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The Good News about Genes and Mental Disorders

Nous

Well-Known Member
Premium Member
In a recent article published in Issues in Science and Technology, neuroanatomy professor Jonathan Leo combs through the findings of the largest genetic investigation of any mental disorder, a multi-national genome-wide association study involving almost 37,000 persons diagnosed with schizophrenia and more than 113,000 controls: http://issues.org/32-2/the-search-for-schizophrenia-genes/ . The researchers identified 108 loci with statistically significant associations, yielding a risk score that could account for about 3.4% of the variance. That isn't a typo: https://dash.harvard.edu/bitstream/handle/1/13890642/4112379.pdf?sequence=1

Of course, it is true that the study design may have failed to capture some loci, perhaps even some important ones. Conversely, the miniscule risk score may even be falsely inflated due to the same (or different) flaws in the study's methodology. The authors reveal that of the 49 ancestry-matched case-control samples that were constructed, 46 were for people of European ancestry and 3 for East Asian ancestry. The 3 family-based samples were exclusively of European lineage. These omissions are highly interesting, possibly informative, given the well documented history of racism in the handing out of psychiatric diagnoses in Europe and the US, especially schizophrenia diagnoses given to people of African and Latino descent: http://pb.rcpsych.org/content/25/7/244 ; http://www.tandfonline.com/doi/abs/10.1080/09540269974429?journalCode=iirp20 ; http://tps.sagepub.com/content/33/3/297.abstract ; https://www.amazon.com/Protest-Psychosis-Schizophrenia-Became-Disease/dp/0807001279 . Examining the records of 135,000 US veterans, Blow et al. found that, despite similar symptom presentations, African Americans were more than 4 times more likely than whites to be diagnosed with schizophrenia (instead of bipolar disorder), while Hispanic Americans were 3.15 times more likely to recieve a diagnosis of schizophrenia than whites: https://www.researchgate.net/profil..._psychoses/links/53d24ac30cf220632f3c898f.pdf As the article notes, people diagnosed with a psychotic disorder are treated quite differently than those given a mood disorder (bipolar) diagnosis. People diagnosed with a psychotic disorder are prescribed more toxic, more debilitating drugs and are more often subjected to forced drugging and confinement. The diagnosing of and prescribing "treatments" for mental disorders are obviously not scientific endeavors. Psychiatry is a system of social control, not a science.

In any case, it's difficult to imagine that discovery of any heretofore undiscovered genetic associations could possibly lead to the conclusion that genes are anything more than an insignificant contributor to the development of symptoms diagnosed as schizophrenia (or any other mental disorder). As professor Leo notes:

As more and more variants are implicated, the results become even more watered down. For instance, a recent algorithm to examine the polygenic risk of schizophrenia estimated that there are 20,000 single nucleotide polymorphisms (SNPs), or differences in single DNA components, implicated in schizophrenia. Commenting on these results, Alkes Price from the Harvard School of Public Health noted that because so many regions are implicated, there is the concern that “GWAS will ultimately implicate the entire genome, becoming uninformative.” A clinically useful signal appears impossible to distinguish from the noise.

Even if you completely agree with the 108 loci study’s methodology and all its inherent assumptions, there is no way to conclude that the researchers have discovered “schizophrenia genes.” In fact, they have disproved their existence. For each of the 108 loci there is a very small difference between the percent found in those diagnosed with schizophrenia and the control sample. Take the very first one: it’s found in 86.4 percent of the patients, and in 85 percent of the control group. This is a minor difference, and whether or not you have the variant tells you nothing about your risk of being diagnosed with schizophrenia. These genes are neither unique nor specific for people diagnosed with schizophrenia; many of the genes are scattered far and wide, and most of us carry at least some of them. As Kenneth Kendler, a psychiatry professor and geneticist at Virginia Commonwealth University, concluded in a recent paper, “All of us carry schizophrenia risk variants, and the vast majority of us carry quite a lot of them.” It is only by combining all the genetic markers into a single polygenic risk score that researchers can say that an individual has an increased risk of developing schizophrenia. However, even those individuals with a supposedly increased risk were more likely to not develop schizophrenia.​

http://issues.org/32-2/the-search-for-schizophrenia-genes/

Leo proceeds to refer to the findings of the largest GWAS on people diagnosed with major depressive disorder, a 2013 mega-analysis involving more than 32,000 cases and 76,000 controls of European descent, the results of which the authors provide the definitive summary: “ . . . we were unable to identify robust and replicable findings.” http://neurogenetics.qimrberghofer.edu.au/papers/Ripke2013MolPsychiatry.pdf (However, a new, larger GWAS on depression was published a couple of days ago, a meta-analysis involving people who obtained their DNA profiles through 23andMe and reported a history of depression, treatment for depression or no history of depression, combined with samples from two previously published GWAS. The abstract, which is all I've read so far, announces finding 15 loci that reached genome-wide significance. But it does not report a risk score, and Figure 2 seems to show that the vast majority of the variance consists of principle components that are explained by geographical ancestry: http://www.nature.com/ng/journal/vaop/ncurrent/full/ng.3623.html As the title of the paper notes, these findings were also limited to people of European descent. One can easily get the impression that researchers consider inclusion of people of non-European ancestry in GWAS on depression to just muddy the waters. It seems unlikely that the findings of this most recent study are generally applicable across cultures and races/ethnicities.)

Leo also explicates how the rationale for pharmacological regimens for mental disorders rests crucially on the assumption that the cause of mental disorders is largely genetic:

It is impossible to separate genetic theories from the medicalization of psychological stress. The widespread use of psychiatric medications is based on the idea that schizophrenia and other psychological conditions arise, in part, from genetic defects that result in biological alterations such as reduced levels of neurotransmitters, or deficits in neuronal circuits, that need to be fine-tuned with medications. In general, higher genetic contributions to a disease equate to a stronger case for pharmacological treatment, while diseases with a higher environmental component are seen as better candidates for lifestyle changes and therapy. In 1996, in regards to ADHD, Stephen Faraone, a leading psychiatric genetic researcher, stated: “Many parents are reluctant for their children to take psychotropic medication and others find it difficult to maintain prescribed regimes. These problems are mitigated by discussing the genetic etiology of ADHD…” If parents really believe that their child has a measurable chemical imbalance, then just as they would treat their diabetic child, they would surely treat their child diagnosed with ADHD.​

The irony of Faraone's statement here is that an honest discussion of the actual scientific findings on "the genetic etiology of ADHD" would begin and end with the fact that no such genetic etiology has been found: http://adhdnet.com/wp/wp-content/uploads/2014/10/Neale-2010-Meta-analysis-of-genome-wide-JAACAP.pdf , even when the sample is racially/ethnically limited: http://www.ncbi.nlm.nih.gov/pubmed/22012869 . Interestingly, after numerous failed attempts to find genetic associations, publication of GWAS on ADHD seem to have come to an abrupt halt around 2010. Leo notes the disturbing fact that 18 times more children are diagnosed with ADHD in the US than in France.
 

Nous

Well-Known Member
Premium Member
By way of comparison, there are significantly greater genetic associations for obesity than for any mental disorder. In the first place, unlike the case of primary mental disorders, several rare forms of obesity are known to result from certain monogenic mutations, in addition to chromosonal abnormalities such as Prader-Willi and Bardet-Biedl syndromes, which generally include distinct physiological anomalies. There is also the important difference in that at least "obesity" can be defined according to an objective, measurable criterion (body fat percentage), in contrast to primary mental disorders, which are neither defined nor diagnosed on the basis of objective biological criteria. Thus, in any study of people diagnosed with mental disorder(s), the problem of ascertainment always looms. It is an unanswered question whether or not any, or what percentage, of the 37,000 in the above GWAS who were diagnosed with schizophrenia actually have any physiological or biochemical anomaly that could hypothetically cause the symptoms of schizophrenia. (Just as with the diagnosis of schizophrenia, which of the required "Criterion A" symptoms a patient is assessed as having--hallucinations, delusions, disorganized speech, disorganized behavior, or negative symptoms--also show racial/ethnic or cultural patterns: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4140994/ . This fact is no less fatal to the idea that what is diagnosed as schizophrenia is an objective disease than is the fact of racial disparities in schizophrenia diagnoses.) The only known physiological or biochemical abnormalities consistently found in people diagnosed with schizophrenia are those known to be caused by the brain-damaging drugs prescribed to "treat" people with psychotic disorders, tardive dyskinesia being one of the overt manifestations.

In any case, the Harvard School of Public Health webpage "Genes Are Not Destiny" explains the genetic findings related to obesity other than those known rare genetic or chromosonal abnormalities ("common obesity"):

What’s increasingly clear . . . is that genetic factors identified so far make only a small contribution to obesity risk--and that our genes are not our destiny: Many people who carry these so-called “obesity genes” do not become overweight, and healthy lifestyles can counteract these genetic effects.

[. . .]

In 2008, for example, Andreasen and colleagues demonstrated that physical activity offsets the effects of one obesity-promoting gene, a common variant of FTO. The study, conducted in 17,058 Danes, found that people who carried the obesity-promoting gene, and who were inactive, had higher BMIs than people without the gene variant who were inactive. Having a genetic predisposition to obesity did not seem to matter, however, for people who were active: Their BMIs were no higher or lower than those of people who did not have the obesity gene. (15)​

https://www.hsph.harvard.edu/obesity-prevention-source/obesity-causes/genes-and-obesity/

The statement of the university's School of Public Health applies even more to mental disorders than to obesity: genes are not destiny. Professor Leo makes the same point, in addition to the fact that the evidence clearly shows that the genetic contribution to development of the mental phenomena that constitute mental disorders is basically inconsequential. This is good news.

And while the popular justification for the dispensing and consuming psychiatric drugs may rest on imaginary genes, the fact is that non-pharmacological interventions remain the most effective, least toxic and least debilitating methods to counteract the unwanted behaviors and psychological phenomena commonly diagnosed as mental disorders. This is good news. For instance:

"Symptoms, functioning and coping strategies in individuals with schizophrenia spectrum disorders who do not take antipsychotic medication: a comparative interview study"

Method In all, 48 participants with a DSM-IV schizophrenia spectrum disorder who were taking (n = 25) or not taking antipsychotic medication (n = 23) were included. Assessment consisted of self-ratings of symptoms, symptom-related distress and social support combined with a semi-structured interview that assessed general and social functioning, subjective evaluation of symptoms and coping strategies.

Results Symptom severity and distress did not differ between the groups. However, the non-medicated participants had significantly higher levels of general functioning than medicated participants and a longer duration of being non-medicated was significantly associated with a higher level of general functioning. In contrast to the hypotheses, not taking medication was not associated with more effective coping strategies or with higher levels of social support. Medicated participants more frequently reported the use of professional help as a coping strategy.​

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=10378898


"Does treatment of schizophrenia with antipsychotic medications eliminate or reduce psychosis? A 20-year multi-follow-up study"

Method. A total of 139 early young schizophrenia and mood-disordered patients were assessed at index hospitalization and then reassessed six times over 20 years for psychosis and other major variables.

Results. At each follow-up assessment over the 20 years, a surprisingly high percentage of SZ ["schizophrenia patients"] treated with antipsychotics longitudinally had psychotic activity. More than 70% of SZ continuously prescribed antipsychotics experienced psychotic activity at four or more of six follow-up assessments over 20 years. Longitudinally, SZ not prescribed antipsychotics showed significantly less psychotic activity than those prescribed antipsychotics (p <0.05).​

http://journals.cambridge.org/actio...e=online&aid=9336096&fileId=S0033291714000610


"Treatment of Schizophrenia Without Neuroleptics: Psychosocial Interventions Versus Neuroleptic Treatment"

Randomized studies comparing psychosocial treatment programs without neuroleptics to drug-based programs were sought out for review, and six were found. Long-term outcomes were statistically equivalent or superior in the nondrug group in all six studies, even those where the quality of the psychosocial treatment was questionable. In studies with psychosocial interventions that appeared to have higher quality, both short and long-term results were equivalent or superior without neuroleptics. These findings suggest that neuroleptics interfere with long-term recovery and, if appropriate psychosocial interventions are available, are not even necessary for short-term behavior control.​

http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.623.5240&rep=rep1&type=pdf


"What the Multimodal Treatmeht Study Really Discovered About Intervention for Children Diagnosed With ADHD: Implications for Early Childhood"

This paper reviews the Multimodal Treatment Study for ADHD (the MTA study) with a focus on the intriguing results of the Summer Treatment Program (STP) component of the MTA study. Review of the findings of the MTA study in relation to behavioral interventions used in the study and the combination of behavioral interventions and educational approaches used during the STP provides an insight into effective non-drug-based approaches to assist children diagnosed as ADHD. There is an increasing trend towards identifying children with ADHD symptoms in the early childhood period. This review of research indicates that focusing on behavioral, parental, and educational interventions may provide better outcomes for the child in the long term than through the alternative of a reliance on drugs for behavioral modification.

[. . . ]

The findings of the MTA study have been reported widely (MTA Cooperative Group, 1999a, 1999b) and used to support the validity and reliability of the ADHD diagnosis and efficacy of treatment using amphetamine-type drugs (United States House of Representatives, Subcommittee on Early Childhood, Youth and Families, 2000; United States House of Representatives, Committee on Government Reform, 2002).

[. . .]

The findings of the MTA Cooperative Group (l999a, 1999b) are used to promote the use of medication and the belief that treatment with medication is more effective than behavior management, parent training, or educational interventions (United States House of Representatives, Committee on Government Reform, 2002).

[. . . ]

Breggin (2000) in a review of the MTA study revealed 26 major methodological flaws that call into question the scientific validity and reliability of the study and undermine any possible conclusions made from the MTA data. Breggin (2000) indicated that there were no placebo controls or double blind; that blind classroom observers found no differences between the groups; there was no control group of untreated children; 32% of the medication management group was already on medication; medication management group subjects were selectively and not randomly chosen (of 4,521 children screened for the trial only 579 were selected); the medication management group was very small (only 2.7% of the original cohort before screening completed the medication management trial) and had been selectively chosen using response to medication as a factor in allocation to the different treatment groups; the children did not rate themselves as improved; most of the subjects were boys; behavioral treatments were stopped earlier than medications; the behavioral treatments were flawed; most children suffered from adverse drug reactions (ADRs); there were not trained observers for ADRs; there was no improvement in academic performance; there was minimal if any effect on social skills; all the researchers were "well known drug advocates" (Breggin, 2000, p. 69); and the parents and teachers were exposed to "pro-drug propaganda." In conclusion to his review Breggin (2000) stated that "the MTA study does not demonstrate the superiority, or even the usefulness, of stimulant medication in the treatment of children labelled with ADHD or any other presumed psychiatric disorder" (p. 71).​

[My bolding]

http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.489.8846&rep=rep1&type=pdf
 

Nous

Well-Known Member
Premium Member
"Efficacy of antidepressants in adults"

Longitudinal follow-up studies show very poor outcomes for people treated for depression both in hospital [14] and in the community, [15] and the overall prevalence of depression is rising despite increased use of antidepressants. [16] Two studies that prospectively assessed outcome in depressed patients treated naturalistically by general practitioners and psychiatrists found that people prescribed antidepressants had a slightly worse outcome than those not prescribed them, even after baseline severity had been taken into account. [17] [18] No comparable studies could be found that showed a better outcome in people prescribed antidepressants.

[. . . ]

The NICE review data suggest that selective serotonin reuptake inhibitors do not have a clinically meaningful advantage over placebo, which is consistent with other recent meta-analyses. In addition, methodological artefacts may account for the small effect seen. Evidence that antidepressants are more effective in more severe conditions is not strong, and data on long term outcome of depression and suicide do not provide convincing evidence of benefit. In children, the balance of benefits to risks is now recognised as unfavourable. We suggest this may also be the case for adults, given the continuing uncertainty about the possible risk of increased suicidality as well as other known adverse effects.​

https://www.baumhedlundlaw.com/25.pdf


"Relabeling the Medications We Call Antidepressants"

This paper raises the question about whether the data on the medications we call antidepressants justify the label of antidepressant. The authors argue that a true antidepressant should be clearly superior to placebo, should offer a risk/benefit balance that exceeds that of alternative treatments, should not increase suicidality, should not increase anxiety and agitation, should not interfere with sexual functioning, and should not increase depression chronicity. Unfortunately, these medications appear to fall short on all of these dimensions. Many of the “side effects” of these medications have larger effect sizes than the antidepressant effect size. To call these medications antidepressants may make sense from a marketing standpoint but may be misleading from a scientific perspective. Consumers deserve a label that more accurately reflects the data on the largest effects and helps them understand the range of effects from these medications. In other words, it may make just as much sense to call these medications antiaphrodisiacs as antidepressants because the negative effects on libido and sexual functioning are so common. It can be argued that a misleading label may interfere with our commitment to informed consent.​

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3820604/


"Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration"

Background

Meta-analyses of antidepressant medications have reported only modest benefits over placebo treatment, and when unpublished trial data are included, the benefit falls below accepted criteria for clinical significance. Yet, the efficacy of the antidepressants may also depend on the severity of initial depression scores. The purpose of this analysis is to establish the relation of baseline severity and antidepressant efficacy using a relevant dataset of published and unpublished clinical trials.

Methods and Findings

We obtained data on all clinical trials submitted to the US Food and Drug Administration (FDA) for the licensing of the four new-generation antidepressants for which full datasets were available. We then used meta-analytic techniques to assess linear and quadratic effects of initial severity on improvement scores for drug and placebo groups and on drug–placebo difference scores. Drug–placebo differences increased as a function of initial severity, rising from virtually no difference at moderate levels of initial depression to a relatively small difference for patients with very severe depression, reaching conventional criteria for clinical significance only for patients at the upper end of the very severely depressed category. Meta-regression analyses indicated that the relation of baseline severity and improvement was curvilinear in drug groups and showed a strong, negative linear component in placebo groups.

Conclusions

Drug–placebo differences in antidepressant efficacy increase as a function of baseline severity, but are relatively small even for severely depressed patients. The relationship between initial severity and antidepressant efficacy is attributable to decreased responsiveness to placebo among very severely depressed patients, rather than to increased responsiveness to medication.​

http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0050045


"Baseline Depression Severity as Moderator of Depression Outcomes Between Cognitive Behavioral Therapy vs Pharmacotherapy"

In this IPDMA [Individual Patient Data Meta-analysis], we found no evidence that baseline severity of depression, whether patient or clinician rated, moderated the effect of treatment on outcomes. That is, patients with more severe depression were no more likely to require medications to improve than patients with less severe depression, and these findings were robust in sensitivity analyses. There was a modest (<1 point on the HAM-D) main effect of ADM [antidepressant medication] over CBT [cognitive behavioral therapy] on the continuous outcomes (HAM-D and BDI) but no evidence of any interaction, which provides new and important information for the debate about treatments for severe depression. Although guidelines[8,9] suggest that patients with severe depression require pharmacotherapy, we found no evidence that differences between ADM and CBT are moderated by baseline depression severity. Furthermore, robustness analysis on the severe sample alone showed no differential treatment response between CBT and ADM. Therefore, CBT may also be an effective first-line treatment for these patients.​

[Note the consistency of these findings with those of Kirsch et al. above, in which the drug-placebo difference for patients with severe depression was attributable to decreased responsiveness to placebo, rather than to increased responsiveness to the drug.]

https://www.researchgate.net/profil...a-analysis/links/5606a68508aea25fce3735a3.pdf


"Is Exercise a Viable Treatment for Depression?"

Blumenthal and colleagues conducted several RCTs comparing the effects of aerobic exercise to antidepressant medication. In the first SMILE (Standard Medical Intervention versus Long-term Exercise) study (3), 156 older adults with MDD were randomized to four months of either aerobic exercise, sertraline, or a combined exercise and sertraline group. Participants in the exercise conditions exercised in a group setting three times per week at 70-85% of their heart rate reserve. Participants in the sertraline condition were titrated for therapeutic response on sertraline by a study psychiatrist (50-200mg), consistent with standard clinical treatment of depression. Following 16 weeks of treatment, groups did not differ in their level of depressive symptoms, suggesting that exercise and standard antidepressant treatments were equally effective. Interestingly, a follow-up examination of these participants conducted 10 months after the completion of the treatment period showed that participants in the exercise group showed lower rates of depression relapse in comparison with both the sertraline and combined groups. Moreover, participants who reported engaging in regular exercise during the follow-up period were more than 50% less likely to be depressed at their 10-month assessment compared to non-exercisers.

The Duke group (5) later extended these findings by including a placebo control group and by adding a group that exercised at home on their own, without the social interaction facilitated by group exercise that could contribute to the antidepressant effects of exercise. Participants were randomized to either home-based or supervised aerobic exercise, sertraline, or placebo for a four-month period. Home-based exercisers were provided with the same exercise prescription as supervised participants and received an initial home visit to establish their exercise training routine, as well as instructions on how to monitor their heart rates accurately. Results revealed that participants in either exercise or sertraline groups tended to show greater improvement in comparison with placebo participants and these results became statistically significant when “early responders” (i.e. participants who experienced a self-reported improvement in depressive symptoms of > 50% within the first week of treatment), were eliminated from analyses.

In a recent follow-up analysis (2), participants’ depression was reassessed one year after their enrollment in the trial. Interestingly, neither group assignment nor antidepressant medication usage during the follow-up period were significant predictors of depression at this follow-up time-point. Instead, the only significant predictor was regular exercise during the follow-up period. In other words, regardless of initial treatment group assignment or background characteristics, those individuals who reported regular exercise following completion of the intervention were the least likely to be depressed at follow-up.​

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3674785/

(There are plenty more such studies. Ask me for them.)

This is good news. After all, it's expensive, futile and counterproductive to eat drugs that are ineffective and induce chronicity and a plethora of other serious adverse effects.

Perhaps there is more good news about genes, mental disorders and effective interventions. You are invited to present any that you know of. You are invited to present any bad news that you know of. You are invited to present any evidence refuting any of the above.
 

Nous

Well-Known Member
Premium Member
It means "too long, didn't read."

It's a way of asking for a summary. In a few sentences, what is the good news?
Thank you. I forget about the brevity of the modern attention span.

A good summary of the good news can be quoted from professor Leo himself:

Even if you completely agree with the 108 loci study’s methodology and all its inherent assumptions, there is no way to conclude that the researchers have discovered “schizophrenia genes.” In fact, they have disproved their existence.​

http://issues.org/32-2/the-search-for-schizophrenia-genes/

And the same goes for "the genetic etiology of ADHD" and major depressive disorder.
 

First Baseman

Retired athlete
Thank you. I forget about the brevity of the modern attention span.

A good summary of the good news can be quoted from professor Leo himself:

Even if you completely agree with the 108 loci study’s methodology and all its inherent assumptions, there is no way to conclude that the researchers have discovered “schizophrenia genes.” In fact, they have disproved their existence.​

http://issues.org/32-2/the-search-for-schizophrenia-genes/

And the same goes for "the genetic etiology of ADHD" and major depressive disorder.

Thank you. I figured that without the study.
 

First Baseman

Retired athlete
Can you elaborate on how you figured it out?

I didn't say I figured it out. I said I figured it, thought it.

How about if more people figure more on how to feed all the starving people in the world and forget about studies like this?
 

Nous

Well-Known Member
Premium Member
I didn't say I figured it out. I said I figured it, thought it.
Can you elaborate on why you thought it?

How about if more people figure more on how to feed all the starving people in the world and forget about studies like this?
I find it interesting to read and understand scientific studies on most any subject. Doing so does not detract from the importance of any other matter (such a feeding starving people). Certainly humans grow more than enough grain to provide adequate calories to all living humans. However an obscenely large percentage (more than half?) of that grain goes to feed livestock animals. In 1997, professor Pimentel calculated that the grain fed to livestock animals in the US alone could sustain 800 million people: http://www.news.cornell.edu/stories/1997/08/us-could-feed-800-million-people-grain-livestock-eat But obviously that isn't the topic of this thread.
 

Nous

Well-Known Member
Premium Member
Sorry, I got to "brevity" and tuned out. ;)
It isn't really a difficult subject. Obviously many people like to believe that they (and others) are genetically "programmed" to their unwanted behaviors. It's a very crippling belief, besides being unequivocally false.
 

Demonslayer

Well-Known Member
It isn't really a difficult subject. Obviously many people like to believe that they (and others) are genetically "programmed" to their unwanted behaviors. It's a very crippling belief, besides being unequivocally false.

I was just joking. It's a good point for sure.
 

Burl

Active Member
Randomized studies comparing psychosocial treatment programs without neuroleptics to drug-based programs were sought out for review, and six were found. Long-term outcomes were statistically equivalent or superior in the nondrug group in all six studies, even those where the quality of the psychosocial treatment was questionable. In studies with psychosocial interventions that appeared to have higher quality, both short and long-term results were equivalent or superior without neuroleptics. These findings suggest that neuroleptics interfere with long-term recovery...

OK I'll stop recommending drug therapy to schizophrenics.
 

First Baseman

Retired athlete
Can you elaborate on why you thought it?

Can you elaborate on how to feed millions of starving people daily? That's kind of my point. Forget about genes and let's get to more immediate problems that affect millions of people who literally are in great pain. Starving to death is quite painful, did you know that?
 

Nous

Well-Known Member
Premium Member
OK I'll stop recommending drug therapy to schizophrenics.
It seems to be upsetting to many people to be exposed to the actual findings in the peer-reviewed literature concerning the ineffectiveness and counterproductiveness of psychiatric drugs. In the case of neuroleptics, the evidence has long been available that these drugs result in worse outcomes than non-drug interventions, as indicated by the above studies, as well as the famous WHO studies that found that people diagnosed with schizophrenia in developing countries, where neuroleptics were rarely used, exhibited more improvement and better functioning at follow-up years than did people in developed countries, where neuroleptics were (and are) usually used to "treat" people diagnosed with schizophrenia: http://www.mentalhealthexcellence.o...3/10/1992_PsychologicalMedicine_22_131-45.pdf ; and http://psycnet.apa.org/psycinfo/1992-31447-001

Whitaker compiled and reviewed findings from an even earlier era:

"The Case Against Antipsychotics: A Review of Their Long-term Effects"

This paper makes a case that antipsychotics, on the whole, worsen long-term outcomes. The drugs may provide a short-term benefit, and it is clear that once patients are on the medications, there is an increased risk of relapse, for some period of time, when discontinuing the medication. But there is also a long line of research that tells of treatment that may increase a person’s biological vulnerability to psychosis and impair functioning over the long-term.

Sohler’s review also reveals that there is an absence of research that tells of medications that improve functional outcomes over the long term. This absence, given the obvious desire by psychiatry to report such positive results, is compelling evidence on its own that these medications, when it comes to affecting aggregate outcomes, do more harm than good.​

http://psychrights.org/Research/Digest/NLPs/The-Case-Against-AntipsychoticsWhitaker2016.pdf

What is the context in which and the basis for which you have been recommending drugs to "schizophrenics"? Is that how you normally refer to people who have merely received a diagnosis of a psychotic disorder?

What are the Criterion A symptoms of the "schizophrenics" to whom you have been recommending drugs? How do you account for the racial/ethnic or cultural patterns in the assessment of Criterion A symptoms, as found by McLean et al. above?

For that matter, how do you account for the racial disparities in the diagnosis of schizophrenia, as found by Bingham et al.? Do you believe that schizophrenia occurs 4 times more often in African Americans and 3 times more often in Hispanic Americans?
 
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