New ADHD Guidelines Include Broader Age Range

Fran Lowry

October 17, 2011 (Boston, Massachusetts) — For the first time in a decade, the American Academy of Pediatrics has issued an updated set of guidelines for the diagnosis and treatment of attention-deficit/hyperactivity disorder (ADHD) that now include younger, preschool children and adolescents.

The guidelines, "ADHD: Clinical Practice Guidelines for the Diagnosis, Evaluation and Treatment of Children and Adolescents with Attention-Deficit/Hyperactivity Disorder," were released here at the American Academy of Pediatrics National Conference & Exhibition and simultaneously published online October 16 in Pediatrics.


Dr. Mark Wolraich
"We wrote the original guidelines in 2000 to 2001, and they were written for children between the ages of 6 and 12 because that's where most of the available evidence was at the time," Mark Wolraich, MD, CMRI/Shaun Walters professor of pediatrics and chief of the Section of Developmental and Behavioral Pediatrics at the University of Oklahoma Health Sciences Center, Oklahoma City, told Medscape Medical News.

"Over the years, we have heard about the concern for preschool children and adolescents and what should be done with them. We've expanded the age group to include children aged 4 to 18 because there's certainly new evidence to support recommendations for the broader age group," said Dr. Wolraich, lead author of the guidelines.

Increase in Approved Medications

The last 10 years have also seen an increase in the number of medications that have been approved by the US Food and Drug Administration for the treatment of ADHD, and the new guidelines reflect this. They also emphasize the chronic nature of the disorder

"We had pushed for the idea that ADHD was a chronic illness in the initial guidelines, and that clinicians needed to use chronic illness principles in treating it, and this has been further emphasized," Dr. Wolraich said.

Other key recommendations include:

assessing children for other conditions that might coexist with ADHD, such as oppositional defiant and conduct disorders, anxiety, and depression;
making sure that Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, criteria have been met;
obtaining information primarily from reports from parents or guardians, teachers, and other school and mental health clinicians involved in the child's care;
first line of treatment for preschool-aged children 4 to 5 years old should be evidence-based parent- or teacher-administered behavior therapy;
titrating medication doses to achieve the maximum benefit with the least adverse effects; and
for adolescents, the primary care clinician should prescribe FDA-approved ADHD medications with their consent.
"The challenge in adolescents is you no longer have individual teachers as good reporters of their behavior, because they are going from class to class, and no one has them for a long period of time. It tends to be hard to get good information," Dr. Wolraich said.

He added that it is important to start treating children at a young age.

"When we can identify them earlier and provide appropriate treatment, we can increase their chance of succeeding in school. With our greater awareness now about ADHD and better ways of diagnosing and treating this disorder, more children are being helped."

Clinical Judgment Not Enough

Peter Jensen, MD, codirector of the Division of Child Psychiatry and Psychology at the Mayo Clinic, Rochester, Minnesota, told Medscape Medical News that the updated guidelines give more detailed instructions to help primary care physicians manage these patients.


Dr. Peter Jensen
"What's wonderful about the updated guidelines is they provide additional guidance and specificity over the guidelines that were published back in 2000 to 2001," Dr. Jensen said.

"Some of these kids have very complex problems; many also have anxiety and depression. The guidelines take note of this, and they also emphasize the use of rating scales from teachers and parents. They take us a step further," he added.

Providing more detailed guidance on the diagnosis and treatment of children with ADHD is important, he said.

"Many doctors treat ADHD by the seat of their pants," he said. "They are well intentioned, but when we are in the midst of a busy office day and frantic parents, and understaffed, our clinical judgment isn't enough, and we are prone to miss things. If the mom smiles we think all is well. But that is not as accurate as looking at the rating scale from the parents, from the teacher, and talking with Johnnie.

"Clinical judgment is not enough to replace these kinds of tools, and the guidelines add more of that kind of detail and will be more likely to help us keep from making errors of omission and commission."

Dr. Jensen said he suspected that ADHD may be increasing because so many demands for sustained attention are being placed on today's children.

"We expect our kids to learn more, do more, we expect them not just to go to college but to have 3 or 4 hobbies and activities they do in the afternoon and quickly get that homework done, and then we expose them to many different stimuli.

"They have the TV going, and the Game Boy going. All those things are competitors for attention. If you had a society where homework was not important, almost by definition you'd have fewer parents complaining about their child's inattention," said Dr. Jensen.

Dr. Wolraich disclosed that he is a past consultant to Shire, Lilly, Shinogi and Nextwave all of which produce medications for ADHD. Dr. Jensen has disclosed no relevant financial relationships.

American Academy of Pediatrics National Conference & Exhibition 2011. Presented October 16, 2011.

Pediatrics. Published online October 16, 2011

|| Link to PDF File || From Medscape

Vaccines for Addiction Gaining Momentum

Ron Zimmerman

October 17, 2011 — Up to now, vaccines have been used effectively against a variety of infectious diseases, but what if they could be developed to treat and/or prevent addiction?

Take smoking, for example. Someone who wanted to quit would go through their usual lighting up routine, but when nicotine does not arrive in the brain, they would probably extinguish the cigarette and not light another. Without feeling nicotine's effects, it is likely they would view smoking as a waste of money.

Or consider a vaccine against methamphetamine: Snorted or injected, the drug would not give the user a high, so what would be the point of going to the trouble of scoring this illegal drug in the first place?

Now both vaccines, for nicotine and for methamphetamine, have gone beyond the dreaming stage. Recently, the National Institute on Drug Abuse (NIDA) awarded "visionary" grants to 2 scientists who believe that in the not-too-distant future, vaccines will be available not just for smallpox and whooping cough but also for substance abuse.

Two scientists proposing to develop vaccines against methamphetamine and nicotine have been selected to receive NIDA's second Avant-Garde Awards for Innovative Medication Development Research.

The scientists, Thomas Kosten, MD, from Baylor College of Medicine, Houston, Texas, and Peter Burkhard, PhD, from the University of Connecticut, Storrs, will each receive $500,000 per year for 5 years from NIDA to support their research.

Addiction vaccines could be life-changing for the estimated 22 million drug abusers in the United States. NIDA estimates that every year, addiction costs the country $84 billion in direct healthcare costs, lost earnings, crime, and accidents. The cost trend is rising, and researchers hope that addiction vaccines may reverse it, not only by treating addicts but also by immunizing young people before they become addicted.

Just like regular vaccines, substance abuse vaccines work by provoking the immune system to produce antibodies, which then causes the body to suspend and reject the drug before it reaches the brain. That is the goal, but thus far, success in humans has been elusive.


Dr. Thomas Kosten
Dr. Kosten is working on a novel human methamphetamine vaccine, and since at this time there is no US Food and Drug Administration (FDA)–approved medication for methamphetamine addiction, his research could have substantial effect.

Dr. Burkhard's peptide nanoparticle antinicotine vaccine would be administered intranasally, which would be easier and less painful than an injection. He believes his de novo peptide design, coupled with nicotine, will induce a strong immune response against nicotine without the need for other chemicals to enhance it, leading to fewer adverse effects and a less expensive vaccine.

Addiction Interrupted

Both vaccines are expected to enter initial clinical trials within 5 years. They both work essentially in the same way: They induce a patient's immune system to generate antibodies that then bind to the target drug, forming compound molecules that are too large to move from the bloodstream to the brain.

Once the drug is denied access to the patient's brain, it cannot produce the reinforcement or "high" that is the major component of the motivation to continue using it. In short, the familiar addiction cycle — drug use, resultant brain stimulation, and then a subsequent desire for continued drug use — is interrupted.
Once the drug is denied access to the patient's brain, it cannot produce the reinforcement or "high" that is the major component of the motivation to continue using it. In short, the familiar addiction cycle — drug use, resultant brain stimulation, and then a subsequent desire for continued drug use — is interrupted.

The science behind vaccines for addiction goes back to the 1950s, when researchers developed a vaccine against fatal overdoses of the heart drug digitalis.

Then, in the 1970s, at the University of Chicago, researchers working with monkey models were successful in creating antibodies to heroin in their subjects by attaching molecules of heroin to a protein from cow's blood. This is the model on which Dr. Kosten has based his research.

Another major precedent for these 2 new addiction vaccines is the work of California researcher Kim D. Janda, PhD, from Scripps Research Institute in La Jolla, who made headlines in July when his team announced it had produced a vaccine against heroin's effects in rats. His laboratory's rodents stopped helping themselves to the drug after they received a vaccine, and it is thought they did so because the heroin stopped having any effect.

However, that success followed a serious setback in Dr. Janda's work on another vaccine: A phase 2 clinical trial for a nicotine vaccine based on his work had disappointing results. Patients receiving the vaccine only quit smoking at the same rate as those receiving placebo, so the trial was halted.

To date, none of Dr. Janda's vaccines has received FDA approval, and despite successes in animal models in his laboratory, they have not yet produced consistent results in humans.

As Dr. Janda recently told the New York Times: "The big problem plaguing these vaccines right now is difficulty predicting in humans how well it's going to work."

That difficulty was revealed in widely anticipated cocaine vaccine studies, in which a bacterial protein plus a molecule that is a cocaine look-alike trained the immune system to produce antibodies that bind to any cocaine in the bloodstream.

"Like Wiping Out Switzerland"

In a 2010 vaccine study at Columbia University, New York City, conducted by Margaret Haney, PhD, with crack cocaine addicts, the level of antibodies in the volunteers varied widely. Only 38% of the cocaine users produced enough antibodies to quell the drug's effects, and of those, only half stayed off the drug more than half the time.

In a 2008 analysis of 34 behavioral studies in cocaine, methamphetamine, and marijuana addictions, improvement was seen in 67% of the addicts. "You can't expect a medication or vaccine alone to take care of addiction," said Dr. Haney."I am entirely humble about that."


Dr. Nora Volkow
NIDA Director Nora D. Volkow, MD, said Dr. Kosten and Dr. Burkhard were awarded the grants because they have already demonstrated proficiency in the laboratory with vaccines.

"They also have clear plans for initiating clinical trials within an accelerated period of time," said Dr Volkow. And that's the goal of NIDA's Avant-Garde Grant Program: "[T]o support investigators of exceptional creativity who propose bold and highly innovative new research approaches that have the potential to produce a major impact on the treatment of drug abuse."

Seven million people die from smoking addiction every year. That's like wiping out Switzerland. It's a tremendous step forward to have a vaccine to prevent smoking, not only for these 7 million who die but also for the other countless millions who are living with their smoking addiction.
"Seven million people die from smoking addiction every year," Dr. Burkhard told Medscape Medical News, "that's like wiping out Switzerland. It's a tremendous step forward to have a vaccine to prevent smoking, not only for these 7 million who die but also for the other countless millions who are living with their smoking addiction."

Nicotine presents a particular challenge in developing a vaccine against it, as on its own it is completely nonimmunogenic. "So you have to couple it to a carrier to induce an immune response," he added.


Dr. Peter Burkhard
Dr. Burkhard heads the Burkhard Protein Design Group at the University of Connecticut, which has developed proprietary methods to synthetically produce nanosize protein particles.

"Our greatest challenge is generating as strong an immune response as possible to induce the effect we're looking for," he said. "The idea has been around for awhile, and other companies have brought it into clinical trials, where they have shown that it works, but it only works if you have really high levels of antibodies. Most of the clinical trials have failed for this reason, because they were only able to induce antibodies in about 30% of the population. And that's simply not good enough."

Dr. Burkhard's 18-nm particles are produced in his group's laboratory after first being designed on a computer.

"We predict a peptide sequence that is then able to self-assemble into a particle with icosahedral symmetry," he said. "Then we go into the lab to synthesize this peptide by biotech procedures, expressing it in [Escherichia coli], purifying it, and then refolding it. With those nanoparticles, the next step is coupling the nicotine molecule to the nanoparticle."

No Guarantees

Under the NIDA grant timeline, Dr. Burkhard plans to spend the first year and a half developing an effective nanoparticle vaccine, "so that we can be sure that we do get enough antibodies."

It will then take a year to manufacture enough vaccine for his 2-year phase 1 clinical trial. "That's our expertise, developing these nanoparticles that have been shown to be very immunogenic, and we have some 'tricks of the trade' to really tweak the immune system to give us a very strong antibody response. There's no guarantee that it will work, but we have confidence that we can achieve that," said Dr. Burkhard.

In addition to his grant to develop a methamphetamine vaccine, Dr. Kosten already has a cocaine vaccine under development.

Known as TA-CD, for Therapy Addiction–Cocaine Addiction, this vaccine uses an inactivated cholera protein to bind to cocaine in the user's bloodstream. The approach is to prevent the addictive substance from ever reaching the brain, and thereby prevent the chemical cascade that results in a euphoric "high."

It is hoped that without that high, the user's addictive cycle will be broken. In fact, a blinded, placebo-controlled study of 114 participants conducted by Dr. Kosten and his wife, neuroscientist Therese Kosten, PhD, showed that individuals who received the vaccine were twice as likely to reduce their cocaine use by at least 50% compared with those who received placebo. The study is now under review, and the Kostens are seeking FDA approval for a larger, 300-person, multicenter trial.

What is the scientific principle behind the vaccine? Dr. Kosten explained that although most foreign substances in the body trigger an immune-system response, drugs like cocaine fail to do so because their molecules are too small. They slip across the blood–brain barrier precisely because the molecules are so tiny.

When cocaine is bound to a much larger protein...the immune system creates antibodies to both the larger protein and the drug that it carries. Then, the next time the user administers the drug, the body's immune defenses attach onto the cocaine and break it down with enzymes.
However, when cocaine is bound to a much larger protein, such as the inactivated cholera protein that has been widely tested and found to be without adverse effects, the immune system creates antibodies to both the larger protein and the drug it carries. Then, the next time the user administers the drug, the body's immune defenses attach onto the cocaine and break it down with enzymes.

"It's like a big sponge for cocaine," Dr. Kosten told Medscape Medical News. "The drug remains trapped in the blood until it's metabolized and made inactive by the liver and secreted in the kidneys."

Users can thwart the vaccine and their fortified immune system responses by taking more cocaine than their immune system can handle, so the user has to want to slow or stop their cocaine use for the vaccine to be effective in curbing their addiction. And that is why TA-CD is currently thought of as a therapeutic drug, not a preventative, said Dr. Kosten.

Made in China

Other researchers have run into a wall in trying to find a substance that will bind to materials such as tetrahydrocannabinol, or THC, in marijuana, so the body can see that substance.

Dr. Janda has tried to make vaccines against alcohol and marijuana use, but so far the effort has failed. He said that in the case of alcohol, its ethanol molecules have proven to be too small to attach a protein to them, and in the case of marijuana, its main ingredient, THC, hides too well for the immune system to react to it.

Using cholera bacterium as a vector was an essential part of Dr. Kosten's new cocaine vaccine, he said, because it allows the vaccine to avoid potential viral syndromes associated with other vaccines. In addition, most people in Western countries where cocaine abuse is most severe do not have natural immunity to cholera.

In Dr. Kosten's methamphetamine vaccine, he is using a Neisseria meningitis protein as a vector.

Dr. Volkow believes the field of drug abuse treatment is on the cusp of a large paradigm shift.

A successful vaccine will make it easier for addicted individuals to establish and maintain abstinence. It will reduce the chances that isolated lapses into drug taking escalate into protracted relapses. Ideally, a single dose will remain effective for months or longer.
"Vaccines have a unique role to play in a comprehensive strategy to help people overcome addictions. A successful vaccine will make it easier for addicted individuals to establish and maintain abstinence. It will reduce the chances that isolated lapses into drug taking escalate into protracted relapses. Ideally, a single dose will remain effective for months or longer," she said.

Although NIDA views vaccines as a potentially powerful tool to aid addicts from their illegal drugs, pharmaceutical companies are not lining up with research grants, say these researchers.

They believe the pharmaceutical companies do not see much money to be made in a shot that is given once every 6 months, and also perhaps because the companies are not anxious to associate their companies with drug addicts.

"Pharma does not see a profit in these vaccines, and only sees great risk in this population due to their lifestyle and [potential for] overdoses," said Dr. Kosten.

Dr. Kosten is taking his methamphetamine vaccine manufacturing and clinical trial to China, as his greatest challenge has been in finding a domestic manufacturer.

"We've had no success doing this in the United States, but we have had success in China. We will manufacture the vaccine in China and do clinical trials there after getting Chinese FDA approval about 3 years from now. A placebo-controlled study will compare vaccinated [groups] to placebo groups during a 6-month outpatient clinical trial. We'll have the vaccine in humans in 4 years and have a commercial product in 10 years," he said.

From : Medscape

Mental Health Day Celebration (Photos)

Dr. Alinea, Dr. Laguidao & Dr. Dalisay

with Interns

Dr. Amadeo Alinea, Jr.

Dr. Edessa P. Laguidao

Dr. Rodney Dalisay

Dr. Alinea & Dr. Laguidao with Psychiatry Interns

Dr. Felicitas A. Soriano, MD, FPPA

Head, Department of Psychiatry

Giving her Opening Message

Dr. Georgina Gozo-Oliver, MD, FPPA, FPSCAP

Child & Adolescent Psychiatrist

Lecturer : Teen Stress: When Coping Fails

Dr. Teresa Icasiano, MD, FPPA

Visiting Consultant, Department of Psychiatry

Lecturer: Stress in the Workplace

Nursing Staff

Department of Psychiatry

Poster-Making Contestants at Work

Poster-Making Contestants

Poster-Making Judges

1st Prize Winner Mark

explaining his work

Dr. Shamylle Quinto

Poster-Making Judge

Ms. Irmburgh Calleja

Poster-Making Judge

Mr. Romeo I. Ariola

Chairman of the Panel of Judges

Poster-Making Contest

3rd Prize Winner

2nd Prize Winner

2nd Prize Winner

1st Prize Winner

Department of Psychiatry Staff

with the Poster-Making Winners

Dr. Alinea & Dr. Cariaga

with 2nd Prize Winner and her parent

Contestant at Work

Intranasal Insulin Therapy for Alzheimer Disease and Amnestic Mild Cognitive Impairment: A Pilot Clinical Trial

Craft S, Baker LD, Montine TJ, et al
Arch Neurol. 2011;Sept 12. [Epub ahead of print]

Summary

The goal of this randomized, double-blind, placebo-controlled trial was to assess the effects of intranasal insulin administration on cognition, function, cerebral glucose metabolism, and cerebrospinal fluid (CSF) biomarkers in adults with amnestic mild cognitive impairment or Alzheimer disease (AD). At the clinical research unit of a Veterans Affairs medical center, 104 adults (64 with amnestic mild cognitive impairment and 40 with mild-moderate AD) were randomly assigned to receive placebo (n = 30), 20 IU of insulin (n = 36), or 40 IU of insulin (n = 38) for 4 months. A nasal drug delivery device was used to administer all study drugs.

The main study endpoints were delayed story recall score and the Dementia Severity Rating Scale score. Secondary measures were the Alzheimer Disease's Assessment Scale–cognitive subscale (ADAS-cog) score and the Alzheimer's Disease Cooperative Study–activities of daily living (ADCS-ADL) scale. Before and after treatment, 23 participants underwent lumbar puncture and 40 underwent positron emission tomography with fludeoxyglucose F-18 (FDG-PET).

Delayed memory was improved in the group receiving 20 IU of insulin (P < .05). Both insulin groups had preserved caregiver-rated functional ability (P < .01) and general cognition measured by the ADAS-cog score for younger participants and functional abilities measured by the ADCS-ADL scale for adults with AD (P < .05).

Among insulin-treated participants as a group, no changes were detected in CSF biomarkers. However, exploratory analyses revealed that changes in memory and function were associated with changes in the CSF amyloid beta-42 level and tau protein-to- amyloid beta-42 ratio.

Fludeoxyglucose F-18 uptake in the parietotemporal, frontal, precuneus, and cuneus regions decreased in participants receiving placebo, whereas insulin appeared to minimize progression of these deficits. No treatment-related severe adverse events occurred, and the safety profile and compliance were excellent.

Viewpoint

Study limitations of this small, single-site pilot study include younger age in the 40-IU dose insulin group than in the placebo group (although age was a covariate in all analyses), availability of CSF and FDG-PET data for only a subset of participants, and lack of verification of increased insulin levels in CSF directly after insulin administration. In addition, treatment duration was relatively short. Nonetheless, on the basis of these findings, longer trials of intranasal insulin treatment are warranted in patients with amnestic mild cognitive impairment or AD. Further mechanistic studies may help clarify the role of insulin in the pathogenesis of AD.

======================
ABSTRACT
======================

Arch Neurol. 2011 Sep 12. [Epub ahead of print]
Intranasal Insulin Therapy for Alzheimer Disease and Amnestic Mild Cognitive Impairment: A Pilot Clinical Trial.
Craft S, Baker LD, Montine TJ, Minoshima S, Watson GS, Claxton A, Arbuckle M, Callaghan M, Tsai E, Plymate SR, Green PS, Leverenz J, Cross D, Gerton B.
Source
Education, and Clinical Center (Drs Craft, Baker, Watson, Claxton, Callaghan, and Plymate and Mr Arbuckle) and Mental Illness Research, Education, and Clinical Center (Drs Leverenz and Gerton), Veterans Affairs Puget Sound Health Care System, and Departments of Psychiatry and Behavioral Sciences (Drs Craft, Baker, Watson, Claxton, and Leverenz), Pathology (Dr Montine), Radiology (Drs Minoshima and Cross), Medicine (Drs Tsai, Plymate, and Green), and Neurology (Drs Leverenz and Gerton), University of Washington School of Medicine, Seattle, Washington.
Abstract
OBJECTIVE:
To examine the effects of intranasal insulin administration on cognition, function, cerebral glucose metabolism, and cerebrospinal fluid biomarkers in adults with amnestic mild cognitive impairment or Alzheimer disease (AD).

DESIGN:
Randomized, double-blind, placebo-controlled trial.

SETTING:
Clinical research unit of a Veterans Affairs medical center.

PARTICIPANTS:
The intent-to-treat sample consisted of 104 adults with amnestic mild cognitive impairment (n = 64) or mild to moderate AD (n = 40). Intervention  Participants received placebo (n = 30), 20 IU of insulin (n = 36), or 40 IU of insulin (n = 38) for 4 months, administered with a nasal drug delivery device (Kurve Technology, Bothell, Washington).

MAIN OUTCOME MEASURES:
Primary measures consisted of delayed story recall score and the Dementia Severity Rating Scale score, and secondary measures included the Alzheimer Disease's Assessment Scale-cognitive subscale (ADAS-cog) score and the Alzheimer's Disease Cooperative Study-activities of daily living (ADCS-ADL) scale. A subset of participants underwent lumbar puncture (n = 23) and positron emission tomography with fludeoxyglucose F 18 (n = 40) before and after treatment.

RESULTS:
Outcome measures were analyzed using repeated-measures analysis of covariance. Treatment with 20 IU of insulin improved delayed memory (P < .05), and both doses of insulin (20 and 40 IU) preserved caregiver-rated functional ability (P < .01). Both insulin doses also preserved general cognition as assessed by the ADAS-cog score for younger participants and functional abilities as assessed by the ADCS-ADL scale for adults with AD (P < .05). Cerebrospinal fluid biomarkers did not change for insulin-treated participants as a group, but, in exploratory analyses, changes in memory and function were associated with changes in the Aβ42 level and in the tau protein-to-Aβ42 ratio in cerebrospinal fluid. Placebo-assigned participants showed decreased fludeoxyglucose F 18 uptake in the parietotemporal, frontal, precuneus, and cuneus regions and insulin-minimized progression. No treatment-related severe adverse events occurred.

CONCLUSIONS:
These results support longer trials of intranasal insulin therapy for patients with amnestic mild cognitive impairment and patients with AD. Trial Registration  clinicaltrials.gov Identifier: NCT00438568.

PMID: 21911655 [PubMed - as supplied by publisher]

From : Medscape

October Events

6 October
BVH Lecture
"Introduction to Interventional Radiology"
Dr. M. Tamaña
VMMC

11 October : 1800H
PPA 8th Monthly Scientific Meeting
"Basics of Substnace Abuse"
Dr. Katrina Enriquez-Lising / Dr. Monica Cardinez-Tan
The Medical City

12 October
VMMC Celebrates World Mental Health Day
Basilio Valdes Hall
Veterans Memorial Medical Center
|| Activities ||

13 October
Psychopathologic Conference
Dr. Pia Jerez-Bagain
Ward 5 Conference Room
VMMC

18 October : 1800 H
PPA 9th Monthly Scientific Meeting
"Treatment of First Episode Depression : Diligence & Innovation"
Dr. Vicente Cabuquit
UERM

20 October
Psychopathologic Conference
Dr. Glenn M. Cariaga
Ward 5 Conference Room
VMMC

24 October : 1800 H
PCPsych 4th Quarterly Scientific Meeting
"Principles of Psychopharmacology in Special Poplations"
Dr. Georgina Gozo-Oliver, FPPA, FPSCAP
AFPMC Officers Club House

27 October
Psychopathologic Conference
Dr. Orville Jess A. Pandes
Ward 5 Conference Room
VMMC

27 - 28 October
Toxicology for Non-Toxicologists
UP-PGH

Coffee May Keep Depression Away

by : Deborah Brauser

September 26, 2011 — Risk for depression may decrease as coffee consumption increases, new research suggests.

In a 10-year cohort study of more than 50,000 older women, investigators found that compared with those who drank 1 cup or less of caffeinated coffee per week, those who drank 2 to 3 cups per day had a 15% decreased risk for depression, and those who drank 4 cups or more had a 20% decreased risk.

"This is one of the first major studies to look to this relationship," lead author Michel Lucas, PhD, RD, epidemiologist/nutritionist at Harvard School of Public Health in Boston, Massachusetts, told Medscape Medical News.

"People have often worried that drinking caffeinated coffee might have a bad effect on their health, but there is more and more literature, including this study, showing that caffeine may not have the detrimental effect previously thought," said Dr. Lucas.

The investigators note that because this was an observational study, it did not prove causality and "only suggests the possibility" of a protective effect.

"Further investigations are needed to confirm [the findings] and to determine whether usual caffeinated coffee consumption can contribute to depression prevention," they write.

Still, Dr. Lucas said that it might be okay for clinicians to recommend increasing a patient's coffee intake.

"If depressed patients are refraining themselves to 1 coffee per day because they think that's all they should have, why not try suggesting they drink more, as long as it doesn't go over 4 cups a day? We still need a large randomized controlled trial to look at this effect, but as long as it's not over a certain amount, upping the intake shouldn't hurt, and may be helpful."

The study is published in the September 26 issue of the Archives of Internal Medicine.

World's Most Used Stimulant

"Caffeine is the world's most widely used central nervous system stimulant, with approximately 80% consumed in the form of coffee, " write the researchers.



They note that although few prospective studies have looked at the link between coffee consumption and depression, a few cohort studies have found a "strong inverse association" between coffee consumption and suicide.

However, a study from Finland ( Eur J Epidemiol. 2000;16:789-791) found that although the risk for suicide decreased progressively for those consuming up to 7 cups of coffee per day, the risk started increasing when consumption went over 8 cups a day.

"It was surprising to us that more studies on caffeine and depression haven't been done. People who drink coffee know that it may give more energy, and we know that caffeine has an impact on the brain and on serotonin, which has been associated with depression. We wanted to explore these associations by comparing women who drink more coffee to those who drink less," said Dr. Lucas.

The US Nurses' Health Study began in 1976 with 121,700 women between the ages of 30 and 55 years at enrollment. Updated information on lifestyle and medical history are provided every 2 years through mailed questionnaires.

For this analysis, the investigators examined data on a cohort of 50,739 of the study's participants who did not have any depressive symptoms in 1996 (baseline for this analysis) and were followed-up through June 2006.

In addition to evaluating both caffeinated and decaffeinated coffee consumption, the women supplied information on their use of tea, caffeinated and decaffeinated sodas, and chocolate.

Incident or clinical depression "was defined as self-reported physician-diagnosed depression and antidepressant use," report the researchers.

Significant Inverse Effect

Results showed that 2607 incident cases of depression were found during the 10 years of follow-up.

An overall "inverse, age-adjusted, dose-response relationship was observed between caffeinated coffee and depression risk (P for trend = .03)," write the investigators.

"Further adjustment for alcohol intake did not materially affect the results," they add.

The women who consumed 2 to 3 cups of caffeinated coffee per day had a 0.85 relative risk (RR) for depression (95% confidence interval [CI], 0.75 - 0.95), and those who drank 4 or more cups a day had an RR of 0.80 (95% CI, 0.64 - 0.99; P < .001 for both) compared with those who drank or 1 or fewer cups per week.

In addition, the participants in the highest of the 5 caffeine consumption categories (550 mg/day or more) had an RR of 0.80 (95% CI, 0.68 - 0.95; P = .02) compared with the women in the lowest category (100 mg/day or less).

Because only 0.52% of the women drank 6 or more cups of caffeinated coffee per day, the effects of very high consumption were not able to be addressed in this study.

Decaffeinated coffee, caffeinated tea, sugared soft drinks, and chocolate were not significantly associated with depression risk.

Dr. Lucas noted that these factors were examined in the women who used them and not coffee as their main source of caffeine consumption, and because their numbers were relatively small, it may have affected the results.

Overall, this large prospective cohort study of older women (mean age, 63 years at baseline) showed that "risk of depression decreased in a dose-dependent manner with increasing consumption of caffeinated coffee," write the investigators.

Important Contribution

"This study makes an important contribution because it is the first large-scale study to look at this issue in women, and they focused on mental health aspects, as opposed to previous work which has focused on other health conditions," Seth Berkowitz, MD, assistant professor of clinical medicine in the Division of General and Internal Medicine at the University of California, San Francisco, told Medscape Medical News.

Dr. Berkowitz, who is also on the editorial board for the Archives of Internal Medicine, writes in an accompanying editor's note that past research has found no significant effects of caffeine on cardiovascular disease, modest decreases in markers of inflammation, and no or modest protective effects in certain malignant neoplasms.

"Taken together, these results reassure coffee drinkers that there seem to exist no glaringly deleterious health consequences to coffee consumption," he writes.

Dr. Berkowitz told Medscape Medical News that people often say that caffeine gives them more energy or helps them to concentrate more. However, "it is important to quantify in a scientific way" what the effects are on mental activities.

"As clinicians we want to make sure that people aren't doing things that will have them come to harm. And we're looking for things that we may be able to add that can be of benefit. I think in this case, this study adds to the body of evidence that there isn't much harm in coffee consumption. But I don't think we're at the point where we can say, 'drink coffee so you won't get depressed,' because that's not how the study was designed," he said.

"Still, if your patients have questions or are wondering if drinking coffee is bad for them, I think you can provide some assurance that, at least up to the amounts examined here, it doesn't seem to be causing a lot of problems. If they are feeling like it helps them, they should enjoy it in good health."

The study was supported by grants from the National Institutes of Health and from the National Alliance for Research on Schizophrenia and Depression. In addition, Dr. Lucas received a fellowship from the Fonds de recherche en santé du Québec. The study authors and Dr. Berkowitz have disclosed no relevant financial relationships.

Arch Intern Med. 2011;171:1571-1578. Abstract
From Medscape

1st Mental Health Day Celebration in VMMC