Well, you don't need familial heredity for something to be genetic, especially in such complex disorders such as schizophrenia where groups of genes are more likely to be involved rather than just one or two genes. Aside from that, I think there is plenty of theory and research on family dynamics and psychosis that goes back to the '60s and even before (Bateson, Lang) and defenses (Klein, Bion, Rosenfeld). And then there are tones of studies published on social cognition and theory of mind in schizophrenia (just check it out on PubMed). What I've found to be most useful in my own work with psychotic patients is Bannister's serial invalidation hypothesis based on George Kelly's personal construct psychology and Gregory Bateson's double bind hypothesis. These theories are also quite interesting because they fit very well into the now popular theory of mind research.

I think the discussion of "non-genetic schizophrenia" is silly in a way, since no one has proven there is such a thing as "genetic schizophrenia." There is certainly a fair amount of evidence that some are more genetically vulnerable to having the reactions that are called schizophrenia, but there is much more hype than evidence, in fact the evidence is so weak that it is possible to coherently argue that there may be no genetic vulnerability at all - see http://jayjoseph.net/docs/models.pdf

There is on the other hand a great deal of evidence that factors like childhood trauma and mistreatment increase the risk of later diagnosis of schizophrenia - see http://healingattention.org/documents/doc_litreviewpsychosis.pdf for one summary. This is so commonly ignored more due to political convenience than anything else: psychiatrists and others obtain their power by defining schizophrenia as a medical illness, framing it as "definitely genetic" helps with this agenda. The truth is probably much more complex, as is life: people can be pushed toward "schizophrenia" by lots of different factors, and there are also lots of factors that can play a role in recovery. If we recognized this, we would probably become much more effective in treatment.

I agree with the previous comments. Based on heritability patterns, schizophrenia predisposition is likely due to the effect of inheriting a combination of genes, each of which with a relatively small effect on its own (in most cases). Therefore, it is quite possible not to see other schizophrenia cases in the family. There is a large gradient in penetrance, even identical twins of schizophrenia patients, who share exactly the same genes may not develop the disease (let's not talk about epigenetics and de novo mutations for now, there is also something to be said for the fact that 3 out of 4 identical twins do not show an equivalent in utero environment). On the other hand, even relatives of schizophrenia patients who appear healthy often show defects in executive function, which requires the optimal function of the dopaminergic system (measured by the Wisconsin Card Sorting Test) and in sensory gating (measured by prepulse inhibition, PPI), and others. Cumulatively, such evidence points to the involvement of the corticostriatal associative loop, which involves connections between the dorsolateral prefrontal cortex and the caudate nucleus of the striatum (in humans), but I digress. With mutations in genes such as ones for dopamine receptors and other genes involved in neural pathways involving cognition and emotional function, the background on which they are expressed is is often very important. This background is given not only by other gene variants that person carries, but also by the conditions under which neurodevelopment occurred. During neurodevelopment, signals are sent back and forth between neurons, which are necessary for the proper migration, pruning and phenotype development of these neurons. It is generally accepted that activation of the CRH axis by stress (in simplified terms the release of cortisol, this includes both infection of psychological stress) during the second trimester of gestation, increases the chance that the offspring will later develop schizophrenia. However, the greatest effect of environmental perturbation is again seen in individual with family history of the disease, therefore, in individuals that likely carrying genes which predispose them to the disease. (It is, of course, possible to develop schizophrenia-like symptoms without any predisposition at all, such as with chronic PCP use.) Importantly, the effects of CRH axis activation cascade down many signaling pathways (most importantly dopaminergic, but also affecting glutamatergic and GABAergic signaling), which play a very important role in the neurodevelopment of the striatum and the dopaminergic system itself. It was recently shown by the Kellendonk lab at Columbia University that upregulation of dopamine 2 receptor (D2R), even if temporary, and only in the striatum, is able to induce a very schizophrenia-like dyregulation of the frontal cortex. The symptoms of schizophrenia are very varied, reflecting the many possible contributing factors. Ultimately, though, the involvement of the dopaminergic system and the striatum comes on top, with premorbid functional deficit in functions requiring the the optimal function of the striatum and/or the dopaminergic system and with the D2R being one of the top ten genes identified by schizophrenia genetic studies. Possibly the strongest supporting evidence is the correlation between the affinity of antipsychotics for the D2R and their effective dose in treating the disease. No such correlation exists between antipsychotic affinity and their effective dose for other receptors. So, in summary, there are likely many genes, with small effect, ultimately predisposing an individual to a less than optimal function of the corticostriatal associative loop, most likely through a defect in dopaminergic signaling. This can be induced entirely environmentally (we can all be pushed over the edge given enough force), but in most individuals with the disease, it involves both an environmental contribution and a genetic predisposition. (However, there are certain genetic mutations that have a very strong contribution indeed, completing the gradient)

Thank you all for replying! My focus while writing the question was based on the observations of common practices of treating the schizophrenia, where mostly medical models are employed (which I do not wish to be criticized badly) and less emphasis is given on targeting psycho-social factors (which are viewed with less enthusiasm, unless a significant decrease in severity is achieved by medications). Though techniques like CBT are not believed to be used separately without medications but clinicians do get demotivated due to weak compliance by the client and his/her family members (along with the compelling belief that schizophrenia is chiefly biological). In such conditions it is not sufficient to just depend on medications as researches do prove that environmental and personal attributes are one of the major maintenance factors. That implies, in order to be more convinced about the importance of psycho-social factors, one needs to view the whole phenomena of schizophrenia differently, more in light of interaction among environment and cognition (and therefore less on biological correlates). This would sound quite unscientific, as there are always biological differences among schizophrenic and non-schizophrenic individuals.

But its not an issue of just finding the most probable cause, rather how one approaches the illness and views the condition in course of treatment. For example, in chronic cases under in-patient care, medications almost fail most of the times. One can't keep on believing firmly that one day the client would get completely well just by taking proper doses of medicines aimed to target his/her symptoms. One of the major reasons for such persistence being that environment is quite rigid to bring any long term benefit to such patients. Patient's perceptions do not seem to change at all despite taking regular medications. So it becomes necessitating to rely more on those factors which are present consistently in the environment or in the 'mind' of the schizophrenic.

In recent years work on cognitions in schizophrenics has taken a pace among researchers, notable ones being Bentall, Frith, Garety, Chapman, Freeman, Moritz etc. There is an increased focus of study on cognitions not only among schizophrenics but also among psychosis-prone individuals, which is a promising population to provide substantial wealth of knowledge on cognitive factors (source-monitoring, self-monitoring, theory of mind, reasoning, cognitive biases, metacognitions) contributing to the onset of psychotic features. Similarly work on social cognition (social perception, emotional processing, theory of mind, social knowledge) is increasingly recognized as important in relation to schizophrenia-like symptomatology. These factors are quite different from the earlier recognized neuro-psychological factors like executive and motor functions. Addressing such factors in therapy would require more recognition of them, more belief in them, and more evidence of them. More models need to be proposed, more factors need to be recognized, and hence more attention needs to be given. This is possible only when there is a firm belief that particular style of cognition is responsible for maintaining the symptoms. Once this 'style' is known, therapy would be more focused and result-bearing.

Such proposals are consistent with the views that schizophrenia may not have any genetic liability. So when there are no genes involved reliability is formed more for psycho-social factors and less for biological ones. Single-gene may not be there, multiple genes may be involved, but that's a different issue. The belief that reduces therapeutic efficiency is that GENES are responsible, which express neurodevelopmentally at some stage, and hence their role assumes major significance. That is why I asked this question in context of those cases where a clinician is not sure of genetic causality (or sure of absence of it for which I took the case of probably negative familial history), and hence must focus on psychological and social factors which are independent of any genetic predisposition. I presented limited facts which may have brought the confusion that the question is referring to genes running in family alone.

Refining the original question, can we think of schizophrenia and related disorders as constituting chiefly the disordered cognitions and corresponding disordered interaction with environment (or vice versa), hence bringing a persistent change in the person (thereby giving minimal emphasis on biological correlates) ? Because then belief in success of psychotherapy is increased manifold. A clinician can be sufficiently assured that its the environment/cognition which has to be finally engineered and not the biology alone (seems an anti-psychiatric viewpoint!).

Even if you exclude any genetic basis, it changes nothing in terms of the psychiatric treatment of schizophrenia, because symptoms of schizophrenia still have their biological underpinnings and neurological correlates. The reason why psychiatrists use medication instead of psychotherapy is because antipsychotic drugs act faster and show better results, it has nothing to do with a possible genetic basis of schizophrenia. In fact, when chlorpromazine was introduced in the '50s, no one was thinking that schizophrenia is a genetic disease.

I don't think the right psychotherapeutic approach has been developed for patients with schizophrenia. Bion himself says that the progress he had made with his patients was really not progress in the clinical sense (in terms of reducing symptoms, improving functionality, etc.), there was no remission at all. He talks about some sort of "psychoanalytical break-through" (I don't remember precisely the term he used), which may be a great achievement in itself, but is not good enough. I've read a couple of studies that show some efficacy of CBT, but nothing very convincing, and - if I recall correctly - never without antipsychotic therapy.

I've worked with a psychotic patient and therapy was quite successful, but in combination with pharmacotherapy (risperidone). Even though this kind of work fascinates me, I don't think I'm brave enough to do it without antipsychotics. And when I say brave, I mean only one thing - I don't have the stomach to keep someone in therapy for a very long time with uncertain prospects of achieving significant improvement, while at the same time they could probably get better results with drugs alone.

Well a lot of work has been done in recent years about treatment of schizophrenia without antipsychotic medications. I am adding a few common researches most cited and referential, one of the first about drug-free trials.

http://journals.cambridge.org/action/displayAbstract;jsessionid=CBBA2882FECC612754F0539FDEA6C689.journals?fromPage=online&aid=5080908

http://onlinelibrary.wiley.com/doi/10.1002/cpp.269/abstract

http://onlinelibrary.wiley.com/doi/10.1348/147608308X278295/abstract

.

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http://www.ncbi.nlm.nih.gov/pubmed/10356622

Above is a link of an abstract from PubMed of a study titled "Treatment of nonpsychotic relatives of patients with schizophrenia: four case studies".

A question comes to my mind by reading it. Is it possible to attenuate or completely eliminate the pre-psychotic/non-psychotic symptomatic manifestations in individuals (similar sample as above) by giving them very low doses of antipsychotic medicines from an early age (may be beginning of adolescence atleast), provided long term side-effects of such medications are minimum/nil, so that any risk of developing schizophrenia in late adolescence or early adulthood (specifically period of 15 to 25 years) can be avoided or controlled to the highest possible degree?

Please share your views or any studies.

I don't think you can take case reports or case series as credible evidence, as interesting and useful as they may be. They should be the basis for research with large numbers of participants, and nothing more. The CBT study (Morrison et al.) is very interesting with good results, but more studies like that are needed, and with more patients. Also, I think another level of research should be conducted - what specific techniques work and for what? Because the diagnosis of schizophrenia includes a number of very different symptoms; I highly doubt that you could use the same approach for delusions, for hallucinations or the so-called "negative symptoms", and how do you do psychotherapy with someone with thought derailment or tangentiality? These are the aspects that should be explored individually, I don't think it's enough to say "CBT works for psychosis".

As for medicating people who are not yet psychotic, I am never quite able to get to the medical reasons for doing that, because I think ethical implications are quite frightening. At this stage, it seems to me that this kind of thinking additionally blurs the lines between normal and pathological, but in the wrong way - we seem to be expanding pathology. (Foucault would have something to say about this.)

Agreed - medicating people who are at risk of experiencing psychosis has huge ethical implications (despite the potential profits for the pharmaceutical industry that have been behind such attempts). A safer and more effective approach may be this: http://130.192.119.102/puntoinformativo/Informazioni%20per%20chi%20studia/folder.2005-02-08.1542893565/folder.2008-09-26.4056331757/folder.2009-03-10.9315004569/exfile.2009-03-10.5624860382/attach/morrison%202004RCT%20PSICOTERAPIA.pdf

As for the other questions about therapy (mostly cognitive therapy based approaches) for hallucinations, delusions, thought disorder etc - there's quite a lot of literature on these issues, much of which has emerged from UK based researchers and clinicians over the past 15-20 years (some author surnames to search for include Morrison, Bentall, Fowler, Chadwick, Birchwood, Kinderman, Gumley,Tarrier, Garety, Freeman, Turkington, Kuipers, Sensky, Brabban and many others). As you might imagine, standards of evidence vary, but overall it's fair to argue that CBT for psychosis should routinely be provided (as should family interventions). Indeed, in England, the hugely influential National Institute for Health and Clinical Excellence have reviewed the evidence base on 2 occasions, and continue to recommend that CBT and FI should be routinely provided by NHS services http://www.nice.org.uk/CG001 and http://guidance.nice.org.uk/CG82

If a mechanic were to treat his car for not running by adding expensive oil to it rather than put some petrol into it they would be deemed to be a little crazy right..... We are what we eat, it is not disputed that nutritional deficiency of Vit B3, B12, folic acid and Vit C all result in psychosis, Patrick Holford, Ultimate nutrition for the mind 2007. His work is a continuation of Abraham Hoffer and Linus Pauling. Hoffer had a 90% cure of SZ out of over 5000 patients (cure being deemed as in the community, in interpersonal relationships and paying income tax). He theorized that adrenaline oxidizes and becomes a hallucinogen for some people and that food allergies and substance addictions trigger those events. I would add emotional issues, past trauma, spiritual emergence, exhaustion, sleep deprivation and extreme stress. Add to that deficiency in B1 - poor concentration and attention, B5 - poor memory, stress, magnesium - irritability, insomnia, depression, manganese - dizziness, convulsions and zinc - confusion, depression, loss of appetite, poor concentration. It seems to me all these and long chain fatty acids, brains are made of it, omega 3 and 6 oils AND then some CBT and a person may with some kindness, safety, purpose, peer work, light therapy and empowerment to self care never have another episode again. Take a look at what Finland is doing in the no medication and no diagnosis field, from worst in the world to now best outcome. High nutrient supplementation has helped me to come off a small amount of meds and achieve a university degree so I speak from personal experience.

i have never given a serious thought to orthomolecular views that appropriate nutrient intake can cure disorders like schizophrenia, though i know a few people personally who have benefitted from orthomolecular therapeutics (those are cases of addiction). i do keep personal intimation with spiritual emergence beliefs that psychotic-like states can trigger expansion of spiritual experiences. But i have now for some time stopped believing in that manner. What fascinates me more is that certain attitudes/appraisals towards events in the mind make it disturbed, which makes a person distorted in reality (as one might believe that mental phenomena is a greater reality than the reality of outer world in a psychotic state) and hence the person responds with stress to such experiences which makes such psychotic states persistent (stress-diathesis models). Thus a predisposition to think in a particular manner, leading to distortions of mental phenomena and maintenance of such states due to inability to reduce stress accompanied by them makes a person psychotic, chronically if such is the case. so one needs to reduce the stress and understand the mechanisms by which mind is distorted or believed to be functioning, can make a person psychosis-free. in such ways cognitive therapies or even meta-cognitive training can serve to benefit a lot, as these therapies aim for the client to identify and alter the attitudes that he/she holds for mental phenomena.