That is the title of this article I am reviewing today. "People with schizophrenia tend to die up to 30 years earlier than the general population. Many of these untimely deaths are due to physical disorders, including heart attacks and stroke, for which diabetes is a major risk factor. Antipsychotic drugs are known to increase the risk of type 2 diabetes, but there are other things that make schizophrenics particularly susceptible to the disorder, including poor diet and a lack of exercise. However, our latest study found that the risk of developing diabetes in people with schizophrenia remains high even when we take these factors into account. People with long-term schizophrenia are three times more likely than the general population to have diabetes. The link between schizophrenia and diabetes was first made back in the 19th century. This was long before the use of antipsychotics, and in an era when diets were less likely to cause diabetes. This could suggest that there is a causative link between schizophrenia and diabetes. Our study examined whether diabetes risk is already raised in people at the onset of schizophrenia – before they’ve started taking antipsychotic drugs or when they’ve only just started taking them."I do not know if I was susceptible to diabetes before I received this mental illness. My grandma and two aunts had it. Although my parents do not have it or my brothers and sisters. I am susceptible to it and have had it although I tell my doctors it is diet controlled for the last three years.
The article goes on to say: "We pooled data from multiple studies that examined evidence of diabetic risk in blood samples from people with early schizophrenia prescribed little or no antipsychotic medication. Diabetes is characterised by elevated blood glucose. The higher the level of glucose in the blood, the higher the risk of diabetes. We demonstrated that compared with healthy individuals, people with schizophrenia had higher levels of glucose in the blood. We also looked at levels of insulin. Insulin is a hormone that triggers the movement of glucose from blood into tissue. Raised insulin levels are seen in type 2 diabetes. We demonstrated higher levels of insulin, and increased levels of insulin resistance in individuals with early schizophrenia. Hints of a direct role of schizophrenia in diabetes. These results remained statistically significant even when we restricted our analysis to studies where people with schizophrenia were matched to healthy controls with regards their diet, the amount of exercise they engaged in and their ethnic background. This suggests that our results were not wholly driven by differences in lifestyle factors or ethnicity between the two groups, and may therefore point towards a direct role for schizophrenia in increasing risk of diabetes." I walk at least three miles three days out of the week. I also take 1000 mg of cinnamon every morning with breakfast. What the cinnamon does it knock down your diabetes number. Mine before I took cinnamon was 5.6 and after I take cinnamon everyday at breakfast and my number drops to 5.4 which is even better. 5.7 is pre-diabetes. Some places they only sell the cinnamon in 500 mg then you take two. Here I only found it at Rite Aid.
The article ends with: "There are several factors that could increase the likelihood of developing both conditions. These include a shared genetic risk, as well as shared developmental risk factors. For example, premature birth and low birth weight are recognised as risk factors for the development of both schizophrenia and diabetes later in life. Raised levels of the stress hormone cortisol is also a risk factor for diabetes. It is possible that the stress associated with developing schizophrenia, which sees levels of cortisol rise, may also contribute to higher diabetic risk. These findings are a wake-up call that we need to rethink the link between diabetes and schizophrenia and start prevention right from the onset of schizophrenia. It is a case of treating the mind and the body right from the start." That is what they need to do is start checking right away and start people exercising and watching all they eat. I did splurge during the holidays and was worried when I took my labs this December. This disease I do not know why I have it. It was blow to find out I had a mental illness. Then when I stopped smoking and my weight increased and my doctor checked I had diabetes. I do not know if it was the weight gain. Since then I have lost around thirty pounds my walking and taking care of what I eat.
Thursday, January 19, 2017
Wednesday, January 11, 2017
Nerve-signaling protein regulates gene associated with Schizophrenia
That is the title of this article I am reviewing today. "Researchers from the University of California, San Diego, have identified a protein that regulates a gene associated with schizophrenia. The study, published in the Journal of Neurophysiology, was chosen as an APSselect article for January.
Schizophrenia -- a chronic mental illness that affects a person's thoughts, feelings and behavior -- is determined in part by genetic makeup. The DISC1 gene is associated with developing schizophrenia. DISC1 is involved in the growth of nerve cells, proper nerve signaling and the ability of the brain to grow and adjust (neuroplasticity) throughout a person's lifetime. Loss of DISC1 function can interrupt the normal signaling pattern, which may lead to schizophrenia-like symptoms, such as movement disorders, memory problems and reduced expression of emotions."I do not have to bad of memory problems I can still remember numbers great. I also watch how my memory is on other things and I think it is normal. Although I do know people with mental illness that have memory problems. As for reduced expression of emotions I think I fall into that category although I have nothing to base it on.
The article continues: "Caveolin (Cav-1) is a cell membrane protein that promotes nerve signaling and neuroplasticity in the nervous system. In this study, the research team looked at the interaction between Cav-1 and DISC1 in the nerve cells of mice. The team is the first to find that Cav-1 regulates the function of DISC1. Mice that did not express the Cav-1 protein had less DISC1 expression in the brain and showed symptoms on the molecular level similar to that seen in brains afflicted with schizophrenia. When the researchers reintroduced Cav-1 specifically in nerve cells of these mice, DISC1 protein, in addition to proteins critical for synaptic plasticity (the ability of neurons to grow and form new connections), returned to normal levels." Now that sounds promising because if they can find medication that returns synaptic plasticity that would be great for all that have schizophrenia. Even though it would not help me I think it would be great for all other's that suffer this disease.
The article ends: "'The study's findings have significant implications for schizophrenia treatment. 'While pharmacological treatments such as antipsychotics are available for schizophrenia, these classes of drugs show poor efficacy for most patients, especially in reversing cognitive abnormalities,' wrote the researchers. 'Further understanding of how Cav-1 modulates DISC1 to maintain and organize neuronal growth signaling and proper function is of upmost importance to better understand and identify potential molecular targets for treating schizophrenia.'"What they have for medicine now is not all that great. I do OK now but I have to always remember that after I take my medication I could fall asleep in the next two hours a side effect. New medication that help a person grow is of the uppermost urgency.
The article continues: "Caveolin (Cav-1) is a cell membrane protein that promotes nerve signaling and neuroplasticity in the nervous system. In this study, the research team looked at the interaction between Cav-1 and DISC1 in the nerve cells of mice. The team is the first to find that Cav-1 regulates the function of DISC1. Mice that did not express the Cav-1 protein had less DISC1 expression in the brain and showed symptoms on the molecular level similar to that seen in brains afflicted with schizophrenia. When the researchers reintroduced Cav-1 specifically in nerve cells of these mice, DISC1 protein, in addition to proteins critical for synaptic plasticity (the ability of neurons to grow and form new connections), returned to normal levels." Now that sounds promising because if they can find medication that returns synaptic plasticity that would be great for all that have schizophrenia. Even though it would not help me I think it would be great for all other's that suffer this disease.
The article ends: "'The study's findings have significant implications for schizophrenia treatment. 'While pharmacological treatments such as antipsychotics are available for schizophrenia, these classes of drugs show poor efficacy for most patients, especially in reversing cognitive abnormalities,' wrote the researchers. 'Further understanding of how Cav-1 modulates DISC1 to maintain and organize neuronal growth signaling and proper function is of upmost importance to better understand and identify potential molecular targets for treating schizophrenia.'"What they have for medicine now is not all that great. I do OK now but I have to always remember that after I take my medication I could fall asleep in the next two hours a side effect. New medication that help a person grow is of the uppermost urgency.
Thursday, January 5, 2017
New Findings Show Dopamine’s Complex Role in Schizophrenia
That is the title of this article I am reviewing today. "'Recent advances in understanding the role of dopamine signaling in schizophrenia are highlighted in a special edition of the journal Biological Psychiatry. Seven reviews show the complexity of the neurotransmitter’s action, and several articles describe how new insights may eventually improve treatment for the disorder. Dopamine alterations are some of the most well-established research findings in schizophrenia, said Anissa Abi-Dargham, M.D., of Stony Brook University, New York, and a deputy editor of Biological Psychiatry.'Unlike any other neurobiological hypothesis of the disease, the dopamine hypothesis has confirmatory evidence from in vivo studies in patients and from pharmacological therapies, she said.'"Now they are going back to what they said in the first place caused mental illness dopamine. I understand that they have to understand it to find better medicine and therapy.
The article goes on to say: "'Despite this, researchers have yet to fully understand when and how dopamine alterations arise in the brain, or their relationship with the diversity of symptoms in the disease. 'This issue highlights the complexity of the findings in patients with the disorder, and raises the possibility that dopamine alterations can lead to a vast array of consequences on the circuitry, on learning and behavior that can explain the vast array of symptom clusters,' Abi-Dargham said.
The body of work collated in the issue ranges from human studies to animal models. New technology in the form of neuroimaging, genetic, and molecular imaging studies have helped clarify the regional differences of dopamine dysfunction throughout the brain. Importantly, the studies have detailed the timing of dopamine alterations in relation to development, symptom onset, and other neurobiological alterations in the disease. Moreover, animal models have allowed researchers to further refine and test the hypothesis, and explore mechanisms behind the dysregulation.'"I know the consequences they have to find out what caused this problem and how to fix it. What causes dopamine to act up and give a person a mental illness?
The article ends with: "'Clarifying the role of dopamine signaling in schizophrenia also shows promise for improving treatment for the disorder. 'We include here some examples of exciting new targeted therapeutic approaches that are currently under development,' Abi-Dargham said.
Although the dopamine system has long been pegged as the culprit for psychotic symptoms in schizophrenia, a review in this issue using a computational approach provides an explanation for how dopamine dysfunction could lead to the range of symptoms present in the disorder. The therapeutic approaches proposed in the issue aim to find new strategies for targeting dopamine signaling to improve the limitations of current antipyschotic drugs. The new strategies are necessary as the current methods only treat psychotic symptoms and come with a host of major side effects. Researchers say the new focus will be to target new pathways and tap into dopamine’s role in other regions of the brain." I understand that this could cause new drugs to come out without the side effects. I know that even I that function pretty good my medication I have to take with food. I also have take it when I know I want to sleep because after two hours it puts me to sleep. The big thing I still want to know is why I have this disease. I sure would like to know before I die. I know I am lucky in that it did not come for me until my late twenties. So I had some life before this illness and need to understand the why now.
The article goes on to say: "'Despite this, researchers have yet to fully understand when and how dopamine alterations arise in the brain, or their relationship with the diversity of symptoms in the disease. 'This issue highlights the complexity of the findings in patients with the disorder, and raises the possibility that dopamine alterations can lead to a vast array of consequences on the circuitry, on learning and behavior that can explain the vast array of symptom clusters,' Abi-Dargham said.
The body of work collated in the issue ranges from human studies to animal models. New technology in the form of neuroimaging, genetic, and molecular imaging studies have helped clarify the regional differences of dopamine dysfunction throughout the brain. Importantly, the studies have detailed the timing of dopamine alterations in relation to development, symptom onset, and other neurobiological alterations in the disease. Moreover, animal models have allowed researchers to further refine and test the hypothesis, and explore mechanisms behind the dysregulation.'"I know the consequences they have to find out what caused this problem and how to fix it. What causes dopamine to act up and give a person a mental illness?
The article ends with: "'Clarifying the role of dopamine signaling in schizophrenia also shows promise for improving treatment for the disorder. 'We include here some examples of exciting new targeted therapeutic approaches that are currently under development,' Abi-Dargham said.
Although the dopamine system has long been pegged as the culprit for psychotic symptoms in schizophrenia, a review in this issue using a computational approach provides an explanation for how dopamine dysfunction could lead to the range of symptoms present in the disorder. The therapeutic approaches proposed in the issue aim to find new strategies for targeting dopamine signaling to improve the limitations of current antipyschotic drugs. The new strategies are necessary as the current methods only treat psychotic symptoms and come with a host of major side effects. Researchers say the new focus will be to target new pathways and tap into dopamine’s role in other regions of the brain." I understand that this could cause new drugs to come out without the side effects. I know that even I that function pretty good my medication I have to take with food. I also have take it when I know I want to sleep because after two hours it puts me to sleep. The big thing I still want to know is why I have this disease. I sure would like to know before I die. I know I am lucky in that it did not come for me until my late twenties. So I had some life before this illness and need to understand the why now.
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