Look them up. No one knows the biological basis for these "diseases" of the mind. For virtually everything else, ilke epilepsy, there's a clear and defined biochemical mechanism. For schizophrenia and autism, they're just defined in hand-wavy terms where anyone could be diagnosed if they are different enough from the horde in any dimension.
It's basically modern day witch burning. Torture anyone with divergent thinking. Give them vaccines and toxic pills so they become unmotivated and sterilized. Forget evidence, just burn them first and ask questions later. Also if you question this practice, then normaltrash will immediately accuse you of being schizophrenic or autistic yourself, which is another tell that it's not science but normaltrash ideology.
The real cause of schizophrenia is not brain damage, the theory goes, which is known to be a major cause of mental illness. But the brain, it seems, becomes a repository of messages that get shoved into the head when one takes drugs.
In fact, the research behind one of the study's central claims, that taking psychiatric drugs leads schizophrenics to act out more severely, is "nonsense", wrote the BBC's Dr Mark Pimentel in a commentary .
"There are a number of studies that have found that the more psychiatric drugs people take, the more aggressive their mental activities become."
Instead, it's time for more research into precisely why schizophrenics act out with drugs because they have no understanding of what's driving those dangerous delusions and behaviours, such as drugs that mimic a human brain.
The study was based on an experiment published last year in the journal Schizophrenia Research. In it, subjects were fed up to a point with no more medication when they were told to try to find a way into the centre where the drugs were being prescribed. The participants, who had been taking benzodiazepines for the previous year, were told to try to find a way to survive.
All the participants were given a small number of doses of a drug that mimicked serotonin - the part of the brain associated with hallucination - from a drug called rimonabant to see if some of the symptoms of psychosis appeared, such as paranoia and delusions.
The most difficult problem was understanding how the drugs worked, to be seen as an alternative, but not as harmful.
A typical drug experience, when a patient is told they have been hit by a car, is not something they can predict or avoid. In fact , some people experience hallucinations at close range, while others think they are seeing faces.
The drugs - which the researchers used to mimic drugs - had two effects: they blocked the receptor that excites the neurons that light up in the brain, which are the nerve cells that control the feelings of fear and emotion like fear and anxiety.
But the drug also prevented the nerve cells in the brain from re-establishing themselves after being shut down for about 10 minutes. After this, people were able to think about all sorts of stimuli again.
The effects lasted about 20 minutes after the drugs were discontinued, which is well below the time needed for people to develop hallucinations.
It seems that the drug effectively blocks the ability of the amygdala to go into a survival mode as it tries to deal with the unexpected and fearful experience.
Some other research has found that when subjects try to resist the fear of an unexpected situation they can develop an uncontrollable and even uncontrollable fear, called an anxiety attack.
Mr Mather said: "I found this effect because it's in the same area of the brain, it's the same area that is activated when you are frightened.
"The amygdala is a very complex organization. It is a very big system, it is very powerful with a very powerful system in the brain.
"In the present experiment, we found that what it was controlling was to slow down the amygdala in a very important part of the brain, which has important functions.
"The idea being that it made the brain think less."
Mr Mather said the study has implications for people experiencing sudden changes that may include nightmares, panic attacks, phobias or OCD.
"I think we also want to talk about mental disorders like anxiety and depression. The amygdala is certainly one of the most important parts of the brain."
He is also interested in learning more about the changes caused by psychedelics and its effect on mental health.
"It will be interesting to discover how the psychedelic environment can affect the brain and what brain changes that occur within the psychedelic process and its consequences for those who take it."
Dr Mather's research comes against the backdrop of a growing interest in the role of the amygdala in mental health.
More than 500 research papers have been published in neuroscience, anxiety and mood neuroscience in recent years, but not all of them explain why the area of the brain involved in emotional responses is so important for the development of a person's sense of well-being.
The findings, published in the Journal of Neurochemistry in the current issue of the Journal of Neuroscience, suggest that the amygdala's ability to control anxiety in autism may not always be as stable after brain injury and may have a lasting impact on the brain's ability to respond to stress and negative emotions, the authors said.
Most previous studies on stress and depression in autism focused on what happens after the birth of a baby or after mental illness is chronic. But scientists have not known what happens during pregnancy, postpartum or after birth, said co-lead author Dr. Eric Kandel, assistant professor of psychiatry, psychology and neuroscience at Vanderbilt. So while those areas are not necessarily affected in this way, they are.
"Our finding of persistent effects after brain injury and the long-lasting effects of postpartum depression suggest that the amygdala is involved in coping strategies after childbirth," he said.
The team focused on the amygdala because many of their previous studies had focused on other brain structures such as the prefrontal cortex (which controls thinking, action, motivation, emotional feelings and behavior) and the brain stem.
"We have a lot going for us," Kandel said. "Just like we had a little bit of prenatal or postpartum depression and the effect persisted after the birth, we have a lot of behavioral responses to a pregnancy that persists into the postpartum period."
After a short period of observation, the researchers tested participants in a game where they were required to move a stick or another object in a set distance in a "free-running" manner. "We had several tests to demonstrate this," Kandel said.
Once the players knew the distances they needed to move the sticks, they were allowed to play against others to see who had the greatest number of moves. In order get the greatest number of moves, players needed to have played for longer distances. By measuring participants' brain activity, Kandel and colleagues found that those who responded to this game with greater brain activity had greater effort to avoid stepping on the "free" stick.
"With training, we believe that the longer a player is on the free-running stick, the more skillful he is able to get at moving his stick in the same direction as other players can get the same amount of stick-moving efficiency," Kandel said.
But the participants' brain activity wasn't the only thing that wasn't affected by the game speed.
The brain's own response to pain also changes with the amount of stick movements — even when it's not being forced by the goal stick.
The more you push yourself, whether on an exercise ball or the ice, the more muscle you use to "push" your body. And those muscle-building changes keep the brain in full function even after the puck comes out of the net.
"One of the most remarkable things about this study is that the participants on the free-running stick were the most active over the course of the experiment," says Dr. Kevin P. Miller of the Scripps Research Institute, who published a commentary on the study in the February issue of Nutrition & Health. "After the team measured their brain activity, they found the subjects were the most active and had the most sustained effects on their brain that I've ever observed, even after several hours of exercise."
Another key finding: The "free" running stick was enough that participants could do what they were supposed to do, despite feeling fatigued.
"After they were instructed to run the free-running test in a way that their brain would respond, they were able to continue performing that activity for longer than it takes a person to sit and have lunch in a normal sitting chair," says study author William Shafer, a researcher at the National Institute of Mental Health and the University of California, San Diego, part of the Johns Hopkins University School of Medicine.
In other words, the researchers say that because the researchers trained their subjects by giving them a challenge using just an electronic stick -- meaning they don't take physical strain -- a free-running session could provide them with more brain stimulation than a typical brain training session.
"Our findings, especially in relation to the effect of exercise on blood flow, could have significant implications for patients who suffer from functional impairments, such as dementia," Shafer says.
While the researchers note that they did not measure activity of the brain as part of their study, they suggest that they are using the method to identify different brain regions for different tasks. Thus, they could apply brain stimulation through different stimulation techniques in a similar setting.
For example, brain stimulation could be used to alter blood flow in parts of the brain that are "red" in an older person's brain. Red-blood cells, which have been associated with blood flow, are associated with the brain's memory functions. If the stimulation is applied to those areas, the "red-blood cell function" appears to decline.
The researchers note that although a study would be necessary to validate their study's findings using their method, the results should be viewed in the context of current research.
In addition to Hagen, Moulton, and Möller, the research team included Dr. David Nissenbaum of Harvard, Dr. Charles R. Weigand of the University of Arizona, and Dr. David Nissenbaum. The study was funded in part by grants from the National Institutes of Health.