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March 25, 2002
Q
"Can I cure my depression with a change in diet?"
A That is not likely, but there is a
recent study that indicates that with a dietary change "major
depression refractory to treatment with conventional antidepressants
may improve with the omega-3 fatty acid ethyl ester of
eicosapentaenoic acid (E-EPA)."
"Omega-3 fatty
acids…are derived from fish oil, and epidemiologic evidence suggests
some relationships between ingestion of fish oil and both cardiac
disease and depression in different cultures"... "Countries with
high rates of fish oil consumption have low rates of depressive
disorder."
"It is not possible to distinguish whether E-EPA augments
antidepressant action in the manner of lithium or has independent
antidepressant properties of its own," the authors write.
Am J Psychiatry. 2002;159(3):477-479
March 26, 2001
Q
"I have a patient who I thought was depressed but may be
suffering from Bipolar II Disorder...in which she becomes agitated,
irritable, restless, does not sleep and gets into letter writing
campaigns and unrealistic spending sprees?"
A
"You may be quite
correct. There was a recent discussion of this topic in which it was
stated that depressed patients have "hidden" episodes of
mild mania that qualify them for a diagnosis of bipolar II disorder.
The disorder is distinct in its clinical features and course from
both depression and bipolar I, and it may be different in terms of
response to treatment -- yet it is frequently missed by clinicians,
according to a report in the March edition of Psychiatric
Services. There is evidence that the diagnosis of bipolar II is
often missed, and the reason may be that the expression of mania is
not as dramatic as in bipolar I patients."
The tell-tale signals
that can flag hypomania: Decreased sleep in the absence of fatigue,
increased energy and a subjective sense on the part of patients that
they are thinking faster than others, and extravagance in important
areas of life, such as spending.
A critical and
potentially tragic consequence of missing bipolar II may be that
patients are treated with tricyclic antidepressants, which can cause
accelerated cycling. Evidence suggesting an increased number of
suicides among patients with bipolar II disorder -- though it may
not be the condition itself but the failure to identify it that puts
the patient at risk.
The most important
point, he says, is that bipolar II patients should be treated with
mood stabilizers. Clinicians treating them with antidepressants
increases cycling in bipolar I patients. It's reasonable to assume
the same is true in bipolar II."
March 19, 2001
Q
"I have Tourette's syndrome, and I have been told that it is
very similar to obsessive compulsive disorder (OCD). Is that
true?"
A
"Similar
to recent findings in Tourette's syndrome and focal dystonia, a
recent study reports significantly decreased intracortical
inhibition (ICI). There is also decreased active and resting motor
evoked potential threshold in OCD patients, another indication of
increased cortical excitability. Neither abnormality appeared
medication related. The decreases in ICI and motor threshold were
greatest in OCD patients with comorbid tics, but remained
significant in patients without tics. The data suggest abnormal
cortical excitability in obsessive-compulsive disorder. These
findings are congruent with the hypothesis that Tourette's syndrome
and obsessive-compulsive disorder (OCD) are analogous disorders with
overlapping dysfunction in corticobasal circuits. Patients with
tic-related OCD may have more abnormal motor cortex excitability
than OCD patients without tics."
Neurology 2000 Jan 11;54(1):142-7
March 12, 2001
Q
"I have a few drinks, sometimes more, at night to relax and
even though I feel pretty relaxed, I do not sleep well at all. In
fact, I think I have insomnia. Any thoughts on that or input?"
A
"Insomnia
may be a marker for severity of alcoholism as well as a predictor for
relapse, according to a study in the March issue of the American
Journal of Psychiatry. In the study of the patients available for
follow-up, 60% of those with insomnia at baseline relapsed, twice as
many as those without insomnia. Additionally, patients with insomnia
had more severe alcohol dependence and a higher incidence of comorbid
depression.
In many alcoholics, sleep
disorders or insomnia can persist for months or even years.
It also is important to
determine if the insomnia is associated with another diagnosis -- such
as depression or anxiety, which also require treatment."
March 5, 2001
Q
My wife has panic disorder. She has chest pain as part of this
disorder, and I am certain this will ultimately precipitate a heart
attack."
A Among
women with chest pain, those who have a history of anxiety disorders
have a lower probability of actually having coronary artery disease
(CAD) than those who do not, according to a report in the March 1st
issue of the Journal of the American College of Cardiology.
A history of anxiety disorder was independent of
standard CAD risk factors and noninvasive stress testing results in
predicting a lower risk of CAD among these women
February 26, 2001
Q
"Can psychological problems be solved over the internet? I see
many websites that claim they can do that."
A
A recent article on WebMD refers to "more and more Americans are
using the Internet to access mental health counseling. Web sites for
emotional problems abound with trendy sounding names...it's
estimated they get millions of hits -- many from the estimated one in
five of us suffering from mental illness, and all at the price of
$30-80 per hour session, which can be much less than traditional
psychotherapy....Confidentiality of
e-discussions between therapists and patients also must be addressed,
so people will feel free to reveal their innermost thoughts
online...to protect these particularly vulnerable people from being
exploited by fraudulent operators.... Although
the Food and Drug Administration has made an effort to crack down on
illegitimate online pharmacies that prescribe drugs without proper
medical supervision, apparently no federal regulation specifically
targets these mental health web sites.
And bad advice may come at
a high price....Online counseling tends to focus on problems like
depression, marital or sexual issues, and anxiety. Because of the
distance between the patient and practitioner, it may be more
difficult to handle emotional crises such as suicidal or violent
tendencies..."
February 19, 2001
Q
"My ex-husband has a long criminal behavior. He had custody of
our son until he was five years old. Now, at 15, our son is exhibiting
the same behaviors. Was this inherited?"
A Are
aggression or antisocial behavior genetic? Yes, but only to some
extent, and the link to genes will not be as easily made. In the most
recent Science, it was stated: "The genetics of behavior
offers more opportunity for media sensationalism than any other branch
of current science. Frequent news reports claim that researchers have
discovered the 'gene for' such traits as aggression, intelligence,
criminality, homosexuality, feminine intuition, and even bad
luck.
Such reports tend
to suggest, usually incorrectly, that there is a direct correspondence
between carrying a mutation in the gene and manifesting the trait or
disorder. With the recent completion of the cataloguing of the genome
by government and private-sector scientists, -- the crowning
achievement of the massive Human Genome Project -- the question of its
utility in understanding a range of behavioral traits is being asked
even louder. Most result from a complex combination of multiple genes
interacting with the environment over time.
These
"complex" conditions include depression, schizophrenia,
Alzheimer's, alcoholism, and a host of other disorders. Eventually,
even the more difficult nuts to crack -- like schizophrenia,
Alzheimer's, or alcoholism -- will succumb, to the extent that we will
know not just what the genes actually are but what they do. These
genes will be very common in the population, and there will be
multiple genes, so that depression, for instance, will result from a
combination of them. It is "somewhat realistic" to expect a
genetic understanding of personality traits.
Nearly all
behaviors that have been studied show moderate to high heritability,
sometimes to a greater degree than many common physical diseases. And
on some domains -- for instance, neuroticism- stability and
introversion-extroversion -- there already is a degree of consensus
about the effect that genes exert. A striking finding is that the role
environment plays in such behavior is of the "nonshared"
type -- that is, environmental factors tend to make people different
from, rather than similar to, their relatives."
February 12, 2001
Q "I
injured my back, and they have me on Oxycontin. I feel like I am
getting hooked on it. What is the current thinking about this
drug?"
A
"The official name is OxyContin (oxycodone HCL), but on the
street it's known as "oxycotton."
When taken in pill form,
as intended, oxycodone HCL is a slow-release narcotic prescribed for
pain caused by cancer, severe arthritis, sickle cell disease, and
nerve damage. The active ingredient in the drug is a morphine
derivative, the same as that also found in oxycodone (Percodan).
But when bought on the
street, oxycotton is crushed and snorted to deliver a powerful and
fast high that many users say is better than heroin.
Purdue Pharma, maker of
OxyContin, has known for about a year that the medicine is being
abused.
The drug's growing bad
reputation is a cause of concern and even fear to those who take it
for medicinal reasons.
Some pharmacies will not
stock the drug for fear the stores will be broken into. And some
physicians are reluctant to write prescriptions for it because they
worry that they will become the target of investigations by law
enforcement agencies.
This drug makes it
possible for chronic pain patients to live their lives normally. It
makes a profound difference in the quality of their lives.
Many report increased
tolerance (and therefore use) of the drug. Others report severe
withdrawal symptoms when discontinuing, and unlike heroin or cocaine,
OxyContin has appeared rapidly in rural areas leading to sweeping
arrests in Virginia and Kentucky."
February 5, 2001
Q
"I sleep very poorly and read that this is actually an epidemic
in America?"
A
"In a recent
article, it was written (Impact on Individuals and Society) `Insomnia
exacts a considerable toll on US society. It is estimated that the
total direct cost of insomnia in 1995 was $13.9 billion. This includes
the cost for prescription and nonprescription medications, visits to
healthcare providers, and nursing home care to treat insomnia
specifically. In addition to direct costs, insomnia is associated with
indirect costs that result from decreased economic output because of
morbidity and mortality related to insomnia. For instance, current
insomnia is associated with significantly greater functional
impairment, impaired memory and concentration, decreased ability to
accomplish daily tasks, and diminished capacity to solve problems.
Insomnia has also been linked to greater work absenteeism, greater
general medical service use, and poorer overall health, and increased
health concerns. Insomnia is also associated with a higher risk for
emotional difficulties, decreased enjoyment of interpersonal
relationships, and decreased perceived mood as well as wellness. It is
also associated with increased risk of motor vehicle accidents. An
important, yet largely unanswered, question is the degree to which
insomnia is linked etiologically to these impairments in daytime
functioning and the degree to which these abnormalities could be
reversed following the effective management of insomnia. Data from
some investigators showing cognitive impairment in "pure
insomniacs" support a causal hypothesis, yet more work needs to
be done in this regard."
January 29, 2001
Q
My sister's teenage daughter is depressed. We wonder if she inherited
this from her mother or whether just being around my sister was
sufficient for her to become depressed?"
A
"Depression in adolescents
runs in families, according to a large, population-based longitudinal
study reported in January's Archives of General Psychiatry.
This family study of a
large community sample from the Oregon Adolescent Depression Project
in Portland assessed 1,709 adolescents from nine high schools between
1987 and 1989. Additional assessments were performed 1 year later in
1,507 adolescents, and then 7 years later in 940 of the original
subjects.
Adolescents with Major
Depressive Disorder (MDD) were 72% female and had mean age at onset of
14.9 years. Twenty-six percent had a history of recurrent major
depressive episodes, with mean duration of the longest episode 6
months.
Relatives of adolescents
with MDD had elevated rates of MDD, with hazard ratio (HR) 1.77. Rates
also were elevated for dysthymia (HR 1.79), and alcohol abuse or
dependence (HR 1.29), but not anxiety disorders, drug abuse or
dependence, or antisocial and borderline personality disorder.
The increased rate of
alcoholism in relatives of adolescents with MDD appeared to be due to
comorbidity of alcohol abuse or dependence with MDD.
While relatives of
probands with anxiety, substance use disorders and disruptive behavior
disorders did not have an elevated rate of MDD, anxiety and substance
use disorders did tend to aggregate in these families.
Whether familial
aggregation represents genetic or environmental influences is still
unclear.
During childhood, shared
environmental factors such as parenting styles and family milieu may
influence psychological status. In the relatives of female
probands in the Oregon study, the rate of MDD was significantly higher
in females than in males, but in the relatives of male probands, the
rates of MDD were similar for males and females. This may suggest
different etiological factors for MDD in males and females, or
cultural transmission, with same-sex relatives having a greater impact
than opposite-sex relatives through identification or modeling.
As adolescence typically
may be associated with erratic moods, rebellious or even
self-destructive behaviors, and withdrawal from family activities, it
becomes important to distinguish "normal" adolescence from
MDD. The combination of irritability and social withdrawal is
particularly ominous ( September 2000 issue of the European Journal
of Child and Adolescent Psychiatry.)"
January 22, 2001
Q
"My sister-in-law goes
from one depressed period to the next. She is seldom not depressed. In
fact, it seems in the last several years, her depression only relents
for about a month or so, about twice a year. What is causing this, and
what are the risk/concern issues?"
A
"In
a recent discussion of this topic, it was stated: "The
lifetime risk of developing a depressive episode now approaches 15%
and the World Health Organization ranks depression as the world's
fourth greatest public health problem. This situation is growing even
more problematic, because the age of onset of a first-episode
depression is becoming progressively younger and, with early onset,
comes greater risks of recurrence and chronicity. Thus, the already
considerable public health burden of recurrent depression will most
certainly increase in the future.
Between 50% and 70% of those who have
experienced one episode of major depression will experience another at
some later point, which represents a 5- to 10-fold elevation of risk
when compared with the general population. For bipolar depression, in
which recurrence rates of 90% are expected without effective
preventive treatment, the increase in risk of recurrence is 14- to
18-fold when compared with that in the general population. Chronic
minor depressive disorders (ie, dysthymia) are similarly associated
with a marked increase in the risk of subsequent major depressive
episodes.
Episodes of recurrent depression may
lead to adverse economic, interpersonal, and medical consequences. For
example, the impact of depression on a family can be detected not only
during the depressive episode, but also years after symptomatic
remission. Impairment of vocational functioning may similarly persist
despite response to treatment. Complications such as alcoholism or
substance abuse also may develop during an untreated depressive
episode. In addition, depression complicates the course of chronic
general medical illnesses such as diabetes and atherosclerotic heart
disease.
Most initial depressive episodes are
temporarily related to stress, which highlights the role of
stress-diathesis vulnerability interactions, suggesting that certain
critical factors impinge on a person's life, which may in turn become
a catalyst for the development of an illness in those who are
genetically predisposed. Women have about 1.7 times the lifetime risk
of developing a major depressive episode. Other relevant risk factors
include a family history of affective disorder or alcoholism, a
pattern of cognitive distortions, personality disorders, chronic
medical problems, and a history of early trauma or abuse.
The relationship between stress and the
onset of depressive episodes appears to become less pronounced in more
highly recurrent episodes, and new episodes often begin to appear
"out-of-the-blue." Some researchers have suggested that the
apparent tendency for recurrent depressive episodes to become
autonomous results from changes in brain stress-response mechanisms.
People with recurrent depression, for example, have a greater
likelihood of hypothalamic-pituitary- adrenocortical dysregulation and
more pronounced alterations of sleep neurophysiology. Other recurrent
disorders have a seasonal pattern, with fall and winter more commonly
associated with depressive episodes. Although the precise mechanism of
seasonal vulnerability has not been elucidated, these recurrent
depressions are thought to be triggered by changes in the length of
the photoperiod."
January 15, 2001
Q
"Is my depression due to
my having inherited it or because of all the bad things that happened
when I was younger?"
A
In a recent article,
it was written that: "Our concept of the etiology of depression
has changed from very simplistic models to complex ones. It is
becoming increasingly evident that depression is a heterogeneous,
systemic illness, involving an array of different neurotransmitters,
neurohormones, and neuronal pathways. The notion that depression is
the result of a simple hereditary process or traumatic life event that
ultimately leads to a single neurotransmitter deficiency is simply
unsubstantiated by the evidence.
It is now assumed that depression may result
from a complex interaction between genetic predisposition to the
illness and early untoward life events such as child abuse or neglect.
Such interactions undoubtedly induce significant changes in the CNS.
Specifically, these interactions result in hyperactive CRF and NE
systems, which are the main moderators of the stress response. The CRF
and NE systems exert wide influences on multiple regions of the CNS,
as well as the periphery, via the HPA axis and the autonomic nervous
system. These neurobiological perturbations may persist into
adulthood, leading to a hypersensitive stress response system, which
overreacts to all forms of stress in adults, including mild stress or
daily life events. It is hypothesized that this hypersensitive stress
response system underlies, in part, the neurobiological vulnerability
to depression and anxiety. After exposure to repetitive or chronic
stress, genetically vulnerable individuals likely develop mood and/or
anxiety disorders. The current limitations of this theory are that
many depressed patients apparently lack 1 of the above-mentioned risk
factors (ie, genetic predisposition or early trauma).
There are many neurobiological substrates for
depression that we have not reviewed. Research has provided evidence
about the potential role of substance P, a neuropeptide, in the
pathogenesis of depression. Moreover, there is some evidence
supporting a role of dopamine circuit dysfunction in depression.
Interestingly, nomifensine, a selective dopamine reuptake inhibitor,
was an effective antidepressant, but was removed from the market
because of an unacceptably high rate of hemolytic anemia in a small
number of patients. Also, several studies have documented that
increased cholinergic activity might be associated with depressed
mood; however, the role of acetylcholine in the development of
depression remains obscure. Because neurotransmitters ultimately
produce their effects via alterations in intracellular mechanisms,
such as second messengers and neurotropic elements (factors and gene
expression), these factors have received more attention in the last
decade.The new findings in the neurobiology of depression have led to
a better understanding of the action of antidepressants, which have
been found to return the alterations of the CRF system back to normal.
Also, there has been an active search for newer agents to target the
newly discovered neurotransmitters. Novel agents, such as CRF receptor
and NK-1 antagonists, are still experimental, but they hold promise
for a better antidepressant treatment, especially for refractory
patients, and they have a more tolerable side-effect profile compared
with that for the currently available agents.
The new discoveries regarding the
"stress-diathesis model" of depression have stimulated
renewed interest in the paramount role of child abuse and other early
untoward life events in the pathogenesis of depression. Because
multiple studies have shown the long-term deleterious effects of early
trauma on vulnerability to depression, and because child abuse is
tragically a common societal problem (at least 1 million cases
verified each year in the US), identification of and intervention for
such vulnerable individuals is an important goal."
January 8, 2001
Q
"I am having a terrible time with sleeplessness. I feel horrid. I
have signed up for a sleep center here in my city. Several of my
friends also have trouble with sleep. How common is our problem?"
A
Insomnia exacts a considerable toll
on US society. It is estimated that the total direct cost of insomnia
in 1995 was $13.9 billion. This includes the cost for prescription and
nonprescription medications, visits to healthcare providers, and
nursing home care to treat insomnia specifically. In addition to
direct costs, insomnia is associated with indirect costs that result
from decreased economic output because of morbidity and mortality
related to insomnia. For instance, current insomnia is associated with
significantly greater functional impairment, impaired memory and
concentration, decreased ability to accomplish daily tasks, and
diminished capacity to solve problems. Insomnia has also been linked
to greater work absenteeism, greater general medical service use, and
poorer overall health, and increased health concerns. Insomnia is also
associated with a higher risk for emotional difficulties, decreased
enjoyment of interpersonal relationships, and decreased perceived mood
as well as wellness. It is also associated with increased risk of
motor vehicle accidents. An important, yet largely unanswered,
question is the degree to which insomnia is linked etiologically to
these impairments in daytime functioning and the degree to which these
abnormalities could be reversed following the effective management of
insomnia. Data from some investigators showing cognitive impairment in
"pure insomniacs" support a causal hypothesis, yet more work
needs to be done in this regard.
January 1, 2001
Q
"I know that alcoholism
runs in families. My husband rarely drank alcohol when we dated, but
his daily increase of alcohol is increasing. He, of course, denies
this as a problem even after his second DUI and a job loss last year.
Is there any physical test for alcoholism?"
A The
Anglo-Scandinavian diagnostics company Axis-Shield has received US
Food and Drug Administration approval for a new test that detects
people at risk of alcohol-related disease, the company announced.
The carbohydrate-deficient transferrin
(CDT) test is already sold in Europe and will be marketed early next
year in the US by the Californian company BioRad.
Alcohol abuse is far bigger than drug
abuse. The marker is that it whether you are drinking more
alcohol than your body can take."
The test, which costs between 3 and 4
British pounds sterling, would be used at first mainly to monitor the
health and compliance of patients in alcohol treatment centers but
might later be used to check airline pilots or by consumers generally.
The company said sustained heavy daily
intake of alcohol results in elevated levels of CDT, which are
maintained for several weeks even when people stop drinking.
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