet hypogalactorrhea is not a symptom of schizophrenia.

>>9864823
tl;dr version of the above post:
- DRD2 might possibly alleviate a narrow subset of schizophrenia symptoms
- whether they actually do has not been determined yet, due to bad research methodology
- DRD2 do not improve some of the core symptoms of schizophrenia
- iatrogenic DRD2 hyperactivity (induced by respective agonists) does not mimic schizophrenia
- iatrogenic DRD2 hyperactivity reliably produces symptoms which are not usually seen in schizophrenia
- DRD2 theories of schizophrenia are plain WRONG

>>9864823
overall, the DRD2 theory is once again deeply flawed logic. reading all this rambling on "cognitive distortions" and "correct reasoning", i find it both ironic and hilariously they do not even understand simple sentential logic themselves.

if A implies B, you cannot decude that B also implies A.

now let A be "DRD2 hyperactivity" and B "hallucinations/delusions". just because DRD2 agonists can cause hallucinations, this does not mean a particular hallucination has to be the consequence of DRD2 hyperactivity.

>>9864829
this is very interesting indeed, thank you very much and keep on the good work!

>>9864880
this another very important methodical flaw of trials i completely missed in the op! thank you!

most mental health patients have both mental (= 2 or more mental health conditions) and "somatic" comorbidities, which frequently meet the exclusion criteria for clinical trials. almost all of the past and contemporary research focuses on "single issue" probands, which are a but a small subset of patients with their respective condition and in no way representative.

common cooccurrances: depression + anxiety, depression after a stroke, depression + cardiovascular disease, depression + dementia, schizophrenia + addiction, schizophrenia + diabetes, etc.

>>9864889
>>9864891

>- iatrogenic DRD2 hyperactivity (induced by respective agonists) does not mimic schizophrenia

The final deathblow to the dopamine hypothesis: D2 receptors form heterodimeric compounds with A2a receptors. A2a antagonism exerts the same physiological effects as D2 agonists.

>https://onlinelibrary.wiley.com/doi/abs/10.1111/gbb.12432

Xanthine derivates such as caffeine tend to be A2a antagonists.

>https://www.nature.com/articles/tp201798

If the dopamine hypothesis were true, coffee or energy drink consumption would
a) cause transient schizophrenic symptoms in healthy controls.
b) exacerbate schizophrenia.

Neither of which it does.

Dopamine hypothesis BTFO!

if the dopamine theory of schizophrenia is wrong why do Parkinsonian patients with top low levels of dopamine who take L dopa to compensate often end up psychotic and exhibit schizophrenia like symptoms if they take too much of it?

dopamine theory is crude and reductive and a bit of a broad stroke, there is more at play sure, but fundamentally it is not wrong

>>9865226
>if the dopamine theory of schizophrenia is wrong why do Parkinsonian patients with top low levels of dopamine who take L dopa to compensate often end up psychotic and exhibit schizophrenia like symptoms if they take too much of it?

because dopamine agonists can actually cause hallucinations and delusions. which does not imply that hallucinations and delusions in schizophrenia are caused by this mechanism. there are several other modes of action known to induce hallucinations (5-HT2a full agonist, mGluR2 antagonists, GABAa negative allosteric modulators, etc.)

read:
>>9864889
>>9864899

fun fact: L-DOPA + peripheric amino acid decarboxylase inhibitor improve cognitive ability and motivation in Parkinson's, whereas schizophrenics suffer from cognitive impairment and avolition. how do you explain that, when dopaminergic theories predict the exact opposite?

>dopamine theory is crude and reductive and a bit of a broad stroke, there is more at play sure, but fundamentally it is not wrong

yes, it is.

additional health-related parameters, you would expect in schizophrenia if the DRD2 hypothesis were true, yet cannot be observed:
- decreased/delayed breast/mammary growth in females
- hypo- or agalactorrhea
- mania
- elevated mood
- excerbation by caffeine
- lower incidence of osteoporosis
- lower indicence of breast cancer (or any other prolactine-dependent tumor)
- lower incidence of Parkinson's disease

there are even case presentations of schizophrenia + Parkinsonian comorbidity, which totally kills ANY dopamine theories: https://www.ncbi.nlm.nih.gov/pubmed/21762841

>>9865292
>there are even case presentations of schizophrenia + Parkinsonian comorbidity, which totally kills ANY dopamine theories:
schizophrenics develop pseudo Parkinsonian symptoms after years of nuking their brains with antipsychotics though, afaik

>>9865292
Any 5ht2a agonism causes hallucinations as in the case of lsd and others
Idk if you know this but sigma receptors are also lower in schizophrenics and sigma receptors are crazy. Really interesting looking into them and how they pretty much avoid neurotoxicity for many drugs but instead different ways. For instance; methamphetamine neurotoxicity is nullified in mice by sigma antagonism but mdma neurotoxicity is cured by dextromethorphan in non human primates by the sigma agonism by my speculation and the sigma receptor agonism could even be responsible for cocaine 's lack of neurotoxicity and partial neuroprotectiveness. The two receptors are even unique in their brain pathways too. Wouldn't be surprised if sigma receptors had something to do with schizophrenia. I also learned about a theoretical limit to psychosis that may vary amongst people so a level of dopamine in one person could make another psychotic
As well aren't adhd and schizophrenia incompatible together. They're both canonically dopamine disorders on opposite spectrums

As well I agree with your skepticism of the dopamine theory of schizophrenia but it is by far the best working theory we have if very rudimentary and poor (as seen by the comments on brain matter loss and parkinsonism introduced by antipsychotics among other terrible side effects). Here are some links that I found interesting

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3554477/
Introduces the idea of different limits of psychosis in response to dopamine levels

https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1600-0447.1985.tb05066.x

http://cochranelibrary-wiley.com/doi/10.1002/14651858.CD004964/abstract

These two deal with amphetamines (dopamine releasers) actually easing negative symptoms in some schizophrenics which lends doubt to the strict dopamine imbalance and leads to more of a brain imbalance

>>9863484
talk to your psychiatrist about amphetamines too
my post above went into how your negative symptoms could be alleviated and if they help you won't have anhedonia which is probably your biggest sadness from what i believe

>>9865409
5-HTR2a is a curious case, since some but not all agonists exert hallucinogenic properties. serotonin syndrom can lead to delirium, which is quite different from the effects of ergoline derivates such as LSD (synaesthesia, entactogenic effects, derealisation), which in turn differ alot from distressing, unpleasant hallucinations as seen in schizophrenia.

hallucinogenic 5-HTR2a agonists somehow act on mGluR2 or its respective G protein with the exact mechanism not being well unterstood, whereas serotonin itself and other non-hallucinogenic agonists do not. seems like the classic "liquid mosaic" model of phospholipide bilayers with virtually limitless surface motility is disproven, since 5-HTR2a forms heterodimers with mGluR2:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3531745/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3064746/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2743172/

i have to admit i do not unterstand sigma receptors at all. the greek letter implies it used to be considered an opioid receptor for its antitussive properties, but does not show affinity for any endogenous opioid. apparently, it is a homologue of some yeast ergosterol isomerase and therefore part of the steroid system:
https://www.cell.com/trends/pharmacological-sciences/abstract/S0165-6147(96)01037-1

its endogenous ligands are dehydroepiandrosterone, pregnenolone (both agonists and both have published trials that suggest an effect on negative symptoms of schizophrenia!) and progesterone (antagonist).

the sigma receptor is "upstream" of the IP3 receptor, which controlls the intracellular Ca2+ homeostasis between endoplasmic reticulum and cytoplasm. this could explain a narrow therapeutic margin, since both intracellular Ca2+ excesses and deficits have deleterious consequences (excitotoxicity and long-term depression, respectively). but this entirely speculative on my part.
https://www.ingentaconnect.com/content/ben/cmc/2003/00000010/00000020/art00003

>>9865460
the only variant of the dopamine hypothesis that has not been thoroughly disproven sounds like:

"since DRD2 agonists can cause hallucinations and delusions, MAYBE there is a SMALL SUBSET of schizophrenics that MAYBE have a SMALL SUBSET of their symptoms caused by excess dopamine. so MAYBE DRD2 antagonists could be helpful for a SMALL SUBSET of symptoms in a SMALL SUBSET of schizophrenics, if we ever obtained credible evidence on their effectiveness by testing versus active placebos and the benefits outweighted the very severe and common adverse effects."

I love this kind of threads, is there a way to store it or archive it in my cellphone? I'm using Clover to browse /sci/

>>9865711
4plebs does not archive /sci/, AFAIK.

For your own use: https://pdfmyurl.com/

>>9865711
>>9865828
>>/sci/

>>9861766

There's another psych-related thread where an anon LARPing as a psychotherapist argues placebo gains are rightfully attributed to the therapy.

>>9864669

>Ask yourself this though - what is the placebo effect and how does it relate to psychotherapy? The placebo effect is someone believing they feel better. The positive effect of psychotherapy is someone feeling better. What is the difference between believing you feel better and feeling better when it comes to mental disorders? If the answer is longevity, there are many longitudinal studies on these therapies which show improved functioning over many years compared to a control group. I would say that is good enough evidence.

Statistical significance is JACK SHIT in clinical trials. You give people an antitussive and they cough on average, say, 100 times in a period of time. On placebo they cough just 95 times. You have a MAD sample size. The difference is HIGHLY significant. Do you recommend that stuff? Hell, NO! Why not? Because the difference is MEANINGLESS. The improvement is not even noticable. Well, unless you do a tally on how often you cough.........

A good point was raised on another thread:

>>9864669

>A clinical trial is an experiment. Experiments require ceteris paribus conditions: In order to see whether a certain variable affects another, you need keep all other parameters possibly affecting your target variable constant. In short: Clinical trials need blinding in order to eliminate differences in Placebo/Nocebo effects as possible confounders. Any unblinded clinical trial is quackery. Homeopathy, faith healing and alternative medicine are quackery, until a randomized, placebo-controlled, double-blinded trial with a sound methodology establishes its effectiveness for a particular health issue. It is simply not enough for symptom relief to coincide with treatment, the treatment needs to be a cause of recovery. If psychotherapy did not meet that standard of evidence, it would be quackery as well. It's really as simple as that. And currently, I honestly do not see any kind of psychotherapy meeting this standard.

>>9861775
Schizophrenia is caused by a germ or a virus.

>>9867376
schizophrenia is associated with early life Epstein Barr virus and toxoplasma gondii exposure, and there are some contradictory result for herpes simplex:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4561501/
http://journal.bums.ac.ir/browse.php?a_id=1972&sid=1&slc_lang=en
https://academic.oup.com/schizophreniabulletin/article/44/suppl_1/S62/4957225

the link to toxoplasmosis is especially well established: https://www.ncbi.nlm.nih.gov/pubmed/29843964

and the effects might be somehow mediated by NMDA receptors:
https://www.ncbi.nlm.nih.gov/pubmed/26969530
https://www.ncbi.nlm.nih.gov/pubmed/28763062
https://www.ncbi.nlm.nih.gov/pubmed/28360866

>>9866967
It's amusing you bring up antitussives as your example. Did you know codeine was once considered the gold standard for cough medicine at one point. Also, the most popular cough medicine ingredient right now (dextromethorphan) gets you high too. I'm pretty sure antitussives aren't an actual thing and are just drugs that get you high that distract you from coughing amusingly. When I had a cough and took mdma I noticed that I didn't really cough or had an urge to while high.

>>9867421
The urge to cough is like itching I think, mild pain that you relieve with abrasion. It makes sense that painkillers would reduce the need to cough, I wonder if painkillers were also used for severe itching before anti-histamines were around.

>>9867437
Interesting, all the drugs I listed also pain relief to some degree (dxm is even closely related to opioids). That actually makes more sense than my theory
Thanks anon

>>9867487
opioids are not only analgetics, but also respiratory depressants, thus slighty relieving your pharynx from breathing.

>>9861757
I'd love to see the OP challenged on psychotherapy!

1) Does anyone here argue that psychotherapy does in fact work for at least some kind of mental illness?

2) Are there any trials with both proband- and examiner-sided blinding? Or any other method of testing it's effectiveness that circumvents the differential placebo/nocebo effect problem?

3) Is there any logically coherent, psychotherapeutic disease theory that relies on empirically well founded premises?

Come on, anons, convince me that psychotherapy is not just a meme!

psychotherapy presumes that we are in control of our apparent intentionality. of course, we aren't in control in any meaningful sense, therefore psychotherapy is fundamentally flawed from its core.

psychiatry is a more interesting field, but as you've noted, it has a lot of problems.

https://westhunt.wordpress.com/2018/07/14/alzheimers-or-did-i-already-say-that/

>>9864745
>i do not actually deny psychiatry or clinical psychology. in fact, i am a fierce proponent of at least the former's approach. i do argue however, that a vast proportion of comtemporary theories und research methods are rubbish and the resulting treatments are likely quackery.

I would argue this for almost all of psych at the moment, luckily the discipline is having a replication crisis which is hitting it hard that will ultimately help the field discern the bullshit from the good stuff.

lmao we know so little about conciousness that anyone speaking with concreteness about the mind is very obviously ignorant of his own underlying ignorance.

bump and test
[math] /partial [/math]
ð

>>9863138
>SSRI
Poison for the brain

>>9868947
it's simply astonishing how a scam of this magnitude could have stayed unnoticed for so long.

the replication crisis and outright data forgery (Diederik Staple, Karen Ruggiero, Jens Forster) is more of a differential/social psychology thing. clinical psychology does overtly circulate logically implausible theories based on false premises.

a simple method to examine, whether a particular hypothesis can possibly be true, is counterfactual analysis: you assume the hypothesis in question IS true and then "mold" reality from it, in order to see any inconsistencies with actual reality.

if cognitive theories of mood and motivation were true, an individual with bipolar disorder would be convinced of a heigthened self-efficacy and a lack thereof in rapid succession, with this circle repeating itself multiple times. yet, even the current reasearch with flawed methodology shows either no effectiveness or miniscule effect sizes for bipolar disorder and especially the manic component of it.

if the cognitive theory of mood were true, depression sufferers would be expected to be in a perfectly normal mood, whereas everyone else should be (hypo)manic due to unrealistically high self-efficacy:
https://link.springer.com/article/10.1007%2FBF01663996
https://link.springer.com/article/10.1007%2FBF01173473
https://link.springer.com/article/10.1007%2FBF01187168
http://psycnet.apa.org/record/1979-26183-001
http://psycnet.apa.org/record/1978-21241-001
http://psycnet.apa.org/record/1978-05783-001
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3565123/

you can allege a myriad of such examples and rarely will the prediction according to clinical psychologist theories correspond to reality.

>>9869066
>Poison for the brain

care to elaborate?

i've read some anecdotal case reports about emotional blunting (rather than general mood elevation) and erectile dysfunction persisting even after discontinuation. but without larger sample sizes and controll groups you can't possibly tell, whether this is due to SSRIs themselves or just chronic depression that (unsurprisingly) hasn't responded to SSRIs.

>>9861757
Understand that current methods follow the market of drugs and funded research. If you want to come up with revolutionary treatments you should create a personality theory that lists all facets of a normal pathology and their average neural pathway prevalence in the most healthy individuals. Think of it as of neropersonology.

>>9869132
>without larger sample sizes and controll groups you can't possibly tell, whether this is due to SSRIs themselves or just chronic depression that (unsurprisingly) hasn't responded to SSRIs.
But isn't the null hypothesis that the SSRIs do nothing?

>>9869162
>But isn't the null hypothesis that the SSRIs do nothing?

yes, of course. from a scientific stance, every effect, be it beneficial or adverse, needs evidence.

however from a user's perspective, serious or long-term adverse effects need evidence of absence (or neglectable incidence), because harm avoidance is a first priority. if there are no well-established treatments for your disease, you might even want to skip evidence of effectiveness altogether and try things that have some proof of concept (putative mechanism of action, effectiveness in animal models, casuistics, anecdotal stuff), as long as there are no serious side effects.

>>9869232
That's a good point
It's important for an individual to have the option when all else has failed to try whatever might work.

>9869162
by the way, SSRIs have no evidence of effectiveness due to unblinding by adverse effects. this however does not PROVE they are ineffective: you simply cannot conclude anything from most past and recent trials due to flawed methodology! as far as proof of concept (POC) is concerned, there is even some to the contrary, i.e. sepiapterin reductase NOT causing depression and serotonine syndrome NOT elevating mood.

DRD2 antagonists have no evidence of effectiveness for the same reasons. they do however present a POC for a few symptoms: DRD2 agonists can cause hallucinations and delusions. yet, there is also POC to the contrary for some other symptoms: avolition, anticipatory anhedonia and cognitive deficits can be caused by a lack, rather than an abundance, of dopamine.

>>9869232
>>9869238

This is especially relevant for mental health concerns. If you recover from mental illness you presumably do so thanks to spontaneous remission. An unknown fraction of people affected by Schizophrenia might have a share their positive symptoms reduced by antidopaminergic drugs at the expense of Hyperprolactinemia, Osteoporosis, obesity and Diabetes but this is largely irrelevant. For those who are not so lucky as to recover spontaneously, they are well advised to try everything available to them, hoping they will eventually find something that works by chance.

so if i have depression, it's impossible to cure it?

>>9869625
>so if i have depression, it's impossible to cure it?

in all honesty: nobody really knows as of now. but you can savely assume depression has nothing to do with serotonine.

there have been some trials of ketamine, but they are at a high risk of being unblinded by adverse effects as well, i.e. unreliable.

rimonabant (CB1 antagonist) can CAUSE depression, so maybe CB1 agonists (e.g., N-palmitoyl-ethanolamine) can help in a few select cases.

but the most promising candidate for an actual antidepressant effect is minocycline (see above!), if you ask me.

if someone wants to do some reading on his own:

>http://stoa.usp.br/vahs/files/-1/16166/Handbook+of+behavioral+neurobiology+of+serotonin+-+cap+do+Chico!.pdf

>>9869661
Is that more neurology heavy or psych?

am brainlet but possibly smart enough to educate myself to the point of understanding this stuff. thanks for posting OP.

there's so much info out there I don't know who to believe. I try to maintain a healthy distrust until proven otherwise...

came from:
>>>/r9k/46811628

>>9869674
The most important thing is don't believe one way or another.
There's a lot that is assumed so unfortunately most knowledge about the field must be done with independent research
Thankfully OP has presented plenty of that in this thread

>9869663
neither nor. it's biochemistry, neurophysiology + behavioral neuroscience (the mostly non-quackery part of biological psychology)

some chapters circulate the serotonergic theory of depression as well, since they take clinical psychological and psychiatric research for granted. other than that, it's a very good read.

>>9869681
Sounds interesting. Thanks for the link!

>>9869674
>I try to maintain a healthy distrust until proven otherwise...

that's a very healthy attitude! don't let yourself be drawn into nonsensical stuff by science babble, "muh scientific consensus" or evidence you haven't checked for plausibility yourself!

>>9869687
So do you think Ketamine shd be effective in the long term treatment of depression?

Also, could ketamine in low doses with certain procedure be used as a cognitive enhancer? I've read that it boosts BDNF and works w/ AMPA receptors, similar to many nootropics

>>9869934
there are several short-term trials of ketamine, but as i said, i wouldn't trust them to much, since it has very common and very noticeable side effects.

apparently, ketamine has no antidepressant effects of its own, but is merely a prodrug, which is consistent with fellow NMDAR antagonists phencyclidine and dizocilpine not exerting any antidepressant action. its active metabolite is probably hydroxynorketamine: https://www.nature.com/articles/nature17998

hydroxynorketamine is an AMPAkine (unknown mechanism that is apparently somehow mediated by ERalpha estrogen receptors), a negative allosteric modulator of nicotinic acetylcholine repectors (NAChR) and an mTOR activator:
https://www.sciencedirect.com/science/article/pii/S0014299912009545?via%3Dihub
https://www.ncbi.nlm.nih.gov/pubmed/29621538
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4061505/

interestingly enough, minocycline also exerts indirect effects on mTOR via the PI3K -> Akt/PKB -> mTOR pathway.

while ketamine has some interaction with the TrkB/ERK pathway, i wouldn't recommend it for a) its adverse effects and b) its involvement with NMDAR-mediated long-term depression.

if you're looking for a TrkB agonist, i'd start with deprenyl/selegiline, N-acetylserotonin (readily crosses the blood-brain-barrier, AFAIK), or flurane type anesthetics: https://www.ncbi.nlm.nih.gov/pubmed/28798343

fluranes are also implicated in malign hyperthermia via ryanodine receptors, which in conjunction with IP3 regulate Ca2+ influx from endoplasmic reticulum into cytoplasm. i'm starting to believe, some cases of depression might have something to do with intracelluar Ca2+ homeostasis.

>>9870004
What do you think about its BDNF boosting effects? Also do you think it could be potentially cognitive enhancing?

>>9870096
>What do you think about its BDNF boosting effects?
BDNF's primary target is TrkB, so i'd go with selegiline (very benign side effect profile) and N-acetylserotonin (not a prescription drug) frist before trying ketamine.

>Also do you think it could be potentially cognitive enhancing?
NMDAR ligands and cognitive function likely have a non-linear dose-response relationship and a very narrow therapeutic margin. if one's cognitive ability is limited by a lack of synaptic pruning, ketamine might help. if long-term potentiation is the limiting factor, it might have deleterious effects. this is a very complex pharmacogenetic issue with a severe lack of research...

>>9867401
>owning cats causes schizophrenia
Based feline friends

Please help >>9870924

>>9871021
>anime OP
Dropped

>>9870574
Alright, so Ketamine apparently causes memory deficits with repeated dosages over a long time.

Do you think these damages would be somewhat reversible?

If I remember correctly, the mechanism of neurotoxicity is the upregulation of NMDA receptors which causes excitotoxicity when Ketamine is withdrawn.

>>9871260
The damage from ketamine is indeed reversible according to a study I found but can't link because it's inconvenient for me to find it. I found it cited on Wikipedia and it basically said everything was reversed through abstinence except some permanent delusional thinking patterns they scored higher on than controls

>>9871260
>If I remember correctly, the mechanism of neurotoxicity is the upregulation of NMDA receptors which causes excitotoxicity when Ketamine is withdrawn.

this is one possible result, the other being neurodegerative effects of the antagonism itself, so called "Olney's lesions". they have been shown only in animal models as of now and even there they remain controversial. nevertheless, this something to be kept in mind when considering ketamine.

overview: https://en.wikipedia.org/wiki/Olney%27s_lesions

>>9871267
>>9871404
This is all quite interesting. Where do you learn about this kinda stuff? Any books or resources?

>>9871415
at first i crossread everything regarding a particular receptor/molecule/pathway on wikipedia, check their sources (usually it's either the original article or large reviews) and proceed from there. https://sci-hub.tw can be used to access almost any paper.

alternatively, i look for either introductory textbooks or large, comprehensive handbooks on http://gen.lib.rus.ec to gradually get the "bigger picture". textbooks provide a low-level entry into a particular field and only mention the general consensus (= what all alleged "experts" agree on). handbooks come with a myriad of details and tend to cite the original sources for a more rigorous look. (this is how i got into psychotherapeutic theories and research)

if you have read large pieces of information, they successively "connect" and your overall view becomes more "holistic", i.e. you can check newly read material for plausibility and consistency with what you've already learnt, start making some low-level predictions and so on. this is especially true for anything physiology-related.

>>9871415
>>9871537
psychotherapy manuals are exceptionally hilarious. there is a book by some guy named James MacCullough on the "Cognitive Behavioral Analysis System of Psychotherapy", in short "CBASP", which he invented.

in this book (forgot the exact title) he depicts certain "problematic" situations that frequently occur within psychotherapy settings, e.g. the "therapist" being late because of a "psychiatric case of emergency".

fun fact: there a single instance of psychiatric emergency, which is acute suicidality. however, psychotherapists can do nothing about it, since they may not prescribe any drugs, they are not legally authorized to restrain people against their will in most legal spheres and there are no quick-acting psychotherapeutic interventions for suicidality, if any.

now, the way the belated "therapist" is supposed to react to his paying client's complaints according to MacCullough:
1) point out that the client should be glad, he wasn't even later than he currently is
2) ask whether his complaints show that he actually values the "therapeutic relationship", because he hadn't made the "therapist" feel that way in the past sessions
3) ask what the client thinks how his complaints made him (the "therapist") feel, in order to reveal the client's "lack of empathy" to him

reading this was a HUGE eye-opener for me, which fully convinced me that psychotherapy is quackery.

>>9871574
Those last two steps come off as a bit manipulative and abusive to me with how they take the spotlight off the emotional suffering of the client and redirect it to the therapist. This guy is actually respected among the psychology community?

>>9871582
>Those last two steps come off as a bit manipulative and abusive to me with how they take the spotlight off the emotional suffering of the client and redirect it to the therapist.

you might laugh, but this is actually the rationale behind his theory! he argues that chronically depressed persons are stuck in a "preoperational stage" of mental development. according to him, they don't unterstand that their own actions/words have consequences on other's feelings and therefore also their actions towards the depression sufferer.

tl;dr: chronically depressed people act out, don't get that they're pissing off others, receive negative reactions, don't see them as a consequence of their very own behavior, blame others and act out even more.

he essentially claims chronically depressed indivuals had no basic unterstanding of the causality principle as if they had an IQ in the low twenties, which is unbelievably dimwitted.

furthermore: if he were right, socially isolated people would be expected to have perfectly normal mood, since there are no unpleasant interpersonal experiences perpetuating the cycle.

>This guy is actually respected among the psychology community?

yes, there were several trials of his "therapeutic" approach since the mid nienties. all of them without any blinding, of course...

>>9871602
Don't chronically depressed people often isolate themselves because they don't want to bring other people down? That would show that they do understand they have an effect on others and throw a wrench into his theory immediately. If they blamed others for their the consequences of their own behavior, you'd also expect to see narcissistic traits accompanying depression, but the opposite happens and self-hatred rather than self-idolization is seen in depression. I've never understood why psychologists always want to take disorders with biochemical causes and make them into a sort of personality disorder. I've read about the same thing happening with schizophrenia, though I think it was referring to several decades ago, I'm not sure how many modern psychologists are still doing that.

>>9871663
you raise a lot of valid points.

current psychiatric research circulates biomedical theories which are not just reductionist and incomplete, but plain wrong: rigorously applied, they make plenty of predictions that do not align with reality. clinical psychology chooses to ignore biomedical causes altogether and purports the notion, mental illness is caused by its very own symptoms. of course, without explaining where they came from, if not from some kind of biological alteration.

the common principle of ANY cognitive psychotherapy: talk them into dissimulation and hope this miraculously turns into some kind of self-fulfilling prophecy. due to the episodic nature of most mental health issues and the high placebo responsivity of some, remissions sometimes randomly cooccur with "treatment", so this medical scam remains unnoticed.

personality disorders are another curious case. there is little, if any, original research on them, the cluster model (partioning personality disorders into "eccetric", "dramatic" and "anxious" clusters) has literally no valid empirical support and most of the particular personality disorders are severely lacking in terms of construct validity. there is a single "approved" treatment option for about a dozen personality disorders: "Dialectical Behavioral Therapy" for borderline personality disorder, which is some esoteric stuff alleged derived from zen buddhismus. given the current state of evidence, personality disorders are rather an insult rather than a medical diagnosis.

>>9871924
To be fair, odd personality types found a link between autism and schizophrenia on an organic basis.

>>9871537
>>9871574
Thank you mate. You seem quite knowledgeable.

Do you have experience with cognitive enhancers or "nootropics"? I've thought of giving them a try for a long time, since my memory/reaction has gotten pretty bad over the last while, it's mostly words that I forget.

>>9872173
as you can see in this very thread, i frequently omit words, mix up syllables, miss out on adverbial -ly or third person -s. the only thing that did improve concentration, cognitive ability and motivation for me so far was minocycline, which is very hard to come by due to restrictive European medical drug laws.

i might start another thread about nootropics in the near future, since this is my original interest and all of the mental health stuff is merely a byproduct. sadly, i can only present anecdotes on them and no actual evidence, which, ironically, is the very thing i criticize about psychiatry and clinical psychology...

>>9872621
>i might start another thread about nootropics in the near future, since this is my original interest and all of the mental health stuff is merely a byproduct. sadly, i can only present anecdotes on them and no actual evidence, which, ironically, is the very thing i criticize about psychiatry and clinical psychology...

That would make for a great interesting thread, especially if you go into detail like you did with this one. Anyway, I ordered some Phenylpiracetam and L-Theanine hoping that they'd improve my cognition, do you have experience with those?

Also, what do you think about the upregulation of dopamine receptors by microdosing amphetamines? I've heard that this is a thing, and it lasts quite long.

in rats
https://www.ncbi.nlm.nih.gov/pubmed/2440058

rhesus monkeys
https://www.nature.com/articles/1395233

Surely if this is replicated in humans (if it's possible?), it would have some bad effects aswell as some good ones like increased motivation etc?

>>9861757
can someone screencap this and post the screencap?

>>9872621
>i might start another thread about nootropics in the near future, since this is my original interest and all of the mental health stuff is merely a byproduct. sadly, i can only present anecdotes on them and no actual evidence, which, ironically, is the very thing i criticize about psychiatry and clinical psychology...
Just preface the thread with an honest explanation of the limited knowledge about them and most people won't mind
Most people here who actually care about empiricism are more than willing to talk about less-evidenced topics so long as they're presented as such.

>>9863481
>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3314969
Pretty interesting to see how results are becoming gene-specific thanks to improvement in genomics.

>>9872639

>Pretty interesting to see how results are becoming gene-specific thanks to improvement in genomics.

Expect much more of this within the next decade. The chinese are currently genotyping their child prodigies in order to unveil the genetic architecture of intelligence.

>https://www.youtube.com/watch?v=1dVv5RMwzuo

Just imagine what happens if the allele frequencies of intelligence-related genes turn out to be not equally distributed among different peoples/races. And the implications of this knowledge for the U.S. and for the immigration-heavy countries of Western Europe.

>>9869115

>if cognitive theories of mood and motivation were true, an individual with bipolar disorder would be convinced of a heigthened self-efficacy and a lack thereof in rapid succession, with this circle repeating itself multiple times. yet, even the current reasearch with flawed methodology shows either no effectiveness or miniscule effect sizes for bipolar disorder and especially the manic component of it.

Another thing about CBT's theoretical framework:

Why would it only apply to depression and to none of the other mental diseases?

If causation of mental illness by distorted thoughts was a thing...

a) Why wouldn't hallucinations disappear when you convince them their perpeceptions aren't real?
b) Why wouldn't anxiety or panic disappear when you convince them their fears are baseless?
c) Why wouldn't addictions cease to cause substance craving when they really want to quit?
d) Why wouldn't mania stop when you convince them their perceived self-efficacy is exaggerated?

>>9861960
Of course thoughts and emotions are physical. They're a bunch of chemical reactions happening in the brain.

>>9872889
>Of course thoughts and emotions are physical. They're a bunch of chemical reactions happening in the brain.

i hold that both thoughts and emotions are consequences of these chemical reactions/electrochemical gradients, but not identical to them.

suppose a certain thought always coincides with a certain physical state/process in someone's brain. now you recreate exactly the same state/process in vitro. is it still connected to the same thought? likely not, because whatever is in your Petri dish cannot think or feel. therefore, the underlying physical state/process does not equal the thought, since the state/process can occur without its respective thought (but NOT vice versa). the state/process is necessary, but not sufficient for the particular thought content.

thoughts and emotions are pieces of information, both of which are not physical, yet real. they are emergent properties of an actual physical state/process.

this is similar to numbers. numbers are real, yet not physical. numbers are slightly different in one regard, though: they are preexistent and therefore inpendent from physical entities whatsoever. the concepts of "four" or "ten" exist even without anyone being aware of them or any physical entity existing/any event happening four- or tenfold.

unlike numbers or abstract constructs, thoughts and emotions require a physical cause, yet cannot exert consequences of their own, due to not being physical themselves.

>>9872629
i haven't tried any racetams yet and theanine was very underwhelming. i didn't notice any effect at all, even at high dosages.

to be honest, i don't know enough to give a reasonable opinion on microdosing. the rationale behind microdosing is usually "hormesis": a phenomenon, where otherwise deleterious/toxic substances are supposed to exert beneficial effects at miniscule dosages. the mere existance of hormesis is highly controversial and, in all honesty, i really don't know what to think of it...

Nootropics: PDE4b inhibitors!
>https://mentalhealthdaily.com/2015/08/18/genetically-modified-mice-pde4b-inhibition-increases-intelligence-reduces-anxiety/

Drugs won't save me and therapy won't either. Great.

imagine being this big of a brainlet to not accept your own mental illness diagnosis and believe you can redefine the entire field to make yourself sane.

the state of the 21st century boomer.

>>9873162
Imagine being a big enough brainlet to think pharmaceuticals is anything more than one big lobby to make billions off of stupid goyim.

>>9873213
>america is the only country in the world

lemao

>>9861778
>antagonists cause Olney's lesions

>>9871260
>>9871267
https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1360-0443.2009.02761.x
the wikipedia has a better summary but was effectively what i said. you can and should email the publisher about reading it fully to learn more as they'll just give you access
>>9871415
like what that other dude said i just read the wikipedia on things i'm interested in and then follow the studies for more information

>>9873162
Fuck

>>9873391
>https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1360-0443.2009.02761.x

try http://sci-hub.tw for papers.

regarding SSRI effectiveness: there are several psychometric tests for depression.

>http://psycnet.apa.org/buy/1996-10085-001
>https://pdfs.semanticscholar.org/0103/b59438cf304ea685a305812ee790ae65cde4.pdf

according the the article linked above, depression sufferers (n = 135) score a mean of 22.39 on the Hamilton Depression Rating Scale (HDRS) with a standard deviation of 3.69, whereas healthy controls (n = 117) score 3.67 on average (SD = 3.11). the weighted mean standard deviation is (117 * 3.11 + 135 * 3.69) / (117 + 135) = 3.42. the difference of the mean values is 22.39 - 3.67 = 18.72. the effect size of depression is 18.72 / 3.42 = 5.47.

similarly, the Hamilton Depression Inventory 17 (HDI-17) indicates 3.99 (SD = 2.99) for the control group and 22.22 (SD = 5.12) for major depression. in this case, the weighted mean standard deviation is (117 * 2.99 + 135 * 5.12) / (117 + 135) = 4.13, the difference of the mean values being 22.22 - 3.99 = 18.23. here, the effect size of depression is 18.23 / 4.13 = 4.41.

according to comtemporary psychiatric research, the currently available antidepressants have effects sizes of about 0.3 - 0.5 (several sources, just search for "depression effect size" on PubMed) and this is without taking publication bias into account. (trials showing negative result are far less frequently published than "successful" trials, thus skewing meta analyses.)

even if one were to accept current psychiatric research, in spite of the flaws pointed out in this very thread, comtemporary antidepressants remove only ~5,5% (0.3 / 5.47) to ~12% (0.5 / 4.41) of overall depression symptomatology!

to use the antitussive analogy once again: in given period of time, a healty individual coughs 18 times on average, whereas people coming down with a cold cough 118 times. now, is a medication reducing the number of average coughs to 106 really worth it?

>>9861828
Brain regions for sight and hearing predate brain regions for feelings, therefore, nothing you see can make you sad.

Makes sense right?

op do you have any interesting info about lithium monotherapy and bipolar disorder?

I'm hopefully going into med school next year and am interested in psychiatry. I have the intention of fixing the field and starting from a better approach. Is this possible in principle? Or is the nature of the study that it is impossible to get a good grip on?

>>9874267
i hate to say it anon but the entire field of psychiatry is bought and sold twice over by big pharma, you will never make a meaningful change to the field as a whole and will be written off as a quack if you try

psychiatry and big pharma have a reciprocal revolving door of mutually beneficial interlocking interests and they are pretty blatant about it

>>9874257
> op do you have any interesting info about lithium monotherapy and bipolar disorder?

the two main biological activities of Li+ are a) disruption of inositolphosphate metabolism and b) inhibition of glycogen synthase kinase 3beta.

>http://bioclima.ro/LITHIUM.pdf

i haven't really looked into bipolar disorder other than testing cognitivist predictions, because there's MUCH more literature on unipolar depression. i have to admit, though, that DRD2 antagonists have a considerable proof of concept for the treatment of mania, since they are very capable of decreasing motivation and anticipatory pleasure.

>>9874267

>I'm hopefully going into med school next year and am interested in psychiatry. I have the intention of fixing the field and starting from a better approach. Is this possible in principle? Or is the nature of the study that it is impossible to get a good grip on?

well, you can always try, but, frankly, i don't see much of a chance for you to succeed... if you do rigorous scientific research, prepare to be ostracized and libeled by your future collegues and fellow "experts". it's not even a "big pharma" thing! academic psychiatrists and psychologists have pushed bad research and false narratives for more than half a century now. they can't just quit and admit "oops sorry dudes, we were wrong about most things, let's start all over again!" without a massive loss of face that utterly destroys any credibility they have left.

if you decide to get into psychiatry, better keep your scientifically-supported-yet-unorthodox insights for yourself and always keep track of the biochemical and neurophysiological literature!

>https://www.sciencedirect.com/science/article/pii/S1551714415300033

This article argues antidepressants would require approximately twice their currently estimated effect size to cause "minimal improvements" when evaluated in terms of clinical, rather than statistical significance.

Do anyone have an informed opinion on anxiety disorders, OCD and other niche diagnoses? And what about the evidence on non-CBTish psychological treatments, transcranial magnetic stimulation and electroconvulsive therapy?

>>9872631
>can someone screencap this and post the screencap?

^

>>9874257
It has its origins in total quackery- lithium carbonate dissolves urate kidney stones. it was eventually found to work as a mood stabilizer, and a lot of research has focused on its action on glutamate in the brain. it does require significant medical monitoring because it can cuck your kidneys, thyroid, etc. and an overdose is not that hard to stumble into by accident, from a patient's perspective.

Speaking of which, lithium helped return me to society and has helped keep almost neurotypical for the better part of a decade. the regular blood tests are a nuisance, but nothing bad has happened and i have not had a legit manic episode since my late teens.

>>9874732
Social worker here who has practiced as a therapist for about three years now- CBT is becoming notorious for being seen as a silver bullet by practitioners who do not have the constitution to do therapy. It is extremely soothing for the clinician to practice in a way that is really remote and focused on diagrams and homework.

The real shit is Marsha Linehan's work in Dialectical Behavior Therapy. The problem is that although it looks like its principles can be widely applicable, there is also an issue with practitioners creating diet DBT treatments that water down the real thing and people using its principles in everything they do which isn't the point (see last article).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2963469/
http://journals.sagepub.com/doi/abs/10.1177/1087054714535951
https://onlinelibrary.wiley.com/doi/abs/10.1002/jclp.22114

Here is an interesting paper about ECT, also. FYI, I am only familiar with ECT being recommended as a second or third-line treatment when outpatient prescribing and concurrent therapy have not stopped the mayhem and hospitalizations over a number of years.
https://www.sciencedirect.com/science/article/pii/S0006322315001547

>>9876616
>Social worker here who has practiced as a therapist for about three years now- CBT is becoming notorious for being seen as a silver bullet by practitioners who do not have the constitution to do therapy. It is extremely soothing for the clinician to practice in a way that is really remote and focused on diagrams and homework.

thanks alot! do you see yourself as some kind of "expert tier placebo-ist" or do you think there is some substance to clinical psychological theories, which i missed/misrepresented in the OP? also, can you think of any method to scientifically evaluate the effectiveness of psychotherapies that circumvents the unblind/placebo/nocebo-problem?

>>9876555
I'm glad to hear that anon, I'm bipolar myself and am currently staring into the abyss.

>>9876706
sure! here are some disjointed thoughts on the subject. I will leave aside some of the epiphenomena discussion because I would really challenge the premise that thoughts and feelings do not have consequences. example: my cat becomes frightened by thunder and lightning outside my apartment. while the thunder and lightning do not bother me, I am sad that my cat is hiding under the bed and will not let me console him. did the physical process going on outside in the storm ultimately cause me to be sad? yes, with a few detours that track so well with the feelings that I am describing that trying to suggest that the feelings themselves were not causally involved does not make much sense. i really h8 dualism btw.

back to therapy.
one of the best predictors of success in psychotherapy is what people have decided to call a "therapeutic alliance." the short version of it is that you need trust and rapport to get anything done. CBT is useful in certain circumstances, e.g. for someone with moderate depression who is functional enough to do something about it, or the worried well who want to fix problematic ways of relating to their families, and so on. what something like CBT can't do is coerce someone into thinking, feeling, and acting differently. no model of therapy can do that. even theories that capture something accurately (and I think CBT speaks to some people's schemas, ways of dealing or not dealing with depression and anxiety really well) or mostly accurately do not always have any purchase in practice, because the person has to be ready to put in some work.

that's a long way of saying that it is hard to suss out what you would call the placebo effect and what you wouldn't in an arena where the idea is to foster connection and healing in part through the expectation that any of it is really possible.

for context, i am also >>9876555 this poster, and i benefit from therapy and medication in addition to practicing it professionally.

thanks again for your answer! i'm honestly surprised the thoughts-cannot-have-consequences stuff turned out to be the most controversial part of the op so far!

i've read a lot about the the dodo bird verdict and the common factors theory, but all of this seems to implicitly assume that psychotherapy does actually work and there's merely confusion about its "active ingredients". still, psychotherapy as some kind of "rent a friend" endeavour sounds alot more plausible than any practitioner-side theory, be it cognitive, behavioral or "psychodynamic". then again, this would imply there's nothing specific about psychotherapy and likely any amicable human contact would do the same, as long as it's equally intense and time-demanding.

the only way to reliably test its effectiveness i can possibly think of, is an RCT with psychotherapy-naive participants and a control group "treated" by non-psychiatric health professionals, non-medical practioners, attorneys, social workers, etc. (any social, "talkative" profession, really) without prior psychological/psychiatric education/experience. these non-psychotherapeutic "practitioners" have to be instructed to avoid the specific modes of action according to the respective therapy's theoretical framework, but otherwise they should provide equally effortful and time-demanding sessions.

any opinion on psychoanalytic and psychodynamic therapies?

and have you ever tried to taper off/discontinue your medication/therapy? if so, did you notice any deterioration?

>>9876952
I can tell you that any and every training program will tell practitioners-to-be how important boundaries are- the "rent a friend" endeavor does not, or should not, capture how an effective therapist does their work. you are paying for someone's time, but you're paying for someone's careful attention to things you want to change or problems-in-living that you're having, not their friendship.

that's actually a great jumping-off point for some thoughts on psychodynamic work. I do not believe that there is some distinct object called "the unconscious" and I am not a big believer in Jung's and Freud's trippy screeds. they're interesting, but they don't really inform anyone's practice.

what I do believe in is being keenly aware of transference and countertransference. all that means is that everyone is living their history all the time, and that both the client and the therapist bring past associations, defense mechanisms, and insights that are based on their history. how the client sees you, how you see the client, and the way your rapport does or does not develop and grow comes from somewhere. you can't stomp it out, but you can name it and use insights you gain from it to work on actual problems.

this is related to the idea of psychotherapists offering careful attention and insight rather than friendship. here is an example of managing countertransference: feeling the impulse to disclose how my own problems relate to someone's, or wanting to talk about what we may have in common. a friend might offer an anecdote about their own life, a therapist might note for himself "I could have a blind spot re: this client's behavior, because it calls something up for me."

i am on a lower dose these days at 28 than i was at 20, but i have gone lower. i take 300 mg three times a day- this has been fine, and i have been on it for about a year and a half. i was on an extended release (600mg twice daily) before that for 2 years but that was a no-go (continued)

>>9876952
>>9876997
(continued)
moving to the XR kicked off a hypomanic episode that was a bear to deal with. thankfully there were no professional consequences and no enormous personal ones. i did almost lose the security deposit on an apartment, though.

i have talked about lithium a lot, but i was on seroquel as well off and on. it calmed that hypomanic episode down, for example, but i was then tapered back off. that's happened about three times now, i think. it helps hit the brakes on an episode, but i hate being on it for long: drowsiness and constipation are the side effects I tend to get. the taper makes me nauseous, also.

>>9861757
OP do you spend alot of time just writing these notes and thinking about this and these are your summary of notes?

>>9861811
but do you realise theres flaws in your reasoning as well in some of these statements though obviously not in alot of them.

>>9861828
thats because it is wrong. limbic regions are very important for thought and cognition.

>>9877111
>OP do you spend alot of time just writing these notes and thinking about this and these are your summary of notes?

when i started reading about motivational improvement, i was prepared to take notes on what i thought i was going to find. this quickly shifted to "noting down what's wrong with contemporary psychiatry/clincal psychology", when most of the stuff turned out to be bad research or outright quackery. for the op, i assorted my stuff into categories, dropped everything i deemed too speculative and kept what i considered either a) supported by evidence, b) derived from logical inference or c) undemonstrable, yet very important to discuss.

>>9877121
>but do you realise theres flaws in your reasoning as well in some of these statements though obviously not in alot of them.

i'm afraid this is impossible to completely avoid, especially if you're doing this kind of stuff entirely on your own. would you mind pointing out the cases of false statements/flawed reasoning on my part? (a few cues on why they are wrong would suffice, no need to write a wall of text!)

on a further note, i do NOT aim to discredit psychiatry/clinical psychology by cherry-picking cases of bad research, because i have emotional/moral objections to the whole enterprise or something like that. in fact, i'd love to see anything of it actually working (and being scientifically evidenced to work).

>>9877121
>thats because it is wrong. limbic regions are very important for thought and cognition.

while i think i'm fairly well-versed in neurophysiology and anything biochemistry-related, i don't know much about neuroANATOMY to be honest. is there any original research connecting conscious thoughts and/or executive functioning to the limbic system?

>>9878123
>is there any original research connecting conscious thoughts and/or executive functioning to the limbic system?
Other anon here. I haven't done much research on this specifically, however I recall a Stanford lecture about it.
I believe it was describing how the vast majority of emotion in mice was processed through the limbic system.
Here's the whole video:
https://www.youtube.com/watch?v=CAOnSbDSaOw&list=PL848F2368C90DDC3D&index=14

>>9877009
>i am on a lower dose these days at 28 than i was at 20, but i have gone lower. i take 300 mg three times a day- this has been fine, and i have been on it for about a year and a half. i was on an extended release (600mg twice daily) before that for 2 years but that was a no-go (continued)

what kind of lithium salt are you taking? (for me to calc the amount of substance)

oh, and would you mind telling me your height and weight?

have you ever experienced electrophysiological side effects (convulsions, kidney disease, etc.)?

>>9872986
>sense made in this post
less than 1

>9878158
please elaborate!

>>9878123
well the easiest way to show you is that while damage to the lateral prefrontal causes executive deficits in humans, its in limbic areas that causes it in rats. plus if you look at the structure of the brains neuroanatomy, its considered that from each sensory area you get a structurally hierarchical trend going from granular to agranular areas which basically means that every sensory or sensorimotor modality has a limbic part to it. you also cannot deny that traditionally limbic areas like the hippocampus or parts of the thalamus are also important for cognition or memory.

>>9878756

>you also cannot deny that traditionally limbic areas like the hippocampus or parts of the thalamus are also important for cognition or memory.

any recommended reads?

>https://www.ncbi.nlm.nih.gov/pubmed/27068570

Untreated patients with schizophrenia do actually have ELEVATED prolactine levels, contrary to what is to be expected in cases of excess dopamine or increased D2 signaling!

Dopamine hypothesis BTFO once again!

>>9878770
theres alot that i would recommend i dont know where to start.
http://www.its.caltech.edu/~squartz/buckner.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4401581/
https://www.frontiersin.org/articles/10.3389/neuro.01.023.2009/full

basic idea is that the hippocampus provides a model/map that represents objects/concepts in our sensory experiences and the relations/contexts them. this maps literally everything from abstract concepts to sound to space to social hierarchies to value. its what allows us to navigate space, remember things that have happened in the past, predict things in the future or imagine things, perform theory of mind tasks, make complex decisions/plan and even for things like mind wandering and dreaming.

>>9878770
cont. the thalamus would naturally be cognitive because though its considered limbic its functions naturally link to the cortical areas it connects with - the thalamus has areas which map with every single part of the neocortex. so areas connected to e.g. prefrontal areas are naturally associated with the same functions normally.

https://s3.amazonaws.com/academia.edu.documents/46438178/Deficits_of_memory_executive_functioning20160613-12337-ofifyd.pdf?AWSAccessKeyId=AKIAIWOWYYGZ2Y53UL3A&Expires=1532009839&Signature=gauOLTQ%2Bgiz8y4avMF4GyCtr0B0%3D&response-content-disposition=inline%3B%20filename%3DDeficits_of_memory_executive_functioning.pdf

BUMP

>>9878825
It's a pathogen. Schizophrenia is caused by a pathogen.

>>9861757
>wall of text
nope.jpeg

>>9880384
>It's a pathogen. Schizophrenia is caused by a pathogen.

Any further information? Toxoplasma gondii, Epstein-Barr-Virus, anything else?

We already know, psychosis is not entirely a mental or neurological disorder. There are non-CNS alterations as well.

>https://www.ncbi.nlm.nih.gov/pubmed/29743584

>>9880408
>Any further information?
No, because the damn retards aren't looking for it. They keep chasing dumb non-pathogenic theories. Find the damn virus.

>>9880485
>it's a virus
why do you say this?

modern psychotherapy is bunk (see: second wave and before) for the reasons you listed because psychological problems are caused by a resistance to(and indulgence in) normal phenomena, not the phenomena themselves

>>9880597
The frequency of schizophrenia is consistent with a pathogenic source:

It is far too debilitating to be a syndrome, which means that unless it is a very recent disease, it would have been weeded out from the population by now, being reduced to the point where it can only occur at about the same rate as novel mutations. On the other hand, by the same argument, if schizophrenia genes had some sort of heterozygote advantage, we would see it at higher frequencies in the population, unless it is a very recent disease. But by all available evidence, schizophrenia is old. Therefore, it is caused by an external factor, the most likely source of impairment being pathogens, since schizophrenia seems to have no relation to other forms of environmental insults to the brain (like hits, depravation or extreme temperature conditions).

>>9880654
As for why schizophrenia doesn't seem to be contagious: the pathogen might have a very complex transmission method which makes it very hard to spread. We know for a fact that certain ulcers are caused by pathogens for example, yet cancer isn't exactly a contagious disease. This might explain why it seems to run in the family (having already ruled out a genetic cause given the frequency at which it occurs humans).

>>9880654
>>9880669
The interesting thing about how it runs in families from my perspective is how large the degree of difference is depending on whether one or both parents are diagnosed.
The occurrence in a general population is about 1%.
When only one has it, the chances of the child also being diagnosed is 10%.
This is significant in and of itself, however when both have it, this gets raised all the way to about 40%.
As a person outside of the field of study I need to ask:
Is this consistent with other genetically inheritable neurodegenerative diseases such as Parkinson's?
If not then would that be further evidence that such a pathogen exists?

>>9880721
Read this: https://muse.jhu.edu/article/44812/summary (use sci-hub.tw to get the full article)

>>9880408

this doesnt necessarily mean schizophrenia is not an entirely non-cns disorder. it is well known that your brain has a heavy top-down influence on your bodies regulation through organs the hypothalamus and also the limbic system heavily affected in schizophrenia.

>https://www.ncbi.nlm.nih.gov/pubmed/29743584

this article is about stress but highlights how cognition can affect the rest of the body and how things like stress are associated with physical disease.

>>9880654
i think its abit presumptuous to say it would have been weeded out by now. surely some pathogens are more frequent than schizophrenia and some other genetic syndromes have a lower frequency possibly?

theres alot of evidence for specific genes involved in schizophrenia.

schizophrenia has one of the most stable windows of onset of any disorder which makes people think it is a developmental disorder.

also bare in mind schizophrenia as a syndrome seems far too heterogenous to be caused by a pathogen?

pathogens may have an input somewhere to these types of symptoms but i doubt they would be the only ones.

>>9880864
>i think its abit presumptuous
No. The math is pretty straightforward.

>theres alot of evidence for specific genes involved in schizophrenia.
It's all correlational; no causal link is established. Genes are also involved in how susceptible you are to the flu. Doesn't mean that flu is genetic.

>>9880726
Very interesting, and there does look to be plenty of evidence that warrants more research.
Although it's important to note that this article isn't attempting to imply that all cases of schizophrenia are caused by such pathogens. Only that there should be more effort in distinguishing based on potential categories of causation rather than phenotypic expression alone.
>"Because the etiology of schizophrenia is unclear and diagnoses are made on the basis of phenotypic similarities rather than etiological evidence, it is likely that schizophrenia will eventually be recognized as a collection of illnesses with distinct etiologies."
>"...a scientific approach to the causation of schizophrenia needs to put a greater emphasis on tests that distinguish hypotheses of genetic causation from those of infectious causation."

>>9873162
Racial anthropology was based on physical observation of races with clearly distinct traits and a growing scientific background and is now considered obsolete and "pseudoscientific"

https://en.wikipedia.org/wiki/Scientific_racism

they even gave it a bad boogeyman name "muh racism"

psychology is considered a science and perfectly rational despite describing none of its syndromes other than vague subjective observation.

Makes you think

The stuff that makes me lose my shit too often, is when i see a certain topic discussed and then i read its proposed causes and it starts off like this:

"The causes are thought to be neurological, genetic and psychological"

who the fuck writes this stuff? i've see it from "serious" "professionals" too

Even mainstream medical quality control institutions agree with SSRIs being useless (either ineffective or benefits too small to be noticed): >>9876105

>>9880886
isnt it presumptuous to think schizophrenia fits into the assumptions of those math models.

and yes youre right it is correlational but id say there is alot more evidence that schizophrenia has a heavy genetic input and is very multifaceted in its causes... than that schizophrenia is solely produced by some kind of pathogen.

>>9881898
>>9880886
also have to bare in mind that genes involved with schizophrenia risk are implicated in some of the theoretical mechanisms which is interesting

>>9881898
>isnt it presumptuous to think schizophrenia fits into the assumptions of those math models
No. It's standard population genetics accounting. To claim that were schizophrenia genetically caused it would not obey the same rules is special pleading.

>>9881923
well desu is it even a threat to fitness? offspring still have relatively small chance of getting schizophrenia.

i just wonder if population genetics can actually model how these processes would work in mental disorders since the brain is so complicated and we don't even understand the brain or what schizophrenia is yet. by saying that it would be weeded out by now is assuming an overly simplistic relationship between the genotype and the phenotype.

>>9881984
>well desu is it even a threat to fitness?

>>9882007
if offspring have a relatively low chance of getting it, is it? 10% chance of having schizophrenia given 1 of your parents having it. and infact, realistically, schizophrenia onset is often so late that many or some people would have already had kids. that would especially be the case a few decades ago when it was normal to have kids in your early 20s. would a given gene that gives risk for schizophrenia gives a higher fitness outside the context? desu we dont even know the selection pressures on the brain so its completely speculative.

>>9882018
what about theories of a schizophrenia spectrum, where minor expressions of it may be beneficial while full blown expressions of it are detrimental?

>>9882024
ive no idea about that, ive always got the impression that its all bad but i thinking that the genes for schizophrenia will always first of all be coding for other cognitive traits. youre balancing what fitness these give vs schizophrenia and its all context dependent.

>>9863395
I dont know from SSRIs but I can tell you this:

Taking just 5 pills of Wellbutrin permanently changed my personality, it basically nullified severe depression/anxiety/pain/PTSD symptoms that I had had for many many years, it was so ridiculously horrible it's impossible to describe, I can't even remember it now, but it was every single day.

It also changed my emotional states in qualitative ways. I'm flatter now. Also my spaciness and my excitability (I had mild dissociation and maybe "bipolar type 2" - anyway I had intense "mood" and perception shifts). I'm also still "depressed" - whatever that really means. Of course affected my thinking (which i've been working on for a long time) changed as well, and that's disappointing.

It took me a couple weeks of trying to mentally go back to the "old me" before realising it's not going to happen. It sucks but this is what I have now. Google "wellbutrin erased my soul" or something like that and you'll see a guy describing something similar.

You might say I'm glad to be relieved of intense suffering, but I also don't have any sense of excitement or 'significance' or interest. Everything lasts for about 1-2 seconds then quickly fades. I wouldn't believe or understand this shit if someone told me. I feel like I have motivation and health now, but no emotions, positive or negative or anything.

I have absolutely no idea what happened, but I'm just assuming the Wellbutrin either fried something, or forced growth of new receptors, or kickstarted something. My gut tells me that since I feel kinda flat & dead, that it did some serious damage. And it's not reversing, as far as I can tell.

These drugs are seriously heavy-duty and dangerous. DO NOT take them unless you're prepared to kill yourself otherwise.

>>9882112
>5 pills
you understand your prescribing psychiatrist always tells that these medicines take "weeks" to build up in your brain?

I took wellbutrin for months and didn't notice anything at all then just quit it cold turkey one day, I'm a bipolar headcase though

>>9882112
Wow. What a roller-coaster of a post.
It was only half-way through that I realized I was reading a real life horror story.
Sorry to hear and I hope you get better.
What did your psych say about this?

>>9882112
like everyone knows, you cant prove a negative, so if your psych tells you "I HAVE PLENTY OF "PATIENTS" ON WELLBUTRIN AND THEY'RE FINE, SO WELLBUTRIN IS HARMLESS"

do not believe her lies, a good portion of those people are getting brain damage

>>9882112 #
>5 pills
you understand your prescribing psychiatrist always tells you that these medicines take "weeks" to build up in your brain, right?

I took wellbutrin for months and didn't notice anything at all then just quit it cold turkey one day, I'm a bipolar headcase though

>>9882123
>do not believe her lies
I got a chuckle from you using "her" there.
Out of curiosity was that due to your gender or an assumption based on probability in the field?

>>9882112
ive never known antidepressants to change my personality. i also feel sometimes its difficult to tell whether the personality changes people experience on these drugs might be a part of just how people have changed since theyve started having problems? i.e. part of their mental illness

>>9882118
Yes, those are 100% total flat lies as well. It starts 'working' a couple hours after you take it. Lexapro starts working immediately too. Different people are different. These drugs are very complicated. If anyone ever tells me 'hurr hurr it doesnt work for weeks' i'm going to kill them and eat their fucking family.

Wellbutrin in particular, is kind of like taking extended-release cocaine or something - it's said to give your brain a lot of dopamine molecules.

>>9882119
I dunno if i made it clear, I'm a LOT better than before, a lot of my suffering is permanently relieved. I'm now able to work shitty jobs and support myself, which I definitely couldn't do before without blowing my brains out.

Just a shame that my brain, personality and thoughts had to be a casualty. It is really 100% true what they say about these "drugs" (i'd never call them "medication") killing originality but I was really at my wits' end before taking it. Realise that 98% of people are just gonna go I FEEL BETTER NOW! and not perceive huge changes in their internal mental states, so by most peoples' measure, I am a success story.

Psych said this doesn't usually happen... she compared it to an electro-shock therapy treatment, where it keeps working after you stop. She acknowledged my issues but she didn't really care or anything. I still see her every week, she's paid to pretend to listen to me. It's pretty sickening.

>>9882126
My therapist's female man, and all the other "psychotherapists" in the office are female except 1 dude.

>>9882128
My sister, who has been on anti-depressant SSRIs as well as Clonazepam for sever anxiety attacks, once described to me her recognition that she was emotionally lacking.
This was after her 2nd attempt of getting off of them (and she still hasn't been able to years later), so the side-effects were starting to wear off.
She explained it as follows (paraphrasing, of course):
"All the time I had spent taking those pills, I had never noticed what my true personality was. It's only coming off of them that I realize that this person who I was before starting the medication was a giant bitch."
The "giant bitch" part is verbatim by the way.
What these pills seem to do is keep you in one solitary state of mind.
This hinders any potential growth that is normal in people as they grow. And I must say it's very obvious that she's still stunted emotionally.
Now of course this is just an anecdote, so I'll ask:
>Have you ever tried to get off of them?
>And if so, did you experience such a realization as to find the personality you thought you had was foreign?

>>9882144
>My therapist's female man, and all the other "psychotherapists" in the office are female except 1 dude.
Nearly 3/4 of new PhDs in the field are women.
This brings up a good question though: Is it better for an individual to get psychological help from somebody of the same gender?
If this is the case then that might at least partially explain the large discrepancy in mental illnesses observed in men as opposed to women.

>>9882157
I've had psychotherapists of both genders, males are better by a country mile

>>9882166
It's my guess that men would be better with men, and women with women.
I would assume that many of the mistaken autism diagnosis, for example, could be better recognized as regular male activity by a man than by a woman.

>>9882166
how so

>>9882146
i havent taken them for over a year, ive just never noticed anything ever. been on and off 6 years.i just feel its hard to pinpoint whether these changes are to do with the pills or just how your personality/emotions change with your mental illness.

>>9882191
>its hard to pinpoint whether these changes are to do with the pills or just how your personality/emotions change with your mental illness.
That's an interesting perspective I had not considered. One interesting thing about these meds is that they're usually prescribed indefinitely while only even attempting to ease the symptoms.
Does you psychiatrist ever talk about doing things that would eventually get you off of them? Or is it more assumed to be a sort-of life sentence?

>>9882166
>I've had psychotherapists of both genders, males are better by a country mile

Did psychotherapists (of either gender) accomplish something for you?

>>9882229
ive just thought that because when people come on and off pills must be usually correlated with changes in their overall symptoms. people come on pills when it gets worse and maybe that has some long term effects. when your sister came off maybe because she felt better she had this revelation.

Are depression and negative symptoms of schizophrenia even distinct entities?

Agonists at the kappa opioid receptor can cause hallucinations, dissociation AND dysphoria!

>https://en.wikipedia.org/wiki/%CE%9A-opioid_receptor#Function

>>9882985
>Are depression and negative symptoms of schizophrenia even distinct entities?
Based on my admittedly limited understanding I believe they're fundamentally similar but with enough difference to classify them separately. In particular if my memory serves depression doesn't generally involve the same kind of linguistic challenges

thanks to bone juice anon, i spent the last few days looking further into psychotherapy research and finally found a 1983 meta analysis comparing psychotherapy to placebo treatment.
>http://psycnet.apa.org/record/1984-12811-001
>A qualitative analysis of the studies in terms of the type of patient involved indicated that those using psychiatric outpatients had essentially zero effect sizes and that none using psychiatric inpatients provided convincing evidence for psychotherapeutic effectiveness.
>essentially zero effect sizes

keep in mind psychotherapy's effect sizes have plummeted since the seventies, so the meta analysis above is likely overestimating its effectiveness, if anything.
>https://uit.no/Content/418448/The%20effect%20of%20CBT%20is%20falling.pdf

another curious finding is that psychotherapist's (the practitioner's, not the treatment's!) effectiveness slighty, but significantly DECREASES with experience. in other words: the average psychotherapist gets worse, not better, by practicing!
>https://www.ncbi.nlm.nih.gov/pubmed/26751152

in general, the scientific quality of psychotherapy trials and meta analyses is astonishingly low. out of 196 meta analyses, 66% turned out to be too heterogenous to produce credible results, 36% had too small sample sizes, 48% had an "excess of significant findings" (which is a more polite synonym for "massaged data") and only 7% met the criteria for sufficient quality (which i still disagree with due to lack of blinding).
>https://onlinelibrary.wiley.com/doi/full/10.1111/acps.12713

yet, there are even claims psychotherapy had severe adverse effects (though i'm as sceptical about this as i am about its effectiveness).
>https://www.sciencedirect.com/science/article/pii/S0092656616302410
>Overall, therapy experiences were associated with significant increases in undesirable traits and markers (e.g., chronic stress, depression, neuroticism), and significant decreases in desirable traits (e.g., self-esteem, conscientiousness).

i'm currently half-way through "The great psychotherapy debate: The evidence for what makes psychotherapy work" by Wampold/Imel.

>The issues include the fact that psychotherapy trials cannot be blinded, the placebo is not indistinguishable from the treatment, the placebo and treatments effects are of the same class (i.e., are both psychological), and the incidental components in the placebo (e.g., the relationship) are active and necessary for the delivery of the purportedly active specific ingredients. Consequently, such controls are labeled as pseudo-placebos.

>treatments intended to be therapeutic outperform pseudo-placebos, which in turn are superior to no treatment. However, when pseudo-placebos are given faithfully, permit the therapist to be caring and empathic, and are structurally equivalent to treatments, then the efficacy of the pseudo-placebos approaches that of active treatments.
>the efficacy of the pseudo-placebos approaches that of active treatments.

(both p. 252)

in spite of the book title, they admit there no specific effect of psychotherapy. psychotherapy is apparently nothing more than an attempt to maximize placebo effects.

interestingly, baseline mu-opioid receptor binding predicts both placebo response and antidepressant response, and both opioid release upon placebo administration and placebo response predict antidepressant response:
https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2443355

right now, i'm very much inclined to say there's currently no specific treatment for depression that somehow exceeds an equally administered placebo.

>>9882190
just general relatablity
>>9882920
honestly no, my world view is far too nihilistic/cynical for their cheap pseudo brainwashing "think positively" CBT techniques to have much of an effect on me

>>9883299
You know when you go jogging and after you feel slightly euphoric, and it feels like a short antidepressant? Why can't they put that in pill form, give you more dopamine or something.

pls gib tldr

>>9884106
>pls gib tldr

- neither depression and schizophrenia are valid disease entities, but mulitple diseases clumped together for diagnostic purposes
- theories about these circulated by both psychiatrists (dopamine hypothesis for schizophrenia, serotonin hypothesis for depression) and clinical psychologists (negativity bias and cognitive distortions as causes rather than symptoms) are logically inconsistent and provably wrong
- SSRIs and psychotherapy for depression and DRD2 antagonists for schizophrenia may not exceed placebo in effectiveness (no credible evidence)
- the overall quality of psychiatric and clinical psychological research is very low
- the validity of trials is severely impaired due to a lack of blinding
- even when assuming the contemporary low-quality research to be trustworthy, SSRIs and DRD2 antagonists exert very low effect sizes and miniscule response rates even when compared to inert placebos: the possible benefits are not "clinically significant"

>>9867376
Schizophrenia is the most heritable mental illness.

>>9885411
>Schizophrenia is the most heritable mental illness.

Are you suggesting a genetic disease with imcomplete penetrance?

Go to bed Tom Cruise

Pitchman we alredy warned you to not post this

Tom Cruise is a horrible actor, but this is a good thread!

>>9885641
>>9886105
The ultimate secret of Scientology is that they work for the CIA.

Interesting discussion here: >>9880330

If neither drugs nor psychological treatments work, what are you supposed to do with mental illness then?

>>9887500
>If neither drugs nor psychological treatments work, what are you supposed to do with mental illness then?

either go ahead try everything with some proof of concept and tolerable side effects or hope for spontaneous remission.