Hello everyone! I hope everyone is doing well today. I wanted to bring you some more bipolar news that I have come across on the internet on PsychCentral's website. Apparently there is a link between elevated AND decreased cortisol levels and the poor quality of life of bipolar patients according to a Swedish study. Below are excerpts from the article as well as a link to the source page.
"New research suggests depression is almost twice as common, and poor quality of life almost five times as common, in people with bipolar disorder who have elevated or low levels of the stress hormone cortisol in the blood. Researchers at Umeå University, Sweden, discuss this finding in a study published in the journal PLOS ONE.
“In bipolar depression the stress system is often activated, which means that the affected individuals have elevated cortisol levels in the blood,” said Martin Maripuu, a Ph.D. student and physician at the psychiatric clinic, Östersund Hospital. “We have now been able to show that both over- and underactivity in the stress system, with corresponding elevated or reduced cortisol levels, can impair mental health in terms of depression and poor quality of life in these patients.”
As many of us know, bipolar disorder is a lifelong disease that causes recurrent episodes of both mania and depression. Stress is a known trigger for these episodes, and depression and mania also adds to the accumulated stress load. One of the body’s main stress systems is the hypothalamic-pituitary-adrenal axis, which regulates cortisol. Cortisol is a hormone that helps us cope with various stressful situations, such as pain, illness and stress at work. Stress causes overactivity in the stress system, resulting in elevated levels of cortisol. If the stress continues in the long-term, it is believed to cause an underactivity in the stress system, which results in low cortisol levels. Previous studies have shown that the stress system is often overactive in patients with bipolar depression."
"Prevalence of low quality of life was six times more common in the group with low cortisol levels and nearly five times more common among those with high cortisol levels, compared with those who exhibited normal activity in the stress system.
The study also shows that people who had low cortisol levels, on average, have had their disease longer than those with high cortisol levels, which could suggest that chronic stress in bipolar disorder can lead to an “exhaustion” of the stress system with reduced cortisol levels as a result. The researchers also believe that the low cortisol levels, once developed, can contribute to a more chronic, manifested state of the disorder."
The researchers think these results are important because they think that in the future they could contribute to a more personally tailored medical treatment of bipolar disorder. "The results may also ultimately lead to the development of new drugs that work by normalizing the stress system and cortisol levels,” said Maripuu.
Source
Let's hope the devlopment of new treatments is sooner rather than later. Have a great Thursday everyone!
Thursday, June 19, 2014
Thursday, June 12, 2014
Possible Therapeutic Target for Select Brain Disorders - including bipolar
Hello Everyone! I found another intersting article about new developments in the treatment of bipolar disorder. I found this information on the National Institute of Health's site. Apparently scientists have been studying different areas in the brain that have not received much attention in the past and finding links between deficiencies in the areas and schizophrenia and bipolar disorder.
"Researchers have found in mice that a formerly obscure region of the hippocampus called CA2 is important for social memory, the ability of an animal to recognize another of the same species. Identifying the role of this region could be useful in understanding and treating disorders characterized by altered social behaviors such as schizophrenia, bipolar disorder, and autism. Funded in part by the National Institute of Mental Health (NIMH), the study was published last month online in Nature."
Results of the Study
"Normally when a mouse encounters another mouse it does not know, it gives it a “sniff test” and is more interested in this new mouse versus a familiar acquaintance. The CA2-inactive mouse, however, shows no recognition of mice it has seen before and ends up sniffing indiscriminately familiar and novel mice. The mice showed no loss in the ability to discriminate social or non-social odors, such as food buried deeply in its litterbox. Although a pronounced loss of social memory is seen in the CA2-inactive mice, the mice did not experience changes in other hippocampal-specific behaviors such as spatial and contextual memory, and could still distinguish between novel and familiar inanimate objects."
Significance
“Because several neuropsychiatric disorders are associated with altered social behaviors, our findings raise the possibility that CA2 dysfunction may contribute to these behavioral changes,” said Siegelbaum.
"Individuals with schizophrenia and bipolar disorder have lowered numbers of CA2 inhibitory neurons. Similarly, individuals with autism have altered signaling of vasopressin, a social behavior hormone that interacts with a specific class of receptors found predominantly in this region. However, the CA2-inactive mice did not display classic symptoms of autism as they had normal levels of sociability, providing evidence that sociability and social memory involve different brain functions. Techniques such as the one detailed here are examples of research tools that the NIH Brain Research through Advancing Innovative Neurotechnologies (BRAIN ) Initiative hopes to build upon to further our understanding of the human brain."
What’s Next
"Siegelbaum’s group hopes to use the same genetic technology to examine whether there are changes in CA2 function in mouse models of psychiatric disorders such as autism and schizophrenia. If so, they plan to screen for drugs that restore normal CA2 function and ask whether this drug treatment helps reverse any behavioral changes seen in the mice. Such research offers the possibility of finding new drug targets and approaches for treating the behavioral changes associated with these disorders."
Reference
Hitti FL, Siegelbaum SA. The Hippocampal CA2 Region is Essential for Social Memory. Nature , published online February 23, 2014.
Grant 5F30MH098633-02
Link to Source page
I hope you found this informative. Sooner or later researchers should be able to find something to truly help us with our mental illnesses. This study makes me hopefully it will be sooner rather than later. Have a great Thursday!
"Researchers have found in mice that a formerly obscure region of the hippocampus called CA2 is important for social memory, the ability of an animal to recognize another of the same species. Identifying the role of this region could be useful in understanding and treating disorders characterized by altered social behaviors such as schizophrenia, bipolar disorder, and autism. Funded in part by the National Institute of Mental Health (NIMH), the study was published last month online in Nature."
Results of the Study
"Normally when a mouse encounters another mouse it does not know, it gives it a “sniff test” and is more interested in this new mouse versus a familiar acquaintance. The CA2-inactive mouse, however, shows no recognition of mice it has seen before and ends up sniffing indiscriminately familiar and novel mice. The mice showed no loss in the ability to discriminate social or non-social odors, such as food buried deeply in its litterbox. Although a pronounced loss of social memory is seen in the CA2-inactive mice, the mice did not experience changes in other hippocampal-specific behaviors such as spatial and contextual memory, and could still distinguish between novel and familiar inanimate objects."
Significance
“Because several neuropsychiatric disorders are associated with altered social behaviors, our findings raise the possibility that CA2 dysfunction may contribute to these behavioral changes,” said Siegelbaum.
"Individuals with schizophrenia and bipolar disorder have lowered numbers of CA2 inhibitory neurons. Similarly, individuals with autism have altered signaling of vasopressin, a social behavior hormone that interacts with a specific class of receptors found predominantly in this region. However, the CA2-inactive mice did not display classic symptoms of autism as they had normal levels of sociability, providing evidence that sociability and social memory involve different brain functions. Techniques such as the one detailed here are examples of research tools that the NIH Brain Research through Advancing Innovative Neurotechnologies (BRAIN ) Initiative hopes to build upon to further our understanding of the human brain."
What’s Next
"Siegelbaum’s group hopes to use the same genetic technology to examine whether there are changes in CA2 function in mouse models of psychiatric disorders such as autism and schizophrenia. If so, they plan to screen for drugs that restore normal CA2 function and ask whether this drug treatment helps reverse any behavioral changes seen in the mice. Such research offers the possibility of finding new drug targets and approaches for treating the behavioral changes associated with these disorders."
Reference
Hitti FL, Siegelbaum SA. The Hippocampal CA2 Region is Essential for Social Memory. Nature , published online February 23, 2014.
Grant 5F30MH098633-02
Link to Source page
I hope you found this informative. Sooner or later researchers should be able to find something to truly help us with our mental illnesses. This study makes me hopefully it will be sooner rather than later. Have a great Thursday!
Wednesday, June 11, 2014
Inflammation and Depression - new study
Hello Everyone! I hope you are doing well this week. Today I wanted to cover an article I just found online about the effects of inflammation and persistence of depression.
"Researcher N. Vogelzangs et al. reported in a 2014 article in Neuropharmacology that inflammatory and metabolic dysregulation in antidepressant users predicted an outcome of depression two years later. Elevated levels of the marker of inflammation Il-6, low HDL (or “good”) cholesterol, high triglycerides, and high blood sugar were associated with poor response to medication and chronicity of depression. Of 315 people treated with antidepressants (average age 43), 138 were in remission at 2 years, while 177 (56.2%) were still depressed. People with four or more types of inflammatory or metabolic dysregulations had a 90% chance of still being depressed at 2 years."
I found this very interesting, that maybe with a change in diet I could help curb my depression. The article is continued below.
"Among inflammatory markers including CRP and TNF-alpha, IL-6 alone was associated with chronic depression. Il-6 can cross the blood-brain barrier. We have previously reported that researcher Scott Russo found that in rats in a depression-like state known as defeat stress (brought about by repeated defeat by a larger rodent), blocking Il-6 can prevent depressive behaviors such as social avoidance or loss of preference for sucrose.
Like inflammation, metabolic abnormalities also complicate depression. Lipid dysregulation and hyperglycemia are associated not only with depression persistence, but also with the new onset of depression in humans.
Vogelzangs et al. conclude that these data “ suggest that inflammatory and metabolic dysregulation worsens depression course owing to reduced [antidepressant] response and that alternative intervention treatments may be needed for depressed persons with inflammatory and metabolic dysregulation.”
It is noteworthy that a 2014 meta-analysis of the anti-inflammatory drug celecoxib (Celebrex) published by Farhad Faridhosseini et al. in Human Psychopharmacology, showed that the drug, often prescribed for arthritis, is effective for unipolar depression when added to patients’ regular treatment.
It remains to be ascertained whether celecoxib’s effects are seen in depression in general, or if they pertain only to the 30% of depressed patients who show inflammation at baseline. Typical markers of inflammation include Il-6, CRP, TNFa, and Il-1.
Statins, prescribed to lower cholesterol, also have anti-inflammatory effects, and are also effective in preventing depression.
Determining treatment approaches for those patients showing signs of inflammation or metabolic irregularities remains a high priority for study. The preliminary data noted here suggest that treating these dysregulations in those with depression may be useful."
Source
I'm not one for taking more medications, but if an anti-inflammatory drug could help my depression I'd give it a try. Always discuss changes to your medication with your prescribing doctor first, especially to avoid drug interactions.
I hope you found this information useful and enlightening. Have a great Wednesday! Hump Day!
"Researcher N. Vogelzangs et al. reported in a 2014 article in Neuropharmacology that inflammatory and metabolic dysregulation in antidepressant users predicted an outcome of depression two years later. Elevated levels of the marker of inflammation Il-6, low HDL (or “good”) cholesterol, high triglycerides, and high blood sugar were associated with poor response to medication and chronicity of depression. Of 315 people treated with antidepressants (average age 43), 138 were in remission at 2 years, while 177 (56.2%) were still depressed. People with four or more types of inflammatory or metabolic dysregulations had a 90% chance of still being depressed at 2 years."
I found this very interesting, that maybe with a change in diet I could help curb my depression. The article is continued below.
"Among inflammatory markers including CRP and TNF-alpha, IL-6 alone was associated with chronic depression. Il-6 can cross the blood-brain barrier. We have previously reported that researcher Scott Russo found that in rats in a depression-like state known as defeat stress (brought about by repeated defeat by a larger rodent), blocking Il-6 can prevent depressive behaviors such as social avoidance or loss of preference for sucrose.
Like inflammation, metabolic abnormalities also complicate depression. Lipid dysregulation and hyperglycemia are associated not only with depression persistence, but also with the new onset of depression in humans.
Vogelzangs et al. conclude that these data “ suggest that inflammatory and metabolic dysregulation worsens depression course owing to reduced [antidepressant] response and that alternative intervention treatments may be needed for depressed persons with inflammatory and metabolic dysregulation.”
It is noteworthy that a 2014 meta-analysis of the anti-inflammatory drug celecoxib (Celebrex) published by Farhad Faridhosseini et al. in Human Psychopharmacology, showed that the drug, often prescribed for arthritis, is effective for unipolar depression when added to patients’ regular treatment.
It remains to be ascertained whether celecoxib’s effects are seen in depression in general, or if they pertain only to the 30% of depressed patients who show inflammation at baseline. Typical markers of inflammation include Il-6, CRP, TNFa, and Il-1.
Statins, prescribed to lower cholesterol, also have anti-inflammatory effects, and are also effective in preventing depression.
Determining treatment approaches for those patients showing signs of inflammation or metabolic irregularities remains a high priority for study. The preliminary data noted here suggest that treating these dysregulations in those with depression may be useful."
Source
I'm not one for taking more medications, but if an anti-inflammatory drug could help my depression I'd give it a try. Always discuss changes to your medication with your prescribing doctor first, especially to avoid drug interactions.
I hope you found this information useful and enlightening. Have a great Wednesday! Hump Day!
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