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Friday, August 29, 2014

Don't Get Emotional: You might get treated for 'mental illness'!

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Editors Note: This article appeared in Salvo 27, Winter 2013 edition and is used by permission. 

Winding up a fourteen-year process, the new Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), was released earlier this year. Originally billed as rolling out a new psychiatric paradigm, the chaotic and secretive project ended up being rushed to print without field testing.[1] The nondisclosure agreement that contributors were required to sign was publicly criticized by the chair of the DSM-III task force.[2] Though the new manual was welcomed by some as another step in catching people who have been falling through the cracks, the overwhelming response was negative.
The DSM, which classifies hundreds of mental disorders, is the bible of psychiatry. Insurance companies rely on its detailed codes to determine reimbursement, and it influences the way doctors prescribe drugs.
DSM-5 added ten new mental illness diagnoses and loosened the criteria for many others. Allen Frances, M.D., chair of the DSM-IV task force, denounced many of the changes as seeming “clearly unsafe and scientifically unsound,” and asserted that blind adherence to the new criteria would lead to “massive over-diagnosis and harmful over-medication.”[3] Current odds are that, based on the DSM-5, half the population will have a diagnosable disorder in their lifetime.
A few examples illustrate the appropriateness of Dr. Frances’s concerns: Per the DSM-5, recurring overindulgence is now Binge Eating Disorder. Children with temper tantrums suffer from Disruptive Mood Dysregulation Disorder. There’s a diagnosis for a specific obsessive-compulsive behavior called Hoarding Disorder, and another (my personal favorite) for Caffeine Withdrawal. Being grumpy in the morning until I sip my Nespresso coffee isn’t a character issue for me anymore; it’s a mental problem. At the other extreme, of course, is Caffeine Intoxication.
This pattern portends two disturbing trends. One is toward the homogenization of the human personality by narrowing the range of what is considered normal. People who are anxious under stress, collapse in a crisis, or get despondent with grief—all common reactions—may now be regarded as abnormal. A diagnosis can lead to judging, labeling, and stigmatizing a person. Or it can lead the diagnosed person to seek personality-altering drugs so he can fit in.
In the “new normal,” what will be lost? Perhaps the spectacular human diversity that builds civilizations and cultures. The great figures of history were not well-behaved schoolchildren. Most great artists were not cheerful, compliant extroverts. And great discoveries were not made by mild-mannered, complacent researchers.
The second trend—toward medicalization—results when more and more aspects of human experience and behavior are seen as problems to be solved by medicine. The emotions elicited by the normal challenges of life, such as grief, sadness, depression, and irritability, are pathologized, treated as a disease to be cured, not a character-forming occasion. The root of the problem is a shift in our understanding of the boundaries of normality, health, and human flourishing.
At its 20th annual conference held earlier this year, the Center for Bioethics and Human Dignity addressed “Health and Human Flourishing.” Speakers expressed the concern that medicine and technology have veered from repairing injury and curing disease to expanding human capacities and “correcting” the effects of normal human experience. Dr. Allen Verhey cited our cult of health, where “hospitals and exercise facilities are the temples, and doctors and dieticians are the priests.”
Christians recognize that health is a good thing, but it is not the greatest good. Rather, Dr. Verhey said, it is in responding to God’s grace and goodness with doxological gratitude, in remaining joyfully hopeful about our future, knowing that the Spirit is drawing all things toward God’s good ends, and in loving both God and neighbor, that we realize true human flourishing.

[1] Allen Frances, “DSM-5 Is Guide, Not Bible—Ignore Its Ten Worst Changes,” Psychology Today, December 2, 2012.
[2] Benedict Carey, “Psychiatrists Revise the Book of Human Troubles,” The New York Times, December 7, 2008.
[3] Frances.
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Tuesday, August 26, 2014

Losing Sleep

Losing Sleep | HMS

Losing Sleep
‘Sleep switch’ neurons diminish with age and Alzheimer’s disease
August 20, 2014
As people grow older, they often have difficulty falling asleep and staying asleep, and tend to awaken too early in the morning. In individuals with Alzheimer’s disease, this common and troubling symptom of aging tends to be especially pronounced, often leading to nighttime confusion and wandering.
Now, a study led by researchers at Harvard Medical School, Beth Israel Deaconess Medical Center and the University of Toronto/Sunnybrook Health Sciences Centre helps explain why sleep becomes more fragmented with age. Reported online in the journal Brain, the new findings demonstrate for the first time that a group of inhibitory neurons, whose loss leads to sleep disruption in experimental animals, are substantially diminished among the elderly and individuals with Alzheimer’s disease, and that this, in turn, is accompanied by sleep disruption.
“On average, a person in his 70s has about one hour less sleep per night than a person in his 20s,” explained senior author Clifford Saper, the HMS James Jackson Putnam Professor of Neurology at Beth Israel Deaconess. “Sleep loss and sleep fragmentation is associated with a number of health issues, including cognitive dysfunction, increased blood pressure and vascular disease, and a tendency to develop type 2 diabetes. It now appears that loss of these neurons may be contributing to these various disorders as people age.”
Clifford Saper. Image: BIDMC Media ServicesClifford Saper. Image: BIDMC Media ServicesIn 1996, the Saper lab first discovered that the ventrolateral preoptic nucleus, a key cell group of inhibitory neurons, was functioning as a “sleep switch” in rats, turning off the brain’s arousal systems to enable animals to fall asleep. “Our experiments in animals showed that loss of these neurons produced profound insomnia, with animals sleeping only about 50 percent as much as normal and their remaining sleep being fragmented and disrupted,” he explained.
A group of cells in the human brain, the intermediate nucleus, is located in a similar location and has the same inhibitory neurotransmitter, galanin, as the vetrolateral preoptic nucleus in rats. The authors hypothesized that if the intermediate nucleus was important for human sleep and was homologous to the animal’s ventrolateral preoptic nucleus, then it may also similarly regulate humans’ sleep-wake cycles.
In order to test this hypothesis, the investigators analyzed data from theRush Memory and Aging Project, a community-based study of aging and dementia which began in 1997 and has been following a group of almost 1,000 subjects who entered the study as healthy 65-year-olds and are followed until their deaths, at which point their brains are donated for research.
“Since 2005, most of the subjects in the memory and aging project have been undergoing actigraphic recording every two years. This consists of their wearing a small wristwatch-type device on their non-dominant arm for seven to 10 days,” explained first author Andrew S. P. Lim of the University of Toronto and Sunnybrook Health Sciences Centre and a former member of the Saper lab. The actigraphy device, which is waterproof, is worn 24 hours a day and thereby monitors all movements, large and small, divided into 15-second intervals. “Our previous work had determined that these actigraphic recordings are a good measure of the amount and quality of sleep,” he added.
The authors examined the brains of 45 study subjects (median age at death, 89.2), identifying ventrolateral preoptic neurons by staining the brains for the neurotransmitter galanin. They then correlated the actigraphic rest-activity behavior of the 45 individuals in the year prior to their deaths with the number of remaining ventrolateral preoptic neurons at autopsy.
“We found that in the older patients who did not have Alzheimer’s disease, the number of ventrolateral preoptic neurons correlated inversely with the amount of sleep fragmentation,” said Saper. “The fewer the neurons, the more fragmented the sleep became.” The subjects with the most neurons (greater than 6,000) spent 50 percent or more of total rest time in the prolonged periods of non-movement most likely to represent sleep while subjects with the fewest ventrolateral preoptic neurons (fewer than 3,000) spent less than 40 percent of total rest time in extended periods of rest. The results further showed that among Alzheimer’s patients, most sleep impairment seemed to be related to the number of ventrolateral preoptic neurons that had been lost.
“These findings provide the first evidence that the ventrolateral preoptic nucleus in humans probably plays a key role in causing sleep, and functions in a similar way to other species that have been studied,” said Saper. “The loss of these neurons with aging and with Alzheimer’s disease may be an important reason why older individuals often face sleep disruptions. These results may, therefore, lead to new methods to diminish sleep problems in the elderly and prevent sleep-deprivation-related cognitive decline in people with dementia.”
This work was supported by a Dana Foundation Clinical Neuroscience Grant and National Institutes of Health grants P01AG009975, P01HL095491, R01NS072337, R01AG017917, R01AG024480, R01NS078009, R01AG043379 and R01AG042210. Other support came from grants from the Canadian Institutes of Health Research, the Illinois Department of Public Health and the Robert C. Borwell Endowment Fund.
Adapted from a Beth Israel Deaconess news release.