That is the title of this article I am writing about. "How quickly a smoker metabolizes nicotine could determine which type of cessation strategy has the best chance of success, according to a new study that represents one of the largest pharmacogentic analyses of tobacco dependence to date. The study found that smokers with normal metabolism levels had better quit rates with varenicline therapy, which does not involve nicotine replacement, compared to a nicotine patch. For people with slow metabolism, the patch may be the better option." I quit seventeen years ago. I used wellbutrin and did it have the side effects. It had so many side effects that I did not even notice or crave cigarettes. My mouth was something awful tasting. The was one of the only medicines that I had so many side effects. My friend gave me a list of the side effects because he had taken a class on stopping smoking. I had every one on that list.
The article goes on to say: "It has been known that smokers clear nicotine from their bodies at different rates, but until now it wasn't known if this measurable trait -- the nicotine metabolite ratio (NMR) -- could be used to optimize treatment and improve outcomes. The study researchers randomly assigned 1,246 smokers (662 slow metabolizers and 584 normal metabolizers) to 11 weeks of the nicotine patch and placebo pill, varenicline and placebo patch, or double placebo; all participants also received behavioral counseling." I know I had never tried to quit before that one I did. I know when I used to go to jail I could not be without my cigarettes. I would buy two for one or if no one had any smokes but roll your owns that is what I would smoke . The idea that I would quit never came to mind. I finally quit because I wanted to seem my granddaughter at my house and daughter did not want her around smoke. It was time anyway because I had a bad cough and this guy in the elevator told me I would not live that long if I kept smoking so it seemed like the right time.
The article ends witth: "After 11 weeks of treatment, normal metabolizers taking varencline were about twice likely not to smoke as those using the nicotine patch. And while slow metabolizers displayed similar effectiveness rates on varencline or the patch, they reported far fewer side effects for patch therapy." Those side effects can be rough. That is why people with mental illness do not always take their medication because of all the side effects especially weight gain.
Tuesday, January 27, 2015
Tuesday, January 20, 2015
United States: Mental health care lacking in state, federal prisons
That is the title of this article I am writing about. "significant portion of state and federal prisoners are not receiving treatment for mental health conditions, according to research by The University of Texas Health Science Center at Houston (UTHealth) School of Public Health. The study was published recently in the American Journal of Public Health.
Mental health disorders among prisoners have consistently exceeded rates of disorders in the general population. Twenty six percent of prisoners reported a mental health diagnosis in the study, compared to 18 percent in the general population in 2012, according to the National Institutes of Health.
State and federal courts mandate that inmates must have access to adequate health services in prison. However, that mandate usually covers only “severe or serious” mental illnesses, according to the paper. 'Individuals with untreated mental health conditions may be at higher risk for correctional rehabilitation treatment failure and future recidivism after release from prison,' said Jennifer Reingle, Ph.D., principal investigator and assistant professor in the Division of Epidemiology, Human Genetics and Environmental Sciences at UTHealth School of Public Health Dallas Regional campus." That many in prison have mental health issues. I have a mental illness and know from experience that all lot of these prisoners with mental health issues do not know they are acting out in prison. Of course there is recidivism how can you treat someone who does not take their medication when they do not understand why.
The article goes on to say: "Data was obtained from a 2004 national sample of state and federal prisoners, which included 14,499 participants in state prisons and 3,686 in federal prisons. Participants self-reported whether they had been taking medication for a mental health condition upon entering the facility and whether they were still taking medication while in prison, marking treatment continuity.
At the time of admission, 18 percent of each sample was taking medication for a mental health condition, but only 52 percent of that subset of the population in federal prisons and 42 percent in state prisons received medication during their sentence.
Depression was the most prevalent mental health condition, reported by 20 percent of inmates, followed by mania, anxiety and post-traumatic stress disorder.
'Screening tools are not consistent across prisons and inmates could be diagnosed with different conditions or not diagnosed at all when they get transferred to a new location,' said Reingle. “A standardized mental health screening process could benefit the inmates and the prison system as a whole.” They are not all taking medication. They do not understand it would help them better. It is a different atmosphere in prison than in the outside world. You are just passing time make it go by.
The article ends with: "This study also found evidence of racial disparities in medication continuity. African American participants were 36 percent more likely than other inmates to have medication continuity in prison, regardless of their diagnosis. African Americans were also more likely to suffer from schizophrenia than Caucasians. Participants with schizophrenia were more than twice as likely to get medication in prison and have treatment continuity.
Since some mental health disorders such as schizophrenia influence behavior, those prisoners may receive medication to maintain security in the prison environment, Reingle said. Since depression does not pose a significant security risk, it’s less likely that depressed prisoners will be easily identified and treated, she added.
Previous studies suggest that former offenders who were diagnosed with a mental health condition were 70 percent more likely to return to prison, whereas in the general prison population, the rate is about 50 percent.
In the study, researchers concluded that of the participants who were taking medication for a mental health condition in prison, 61 percent used no other form of treatment. A more holistic, multidimensional approach to treatment, such as counseling or group therapy, may lead to better outcomes and lower recidivism rates in this population, said Reingle." I see at least the ones with schizophrenia are getting medication although all of them should without regard to their diagnosis. I can see why they return what else are they going to do unless they receive help to adjust with medication and a chance to rehabilitate.
State and federal courts mandate that inmates must have access to adequate health services in prison. However, that mandate usually covers only “severe or serious” mental illnesses, according to the paper. 'Individuals with untreated mental health conditions may be at higher risk for correctional rehabilitation treatment failure and future recidivism after release from prison,' said Jennifer Reingle, Ph.D., principal investigator and assistant professor in the Division of Epidemiology, Human Genetics and Environmental Sciences at UTHealth School of Public Health Dallas Regional campus." That many in prison have mental health issues. I have a mental illness and know from experience that all lot of these prisoners with mental health issues do not know they are acting out in prison. Of course there is recidivism how can you treat someone who does not take their medication when they do not understand why.
The article goes on to say: "Data was obtained from a 2004 national sample of state and federal prisoners, which included 14,499 participants in state prisons and 3,686 in federal prisons. Participants self-reported whether they had been taking medication for a mental health condition upon entering the facility and whether they were still taking medication while in prison, marking treatment continuity.
At the time of admission, 18 percent of each sample was taking medication for a mental health condition, but only 52 percent of that subset of the population in federal prisons and 42 percent in state prisons received medication during their sentence.
Depression was the most prevalent mental health condition, reported by 20 percent of inmates, followed by mania, anxiety and post-traumatic stress disorder.
'Screening tools are not consistent across prisons and inmates could be diagnosed with different conditions or not diagnosed at all when they get transferred to a new location,' said Reingle. “A standardized mental health screening process could benefit the inmates and the prison system as a whole.” They are not all taking medication. They do not understand it would help them better. It is a different atmosphere in prison than in the outside world. You are just passing time make it go by.
The article ends with: "This study also found evidence of racial disparities in medication continuity. African American participants were 36 percent more likely than other inmates to have medication continuity in prison, regardless of their diagnosis. African Americans were also more likely to suffer from schizophrenia than Caucasians. Participants with schizophrenia were more than twice as likely to get medication in prison and have treatment continuity.
Since some mental health disorders such as schizophrenia influence behavior, those prisoners may receive medication to maintain security in the prison environment, Reingle said. Since depression does not pose a significant security risk, it’s less likely that depressed prisoners will be easily identified and treated, she added.
Previous studies suggest that former offenders who were diagnosed with a mental health condition were 70 percent more likely to return to prison, whereas in the general prison population, the rate is about 50 percent.
In the study, researchers concluded that of the participants who were taking medication for a mental health condition in prison, 61 percent used no other form of treatment. A more holistic, multidimensional approach to treatment, such as counseling or group therapy, may lead to better outcomes and lower recidivism rates in this population, said Reingle." I see at least the ones with schizophrenia are getting medication although all of them should without regard to their diagnosis. I can see why they return what else are they going to do unless they receive help to adjust with medication and a chance to rehabilitate.
Tuesday, January 13, 2015
IQ takes a hit with longer lasting psychosis
That is the title of this article I am writing about. Last week I did on how the higher IQ the less chance to develop schizophrenia. This one is about how we lose IQ by having psychosis longer. "A 10-year-long Scandinavian study has shed light on a small group of schizophrenic patients who suffer a greater decline in IQ over time than most patients.
Researchers at the University of Oslo and Yale have discovered that people who are diagnosed with schizophrenia often have a more positive illness trajectory than was previously thought. However, a subgroup of the study’s patients who experienced repeated psychosis after receiving treatment demonstrated significant deterioration of verbal recall and working memory ability over time. In other words, those who had a longer duration of psychosis after starting treatment saw their IQs drop more than those who experienced a shorter duration of psychosis.
These findings emphasize the need for patients at higher risk to be monitored more closely in order to detect episodes before they manifest themselves, according to secondary author and University of Oslo professor of neuropsychology Kjetil Sundet. He added that the ultimate goal in treating schizophrenic patients is to notice these warning signs before the onset of even the first psychotic episode." It is the longer you have psychosis after starting treatment. I think we lose some just in having schizophrenia. I know my IQ when I went to high school and when I started college were different.
The article continues: "So far, this study is the longest lasting of its kind to investigate whether the course of IQ is affected by duration of psychosis before treatment and duration of psychosis after treatment. Researchers found that the overall IQ of all 89 patients studied remained stable over time. But when they divided the sample into subgroups based on duration of untreated psychosis (DUP) and duration after treatment (DAT), they discovered that the length of DUP did not affect cognitive ability, while the length of DAT did correlate with cognitive decline. Patients with the longest DAT performed significantly worse on tests of intellectual ability over time compared to those with the shortest DAT. Some patients in the study saw a slight increase in IQ, which explains the overall consistency in IQ.
Additionally, the group with the longest DAT had a slightly lower baseline IQ at the start of the study than other groups, suggesting that lower IQ may indicate increased risk for a more severe course of illness.
This study was inspired by the Early Treatment and Intervention in Psychosis Study, led by co-primary investigators Svein Friis, professor of psychiatry at University of Oslo, and Thomas McGlashan, professor emeritus of psychiatry at Yale University. The main goal of that project was to find out if an Early Detection and Early Intervention program could reduce duration of untreated psychosis, and if that could improve quality of life outcomes, according to Friis.
'Without [McGlashan], this large-scale study would hardly have been possible,” Sundet said. “He inspired and enabled his colleagues to do this research.'" They need to treat people with psychosis sooner than. That would explain to me why I lost some IQ. I was put in jail with my psychoiss was going on and they did not give me medication until I was sentenced and went to the state hospital about six months down the road.
The article ends with: "
Although the results of this study do not provide any causal explanations of the relationship between longer illness duration after treatment and cognitive decline, the authors have offered several possible hypotheses. Because patients with greater intellectual impairments had a lower baseline IQ to begin with, they hypothesized that those patients may have possessed a lower cognitive reserve in general, hindering their ability to inhibit psychotic symptoms.
Alternatively, the researchers have proposed the existence of a distinct subtype of schizophrenia that causes more severe cognitive decline as well as longer psychotic episodes. That hypothesis is based on recent studies on certain patients’ genetic susceptibility to schizophrenia.
Though the findings of this study fall in line with previous schizophrenia-spectrum disorder studies, the study relied largely on human memory for its data, adding an element of uncertainty to the results.
According to Sundet, the general opinion of schizophrenia-spectrum disorders was much bleaker 20 years ago at the beginning of the study, when it was thought that having schizophrenia necessarily meant a major interference with normal life. However, nowadays most patients can live a good life with treatment and medication, and some people suffer only one episode their entire lives, he added.
According to the National Institute of Mental Health, schizophrenia affects 1.1 percent of the U.S. population ages 18 and older. "My memory of numbers is all I have that works great. Remembering anything else and I have to keep reminding myself to remember and that does not been I will. although with numbers I can remember them very well.
Researchers at the University of Oslo and Yale have discovered that people who are diagnosed with schizophrenia often have a more positive illness trajectory than was previously thought. However, a subgroup of the study’s patients who experienced repeated psychosis after receiving treatment demonstrated significant deterioration of verbal recall and working memory ability over time. In other words, those who had a longer duration of psychosis after starting treatment saw their IQs drop more than those who experienced a shorter duration of psychosis.
These findings emphasize the need for patients at higher risk to be monitored more closely in order to detect episodes before they manifest themselves, according to secondary author and University of Oslo professor of neuropsychology Kjetil Sundet. He added that the ultimate goal in treating schizophrenic patients is to notice these warning signs before the onset of even the first psychotic episode." It is the longer you have psychosis after starting treatment. I think we lose some just in having schizophrenia. I know my IQ when I went to high school and when I started college were different.
The article continues: "So far, this study is the longest lasting of its kind to investigate whether the course of IQ is affected by duration of psychosis before treatment and duration of psychosis after treatment. Researchers found that the overall IQ of all 89 patients studied remained stable over time. But when they divided the sample into subgroups based on duration of untreated psychosis (DUP) and duration after treatment (DAT), they discovered that the length of DUP did not affect cognitive ability, while the length of DAT did correlate with cognitive decline. Patients with the longest DAT performed significantly worse on tests of intellectual ability over time compared to those with the shortest DAT. Some patients in the study saw a slight increase in IQ, which explains the overall consistency in IQ.
Additionally, the group with the longest DAT had a slightly lower baseline IQ at the start of the study than other groups, suggesting that lower IQ may indicate increased risk for a more severe course of illness.
This study was inspired by the Early Treatment and Intervention in Psychosis Study, led by co-primary investigators Svein Friis, professor of psychiatry at University of Oslo, and Thomas McGlashan, professor emeritus of psychiatry at Yale University. The main goal of that project was to find out if an Early Detection and Early Intervention program could reduce duration of untreated psychosis, and if that could improve quality of life outcomes, according to Friis.
'Without [McGlashan], this large-scale study would hardly have been possible,” Sundet said. “He inspired and enabled his colleagues to do this research.'" They need to treat people with psychosis sooner than. That would explain to me why I lost some IQ. I was put in jail with my psychoiss was going on and they did not give me medication until I was sentenced and went to the state hospital about six months down the road.
The article ends with: "
Although the results of this study do not provide any causal explanations of the relationship between longer illness duration after treatment and cognitive decline, the authors have offered several possible hypotheses. Because patients with greater intellectual impairments had a lower baseline IQ to begin with, they hypothesized that those patients may have possessed a lower cognitive reserve in general, hindering their ability to inhibit psychotic symptoms.
Alternatively, the researchers have proposed the existence of a distinct subtype of schizophrenia that causes more severe cognitive decline as well as longer psychotic episodes. That hypothesis is based on recent studies on certain patients’ genetic susceptibility to schizophrenia.
Though the findings of this study fall in line with previous schizophrenia-spectrum disorder studies, the study relied largely on human memory for its data, adding an element of uncertainty to the results.
According to Sundet, the general opinion of schizophrenia-spectrum disorders was much bleaker 20 years ago at the beginning of the study, when it was thought that having schizophrenia necessarily meant a major interference with normal life. However, nowadays most patients can live a good life with treatment and medication, and some people suffer only one episode their entire lives, he added.
According to the National Institute of Mental Health, schizophrenia affects 1.1 percent of the U.S. population ages 18 and older. "My memory of numbers is all I have that works great. Remembering anything else and I have to keep reminding myself to remember and that does not been I will. although with numbers I can remember them very well.
Tuesday, January 6, 2015
High IQ May Protect Against Schizophrenia
That is the title of this article I am writing about. "In people with a genetic predisposition for schizophrenia, having high intelligence may help protect them from developing the severe mental disorder, according to a new study by researchers at Virginia Commonwealth University (VCU) and Lund University in Sweden. In fact, people with a lower IQ (intelligence quotient) than their siblings had the greatest risk for developing schizophrenia. The research appears to contradict the popular belief that schizophrenia and brilliance are typically linked. 'If you’re really smart, your genes for schizophrenia don’t have much of a chance of acting,' said first author Kenneth S. Kendler, M.D., professor of psychiatry and human and molecular genetics in the Department of Psychiatry, VCU School of Medicine." I do not know if I follow this belief. John Nash is not the only one that has a high IQ also Ellen Saks. If you follow Colorado and they do find James Holmes not guilty by reason of insanity there will be another.
The article goes on to say: "'What really predicted risk for schizophrenia is how much you deviate from the predicted IQ that we get from your relatives. If you’re quite a bit lower, that carries a high risk for schizophrenia. Not achieving the IQ that you should have based on your genetic constitution and family background seems to most strongly predispose for schizophrenia.' Just like those without the disease, people with schizophrenia vary widely in their intelligence levels. Kendler added that low IQ is one of many risk factors for schizophrenia. For the study, researchers assessed the IQs of more than 1.2 million Swedish males (ages 18-to-20) born between 1951 and 1975. Schizophrenia-related hospitalization was tracked for 24 years until 2010. Subjects with a lower IQ than their siblings were at the greatest risk for developing schizophrenia." If you have a lower IQ than your brothers and sisters than you have a greater chance of developing schizophrenia.
The article ends: "Kendler noted that environmental factors that may lower IQ, such as intrauterine experience, childhood trauma, or early drug use, could contribute to the increased risk.
Having a high IQ, however, doesn’t completely eliminate the risk for schizophrenia. In fact, there are several well-known, brilliant and creative people who have suffered from schizophrenia, including math prodigy John Nash, whose story was made famous in the film “A Beautiful Mind.”
'The question is, might we see some upward bump at that high level of intelligence where really brilliant people have increased risk for the disease and we show no such trend,' Kendler said.
Schizophrenia is one of the most severe and rarest of the mental health disorders, occurring in about one in 100 people. Symptoms of the disease include hallucinations, delusions, paranoia, cognitive impairment, social withdrawal, self-neglect, and loss of motivation and initiative." I never lost my motivation or I would not have been able to complete college. I lost some of my smarts though since I was in high school that is why I had a harder time in college. I believe that no matter what type of IQ you have it is still a bad disease and hard to tell when you are slipping into psychosis.
The article goes on to say: "'What really predicted risk for schizophrenia is how much you deviate from the predicted IQ that we get from your relatives. If you’re quite a bit lower, that carries a high risk for schizophrenia. Not achieving the IQ that you should have based on your genetic constitution and family background seems to most strongly predispose for schizophrenia.' Just like those without the disease, people with schizophrenia vary widely in their intelligence levels. Kendler added that low IQ is one of many risk factors for schizophrenia. For the study, researchers assessed the IQs of more than 1.2 million Swedish males (ages 18-to-20) born between 1951 and 1975. Schizophrenia-related hospitalization was tracked for 24 years until 2010. Subjects with a lower IQ than their siblings were at the greatest risk for developing schizophrenia." If you have a lower IQ than your brothers and sisters than you have a greater chance of developing schizophrenia.
The article ends: "Kendler noted that environmental factors that may lower IQ, such as intrauterine experience, childhood trauma, or early drug use, could contribute to the increased risk.
Having a high IQ, however, doesn’t completely eliminate the risk for schizophrenia. In fact, there are several well-known, brilliant and creative people who have suffered from schizophrenia, including math prodigy John Nash, whose story was made famous in the film “A Beautiful Mind.”
'The question is, might we see some upward bump at that high level of intelligence where really brilliant people have increased risk for the disease and we show no such trend,' Kendler said.
Schizophrenia is one of the most severe and rarest of the mental health disorders, occurring in about one in 100 people. Symptoms of the disease include hallucinations, delusions, paranoia, cognitive impairment, social withdrawal, self-neglect, and loss of motivation and initiative." I never lost my motivation or I would not have been able to complete college. I lost some of my smarts though since I was in high school that is why I had a harder time in college. I believe that no matter what type of IQ you have it is still a bad disease and hard to tell when you are slipping into psychosis.
Tuesday, December 30, 2014
Eye Test Identifies People with Schizophrenia
That is the title of this article I am writing about. "Impaired eye movements have long been associated with schizophrenia. In a new study, researchers have discovered they can distinguish people with and without schizophrenia through the use of simple eye movement tests with over 98 percent accuracy. 'It has been known for over a hundred years that individuals with psychotic illnesses have a variety of eye movement abnormalities, but until our study, using a novel battery of tests, no one thought the abnormalities were sensitive enough to be used as potential clinical diagnostic biomarkers,' say Dr. Philip Benson and Dr. David St. Clair, lead authors on the paper.
The series of tests included smooth pursuit, free-viewing, and gaze fixation tasks." That is cool that they now have another test that can say if you have schizophrenia or not. They have to get people diagnosed early so that they have a better chance of succeeding in life with this mental illness. It took the state hospital to diagnose me. If they could have found out when I had my breakdown in prison it would have saved me a lot of trouble. I do not know if my life would have been better or worse.
The article goes on with: "In smooth pursuit, people with schizophrenia have difficulty following slow-moving objects smoothly with their eyes. Their eye movements tend to fall behind the moving object and then catch-up with the moving object using a rapid eye movement, called a saccade.
In the free-viewing test — in which a picture is shown — those with schizophrenia follow an abnormal pattern as they look at the picture, compared to the general population.
In the fixation task, the individual is asked to keep a steady gaze on a single unmoving target, which tends to be difficult for individuals with schizophrenia. In each of the eye tests, the performance of individuals with schizophrenia was abnormal compared to the healthy volunteer group. The researchers then used several methods to model the data. Combining all the data, one of the models achieved 98.3% accuracy." That is a good accuracy number. I know there a lot of things that the eyes can tell so why not tell if you have schizophrenia or not?
The article ends with: "We now have exciting unpublished data showing that patterns of eye movement abnormalities are specific to different psychiatric subgroups, another key requirement for diagnostic biomarkers.
'The next thing we want to know is when the abnormalities are first detectable and can they be used as disease markers for early intervention studies in major mental illness,' say the researchers.
'We are also keen to explore how best our findings can be developed for use in routine clinical practice,' they add. Typical neuropsychological assessments are time-consuming, expensive, and require highly trained individuals to administer, while these eye tests are simple, cheap, and take only minutes to conduct. A predictive model with such accuracy could potentially be used in clinics and hospitals to aid doctors by supplementing other symptom-based diagnostic criteria." It could be used all over. It would really help.
The series of tests included smooth pursuit, free-viewing, and gaze fixation tasks." That is cool that they now have another test that can say if you have schizophrenia or not. They have to get people diagnosed early so that they have a better chance of succeeding in life with this mental illness. It took the state hospital to diagnose me. If they could have found out when I had my breakdown in prison it would have saved me a lot of trouble. I do not know if my life would have been better or worse.
The article goes on with: "In smooth pursuit, people with schizophrenia have difficulty following slow-moving objects smoothly with their eyes. Their eye movements tend to fall behind the moving object and then catch-up with the moving object using a rapid eye movement, called a saccade.
In the free-viewing test — in which a picture is shown — those with schizophrenia follow an abnormal pattern as they look at the picture, compared to the general population.
In the fixation task, the individual is asked to keep a steady gaze on a single unmoving target, which tends to be difficult for individuals with schizophrenia. In each of the eye tests, the performance of individuals with schizophrenia was abnormal compared to the healthy volunteer group. The researchers then used several methods to model the data. Combining all the data, one of the models achieved 98.3% accuracy." That is a good accuracy number. I know there a lot of things that the eyes can tell so why not tell if you have schizophrenia or not?
The article ends with: "We now have exciting unpublished data showing that patterns of eye movement abnormalities are specific to different psychiatric subgroups, another key requirement for diagnostic biomarkers.
'The next thing we want to know is when the abnormalities are first detectable and can they be used as disease markers for early intervention studies in major mental illness,' say the researchers.
'We are also keen to explore how best our findings can be developed for use in routine clinical practice,' they add. Typical neuropsychological assessments are time-consuming, expensive, and require highly trained individuals to administer, while these eye tests are simple, cheap, and take only minutes to conduct. A predictive model with such accuracy could potentially be used in clinics and hospitals to aid doctors by supplementing other symptom-based diagnostic criteria." It could be used all over. It would really help.
Tuesday, December 23, 2014
Dopamine: Psychotic fire-starter? The Paykel Lecture 2014
That is the title of this article I am writing about. "The eye-catching title of the 2014 Paykel Lecture certainly lived up to its promise of a fascinating talk. Delivered by Dr Oliver Howes of the Institute of Psychiatry, Psychology and Neuroscience (IoPPN – King’s College London), the title made reference to an early paper on the dopamine hypothesis of schizophrenia, where dopamine was referred to as “the wind of the psychotic fire.” An eloquent review of the dopamine hypothesis followed, from the perspective of studies employing positron emission tomography (PET) and magnetic resonance imaging (MRI).
Dopamine is an important neurotransmitter, playing a crucial role in brain processes such as how we predict events and experience rewards. Its over-abundance in the brain has long been posited as a theory for the symptoms of psychosis seen in people with schizophrenia. Brain imaging techniques such as PET, which uses a radioactively labelled tracer, can help us obtain information about all aspects of the dopamine system. We can specifically study dopamine receptors, dopamine synthesis, its transportation or its release from neurons, and these methods have allowed scientists to pinpoint abnormalities in schizophrenia. Using this technology, Dr. Howes and colleagues studied people with schizophrenia who had received very little treatment, and found that the abnormality of dopamine appears to be at the level of synthesis and release from brain cells, rather than at the receptor as was initially believed." Wow they found out where it is released from. They can find out how it works.
The article goes on to say: "But this, Dr. Howes went on to explain, does not tell us whether schizophrenia is caused by an abnormality in dopamine regulation, or whether increased dopamine is a result of having schizophrenia. Therefore, his group decided to conduct research studies with a group of people who were at high risk of developing schizophrenia but do not yet show symptoms adequate for a diagnosis. These people are said to be in the prodromal, or sub-clinical, phase of schizophrenia. Whilst many go on to develop further symptoms, some remain stable at the sub-clinical phase and are able to function perfectly well. A prominent historical example of such a person, Dr. Howes explains, was Joan of Arc. Despite hearing voices (which she attributed to angels), she was able to lead the French army to victory over the British.Thus, using the same PET imaging techniques, Dr Howes and his team found elevated dopamine synthesis in the striatum of people with sub-clinical symptoms, which appeared to be around halfway between controls and people diagnosed with schizophrenia. Further investigation found that this increase in dopamine was in fact specific to those who would go on to develop a full clinical syndrome of schizophrenia, while those with long term sub-clinical symptoms did not demonstrate any increase in dopamine synthesis.
But what is it, Dr. Howes pondered, that the biology of schizophrenia needs to explain? The answer he came up with: Neurodevelopmental and sociodevelopmental risk factors (e.g drugs or stress), and symptoms. Stay away from drugs and you probably will not get schizophrenia. Stress is a hard one to stay away from. That is what brought on my mental illness. Anger, stress that all brought it on not knowing what was going to happen to me.
The article ends:"Based on research ongoing in his group, Dr. Howes (alongside Professor Sir Robin Murray) proposed a model to explain how these risk factors and symptoms might fit into the dopamine hypothesis. They proposed that a combination of genes and hazards to the brain disrupt the development of the dopamine system, and cause it become very sensitive. Social stress then acts on this sensitised system, increasing dopamine release, leading to irregular cognitive processing of events. This in turn leads to a paranoid interpretation of events and eventually psychosis, which in itself is a stressful experience, causing a vicious cycle of stress and increased dopamine release.
While this model both supports and is supported by much of the research into the dopamine hypothesis, there are many questions outstanding, and the hypothesis is far from being finally accepted or refuted. Dr Howes identified that further work needs to be done to understand why approximately one third of people with schizophrenia are resistant to treatment with antipsychotic drugs, which act on the dopamine system. The causes of the ‘negative symptoms’ of schizophrenia (e.g. affective flattening, or a reduced display of emotion) and the relationship with substance misuse (such as cannabis, which was not found to increase dopamine in the striatum when cannabis smokers experienced psychotic like symptoms as a result of their drug use).
Dr. Oliver Howes is a group head and reader in imaging of neurochemical processing in psychosis at Kings College London and at the MRC CSC psychiatric imaging group, Hammersmith Hospital, Imperial College. Dr. Howes has been the recipient of many prestigious awards, including most recently the Schizophrenia International Research Society Rising Star Award 2013." If it can help those people who are resistant to antipsychotics that would be a big help. If it is the dopamine that is causing schizophrenia then why are they resistant to drugs that help the dopamine? I believe we are far away from discovering what actually causes schizophrenia.
Dopamine is an important neurotransmitter, playing a crucial role in brain processes such as how we predict events and experience rewards. Its over-abundance in the brain has long been posited as a theory for the symptoms of psychosis seen in people with schizophrenia. Brain imaging techniques such as PET, which uses a radioactively labelled tracer, can help us obtain information about all aspects of the dopamine system. We can specifically study dopamine receptors, dopamine synthesis, its transportation or its release from neurons, and these methods have allowed scientists to pinpoint abnormalities in schizophrenia. Using this technology, Dr. Howes and colleagues studied people with schizophrenia who had received very little treatment, and found that the abnormality of dopamine appears to be at the level of synthesis and release from brain cells, rather than at the receptor as was initially believed." Wow they found out where it is released from. They can find out how it works.
The article goes on to say: "But this, Dr. Howes went on to explain, does not tell us whether schizophrenia is caused by an abnormality in dopamine regulation, or whether increased dopamine is a result of having schizophrenia. Therefore, his group decided to conduct research studies with a group of people who were at high risk of developing schizophrenia but do not yet show symptoms adequate for a diagnosis. These people are said to be in the prodromal, or sub-clinical, phase of schizophrenia. Whilst many go on to develop further symptoms, some remain stable at the sub-clinical phase and are able to function perfectly well. A prominent historical example of such a person, Dr. Howes explains, was Joan of Arc. Despite hearing voices (which she attributed to angels), she was able to lead the French army to victory over the British.Thus, using the same PET imaging techniques, Dr Howes and his team found elevated dopamine synthesis in the striatum of people with sub-clinical symptoms, which appeared to be around halfway between controls and people diagnosed with schizophrenia. Further investigation found that this increase in dopamine was in fact specific to those who would go on to develop a full clinical syndrome of schizophrenia, while those with long term sub-clinical symptoms did not demonstrate any increase in dopamine synthesis.
But what is it, Dr. Howes pondered, that the biology of schizophrenia needs to explain? The answer he came up with: Neurodevelopmental and sociodevelopmental risk factors (e.g drugs or stress), and symptoms. Stay away from drugs and you probably will not get schizophrenia. Stress is a hard one to stay away from. That is what brought on my mental illness. Anger, stress that all brought it on not knowing what was going to happen to me.
The article ends:"Based on research ongoing in his group, Dr. Howes (alongside Professor Sir Robin Murray) proposed a model to explain how these risk factors and symptoms might fit into the dopamine hypothesis. They proposed that a combination of genes and hazards to the brain disrupt the development of the dopamine system, and cause it become very sensitive. Social stress then acts on this sensitised system, increasing dopamine release, leading to irregular cognitive processing of events. This in turn leads to a paranoid interpretation of events and eventually psychosis, which in itself is a stressful experience, causing a vicious cycle of stress and increased dopamine release.
While this model both supports and is supported by much of the research into the dopamine hypothesis, there are many questions outstanding, and the hypothesis is far from being finally accepted or refuted. Dr Howes identified that further work needs to be done to understand why approximately one third of people with schizophrenia are resistant to treatment with antipsychotic drugs, which act on the dopamine system. The causes of the ‘negative symptoms’ of schizophrenia (e.g. affective flattening, or a reduced display of emotion) and the relationship with substance misuse (such as cannabis, which was not found to increase dopamine in the striatum when cannabis smokers experienced psychotic like symptoms as a result of their drug use).
Dr. Oliver Howes is a group head and reader in imaging of neurochemical processing in psychosis at Kings College London and at the MRC CSC psychiatric imaging group, Hammersmith Hospital, Imperial College. Dr. Howes has been the recipient of many prestigious awards, including most recently the Schizophrenia International Research Society Rising Star Award 2013." If it can help those people who are resistant to antipsychotics that would be a big help. If it is the dopamine that is causing schizophrenia then why are they resistant to drugs that help the dopamine? I believe we are far away from discovering what actually causes schizophrenia.
Tuesday, December 16, 2014
Discovery of novel drug target may lead to better treatment for schizophrenia
That is the title of this article I writing about. "A novel drug target that could lead to the development of better antipsychotic medications has been discovered by researchers. Current treatment for patients with schizophrenia involves taking medications that block or interfere with the action of the neurotransmitter dopamine. However, because this D2-blocking action my cause unwanted side-effects, such as slow gait, stiffness and tremor, the team looked for new ways to interfere with the action of D2 receptors, without causing these side-effects. Scientists at the Centre for Addiction and Mental Health (CAMH) have identified a novel drug target that could lead to the development of better antipsychotic medications. Dr. Fang Liu, senior scientist in CAMH's Campbell Family Mental Health Research Institute and professor in the Department of Psychiatry, University of Toronto, and her team published their results online in the Journal Neuron. Current treatment for patients with schizophrenia involves taking medications that block or interfere with the action of the neurotransmitter dopamine, which acts on dopamine D2 receptors in the brain. However, because this D2-blocking action may cause unwanted side-effects, such as slow gait, stiffness and tremor, Dr. Liu and her team looked for new ways to interfere with the action of D2 receptors, without causing these side-effects." Nobody wants to have side-effects. It could be the reason that a lot of people with mental illness do not like taking the medication. I know when my arm was shaking with stelazine I did not want to take who wants to look like a freak just to be well.
The article goes on to say: " Dr. Liu and colleagues showed that the D2 receptor could combine with a protein called the Disrupted-In-Schizophrenia (DISC1) protein. Then, they showed that levels of this combined protein were higher in post-mortem brain tissues of deceased patients with schizophrenia, suggesting it was associated with the illness. Delving even further, the researchers identified the regions where the two proteins bound together. With this information, they were able to generate a peptide to disrupt the binding of the two proteins, speculating that it may reduce symptoms. In animal models of schizophrenia, they were able to demonstrate that this disruption led to antipsychotic effects, comparable to commonly used antipsychotic medications, but without their side-effects." That would be great news if this new medication really works in people. No side effects will really be big news.
The article ends: "'The most exciting aspect of our finding is not the antipsychotic effect of this peptide, which all current antipsychotics have, but rather the possibility of a lack of the side-effects in humans compared to current medications,' says Dr. Liu. 'We hope that it will lead to a better treatment for schizophrenia patients who experience side-effects from current medications.'These side-effects discourage some patients from taking their medications, which impacts recovery. Schizophrenia is a chronic, often severe and disabling mental illness that affects one percent of the general population. 'Our future steps are to determine how this discovery can be translated into a novel treatment for patients as soon as possible,' says Dr. Liu. 'We are optimistic that our findings will lead to new and better options for treatment for schizophrenia.'" For all those people who do not like to take their medication because of the side effects help might be on the way. They do not say how long though until they find out if it works on people. News this good has been slow in coming we really need more research done. To help people who suffer from this disease. I do not have side-effects anymore. I am glad as I had them in the past and it was hard to take the medication. It got rid of the positive effects but not the negative.
The article goes on to say: " Dr. Liu and colleagues showed that the D2 receptor could combine with a protein called the Disrupted-In-Schizophrenia (DISC1) protein. Then, they showed that levels of this combined protein were higher in post-mortem brain tissues of deceased patients with schizophrenia, suggesting it was associated with the illness. Delving even further, the researchers identified the regions where the two proteins bound together. With this information, they were able to generate a peptide to disrupt the binding of the two proteins, speculating that it may reduce symptoms. In animal models of schizophrenia, they were able to demonstrate that this disruption led to antipsychotic effects, comparable to commonly used antipsychotic medications, but without their side-effects." That would be great news if this new medication really works in people. No side effects will really be big news.
The article ends: "'The most exciting aspect of our finding is not the antipsychotic effect of this peptide, which all current antipsychotics have, but rather the possibility of a lack of the side-effects in humans compared to current medications,' says Dr. Liu. 'We hope that it will lead to a better treatment for schizophrenia patients who experience side-effects from current medications.'These side-effects discourage some patients from taking their medications, which impacts recovery. Schizophrenia is a chronic, often severe and disabling mental illness that affects one percent of the general population. 'Our future steps are to determine how this discovery can be translated into a novel treatment for patients as soon as possible,' says Dr. Liu. 'We are optimistic that our findings will lead to new and better options for treatment for schizophrenia.'" For all those people who do not like to take their medication because of the side effects help might be on the way. They do not say how long though until they find out if it works on people. News this good has been slow in coming we really need more research done. To help people who suffer from this disease. I do not have side-effects anymore. I am glad as I had them in the past and it was hard to take the medication. It got rid of the positive effects but not the negative.
Subscribe to:
Posts (Atom)