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QUESTIONS OF THE WEEK BETWEEN October, 2006 and DECEMBER, 2006 

December 26, 2006

Q What is the best way to get a teenager to quit smoking before he does further damage to his health?

A "The US Centers for Disease Control and Prevention (CDC) has reported in teens and young adults more likely to use unassisted methods for smoking cessation

Young smokers aged 16 to 24 years are more likely to use unassisted cessation methods rather than those recommended by the Public Health Service.

Recommended smoking cessation strategies for adults include talking with a healthcare professional, use of nicotine-replacement products, bupropion therapy, counseling, participating in a program or class, and calling a telephone helpline.

Study results showed that whereas 6 of 11 unassisted methods were each used by at least 36% of respondents, only 1 (talking with a nurse, physician, or dentist) of 13 assisted methods was used by at least 20% of young adults in this age group.

Most (88.3%) relied on decreasing the number of cigarettes they smoked, while 56% tried not buying cigarettes, 51.0% exercised more, 47.5% tried to quit with a friend, 44.5% told others they no longer smoked, and 36.1% switched to light cigarettes.

Women were more likely than men to seek help from health professionals (24.9% vs 15.6%), to quit with a friend (52.1% vs 43.2%), and to use self-help pamphlets or videos (19.5% vs 12.5%). Men were more likely to try nicotine gum (20.3% vs 14.4%), use a strategy of increased exercise (55.7% vs 46.0%), and switch to chewing tobacco, snuff, or other products (18.1% vs 1.6%).

The CDC notes that the high proportion of respondents who tried to quit smoking by switching to light cigarettes (36.1% overall) or other tobacco products (18.0% among men) is a concern due to the associated risk for undermining cessation efforts.

Preliminary evidence suggests that clinical interventions that incorporate cognitive-behavioral approaches are the most promising, particularly in smokers younger than 18 years for whom pharmacotherapy (eg, nicotine-replacement products or bupropion) is not approved by the US Food and Drug Administration."

December 18, 2006

Q Did I not read that people who get depressed after a heart attack are making sure that they have another?

A "Patients with incident depression after a myocardial infarction (MI) have an increased risk of another cardiovascular event compared with post-MI patients who are not depressed.

About one half of post-MI depression episodes represent incident depression, whereas the other half consist of ongoing or recurrent depression.

The researchers examined whether incident and non-incident depression after MI result in different cardiovascular prognoses. They evaluated 468 patients for depression during the year after the index MI. The International Classification of Diseases-10 diagnostic criteria were used to define depression. The patients were followed up for a mean of 2.5 years.

One hundred nineteen patients experienced depression in the year after their MI. Fifty-three (44.5%) were incident depressions and 66 (55.4%) non-incident depressions.

One hundred nine patients (23.3%) experienced a fatal (n = 10) or non-fatal (n = 99) cardiovascular event during follow-up. A cardiovascular event occurred in 21.5% of non-depressed controls, 33.3% with incident depression and 22.6% with non-incident depression.

Patients with incident depression were 65% more likely than non-depressed patients to have a cardiovascular event (p = 0.04). The risk among patients with non-incident depression was increased by 12% compared with the non-depressed controls, a nonsignificant difference. Controlling for confounders did not significantly alter the data.

Findings stress the need for treatment strategies for post-MI depression, which may be closer to cardiac rehabilitation and more focused on the consequences of the MI than a purely depression-oriented approach.

The findings of this study may explain the relatively high effectiveness of psychoeducational interventions, including stress management and relaxation, to prevent cardiac events in coronary artery disease patients. The development of new treatment strategies to treat post-MI depression may also prevent additional cardiovascular events.

J Am Coll Cardiol 2006;48:2204-2208.
 

December 11, 2006

Q Can't you take high blood pressure medication for PTSD?

A The antihypertensive agent guanfacine, which lowers brain norepinephrine activity, does not reduce the symptoms of posttraumatic stress disorder (PTSD). There is evidence from a variety of studies that norepinephrine is over-activated in PTSD. Because of this, experts in the field have recommended guanfacine and clonidine (both alpha 2 adrenergic receptor agonists) as possibly effective in PTSD. However, prior to our study, there were no data from randomized controlled trials.

Guanfacine relative to placebo did not result in greater improvement in PTSD symptoms, depression, general psychological distress, sleep quality or quality of life. The effect size of zero suggests no promise for demonstrating efficacy even with larger samples. Moreover, guanfacine was associated with a number of side effects, including somnolence, lightheadedness and dry mouth.

For chronic PTSD, the key message is to avoid guanfacine and be wary of using a similar drug clonidine -- at least until there are results from randomized controlled studies.

Another antihypertensive medication, prazosin, which has a different mechanism of action than guanfacine and clonidine, has shown promise for the treatment of chronic PTSD in randomized controlled trials.

The important distinction between guanfacine and prazosin is that the latter drug does not lower brain norepinephrine release. Rather, it blocks the effect of norepinephrine on one particular receptor (alpha 1) on the post-synaptic side of the synapse, which may be implicated in anxious arousal." Am J Psychiatry 2006.

December 4, 2006

Q Does my son have to be on Stattera for his ADHD. Are there any non-drug approaches?

A "Children with attention deficit/hyperactivity disorder (ADHD) can be trained through biofeedback, based on electroencephalographic (EEG) parameters, to regulate their brain waves. This learned control is associated with durable improvements in behavior, attention and IQ scores.

Neurofeedback is used to modify activity of the brain, specifically of slow cortical potentials for patients with ADHD. Slow cortical potentials are slow event-related direct-current shifts of the EEG, originating from the upper cortical layer. These shifts "occur as a consequence of external or internal events."

Although previous studies have shown the improved self-regulatory capacities in this patient population, no reports included EEG data during learning and follow-up.

The training was introduced as a computer game. The subjects faced a computer that provided visual feedback in the form of movement of a ball, in which the position of the ball reflected amplitude of brain waves. Auditory feedback was also given and the children received small gifts at the end of a session based on the number of accurate responses.

While viewing a ball on the screen, they were told "to be attentive to the feedback and to find the most successful mental strategy to move the ball into the required goal."

The subjects completed 30 one-hour sessions divided into three phases. Each phase lasted for 2 weeks and the training sessions were held 5 days per week. After each phase was completed, the subjects took a 6 to 8-week break. During the last phase, the children worked on their homework while they applied the self-regulation strategy they had learned.

At the end of the training and at a 6-month follow-up, EEGs indicated that the children had learned to regulate negative slow cortical potentials. Two of the subjects at the end of training and three at follow-up no longer fulfilled the diagnostic criteria for ADHD.

Performance IQ scores on Wechsler Intelligence Scale for Children, and measures of attention improved significantly from screening to follow-up.

With voluntary regulation of slow control potentials, children may learn to flexibly adjust their cholinergic-dopaminergic balance to task requirements. They believe that the acquired skill becomes automatic over time."

Pediatrics 2006;118:e1530-e1540.
 

November 27, 2006

Q "My son was born with low birthrate.  I have read horror stories about the future of such children. Can you point me a direction to start some research?"

A  Please take time to look up this article: "Very preterm or very low birth weight children are more likely to have behavioral and emotional problems when they start school. Children born very preterm (VP; less than 32 weeks' gestation) or with very low birth weight (VLBW, less than 1500 g) are at risk for behavioral and emotional problems during school age and adolescence. At school entrance these problems may hamper academic functioning, but evidence on their occurrence at this age in VP/VLBW children is lacking."

Researchers compared the prevalence of behavioral and emotional problems at age 5 years between VP/VLBW children and children of the same age in the general population. In addition, they examined the association between these behavioral and emotional problems and other developmental problems assessed by pediatricians.

Overall, 13.2% of VP/VLBW children scored in the clinical range of CBCL total problems, compared to 8.7% of children in the general population (odds ratio 1.60). The largest mean differences were observed for social and attention problems. Children with pediatrician-diagnosed developmental problems at 5 years had larger differences, as did children with severe perinatal problems."

Arch Dis Child Fetal Neonatal Ed 2006;91:F423-F428.

November 20, 2006

Q "We have been trying to get pregnant.  No luck so far.  This is very depressing.  Could depression make me infertile?."

"Middle-aged men with depression have reduced levels of bioavailable testosterone as well as circulating total testosterone compared with their counterparts without depression. There has been an interest for many years in regards to the question of reproductive hormones in relationship to depression. There is a logic to this in that the loss of libido is thought to be associated with low testosterone, but there hasn't been much robust research done in the area. Depressed subjects were untreated at the time of enrollment, but they underwent a washout period in the event they had received an antidepressant drug during the index period or for a previous episode of illness. Low testosterone is associated with depression, even when you control for the effects of age. It supports a trend that was generally uninformed by research, that there may be some merit in adding a testosterone supplement in the treatment of depression, particularly if men report low libido. The results show a link between decreased hormonal levels and depression, but it is too premature to support hormonal therapy in the way of a testosterone supplement for depressed men. This does not mean patients should be on testosterone. The next step in research would look at whether treating men with testosterone makes them less depressed. This study did not address that. The finding of reduced bioavailable testosterone does not establish if the decreased expression of testosterone caused depression or was a consequence of the depression, noting depression can cause changes in how hormones are processed in the body. The depression itself may be lowering the bioavailable testosterone, rather than the other way around."

November 13, 2006

Q "Have you heard anything about antidepressants being risky during pregnancy?."

A  “The use of selective serotonin reuptake inhibitors (SSRIs) early in pregnancy seems to moderately raise the risk of congenital malformations in offspring. It's unclear whether the effects were causal or due to factors related to the underlying disease for which SSRIs were prescribed. However, the finding that the association between SSRI use and risk of congenital malformations was stronger during the second or third month of pregnancy is consistent with a causal effect. There was no evidence that the association was specific to particular malformations. Epidemiol 2006;17:701-70.” 

November 6, 2006

Q "I would think that being nervous would be hard on asthmatics."

A "Depressive disorders and anxiety disorders are both associated with worse asthma-related quality of life, but only depressive disorders are associated with worse asthma control.

Having either a depressive (e.g., major depression) or anxiety (e.g., panic disorder) disorder was associated with worse asthma-related quality of life, but only depressive disorders were associated with worse asthma control levels.

These findings were observed independent of age, sex, and asthma severity, which is significant because this means that the worse asthma control and quality of life observed in patients with comorbid depressive and anxiety disorders were not simply due to greater asthma severity in the psychiatric patients.

If depressed patients with asthma are at greater risk for worse asthma control (independently of asthma severity), they could be targeted for more intensive asthma care interventions as well as for psychotherapeutic or behavioral interventions to improve their depressive status.

There are several symptoms of depressive disorders -- e.g., fatigue, lack of energy, and decreased interest in daily activities that may include self-management of chronic asthma -- that may make them less likely to adhere to daily medication regimens ... which we know has a huge impact on control. As such, detecting and treating comorbid psychiatric disorders may have implications for both mental and physical (asthma) health."

Chest 2006;130:1039-1047.

October 30, 2006

Q "You can get sick from anxiety, right?"

A "Patients with physical maladies are at increased risk of having an anxiety disorder as well. Furthermore, the severity of the physical illness and resulting loss of function are exacerbated among patients with comorbid anxiety.

Analyses showed that the presence of an anxiety disorder -- panic disorder, phobia, generalized anxiety disorder, agoraphobia, social phobia, or obsessive-compulsive disorder -- was independently associated with diseases of the respiratory and the gastrointestinal tracts, arthritis, allergies, thyroid disease, migraine, and any past-month physical condition.

The onset of anxiety disorders was more likely to have preceded onset of comorbid physical conditions, and that quality of life and physical functioning were worse when comorbid anxiety disorders existed.

Anxiety disorders and physical illness can turn into a vicious circle. Painful conditions like migraine and arthritis could increase a patient's anxiety about the pain. Or panic attacks may be mistaken for asthma attacks.

Anxiety causes individuals to avoid situations that could precipitate symptoms, leading them to restrict physical pursuits or avoid social activities. Obesity or substance abuse may develop as a result, thereby raising the risk of other painful conditions and physical diseases.

Arch Intern Med 2006;166:2109-2116.
 

October 23, 2006

Q "Aside from damage to your body and making you steal from the family, are there other things that cocaine does to a person?."

A In a recent presentation, it was reported that "A number of studies show that cocaine use negatively affects neuronal functioning of the brain, primarily in the prefrontal cortex but also in a number of other areas in the brain.

The result is a reduced ability to weigh benefits versus drawbacks, and to control behavior.

During fMRI, subjects were asked to identify various amounts of money and rank them in order of value, or "reward."

More than half of the addicts could not differentiate between values. FMRI showed a "disconnect," or a "conflict pattern in response to monetary rewards. There was a decreased response overall...in the prefrontal cortex.

The prefrontal cortex is the region in which impulse control occurs. An inability to distinguish between different values of money "means that this reward system can not be used to change behavior" in cocaine addiction.

Although there is some improvement in function (in the prefrontal cortex) once the drug is removed, it never completely returns to normal."

October 16, 2006

Q "Do many people commit suicide when diagnosed with breast cancer?."

A Importantly, a significant number of people who survive breast cancer later commit suicide. "Breast cancer survivors are 37% more likely to commit suicide than other women, and the elevated risk persists for at least 25 years after diagnosis. Previous studies have looked at suicide risk in breast cancer survivors, but most have not examined the long-term risk.

In an analysis of data for 723,810 breast cancer survivors who were diagnosed between 1953 and 2001. During follow-up through 2002, 836 subjects committed suicide. The standardized mortality ratio was 1.35 for the breast cancer survivors compared with the general population. The excess absolute risk was 4.1 per 100,000 person-years.

After 25 or more years, breast cancer survivors still had a 35% increased risk of suicide. Black cancer survivors were most likely to commit suicide, with a 2.88-fold elevated risk. The risk of suicide rose as cancer stage increased.

At 30 years after breast cancer diagnosis, the cumulative probability of suicide was 0.20%.

Although the cumulative probability of suicide is small, our results suggest that long-term follow-up programs for breast cancer survivors should include resources devoted to psychosocial concerns."

J Natl Cancer Inst 2006;98:1416-1419.

October 9, 2006

Q "Our dad had a stroke and is very slow to mobilize. The doctors say that he should be recovering faster.  Any thoughts?."

A Yes, consider the possibility that he is depressed: "Despite a high rate of depression, which can have a significant impact on stroke survivors' mortality, the majority of clinically depressed stroke patients do not receive antidepressant medication. Researchers found that at 5 years after stroke, almost 20% of survivors suffered from depression, yet only 22% were treated for the condition. Stroke patients suffering from depression have been found to have reduced quality of life and a higher rate of death, so it is important to identify and treat depression after stroke. The low treatment levels found may indicate that physicians are unwilling to prescribe treatments that have not been demonstrated to be an effective and safe treatment for depression among stroke patients. Another factor may be that depression among stroke patients is not being diagnosed. Interestingly, a high proportion of patients (72%) taking an antidepressant were not depressed. This could indicate efficacy of antidepressant therapy or may be because the medications were prescribed for an indication other than depression, such as pain." Stroke. 2006.

 

October 2, 2006

Q "Our family doctor told us that our son's social pressures do not influence his asthmatic attacks ."

 Perhaps you misunderstood what he said, but "Young people with asthma who also have an anxiety or depressive disorder have a significantly increased asthma symptom burden. After controlling for variables including asthma severity, adolescents with anxiety or depressive disorders had significantly more days of asthma symptoms over the previous 2 weeks than those with no anxiety or depressive disorders.

A significant association was observed between the overall number of reported asthma symptoms and the number of anxiety and depressive symptoms reported by the subjects (p < 0.001).

A diagnosis of an anxiety or depressive disorder was "strongly associated" with both asthma-specific symptoms and nonspecific somatic symptoms."

Pediatrics 2006;118:1042-1051.



Past Questions of the Week are available through the educational resources of the  website. If you would like to submit your own question for consideration as a public Question of the Week, please contact the practice.

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©2006 David B. Adams, Ph.D.