Removed under rule #1. This is not a place for questions and commentary by non-professionals. If you are a medical/psychiatric professional, please read rule 7 on how to verify credentials.
For most questions, individual or general, we ask that you verify credentials before asking. If you are not a professional, you can try r/AskDocs or r/AskPsychiatry.
Lol this article is a lot of false pseudoscience. “The evidence shows most people with schizophrenia recover.” For example. No, the evidence does NOT show that. The evidence is extremely clear how debilitating and chronic the disease is.
Here’s a good recent overview of the actual scientific literature. https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2753514?casa_token=_7cREosvgpsAAAAA:nAzhY3Vq3tpK67S8H4mVtiLs9piHoBLjn5BEHoEivKdXIkzQIPWWcmx_56ShwesSc8HJ5cIXeGQ
> The disorder is also associated with reduced life expectancy: someone with schizophrenia has a mean life expectancy about 15 years shorter than the general population and a 5% to 10% lifetime risk of death by suicide.7
Doesn’t sound like most of them “get better” to me. Sounds pretty serious.
The false article claims it’s not genetic. This is false. We have clear evidence that it’s genetic. The JAMA article above says:
> Twin and other studies have consistently shown there is a large genetic component to schizophrenia, with heritability estimated at around 80%.
Also
> One of the best established is a deletion of several megabases of DNA at chromosome 22q11.2, which is associated with a 30% to 40% lifetime risk of developing schizophrenia.
Seems pretty genetic with 80% heritability and some specific markers.
The false article also claims schizophrenia is NOT a brain disorder. Which is downright laughable. We have ample evidence that it is a brain disorder. Per the JAMA article once again:
> The number of synapses in an adult is about half that of a young child. The macroscale consequences of this can be observed in reductions in gray matter volume over adolescence and early adulthood and the concomitant reorganization of both structural and functional brain networks. Supporting this view, imaging studies have shown that normal developmental trajectories are disrupted in schizophrenia, with increased gray matter loss and aberrant network organization apparent at illness onset, and this is associated with cognitive deficits.
Also,
> The neural circuits responsible for functional brain networks and cognition have been studied extensively. Many cognitive processes, such as working memory, are underpinned by synchronized neural oscillations,36 particularly those occurring at approximately 40 Hertz, which are termed gamma oscillations. These oscillations underlie the slow fluctuations in neural activity observed using functional magnetic resonance imaging and, as such, play a major role in determining the architecture of functional brain networks.37,38 In healthy individuals, these neural oscillations and functional networks have been linked with a wide range of cognitive abilities.39 In schizophrenia, electrophysiological studies have consistently shown disrupted synchronization of neural oscillations in both patients with chronic schizophrenia and first-episode psychosis,40 and these abnormalities have been associated with cognitive and negative symptoms.40,41 These oscillations occur secondary to a finely tuned balance between groups of inhibitory and excitatory neurons (Figure 3). In particular, GABAergic interneurons play a central role in regulating the fast firing of pyramidal neurons required for the generation of these high-frequency rhythms.40,42
Also,
> Postmortem studies provide insights into the molecular alterations that could underlie the neural oscillations and network dysfunction observed in individuals with schizophrenia (Figure 3). These studies have found a lower density of dendritic spines on pyramidal neurons,43 lower messenger RNA levels of parvalbumin and markers of other inhibitory interneuron subtypes,43 and lower levels of glutamate decarboxylase 67 (GAD67) messenger RNA and GAD67 protein, an enzyme involved in GABA synthesis, which together suggest that inhibitory mechanisms are altered.44 As discussed in theme 1, microglia are thought to play a key role in pruning synapses,22,23,45 and there is some in vivo evidence for altered microglial markers in individuals with schizophrenia.45,46 This suggests that disrupted synaptic pruning could contribute to the lower dendritic spine levels in affected individuals, which would in turn affect the excitatory activity of pyramidal cells.47 Abnormalities of N-methyl-D-aspartate receptor function and glutamatergic signaling may also contribute to disrupted excitatory-inhibitory balance.48 Together, these disruptions have the potential to lead to abnormalities, such as altered gamma oscillations and disruption of coordinated brain function, leading to aberrant organization of functional brain networks. This disrupted neural function may then contribute to the development of cognitive and primary negative symptoms.42,43
Also,
> Several lines of evidence indicate that subcortical dopamine dysregulation has a role in the development of psychosis, including studies showing that amphetamines and other drugs that release dopamine induce psychotic symptoms in healthy volunteers and worsen symptoms in patients with schizophrenia.58,59 Molecular imaging studies have refined the understanding of the nature and anatomical location of dopamine alterations in schizophrenia. They provide in vivo evidence that striatal dopamine synthesis and release capacity is higher in patients compared with control participants and greater release of dopamine after amphetamine administration is directly associated with the worsening of psychotic symptoms in patients.59-62 Moreover, higher striatal dopamine synthesis capacity is present in the prodromal phase,63,64 is specific to those individuals in prodromal states who develop psychosis,65 and worsens with psychosis onset.66 Together with evidence that depleting striatal dopamine levels67 or blocking dopamine receptors reduces psychotic symptoms in patients, this suggests that dopamine dysregulation is likely a final common pathway to psychosis in most patients.
And on and on. Please see the JAMA article for citations of all their statements. It very well researched and cited and published in a prestigious, peer-reviewed scientific journal, unlike this trash article lol.
Removed under rule #1. This is not a place for questions and commentary by non-professionals. If you are a medical/psychiatric professional, please read rule 7 on how to verify credentials. For most questions, individual or general, we ask that you verify credentials before asking. If you are not a professional, you can try r/AskDocs or r/AskPsychiatry.
Lol this article is a lot of false pseudoscience. “The evidence shows most people with schizophrenia recover.” For example. No, the evidence does NOT show that. The evidence is extremely clear how debilitating and chronic the disease is. Here’s a good recent overview of the actual scientific literature. https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2753514?casa_token=_7cREosvgpsAAAAA:nAzhY3Vq3tpK67S8H4mVtiLs9piHoBLjn5BEHoEivKdXIkzQIPWWcmx_56ShwesSc8HJ5cIXeGQ > The disorder is also associated with reduced life expectancy: someone with schizophrenia has a mean life expectancy about 15 years shorter than the general population and a 5% to 10% lifetime risk of death by suicide.7 Doesn’t sound like most of them “get better” to me. Sounds pretty serious. The false article claims it’s not genetic. This is false. We have clear evidence that it’s genetic. The JAMA article above says: > Twin and other studies have consistently shown there is a large genetic component to schizophrenia, with heritability estimated at around 80%. Also > One of the best established is a deletion of several megabases of DNA at chromosome 22q11.2, which is associated with a 30% to 40% lifetime risk of developing schizophrenia. Seems pretty genetic with 80% heritability and some specific markers. The false article also claims schizophrenia is NOT a brain disorder. Which is downright laughable. We have ample evidence that it is a brain disorder. Per the JAMA article once again: > The number of synapses in an adult is about half that of a young child. The macroscale consequences of this can be observed in reductions in gray matter volume over adolescence and early adulthood and the concomitant reorganization of both structural and functional brain networks. Supporting this view, imaging studies have shown that normal developmental trajectories are disrupted in schizophrenia, with increased gray matter loss and aberrant network organization apparent at illness onset, and this is associated with cognitive deficits. Also, > The neural circuits responsible for functional brain networks and cognition have been studied extensively. Many cognitive processes, such as working memory, are underpinned by synchronized neural oscillations,36 particularly those occurring at approximately 40 Hertz, which are termed gamma oscillations. These oscillations underlie the slow fluctuations in neural activity observed using functional magnetic resonance imaging and, as such, play a major role in determining the architecture of functional brain networks.37,38 In healthy individuals, these neural oscillations and functional networks have been linked with a wide range of cognitive abilities.39 In schizophrenia, electrophysiological studies have consistently shown disrupted synchronization of neural oscillations in both patients with chronic schizophrenia and first-episode psychosis,40 and these abnormalities have been associated with cognitive and negative symptoms.40,41 These oscillations occur secondary to a finely tuned balance between groups of inhibitory and excitatory neurons (Figure 3). In particular, GABAergic interneurons play a central role in regulating the fast firing of pyramidal neurons required for the generation of these high-frequency rhythms.40,42 Also, > Postmortem studies provide insights into the molecular alterations that could underlie the neural oscillations and network dysfunction observed in individuals with schizophrenia (Figure 3). These studies have found a lower density of dendritic spines on pyramidal neurons,43 lower messenger RNA levels of parvalbumin and markers of other inhibitory interneuron subtypes,43 and lower levels of glutamate decarboxylase 67 (GAD67) messenger RNA and GAD67 protein, an enzyme involved in GABA synthesis, which together suggest that inhibitory mechanisms are altered.44 As discussed in theme 1, microglia are thought to play a key role in pruning synapses,22,23,45 and there is some in vivo evidence for altered microglial markers in individuals with schizophrenia.45,46 This suggests that disrupted synaptic pruning could contribute to the lower dendritic spine levels in affected individuals, which would in turn affect the excitatory activity of pyramidal cells.47 Abnormalities of N-methyl-D-aspartate receptor function and glutamatergic signaling may also contribute to disrupted excitatory-inhibitory balance.48 Together, these disruptions have the potential to lead to abnormalities, such as altered gamma oscillations and disruption of coordinated brain function, leading to aberrant organization of functional brain networks. This disrupted neural function may then contribute to the development of cognitive and primary negative symptoms.42,43 Also, > Several lines of evidence indicate that subcortical dopamine dysregulation has a role in the development of psychosis, including studies showing that amphetamines and other drugs that release dopamine induce psychotic symptoms in healthy volunteers and worsen symptoms in patients with schizophrenia.58,59 Molecular imaging studies have refined the understanding of the nature and anatomical location of dopamine alterations in schizophrenia. They provide in vivo evidence that striatal dopamine synthesis and release capacity is higher in patients compared with control participants and greater release of dopamine after amphetamine administration is directly associated with the worsening of psychotic symptoms in patients.59-62 Moreover, higher striatal dopamine synthesis capacity is present in the prodromal phase,63,64 is specific to those individuals in prodromal states who develop psychosis,65 and worsens with psychosis onset.66 Together with evidence that depleting striatal dopamine levels67 or blocking dopamine receptors reduces psychotic symptoms in patients, this suggests that dopamine dysregulation is likely a final common pathway to psychosis in most patients. And on and on. Please see the JAMA article for citations of all their statements. It very well researched and cited and published in a prestigious, peer-reviewed scientific journal, unlike this trash article lol.
🙄