by Peter J. Dorsen M.D., LADC
Dylan Murray et al in Mania and Mortality: "Why the Excess Cardiovascular Risk in Bipolar Disorder?" From Current Psychiatry Reports 2009, 11: 475-480, raises more questions why individuals with bipolar disorder have twice the cardiovascular mortality as the general population(prevalence ratio of 1.6). For one thing, metabolic syndrome is more common in this population.
Just being manic increases your chances for such increased mortality. There is a significant history of sudden death from cardiovascular factors in manic individuals. Confounders include behavior, access to treatment, quality of health care, and underlying pathophysiology. I can relate because I have mentioned previously experiencing an MI requiring angioplasty and two stents three years ago. I did not have any of the criteria for metabolic syndrome that include abdominal obesity, diabetes, dyslipidemia or hypertension.
The authors point out that our U.S. population certainly has its share of both metabolic syndrome and diabetes. Certainly, other studies warn about the dangers as well with associated smoking, an elevated total cholesterol, with specifically a reduced high-density lipoprotein (the “good” cholesterol).
Because of such significant associations, the authors advocate screening bipolar disorder patients for diabetes and metabolic syndrome especially if they happen to be on second-generation antipsychotics. They warn that bipolar disorder appears to negatively affect fat metabolism in women. Bipolar I patients appear to be at higher risk for cardiovascular mortality than bipolar II individuals. They attribute such disparity to a higher incidence of mania in bipolar I disorder. There appears to be less likelihood that the manic patient will have a primary care physician.
There may well be barriers to optimal medical care. Such patients may have difficulties navigating through the health care system. Murray et al suggest better integrated health care. They are suggesting better lines of communication between psychiatrist and primary care giver. They warn as well about QTc prolongation (the repolarization phase of the cardiogram). Ray et al warn about sudden death among atypical antipsychotic users (N Engl J Med 2009, 360:225-235).
Perhaps increased mortality can be attributed to increased smoking, medication-related weight gain, or linking genetic risk or pathophysiologic processes of bipolar disorder to elevated cardiovascular risk. They even ruminate about an overactive inflammatory response in bipolar patients.
These authors note that less than half of psychiatrists actually are monitoring lipid levels or waist circumference. Anyone on second-generation antipsychotics deserves to be monitored for family history of diabetes, body mass-index, weight gain and triglyceride levels. They reflect on compliance as well related to “ limited insight, a negative view of medications, and substance abuse.” They allude to studying cardiovascular risk in youth with bipolar disorder thus eliminating confounding variables.
In their own words, “Further education may improve recognition and screening for traditional risk factors and may result in better cardiovascular outcomes for this at-risk population.”
Tuesday, March 23, 2010
Monday, March 15, 2010
Alzheimer's and Sleep
by Peter J. Dorsen M.D., LADC
Andrew McCaddon, M.D. and Peter R. Hudson, Ph.D. of North Wales U.K, note utiliizing plasma total homocysteine (tHcy) as a marker, B vitamins deficiencies were found to be highly prevalent in the elderly. These writers note reports of elevated levels of homocysteine in individuals with clinically and pathologically confirmed Alzheimer’s disease (AD). Neuroinflammatory oxidative stress occurs early in AD. Amyloid plaques and neurofibrillary tangles represent end-stage of such oxidative stress.
They note as well an accumulation of methylmalonic acid that appears to be associated with lower cognitive function scores. There is an association as well between elevated homocysteine (Hcy) levels and stroke. Folate supplements serve as affective stroke prevention. They note the association of high Hcy and brain atrophy reversible with high-dose B-vitamin supplementation.
They recommend a naturally occurring product, cerefolin. They also report the efficacy of high doses of ORAL vitamin B12 (1-2mg/day). They emphasize assessing folate, B12 and homocysteine levels in ALL dementia patients and TREATING those with abnormal findings. Especially important, is that clinicians screen EVERYONE presenting with cognitive impairment who has co-occurring vascular risks such as high blood pressure, elevated cholesterol, diabetes, who smokes, or high homocystein levels. McCaddon and Hudson offer some novel warnings about and treatments for AD.
Sleep Problems
John W. Winkelman, MD. Ph.D. in Primary Psychiatry 16: 12 (suppl 8), differentiates between insomnia and sleep deprivation (reduced opportunity to sleep –voluntary or imposed. He recommends that someone who has trouble sleeping keep a 1-2 week sleep diary. Winkelman stresses that a polysomnogram (PSG) is NOT recommended routinely for insomnia unless a clinician suspects sleep apnea, periodic limb movement disorder or narcolepsy ( falling to sleep anywhere anytime inappropriately).
Many with insomnia spend more and more time in bed trying to get adequate sleep but don’t. He cites one such patient in whom “sleeplessness and anxiety symptoms are locked in a vicious cycle…”
Andrew Krystal, M.D. in this same monograph addresses treatment. He recommends Cognitive-Behavioral Treatment (CBT) for insomnia. CBT deals with such crucial issues as sleep hygiene, stimulus control, sleep restriction, and cognitive therapy. Cognitive therapy addresses “the maladaptive thought and emotional processes that often occur.” Consider “problem solving” BEFORE bedtime and something relatively simple like progressive muscle relaxation (one of Tim’s favorites). CBT compared more favorably compared with progressive muscle relaxation and imagery.
Utilizing medications like the hypnotic Zolpidem seem to work best with CBT when medication treatment at, let’s, say six months moves to an as-needed regimen. Clinicians aim for the speed of onset of pharmacotherapy with the durability of CBT. Krystal recommends a taper at 2-3 months and ultimately deciding whether to stop the medication altogether based on how well someone does.
These investigators emphasize not to minimize the potential side effects of the benzodiazepines for cognitive or psychomotor impairment and abuse potential, They advise: "initiate periodic tapers." One group cited treated patients three nights a week according to the patients’ preference. They reduced cost and minimized adverse effects. M Vaughn McCall, MD. MS, addresses co-morbid insomnia. “Relentless insomnia may be a prelude to development of a classic mental disorder such as depression.” He notes that it is important to investigate for a primary sleep disorder “ if a depressed insomniac complains of both insomnia and sleepiness.” Insomniacs, he reports, DENY daytime sleepiness complaining instead of "tiredness and exhaustion."
Certainly, appropriate for insomnia AND depression are the SSRIs. Insomniacs and depressed persons may well demonstrate remission on these medications. However, a large number continue to experience insomnia. If this does not resolve, and especially if a patient has hypersomnia (sleeping all the time) in addition to insomnia, they advise other modalities that include CBT-I for making changes in sleep schedules (avoiding going to bed too early or staying there too long); and dealing with distorted ideas about sleep (bedtime anxiety or fearing that they will be unable to fall asleep).
Consider bedtime hypnotic therapy. Evidence-based statistics, at this point, supports adding a FDA –approved hypnotic RATHER than a sedating antidepressant like trazadone. They advise “high level oversight” when using “benzo’s” or non-benzodiazepine receptor agonists (NBBRA’s). Why? Suicide! Note too, that insomnia is an independent indicator for suicidal ideation, behavior or death in depressed patients. Especially dangerous is an overdose of an accumulation of hypnotics and alcohol. As a result, clinicians should prescribe only 1-2 weeks of theses medications.Depression and insomnia often co-occur.These investigators offer some helpful advice that can stabilize both successfully.
Alzheimer's
"Novel treatment options: cognitive decline in Alzheimer’s disease" (Primary Psychiatry 17:1 (suppl 1). As we age, are afflicted with bipolar disorder, and might require a panel of mood stabilizers and more, we certainly can experience a decline in mental function (executive/cognitive as well?). Thirty million individuals will have (some form of ) dementia in 2010!Andrew McCaddon, M.D. and Peter R. Hudson, Ph.D. of North Wales U.K, note utiliizing plasma total homocysteine (tHcy) as a marker, B vitamins deficiencies were found to be highly prevalent in the elderly. These writers note reports of elevated levels of homocysteine in individuals with clinically and pathologically confirmed Alzheimer’s disease (AD). Neuroinflammatory oxidative stress occurs early in AD. Amyloid plaques and neurofibrillary tangles represent end-stage of such oxidative stress.
They note as well an accumulation of methylmalonic acid that appears to be associated with lower cognitive function scores. There is an association as well between elevated homocysteine (Hcy) levels and stroke. Folate supplements serve as affective stroke prevention. They note the association of high Hcy and brain atrophy reversible with high-dose B-vitamin supplementation.
They recommend a naturally occurring product, cerefolin. They also report the efficacy of high doses of ORAL vitamin B12 (1-2mg/day). They emphasize assessing folate, B12 and homocysteine levels in ALL dementia patients and TREATING those with abnormal findings. Especially important, is that clinicians screen EVERYONE presenting with cognitive impairment who has co-occurring vascular risks such as high blood pressure, elevated cholesterol, diabetes, who smokes, or high homocystein levels. McCaddon and Hudson offer some novel warnings about and treatments for AD.
Sleep Problems
John W. Winkelman, MD. Ph.D. in Primary Psychiatry 16: 12 (suppl 8), differentiates between insomnia and sleep deprivation (reduced opportunity to sleep –voluntary or imposed. He recommends that someone who has trouble sleeping keep a 1-2 week sleep diary. Winkelman stresses that a polysomnogram (PSG) is NOT recommended routinely for insomnia unless a clinician suspects sleep apnea, periodic limb movement disorder or narcolepsy ( falling to sleep anywhere anytime inappropriately).
Many with insomnia spend more and more time in bed trying to get adequate sleep but don’t. He cites one such patient in whom “sleeplessness and anxiety symptoms are locked in a vicious cycle…”
Andrew Krystal, M.D. in this same monograph addresses treatment. He recommends Cognitive-Behavioral Treatment (CBT) for insomnia. CBT deals with such crucial issues as sleep hygiene, stimulus control, sleep restriction, and cognitive therapy. Cognitive therapy addresses “the maladaptive thought and emotional processes that often occur.” Consider “problem solving” BEFORE bedtime and something relatively simple like progressive muscle relaxation (one of Tim’s favorites). CBT compared more favorably compared with progressive muscle relaxation and imagery.
Utilizing medications like the hypnotic Zolpidem seem to work best with CBT when medication treatment at, let’s, say six months moves to an as-needed regimen. Clinicians aim for the speed of onset of pharmacotherapy with the durability of CBT. Krystal recommends a taper at 2-3 months and ultimately deciding whether to stop the medication altogether based on how well someone does.
These investigators emphasize not to minimize the potential side effects of the benzodiazepines for cognitive or psychomotor impairment and abuse potential, They advise: "initiate periodic tapers." One group cited treated patients three nights a week according to the patients’ preference. They reduced cost and minimized adverse effects. M Vaughn McCall, MD. MS, addresses co-morbid insomnia. “Relentless insomnia may be a prelude to development of a classic mental disorder such as depression.” He notes that it is important to investigate for a primary sleep disorder “ if a depressed insomniac complains of both insomnia and sleepiness.” Insomniacs, he reports, DENY daytime sleepiness complaining instead of "tiredness and exhaustion."
Certainly, appropriate for insomnia AND depression are the SSRIs. Insomniacs and depressed persons may well demonstrate remission on these medications. However, a large number continue to experience insomnia. If this does not resolve, and especially if a patient has hypersomnia (sleeping all the time) in addition to insomnia, they advise other modalities that include CBT-I for making changes in sleep schedules (avoiding going to bed too early or staying there too long); and dealing with distorted ideas about sleep (bedtime anxiety or fearing that they will be unable to fall asleep).
Consider bedtime hypnotic therapy. Evidence-based statistics, at this point, supports adding a FDA –approved hypnotic RATHER than a sedating antidepressant like trazadone. They advise “high level oversight” when using “benzo’s” or non-benzodiazepine receptor agonists (NBBRA’s). Why? Suicide! Note too, that insomnia is an independent indicator for suicidal ideation, behavior or death in depressed patients. Especially dangerous is an overdose of an accumulation of hypnotics and alcohol. As a result, clinicians should prescribe only 1-2 weeks of theses medications.Depression and insomnia often co-occur.These investigators offer some helpful advice that can stabilize both successfully.
Wednesday, March 3, 2010
Bipolar disorder and Medical Co-morbidities Peter J. Dorsen, M.D. LADC
by Peter J. Dorsen M.D., LADC
Three years ago, I experienced excruciating chest pain with exercise, ultimately underwent angiography, required two stents and angioplasty, and subsequently was found to have experienced a heart attack in the process.
I had been taking lithium for an extended period of time for my bipolar II disorder.
What I could not completely comprehend was why, if I was thin and exercised regularly, did I continue to run a modestly elevated total cholesterol as well as an ongoing upper limit normal LDL (the “bad” cholesterol) and, no matter how fit I thought I was, I could never elevate my HDL (the “good” cholesterol) to a favorable level. I had a significant family history of high cholesterol. I chose not to take a lipid-lowering drug like simvastatin for fear of liver injury. Doctors are the worst patients!
The good news is that I have fared well with a “clean” angiogram one year after my stents and an acceptable fairly recent maximal graduated stress test several months ago. Initially, I had an elevated blood pressure transiently but am now off all blood pressure medications. I have never had any of the other criteria for metabolic syndrome such as diabetes or centripetal obesity. Metabolic syndrome is excess fat in one’s abdomen with a reduced sensitivity to insulin’s effects (insulin resistance), a high blood sugar level, abnormal cholesterol levels, and high blood pressure. Some have referred to such an insulin resistance syndrome as “Syndrome X.”
My BMI and waist circumference have never been excessive. However, metabolic syndrome is especially prevalent in developed countries with over 40% of those over 50 having it. This syndrome has the “apple-shape” in men or post menopausal women versus the “pear-shape” more commonly seen in women as adiposity collecting around the hips.
Aripiprazole (Abilify) has been advertised on TV recently as an adjunctive medication for depression. According to Page CU Expert Opin Drug Saf. 2009 May; 8(3) 373-86, it does have FDA approval for treatment “as adjunctive therapy or monotherapy (manic or mixed episodes) as well as an augmentation therapy of major depressive disorder (MDD).” These reporters state that it has “favorable safety compared to other atypical antipsychotics” with “minimal propensity for weight gain and metabolic disruption.” However they report abnormal body movements(akathisia) “that may limit its clinical use…especially in bipolar disorder and MDD.” It is actually one of the newer “atypical” antipsychotics with all the provisos and considerations that go with that class of drugs.
When I went on the medication, I developed tardive dyskinesia (TD) meaning that my chin began twitching and I developed uncontrollable spastic movements in my right hand. Secondly, it is important that you alert your provider if you have ever had a history of heart failure, a heart attack, high or low blood pressure, or a stroke or seizures if you elect to take this drug. Caveat emptor, “may the buyer beware.” These are not necessarily benign medications!
Here’s an interesting one: there are somewhat anecdotal reports that ginseng of one variety or another, functioning as an anti-oxidant, can lower low density lipoproteins (LDL). Not only is it reputed that ginseng may lower blood sugar in Type II diabetes, but it can decrease the risk of heart disease, improve blood pressure, and decrease symptoms of coronary heart disease. So not try some of this herb?
Wildes et al in J Clin Psychiatry. 2006 Jun; 67(6): 904-15, reviewed 92 studies and found that “(studies) targeting physical inactivity and overeating in bipolar disorders are needed, as are better screening and treatment for binge eating.” The authors want to explain both ” the causes and consequences of obesity…”
McIntyre et al in Ann Clin Psychiatry. 2007 Oct-Dec, advise: “ A comprehensive management approach for depressive disorders should routinely include opportunistic screening and primary prevention strategies targeting metabolically mediated comorbitity (eg. Cardiovascular disease).” Also, they say “ explore innovative treatments for mood disorders which primarily target aberrant metabolic networks.” They go so far as to “propose the notion of ‘metabolic syndrome type II’ as a neuropsychiatric syndrome.”
In an older article, Morriss R, Mohammed FA J. Psychopharmacol. 2005 Nov;19(6 Suppl): 94-101 report that lifestyle, illness and treatment factors in people with bipolar disorder (BD) may confer additional risk of morbidity and mortality to the increasing rates of obesity, metabolic syndrome, diabetes mellitus and cardiovascular mortality in the general population.” They observe increased mortality from cardiovascular causes as well as morbidity from obesity and type 2 diabetes increased compared with the general population. They note an increased risk in people with bipolar disorder as well due to less exercise, poor diet, frequent depressive episodes, and co-morbidity with substance misuse.
Saravane D et al in Encephale. 2009 Sep; 35(4): 330-9 (in French), posit that bipolar disorder is associated with “undue medical morbidity and mortality…with a 15-30 year shorter lifetime…” This is, after all, the same population who have “higher rate of preventable risk factors such as smoking, addiction, poor diet , lack of exercise.” Treatment of such co-morbitities is crucial, they advise as significant “ for their psychosocial functioning and overall quality of life.” Detect medical illness at “the first episode of mental illness.” They admonish: “ identify…crucial modifiable risk factors, such as… obesity, dyslipidemia, diabetes, hypertension, and smoking.
This team relates such metabolic and cardiovascular risk factors in population with significant mental illness “to poverty and limited access to medical care but also to the use of psychotropic mediations.” They advise in the first three to four months of treatment that patients with severe mental illness obtain baseline weight, height, waist circumference, blood pressure, fasting plasma glucose, and a fasting lipid profile. Obtaining a BMI ( Body mass index) which is weight(kg) over height(meters) squared can be extremely helpful.
Getting a baseline EKG is essential if a patient is taking an atypical antipsychotic which can increase your QT interval (the repolarization phase of the cardiogram) and lead to fatal arrhythmias. We need to know about the cardiovascular and metabolic risks of our medications! Prescribing antipsychotics carries responsibility for monitoring metabolic abnormalities as well. An ideal world MUST BE coordination among psychiatrists, GP’s, endocrinologists, cardiologists, nurses, dietitions, our families and US.
It is crucial that clinicians stay vigilant for metabolic syndrome among their stable of bipolar patients. Individuals who develop this complication are susceptible to coronary artery disease ( like I was), high blood pressure, Type 2 diabetes, abnormal fats, fatty liver, gout, polycystic ovaries, and chronic kidney disease. Men with abdominal girth over 40 inches and women over 35 inches may have it.
As Tim has suggested, changes in diet accompanied by a commitment to regular exercise is crucial. Medications that increase the body’s sensitivity to elevated glucose like metformin, thiazolidine, or rosiglitazone WITH exercise can improve sugar utilization. If weight reduction and exercise totally fail and after appropriate screening, bariatric surgery can certainly be a viable alternative. But that subject is for another time and blog.
Three years ago, I experienced excruciating chest pain with exercise, ultimately underwent angiography, required two stents and angioplasty, and subsequently was found to have experienced a heart attack in the process.
I had been taking lithium for an extended period of time for my bipolar II disorder.
What I could not completely comprehend was why, if I was thin and exercised regularly, did I continue to run a modestly elevated total cholesterol as well as an ongoing upper limit normal LDL (the “bad” cholesterol) and, no matter how fit I thought I was, I could never elevate my HDL (the “good” cholesterol) to a favorable level. I had a significant family history of high cholesterol. I chose not to take a lipid-lowering drug like simvastatin for fear of liver injury. Doctors are the worst patients!
The good news is that I have fared well with a “clean” angiogram one year after my stents and an acceptable fairly recent maximal graduated stress test several months ago. Initially, I had an elevated blood pressure transiently but am now off all blood pressure medications. I have never had any of the other criteria for metabolic syndrome such as diabetes or centripetal obesity. Metabolic syndrome is excess fat in one’s abdomen with a reduced sensitivity to insulin’s effects (insulin resistance), a high blood sugar level, abnormal cholesterol levels, and high blood pressure. Some have referred to such an insulin resistance syndrome as “Syndrome X.”
My BMI and waist circumference have never been excessive. However, metabolic syndrome is especially prevalent in developed countries with over 40% of those over 50 having it. This syndrome has the “apple-shape” in men or post menopausal women versus the “pear-shape” more commonly seen in women as adiposity collecting around the hips.
Aripiprazole (Abilify) has been advertised on TV recently as an adjunctive medication for depression. According to Page CU Expert Opin Drug Saf. 2009 May; 8(3) 373-86, it does have FDA approval for treatment “as adjunctive therapy or monotherapy (manic or mixed episodes) as well as an augmentation therapy of major depressive disorder (MDD).” These reporters state that it has “favorable safety compared to other atypical antipsychotics” with “minimal propensity for weight gain and metabolic disruption.” However they report abnormal body movements(akathisia) “that may limit its clinical use…especially in bipolar disorder and MDD.” It is actually one of the newer “atypical” antipsychotics with all the provisos and considerations that go with that class of drugs.
When I went on the medication, I developed tardive dyskinesia (TD) meaning that my chin began twitching and I developed uncontrollable spastic movements in my right hand. Secondly, it is important that you alert your provider if you have ever had a history of heart failure, a heart attack, high or low blood pressure, or a stroke or seizures if you elect to take this drug. Caveat emptor, “may the buyer beware.” These are not necessarily benign medications!
Here’s an interesting one: there are somewhat anecdotal reports that ginseng of one variety or another, functioning as an anti-oxidant, can lower low density lipoproteins (LDL). Not only is it reputed that ginseng may lower blood sugar in Type II diabetes, but it can decrease the risk of heart disease, improve blood pressure, and decrease symptoms of coronary heart disease. So not try some of this herb?
Wildes et al in J Clin Psychiatry. 2006 Jun; 67(6): 904-15, reviewed 92 studies and found that “(studies) targeting physical inactivity and overeating in bipolar disorders are needed, as are better screening and treatment for binge eating.” The authors want to explain both ” the causes and consequences of obesity…”
McIntyre et al in Ann Clin Psychiatry. 2007 Oct-Dec, advise: “ A comprehensive management approach for depressive disorders should routinely include opportunistic screening and primary prevention strategies targeting metabolically mediated comorbitity (eg. Cardiovascular disease).” Also, they say “ explore innovative treatments for mood disorders which primarily target aberrant metabolic networks.” They go so far as to “propose the notion of ‘metabolic syndrome type II’ as a neuropsychiatric syndrome.”
In an older article, Morriss R, Mohammed FA J. Psychopharmacol. 2005 Nov;19(6 Suppl): 94-101 report that lifestyle, illness and treatment factors in people with bipolar disorder (BD) may confer additional risk of morbidity and mortality to the increasing rates of obesity, metabolic syndrome, diabetes mellitus and cardiovascular mortality in the general population.” They observe increased mortality from cardiovascular causes as well as morbidity from obesity and type 2 diabetes increased compared with the general population. They note an increased risk in people with bipolar disorder as well due to less exercise, poor diet, frequent depressive episodes, and co-morbidity with substance misuse.
Saravane D et al in Encephale. 2009 Sep; 35(4): 330-9 (in French), posit that bipolar disorder is associated with “undue medical morbidity and mortality…with a 15-30 year shorter lifetime…” This is, after all, the same population who have “higher rate of preventable risk factors such as smoking, addiction, poor diet , lack of exercise.” Treatment of such co-morbitities is crucial, they advise as significant “ for their psychosocial functioning and overall quality of life.” Detect medical illness at “the first episode of mental illness.” They admonish: “ identify…crucial modifiable risk factors, such as… obesity, dyslipidemia, diabetes, hypertension, and smoking.
This team relates such metabolic and cardiovascular risk factors in population with significant mental illness “to poverty and limited access to medical care but also to the use of psychotropic mediations.” They advise in the first three to four months of treatment that patients with severe mental illness obtain baseline weight, height, waist circumference, blood pressure, fasting plasma glucose, and a fasting lipid profile. Obtaining a BMI ( Body mass index) which is weight(kg) over height(meters) squared can be extremely helpful.
Getting a baseline EKG is essential if a patient is taking an atypical antipsychotic which can increase your QT interval (the repolarization phase of the cardiogram) and lead to fatal arrhythmias. We need to know about the cardiovascular and metabolic risks of our medications! Prescribing antipsychotics carries responsibility for monitoring metabolic abnormalities as well. An ideal world MUST BE coordination among psychiatrists, GP’s, endocrinologists, cardiologists, nurses, dietitions, our families and US.
It is crucial that clinicians stay vigilant for metabolic syndrome among their stable of bipolar patients. Individuals who develop this complication are susceptible to coronary artery disease ( like I was), high blood pressure, Type 2 diabetes, abnormal fats, fatty liver, gout, polycystic ovaries, and chronic kidney disease. Men with abdominal girth over 40 inches and women over 35 inches may have it.
As Tim has suggested, changes in diet accompanied by a commitment to regular exercise is crucial. Medications that increase the body’s sensitivity to elevated glucose like metformin, thiazolidine, or rosiglitazone WITH exercise can improve sugar utilization. If weight reduction and exercise totally fail and after appropriate screening, bariatric surgery can certainly be a viable alternative. But that subject is for another time and blog.
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