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The article ends with: "We now have exciting unpublished data showing that patterns of eye movement abnormalities are specific to different psychiatric subgroups, another key requirement for diagnostic biomarkers.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.
Tuesday, December 30, 2014
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.
Tuesday, December 9, 2014
A Battle Plan to Lose Weight
That is the title of this article I am writing about. "Laura Ward, 41, had always attributed her excess pounds to the drugs she takes for major depression. So Ms. Ward, who is 5-foot-6 and once weighed 220 pounds, didn't try to slim down or avoid dietary pitfalls like fried chicken. But in a clinical trial, Ms. Ward managed to lose more than 30 pounds doing low-impact aerobics three times a week. During the 18-month experiment, she was introduced to cauliflower and post-workout soreness for the first time. She and the other participants attended counseling sessions where they practiced refusing junk food and choosing smaller portions. She drank two liters of Diet Dr Pepper daily instead of eight. Eventually, Ms. Ward, who lives in Baltimore, realized her waistline wasn’t simply a drug side effect. 'If it was only the medications, I would have never lost all that weight,' she said.
People with serious mental illnesses, like schizophrenia, bipolar disorder or major depression, are at least 50 percent more likely to be overweight or obese than the general population. They die earlier, too, with the primary cause heart disease.Yet diet and exercise usually take a back seat to the treatment of their illnesses. The drugs used, like antidepressants and antipsychotics, can increase appetite and weight." I do not have increase appetite as I have cut down the size of my portions I eat. Although when I go out to eat or thanksgiving I might have more. My cutting my portions to half of what I used to eat and cutting down the number and the kinds of soda I lost twenty pounds although I have plateaued. I drink coke zero or Pepsi max as it does not taste bad except if I go to a restaurant that does not have those drinks.
The article goes on to say: "'Treatment contributes to the problem of obesity,' said Dr. Thomas R. Insel, the director of the National Institute of Mental Health. 'Not every drug does, but that has made the problem of obesity greater in the last decade.”
It has been a difficult issue for mental health experts. A 2012 review of health promotion programs for those with serious mental illness by Dartmouth researchers concluded that of 24 well-designed studies, most achieved statistically significant weight loss, but very few achieved “clinically significant weight loss.' But now a trial published online in The New England Journal of Medicine in March has provided the most comprehensive evidence yet that people with serious mental illness can lose weight, despite the challenges. Nearly 300 people with schizophrenia, bipolar disorder, schizoaffective disorder or major depression — including Ms. Ward — were assigned to either a control group given basic nutrition and exercise information or one whose members exercised together and attended weight-management sessions.
The mean difference between the groups at 18 months was a modest seven pounds, but studies have shown that it is enough to reduce cardiovascular risks, the researchers noted. Nearly 38 percent of participants in the intervention group lost 5 percent or more of their initial weight, compared with only 22.7 percent of members of the control group. The difference between the groups could have been bigger, as the control group benefited from one aspect of the intervention: healthier dietary choices offered at the 10 psychiatric programs where the study took place, like baked fish instead of fried. 'This population can make a change,' said Dr. Gail L. Daumit, the study’s lead author and an internist at Johns Hopkins University School of Medicine. 'There’s been a lot of stigma that they can’t do it.' Most other trials had “a narrowly defined population that excluded people with lots of co-morbidities,” said Dr. Caroline Richardson, at Veterans Affairs Ann Arbor Healthcare System in Michigan. But this study 'applies to a lot of people.'" I would like to lose more weight I am happy though that I have not gained it back except a couple of pounds then I lose that again. Although if I could lose thirty more pounds I would be happier.
The article ends with: "The study suggests that weight loss may take a different trajectory for those with mental illness. Weight loss in the intervention group didn’t 'peak early' and then rebound a bit, as sometimes happens in programs targeted to people without mental illness, Dr. Daumit said. Instead, it 'progressed over the course of the trial.' Since the study, Ms. Ward said she had regained at least 15 pounds. Still, every other day she walks for 20 minutes. Dr. Stephen J. Bartels, a professor of psychiatry at Dartmouth and co-author of the 2012 review, said the more effective interventions for people with mental illness combined education and structured activity, focusing on both exercise and diet. Classes and exercise programs seem to work better when they are available where mental health services are provided. And these programs should probably run six months or longer, he said.
Losing weight is challenging for anyone, let alone people with problems with executive function and memory. In Dr. Daumit’s trial, researchers gave cards to carry in wallets and purses that emphasized messages like avoiding sugary drinks. One of the few widely tried health-promotion programs for people with mental illnesses is InShape, available at 10 sites in New Hampshire and 9 programs in 5 other states. One of its tenets is to have patients set their own goals, with the help of a health 'mentor' who also sometimes accompanies them to the gym to get them past any feelings of discomfort.
In a randomized controlled yearlong intervention using InShape, to be published in Psychiatric Services next month, almost half of the 133 participants had either clinically significant weight loss (5 percent or more of body weight) or clinically significant improvements on a six-minute walk, said Dr. Bartels, the lead author. 'Many of them come to feel helpless about how they will avoid gaining weight,' Ken Jue, who started InShape at Monadnock Family Services in Keene, N.H., in 2003. “We try to encourage people and say, ‘You do have some control in this.’" I started walking again. The treadmills in my building are broke. I get left off on the bus farther from my apartment and then walk home. That way I get exercise everyday unless I have to be home at a certain time for something. It's time to lose this weight once and for all time.
Tuesday, December 2, 2014
Fish Oil reduces Smoking, Israeli study suggests
That is the title of the article I am writing about.
"Haifa University researcher finds that omega-3 supplements help reduce the number of cigarettes that addicts smoke in a given day, a new Israeli study found. The study, conducted by Dr. Rabinovitz Shenkar of the University of Haifa, indicated that the fish oil capsules significantly reduced nicotine cravings and helped participants cut down their cigarette consumption by at least 11 percent. According to Rabinovitz Shenkar, head of the addictions program at the University of Haifa's School of Criminology, current medications used to help quit smoking are not effective and carry adverse effects. 'Omega-3, an inexpensive and easily available dietary supplement with almost no side effects, reduces smoking significantly,' Rabinovitz Shenkar said in the study, published in the Journal or Psychopharmacology." Eleven percent that is a lot of cigarettes you will cut down on when you are trying to quit. I quit sixteen years ago. I would not have gained as much weight as I did if I kept smoking. All I bought back then was cigarettes and frozen dinners all on a budget.
The article goes on to say: "Smoke-derived toxicants greatly reduce the level of essential fatty acids in the brain, particularly omega-3, damaging areas of the brain involved with pleasure and satisfaction. Damage in these areas of the brain is directly related to the inability to stop smoking. 'Earlier studies have proven that an imbalance in omega-3 is also related to mental health, depression and the ability to cope with pressure and stress. Pressure and stress, in turn, are associated with the urge to smoke,' Rabinovitz Shenkar said, adding that despite the findings, the connection between these factors has not been studied thus far." Well when I quit I used Wellbutrin and did I have the side effects. I was so bothered by the side effects that I did not have time to worry about my smoking. After thirty days I did not refill the prescription my doctor wrote. I had quit smoking and id not have to take it anymore. I quit for a reason my granddaughter was born and my daughter did not want her around smoking.
The article ends with: "Forty-eight smokers aged 18 to 45 who smoked an average of 14 cigarettes a day participated in the study. They were divided into two groups, one given omega-3 capsules containing omega-3 950, and the other a placebo. The participants were asked to take 5 capsules a day for 30 days, and at no point were they asked to stop smoking. After 30 days, smokers who received the omega-3 capsules were found to cut down their cigarette intake by an average of two a day (roughly 115 in total), also displaying a significant decrease in craving levels. In contrast, the group receiving the placebo showed no significant changes in their craving levels, and did not reduce the number of cigarettes they smoked a day. Rabinovitz Shenkar added that further research will indicate whether the supplement can effectively help smokers quit altogether." That would be nice if it helped someone like me that used to smoke a pack and half a pack a day. That would really help. Also if it could cut down the cravings I am sure a lot of smokers would have a chance at quitting.
The article goes on to say: "Smoke-derived toxicants greatly reduce the level of essential fatty acids in the brain, particularly omega-3, damaging areas of the brain involved with pleasure and satisfaction. Damage in these areas of the brain is directly related to the inability to stop smoking. 'Earlier studies have proven that an imbalance in omega-3 is also related to mental health, depression and the ability to cope with pressure and stress. Pressure and stress, in turn, are associated with the urge to smoke,' Rabinovitz Shenkar said, adding that despite the findings, the connection between these factors has not been studied thus far." Well when I quit I used Wellbutrin and did I have the side effects. I was so bothered by the side effects that I did not have time to worry about my smoking. After thirty days I did not refill the prescription my doctor wrote. I had quit smoking and id not have to take it anymore. I quit for a reason my granddaughter was born and my daughter did not want her around smoking.
The article ends with: "Forty-eight smokers aged 18 to 45 who smoked an average of 14 cigarettes a day participated in the study. They were divided into two groups, one given omega-3 capsules containing omega-3 950, and the other a placebo. The participants were asked to take 5 capsules a day for 30 days, and at no point were they asked to stop smoking. After 30 days, smokers who received the omega-3 capsules were found to cut down their cigarette intake by an average of two a day (roughly 115 in total), also displaying a significant decrease in craving levels. In contrast, the group receiving the placebo showed no significant changes in their craving levels, and did not reduce the number of cigarettes they smoked a day. Rabinovitz Shenkar added that further research will indicate whether the supplement can effectively help smokers quit altogether." That would be nice if it helped someone like me that used to smoke a pack and half a pack a day. That would really help. Also if it could cut down the cravings I am sure a lot of smokers would have a chance at quitting.
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