Psychiatry is far more developed than appears. It is in this way by design.

The following is a collection of research articles which will help to show you that the level of knowledge which exists in psychiatry today far exceeds the level of available treatment options.

The other hypothesis -

1. Glutamate hypothesis in schizophrenia
This paper identifies a link between NMDAR hypofunction and the symptoms of psychosis.

2. (The 5HT Hypothesis of Schizophrenia) The Role of Serotonin in Schizophrenia
This paper states that serotonin blocking agents should also be employed in the treatment of schizophrenia. This is different to what is stated in number seven and eight where a drug which enhances serotonergic activity would provide benefit.

3. Psilocybin induces schizophrenia-like psychosis in humans via a serotonin-2 agonist action

4. The Nicotine Hypothesis

5. Towards a muscarinic hypothesis of schizophrenia

6. (Cannabinoid Hypothesis of Schizophrenia) Lateral Gene Transfer of Foreign DNA: The Missing Link Between Cannabis Psychosis and Schizophrenia

7. New Targets for Schizophrenia Treatment beyond the Dopamine Hypothesis
This study appreciates that the brain is a complex machine involving many different interacting parts and implies that it is an incredibly naive attempt to describe all psychosis as a result of too much dopamine.

Identifying other mechanisms -

8. THE EFFECTS OF METHEDRINE AND OF LYSERGIC ACID DIETHYLAMIDE ON MENTAL PROCESSES AND ON TILE BLOOD ADRENALINE LEVEL
As this study and the one below shows, persons suffering schizophrenia have less functional 5-HT2a receptors.

9. His452Tyr Polymorphism in the Human 5-HT 2A Receptor Destabilizes the Signaling Conformation

10. Anticholinergic Activity and Schizophrenia

11. Decreased Muscarinic Receptor Binding in Subjects with Schizophrenia: A Study of the Human Hippocampal Formation

12. The cannabinoid receptor 1 associates with NMDA receptors to produce glutamatergic hypofunction: implications in psychosis and schizophrenia



The Analysis -

It is clear to see that drugs which act in the manner of depressing a neurotransmitter system causes apoptosis (nerve cell death) in the affected system. While it is equally clear to see that drugs which excite a neurotransmitter system lead to neurogenesis in the affected regions.

1. Exposure to nicotine increases nicotinic acetylcholine receptor density in the reward pathway and binge ethanol consumption in C57BL/6J adolescent female mice

2. The Epigenetic Effect of Nicotine on Dopamine D1 Receptor Expression in Rat Prefrontal Cortex

3. Adaptive Increase in D 3 Dopamine Receptors in the Brain Reward Circuits of Human Cocaine Fatalities

This is substantiated by the scientific discovery of the being that smoking tobacco is known to reduce one's risk of developing Parkinson's disease.

It is also known that anticholinergic agents increases one's risk of developing dementia.

Or that how amphetamine use leads to neurogenesis in affected dopamine pathways.

Outside of the application of (external) agents it is known that exercise is capable of inducing levels of intense nerve cell growth or in the same notion on the proven fact of depression causing losses in nerve cells.

4. Exercise Increases Hippocampal Neurogenesis to High Levels but Does Not Improve Spatial Learning in Mice Bred for Increased Voluntary Wheel Running
As was mentioned earlier, it is shown here that exercise leads to a growth of new neurons.

5. Stress, Depression and Hippocampal Apoptosis
And shown here is that depression causes a loss of neurons.

There is also much discrepancy in the medical literature. For example one is that it is shown in scientific literature that smoking tobacco increases one's risk of developing psychosis in later life. It is then also shown in other journal articles that smoking tobacco causes a down-regulation, that is in the sense of reducing receptor density at the D2 terminals. This contradicts the current hypothesis being humped by every psychiatrist which I have ever met in my life, this is the dopamine hypothesis, which asserts that symptoms of psychosis are due to over expression or an overly energetic D2 receptor system.

All of these claims will be substantiated in the proceeding sections.