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Newborns Need Pain Relief ,Too

Pain Control Recommended for Newborns

Laurie Barclay, MD

November 11, 2009 — Feeding and breast-feeding newborns are found to be the most effective methods of pain relief during heel-lancing, according to the results of a prospective study reported in the November issue of Pediatrics.

“Pain experience can alter clinical outcome, brain development, and subsequent behavior in newborns, primarily in preterm infants,” write Amir Weissman, MD, from Technion-Israel Institute of Technology in Haifa, Israel, and colleagues. “The aims of this study were (1) to evaluate several simple, commonly used methods for pain control in newborns and (2) to evaluate the concordance between behavioral and autonomic cardiac reactivity to pain in term neonates during heel-lancing.”

During heel-lancing for routine neonatal screening of phenylketonuria and hypothyroidism, 180 term newborn infants were randomly selected to 1 of 6 groups: (1) control (no intervention for pain relief); (2) sucking without feeding; (3) holding by mother; (4) ingestion of oral glucose solution; (5) feeding with oral formula; or (6) breast-feeding. Response to pain was assessed with the Neonatal Facial Coding System score; duration of crying; and autonomic variables determined from spectral analysis of heart rate variability before, during, and after heel-lancing.

Compared with newborns in any of the 5 intervention groups, those in the control group with no pain intervention had the greatest levels of pain manifestation. Breast-feeding or feeding with oral formula appeared to be most effective vs all other groups, based on the lowest increase in heart rate (21 and 23 beats per minute, respectively, vs 36 beats per minute; P < .01), neonatal facial score (2.3 and 2.9, respectively, vs 7.1; P < .001), cry duration (5 and 13 seconds, respectively, vs 49 seconds; P < .001), and the lowest decrease in parasympathetic tone (–2 and –2.4, respectively, vs 1.2; P < .02). “Any method of pain control is better than none,” the study authors write. “Feeding and breast-feeding during heel-lancing were found to be the most effective methods of pain relief.” Limitations of this study include low sensitivity of the pain assessment methods, large variability of newborn response to painful stimuli, and the subjective nature of interpreting these data. “Neonatal pain prevention is the expectation of the parents and should be the goal of the medical staff; therefore, family members or staff may be recruited to help during these procedures, and nursing mothers should be encouraged to breastfeed during the procedure,” the study authors conclude. “If family members believe that they cannot withstand the procedure, hear their infant crying, or see the heel-lancing, then bottle-feeding seems to be a good alternative.” The study authors have disclosed no relevant financial relationships. Pediatrics. 2009;124:e921-e926.

WHO Urges Rapid Use of Antivirals in H1N1

New Guidelines on H1N1 Influenza Urge Quicker Use of Antivirals

Robert Lowes

November 12, 2009 — Updated treatment guidelines for H1N1 influenza from the World Health Organization (WHO) urge clinicians to administer antiviral medications as soon as possible to patients in at-risk groups with flu symptoms, patients with pneumonia, and those with uncomplicated influenza-like illness that worsens or fails to improve within 72 hours.

The reason for immediate antiviral therapy is that a mild case of H1N1 influenza can morph into a deadly disease such as pneumonia within 24 hours, according to the revised guidelines released Tuesday.

“The virus can take a life within a week,” Nikki Shindo, MD, a medical officer in WHO’s Global Influenza Programme, said during a press conference today. “The week of opportunity is very narrow in regard to the progression of the disease. The medicine needs to be administered before the virus destroys the lungs.”

Patients in at-risk groups who should receive antivirals once they experience flu symptoms include pregnant women, children younger than 2 years, and individuals with chronic illnesses such as respiratory problems, according to Dr. Shindo.

Dr. Shindo said that earlier WHO guidelines focused on treating severe disease stemming from the H1N1 virus. The updated guidelines, she explained, have more to say about preventing severe disease, especially with the use of antiviral medications. Initial guidance about antivirals had been more conservative because WHO “had almost no experience” in regard to their effectiveness and because supplies were limited, said Dr. Shindo. Now, WHO has more data about the safety and usefulness of the medicine, and supplies are more ample.

The updated guidelines state that clinicians should not delay antiviral treatment for patients with suspected H1N1 influenza for the sake of conducting tests to confirm the diagnosis. In addition, a negative result from some rapid influenza diagnostic tests should not justify withholding antiviral therapy because these tests “miss many infections with pandemic H1N1 virus.”

The first-line antiviral for treating the H1N1 virus is oseltamivir (Tamiflu), according to WHO. If oseltamivir is not available, it is not possible to administer it to a particular patient, or if the virus is resistant to oseltamivir, the guidelines recommend that clinicians use zanamivir (Relenza), which is inhaled.

To ensure easier access to treatment, public health authorities should distribute antivirals through general practitioners and not primarily through hospitals, said Dr. Shindo. “Patients should not have to visit the hospital to get antivirals prescribed,” she said. “This should help ensure that individuals get the care they need faster. This will leave hospitals freer to treat the more severe cases.”

Although Dr. Shindo emphasized the need for the earlier use of antivirals, she said that people not in the at-risk groups who are experiencing only mild flu symptoms do not need to take antiviral therapy. Nor should healthy individuals take it as a preventive measure.

WHO Guidelines Do Not Conflict With CDC Directives

The updated WHO guidelines specify watchful waiting for 72 hours for patients who have uncomplicated influenza-like illness and who do not have an underlying medical condition that puts them at risk. Hallmarks of progressive illness that warrant antiviral therapy include:

* Shortness of breath, hypoxia, and fast or labored breathing in children, which would suggest oxygen impairment or cardiopulmonary insufficiency.
* Altered mental status, unconsciousness, drowsiness, and seizures, which suggest central nervous system complications.
* Evidence of sustained virus replication or invasive secondary bacterial infection.
* Severe dehydration, expressed as decreased activity, dizziness, decreased urine output, and lethargy.

By necessity, this recommendation for follow-up requires patient education, Dr. Shindo said. Clinicians should instruct patients who initially present with uncomplicated influenza-like illness to return for another visit if they develop these or other symptoms of progressive illness — or do not get better — within 72 hours from the onset of symptoms, according to WHO.

The Centers for Disease Control and Prevention (CDC) have not issued any guidance on follow-up care for influenza patients that stipulates a 72-hour time frame, but the agency does advise patients who do not improve within a few days that they might have a complication like a secondary infection, said Anthony Fiore, MD, a medical epidemiologist with the CDC’s National Center for Immunization and Respiratory Diseases.

“I do not see the WHO recommendations as being in conflict [with the CDC directives],” Dr. Fiore told Medscape Infectious Diseases. CDC recommendations on administering antiviral medications are revised on average every 4 to 6 weeks, said Dr. Fiore. “We will look at the WHO guidance and the evidence base used to develop the guidance as part of [our] revision.”

The updated treatment guidelines are available on the WHO Web site.

CDC Update

At a CDC press briefing today, Anne Schuchat, MD, director of the CDC’s National Center for Immunization and Respiratory Diseases, provided an updated estimate of H1N1 cases using data extrapolated from the CDC’s Emerging Infections Program .

The CDC estimates that during the first 6 months of the pandemic (April through October 17, 2009), a total of 22 million people (range, 14 – 34 million) in the United States became infected with H1N1 influenza. Of these, 98,000 people (range, 63,000 to 153,000) were hospitalized; and 3900 (range, 2500 – 6100) died.

The data are also broken down by age group and highlight that fact that numbers of cases, hospitalizations, and deaths are disproportionately higher in people aged 64 years and younger than in older individuals.

These numbers will be updated every 3 to 4 weeks, she said.

Dr. Schuchat also discussed the effect of H1N1 influenza in patients with diabetes, which afflicts about 19% of adults hospitalized for H1N1. According to Dr. Schuchat, people with diabetes should be vaccinated (with the injectable vaccine not the nasal spray) against H1N1. People with diabetes who also have respiratory illness should receive antiviral therapy, which should be initiated prior to availability of test results. Patients with diabetes should also ensure that they have been vaccinated against pneumococcal infections.

To date, 41.6 million doses of H1N1 vaccine have become available. “This is more than we had before but not as much as we had hoped to have by today,” Dr. Schuchat said. Currently, 94 million doses of seasonal influenza vaccine have been distributed, with 114 million doses total expected by the end of the year.

Emma Hitt, PhD, contributed to this report.

H1N1 (Swine)Flu vaccines are now available to parents and caretakers!

We are now offering the H1N1(Swine)Flu vaccine to our patients parents and caretakers. There is a $20 admnistration charge for adults. If you are interested in recieving this vaccine please call the office to schedule an appointment.

Preservative free Swine Flu vaccine for ages 6 months – 35 months has arrived!

Our preservative free H1N1(Swine) Flu vaccines for age 6 months to 35 months has arrived. Please call the office to schedule your childs appointment. Please remember we are trying to accomodate many patients who want their children to have the vaccine and are doing our best to schedule everyone at the earliest time available. We are currently scheduling out 2-3 weeks. Thank you in advance for your understanding.

Cannabinoids Do Not Help Tics in Tourette’s Syndrome

Cannabinoids for Tourette’s Syndrome

Curtis A, Clarke CE, Rickards HE
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Summary
Cannabinoids for Tourette syndrome

Cannabinoid medication might be useful in the treatment of the symptoms in patients with Tourette’s syndrome. At the present time only two relevant studies have been conducted. Both studies used tetrahydrocannabinol (Δ9THC). In both studies Δ9THC was associated with tic reduction. However the sample size was small and a large number of multiple comparisons were made . There were only 28 participants in total, since eight participants took part in both studies. Possibly the patients who derived the greatest benefit and experienced the least adverse effects would be the most inclined to participate in further studies. There were a high number of drop outs/exclusions in the six week study and it is unclear whether intention to treat analysis (ITT) was performed. The results that are reported are analyses done on the patients who remained in the study on the study medication at the correct dose. In reality, patients do opt not to continue treatment if there is limited efficacy or unpalatable side effects. This introduces attrition bias. Whilst there were some significant results, the authors themselves accept that very few of these results are significant if a Bonferroni correction is performed. It is possible that cannabinoid medication has a beneficial effect which is too weak to be detected using ITT and such a small sample size. There is some weak evidence that cannabinoid medication may have an effect on obsessive compulsive behaviour but the measure used was an addition to the TSSL which has not been validated.There were no data on the effect of Δ9THC on quality of life.There is not enough evidence to support the use of cannabinoids in treating tics and obsessive compulsive behaviour in people with Tourette’s syndrome.

This is a Cochrane review abstract and plain language summary, prepared and maintained by The Cochrane Collaboration, currently published in The Cochrane Database of Systematic Reviews 2009 Issue 4, Copyright © 2009 The Cochrane Collaboration. Published by John Wiley and Sons, Ltd.. The full text of the review is available in The Cochrane Library (ISSN 1464-780X).
This record should be cited as: Curtis A, Clarke CE, Rickards HE. Cannabinoids for Tourette’s Syndrome. Cochrane Database of Systematic Reviews 2009, Issue 4. Art. No.: CD006565. DOI: 10.1002/14651858.CD006565.pub2

This version first published online: October 07. 2009
Abstract
Background

Gilles de la Tourette Syndrome (GTS) is a developmental neuropsychiatric disorder characterised by the presence of chronic motor and phonic tics. Drugs currently used in the treatment of GTS either lack efficacy or are associated with intolerable side effects. There is some anecdotal and experimental evidence that cannabinoids may be effective in treating tics and compulsive behaviour in patients with GTS. There are currently no systematic Cochrane reviews of treatments used in GTS. There is one other Cochrane review being undertaken at present, on the use of fluoxetine for tics in GTS.
Objectives

To evaluate the efficacy and safety of cannabinoids as compared to placebo or other drugs in treating tics, premonitory urges and obsessive compulsive symptoms (OCS), in patients with GTS.
Search strategy

We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (in The Cochrane Library Issue 4 2008) , MEDLINE (January 1996 to date), EMBASE (January 1974 to date), PsycINFO (January 1887 to date), CINAHL (January 1982 to date), AMED (January 1985 to date), British Nursing Index (January 1994 to date) and DH DATA (January 1994 to date).

We also searched the reference lists of located trials and review articles for further information.
Selection criteria

We included randomised controlled trials (RCTs) comparing any cannabinoid preparation with placebo or other drugs used in the treatment of tics and OCS in patients with GTS.
Data collection and analysis

Two authors abstracted data independently and settled any differences by discussion.
Main results

Only two trials were found that met the inclusion criteria. Both compared a cannabinoid, delta-9-Tetrahydrocannabinol (Δ9THC), either as monotherapy or as adjuvant therapy, with placebo. One was a double blind, single dose crossover trial and the other was a double blind, parallel group study. A total of 28 different patients were studied. Although both trials reported a positive effect from Δ9THC, the improvements in tic frequency and severity were small and were only detected by some of the outcome measures.
Authors’ conclusions

Not enough evidence to support the use of cannabinoids in treating tics and obsessive compulsive behaviour in people with Tourette’s syndrome.

ADHD Represents Delayed, Not Abnormal Brain Maturation

by
Arline Kaplan MD

Cortical development in children with attention-deficit/hyperactivity disorder (ADHD) generally lags behind that in other children by several years, NIMH researchers reported recently.1 The greatest maturational delay occurs in prefrontal regions important for control of such cognitive processes as attention and working memory, they found.
There has been a long-standing debate as to whether ADHD is caused by a delay in brain development or is partly due to a complete deviation away from typical brain development, said Philip Shaw, MD, PhD, an NIMH staff clinician and leader of the research team.
To help resolve the controversy about the disorder that affects 3% to 5% of school-aged children, Shaw and his colleagues conducted a neuroanatomical MRI study and found evidence suggesting that ADHD is characterized by delay rather than deviance in cortical maturation.
“We looked at the development of the cortex, and we measured its thickness in 446 kids, half… with ADHD and half without the disorder,” Shaw told Psychiatric Times.
The researchers scanned the brains of most of the study participants at least twice at about 3-year intervals. While the participants included preschoolers and young adults, most ranged in age from 7 to 16 years. Among the participants with ADHD, 92% had combined-type ADHD at baseline.
Using computational neuroanatomical techniques, the researchers estimated cortical thickness at more than 40,000 cerebral points from 824 MRI scans. They focused on the age of attaining peak cortical thickness—when cortex thickening during childhood gives way to thinning following puberty, as unused neural connections are pruned for optimal efficiency during the teen years.
“While healthy kids reached peak cortical thickness at age 7 or 8, the kids with ADHD reached… peak cortical thickness a few years later, around age 10,” Shaw said.
The cortical maturation delay in ADHD was most prominent in the lateral prefrontal cortex, the region, according to the research team, that supports such cognitive functions as the ability to suppress inappropriate responses and thoughts, executive control of attention, evaluation of reward contingencies, and working memory. Delay was also found in the temporal cortex.
The only cortical area in which the ADHD group demonstrated slightly earlier maturation was the primary motor cortex.
“It is possible that the combination of early maturation of the primary motor cortex with late maturation of higher-order motor control regions may reflect or even drive the excessive and poorly controlled motor activity cardinal to the syndrome,” the research team wrote.
Although there was a delay in the young people with ADHD, the order in which the different parts of the cortex matured was similar in both groups.
Shaw was asked whether the findings indicate that children will eventually grow out of ADHD. The study findings cannot be interpreted to mean that in ADHD the brain normalizes at age 10 or 12, he said.
“The delay we showed is carried forward into adolescence,” he said. “Also we know from a host of other studies that there are very real persisting structural and functional differences between teenagers with ADHD and those who don’t have the disorder.” Frequently, he said, outcomes reported in previous studies depend on how ADHD is defined. If you use a strict definition, he explained, about one quarter of people who grow up with ADHD will still meet the definition in adulthood. If a broader definition is used, about two thirds of people with childhood ADHD will still have troublesome symptoms in adulthood.
Studies that measure brain volume or function also have detected differences between the brains of young people who have ADHD and those of individuals who do not have the disorder.
“One very striking thing about our findings is that they complement existing imaging studies from other groups that found structural and functional differences, and all of them are pointing to similar parts of the brain,” Shaw said.
Why the delay?
Discussing factors that might underpin the delay, the research team mentioned psychostimulants and genetic factors. Most of those with ADHD in the study were receiving standard treatment with psychostimulants, but there were not enough medication-naive children to analyze them as a separate group, according to Shaw. In the published report, the research team wrote “trophic effects of treatment with psychostimulants in the ADHD group are possible, but unlikely, given our previous reports of no effect of psychostimulants on gray matter volume.”
“Genetic factors will certainly play a role, with a perturbation in the developmental sequence of the activation and deactivation of genes that sculpt cortical architecture,” the team wrote. “In this context, neurotrophins, essential for the proliferation, differentiation, and survival of neuronal and nonneuronal cells, emerge as promising candidates.”
“The numbers needed to do genetic studies are enormous,” Shaw said. “Of course, there are very good multisite collaborative studies going on, which are helping us identify the key genes.”
There are a host of candidates and factors that could control neural growth, Shaw said, acknowledging that dopamine and other neurotransmitters in the brain also are important to the growth of the cortex.
While research continues on possible causes of ADHD, Shaw noted that his team would be using brain-imaging techniques to study what happens to children with ADHD as they grow older.
“There is a large cohort of children who have very persistent ADHD,” he explained. “We want to compare them with the kids who get better from ADHD. That involves scanning the kids a little bit later when they are in their mid-teens.”
Diagnosis and treatment
Brain imaging is not ready for use as a diagnostic tool in ADHD, Shaw said.”It is still too early to use neuroanatomical scans for diagnosis,” he said. “We had to scan hundreds of children to identify subtle differences. They [the differences] are very real, but they are subtle. So the scan of any one child will not tell you a great deal about whether [he or she has] ADHD or not. Currently, the diagnosis of ADHD remains clinical.”
What’s more, the brain imaging study was a “natural history study” and so it did not address treatment, he explained.
“We know the treatments that work for ADHD on the basis of very large clinical studies, including the Multimodal Treatment Study of Children With ADHD and the Treatment of Attention Deficit Hyperactivity Disorder in Preschool-Age Children study,” he said.
While the Shaw et al study is not relevant to issues of diagnosis and treatment, it is nevertheless important in providing another facet of our increasing knowledge about the neurobiology of this disorder, said F. Xavier Castellanos, MD, Brooke and Daniel Neidich Professor of Child and Adolescent Psychiatry and director of research for the New York University Child Study Center.
In his own work, Castellanos said, his group is pursuing some novel methods of functional MRI that may well have diagnostic implications.2,3
Also responding to the Shaw et al study was E. Clarke Ross, chief executive officer for Children and Adults With Attention Deficit/Hyperactivity Disorder, a national advocacy and support organization.
“In a time when a vocal minority denies the mountain of evidence showing ADHD to be a real disorder,” he said, “it is nice to watch brain scans light up on televisions across the country with images actually showing the structural differences in the brains of those living with ADHD.”

Be Aware of Fraudulent "Natural" Flu Treatments

FDA NEWS RELEASE

For Immediate Release: Oct. 19, 2009

Media Inquiries: Christopher Kelly, 301-796-4676 christopher.kelly@fda.hhs.gov
Consumer Inquiries: 888-INFO-FDA

FDA, FTC Issue Joint Warning Letter to Web Site Offering Fraudulent H1N1 Flu Supplements


Agencies continue effort to protect public health from illegal Web activity

On October 15, 2009, the U.S. Food and Drug Administration (FDA) and the Federal Trade Commission (FTC) issued a joint warning letter to a Web site marketing fraudulent supplements that claim to help prevent the spread of the 2009 H1N1 influenza virus.

The warning letter, the first to be issued jointly by the agencies, advises the owners of the site that they must discontinue the fraudulent marketing of their product or face legal action. The letter further advises the owners of the site that they have 48 hours to give the agencies a plan to discontinue their fraudulent marketing.

The FDA and the FTC remind consumers to be cautious of promotions or Internet sites offering products for sale that claim to diagnose, prevent, mitigate, treat or cure the 2009 H1N1 influenza virus. Fraudulent H1N1 influenza products come in many varieties, including dietary supplements, as well as products purporting to be drugs, medical devices or vaccines. Since May 2009, the FDA has warned more than 75 Web sites to stop the sale of more than 135 products with fraudulent H1N1 influenza virus claims.

“Products that are offered for sale with claims to diagnose, prevent, mitigate, treat or cure the 2009 H1N1 influenza virus must be carefully evaluated,” said Commissioner of Food and Drugs Margaret A. Hamburg, M.D. “Unless these products are proven to be safe and effective for the claims that are made, it is not known whether they will prevent the transmission of the virus or offer effective remedies against infection. Furthermore, they can make matters worse by providing consumers with a false sense of protection.”

The FDA and the FTC also warn consumers to take extreme care when buying products over the Internet that claim to diagnose, prevent, treat or cure the H1N1 influenza virus because, in addition to being fraudulent, they could be dangerous.

In collaboration with the FTC, the FDA will continue to work aggressively to identify, investigate and take regulatory action against individuals or businesses that wrongfully promote purported 2009 H1N1 influenza products.

This will include taking joint action, when appropriate, such as the issuance of last Thursday’s warning letter. Additional legal action could include an injunction or issuance of an administrative order by the FTC or seizure of products, an injunction or criminal prosecution by the FDA.

“The FDA continues to consider the sale and promotion of fraudulent H1N1 influenza products to be a possible threat to the public health and in violation of the Federal Food Drug and Cosmetic Act,” said Michael Chappell, acting associate commissioner for regulatory affairs. “The FDA has an aggressive surveillance program to detect fraudulent H1N1-related products and will take prompt action to stop the marketing of fraudulent H1N1 influenza products and will hold those who are responsible for doing so accountable.”

To view the warning letters, visit: http://www.fda.gov/ICECI/EnforcementActions/WarningLetters/2009/default.htm.

There are two antiviral drugs approved by the FDA for treatment and prophylaxis of the 2009 H1N1 influenza virus – Tamiflu (oseltamivir phosphate) and Relenza (zanamivir). Tamiflu and Relenza, in addition to their approved labeling, have been issued Emergency Use Authorizations by the FDA that describe specific authorized uses during this public health emergency.

H1N1 Flu Fraud Widget

This week, the FDA enhanced its efforts to warn the public about potentially deceptive H1N1 influenza products and to report suspected criminal activity with the release of an H1N1 flu fraud widget.

The portable application, embedded in a Web page that can be copied onto any other Web site or blog, will allow the public to play an active role in preventing flu fraud, and is available at http://www.fda.gov/NewsEvents/PublicHealthFocus/ucm186340.htm

Consumers are urged to report any suspected fraudulent products or criminal activity relating to FDA-regulated products associated with H1N1 influenza virus, including the names of Web sites that may be offering these products for sale, to the FDA by visiting: http://www.accessdata.fda.gov/scripts/email/oc/oci/flucontact.cfm

Consumers are urged to purchase and consume only FDA-approved or authorized medical products to diagnose, treat, prevent, or cure infections caused by the H1N1 virus. Consumers also are urged to contact their health care provider if they have any questions or concerns about medical products or personal protective equipment.

For more information:

FDA 2009 H1N1 (Swine) Flu Page
http://www.fda.gov/NewsEvents/PublicHealthFocus/ucm150305.htm

Centers for Disease Control and Prevention – 2009 H1N1 Flu (Swine Flu)
http://www.cdc.gov/h1n1flu/

Fraudulent 2009 H1N1 Influenza Products List
http://www.accessdata.fda.gov/scripts/h1n1flu/

Influenza Antiviral Drugs and Related Information
http://www.fda.gov/Drugs/DrugSafety/InformationbyDrugClass/ucm100228.htm

The Federal Government’s Influenza Web site
http://www.flu.gov/

FTC Warns Internet Peddlers that Potentially Bogus H1N1 Influenza Products May Violate Federal Law—Press Release, May 5, 2009
http://www2.ftc.gov/opa/2009/05/swineflu2.shtm

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RSS Feed for FDA News Releases [what is RSS?]

Page Last Updated: 10/19/2009

Seasonal Flu shots for children 3 years old and younger now available!

Our Seasonal flu shots for children 3 years of age or younger are now available. If your child has not yet recieved this vaccine or is due for their second dose please call the office to schedule their appointment. We do not yet have information on when we will recieve the rest of our Seasonal flu vaccine for patients above the age of 3, as soon as we do we will post it on this website.

The H1N1 (Swine) Flu shots for children 3 years and up are in!!

The shot for children 3 years of age and up for the H1N1 (aka Swine flu) are now available! If you are interested in having your child vaccinated please call the office to schedule an appointment. We are making every effort to get everyone in as quickly as possible, but due to the large number of vaccines we need to administer in a short period of time we have alloted certain times we are scheduling these appointments. Thank you in advance for your understanding and cooperation.
If you have questions regarding the vaccines please follow this link: http://www.cdc.gov/vaccines/pubs/vis/default.htm.for the vaccine information sheets to help you make an informed decision.

Treating Depression or Anxiety without Presciptions?

CAM for your depressed patient: 6 recommended options

Sy Atezaz Saeed, MD

Professor and chair, Department of psychiatric medicine, Brody School of Medicine at East Carolina University, Greenville, NC

Richard M. Bloch, PhD

Professor and director of research, Department of psychiatric medicine, Brody School of Medicine at East Carolina University, Greenville, NC

Diana J. Antonacci, MD

Associate professor and director of residency training, Department of psychiatric medicine, Brody School of Medicine at East Carolina University, Greenville, NC


Americans with depression turn to complementary and alternative medicine (CAM) more often than conventional psychotherapy or FDA-approved medication. In a nationally representative sample, 54% of respondents with self-reported “severe depression”—including two-thirds of those receiving conventional therapies—reported using CAM during the previous 12 months.1

Unfortunately, popular acceptance of CAM for depression is disproportionate to the evidence base, which—although growing—remains limited. As a result, your patients may be self-medicating with poorly supported treatments that are unlikely to help them recover from depression.

In reviewing CAM treatments for depression, we found some with enough evidence of positive effect that we feel comfortable recommending them as evidence-based options. These promising, short-term treatments are supported by level 1a or 1b evidence and at least 1 study that demonstrates an ability to induce remission (Table 1).2

For patients seeking “natural” or nonprescription treatments—or when you wish to augment standard treatments that are not working adequately—you might recommend fatty acids, St. John’s wort, or S-adenosyl-L-methionine (SAMe). Similar recommendations can be made for yoga, exercise, and bibliotherapy, as we discuss here.


Table 1
Evidence these authors required to recommend a CAM treatment

Minimum requirements

Level of evidence

Recommendation

Systematic review showing superiority to placebo or standard treatment
Plus
1 study showing CAM treatment can induce remission

1a +

1b or 2b

A

At least 2 RCTs showing superiority to placebo or standard treatment
Plus
1 study showing CAM treatment can induce remission

1b

1b or 2b

A–

CAM: complementary and alternative medicine; RCT: randomized controlled trial

Source:Reference 2

Reviewing CAM evidence

This article refers to as “alternative” any treatment other than a form of psychotherapy or an FDA-approved medication that substitutes for a standard psychiatric treatment. When used to augment standard psychiatric treatments, these approaches are considered “complementary.”

Our search for evidence on CAM treatments for depressive disorders raised questions about what constitutes acceptable and convincing methodology:

  • Studies often had problems with blinding and suitable placebos. Many were small, with short duration and no long-term follow-up.

  • Comparisons with active treatments that showed no differences were assumed to imply comparability, even though the studies were powered to detect only large differences.

Clinical Point

Multiple RCTs have shown consistent superiority of some CAM treatments over comparison conditions

On the other hand, multiple randomized controlled trials (RCTs) have shown consistent superiority of some CAM treatments over comparison conditions.

Applying the evidence. Because CAM use is widespread, be sure to ask psychiatric patients if they are using CAM treatments. If the answer is “yes,” a risk-benefit assessment is needed. Inform patients who are using poorly supported CAM approaches that they could consider better-supported CAM options as well as standard effective antidepressants.

Monitor patients for an adequately prompt positive response to an evidence-based CAM approach that has shown efficacy for their level of depression. As with any treatment, consider other evidence-based options when CAM treatments are inadequate or unsuccessful in achieving remission of depressive symptoms.

Sufficient evidence of efficacy

Yoga. In their systematic review of yoga’s effectiveness for depression, Pilkington et al3 analyzed 5 RCTs that met 3 criteria:

  • participants had mild to severe depression or depressive disorders

  • yoga or yoga-based exercises alone were used for treatment

  • depression rating scales were used as outcome measures.

They found evidence that yoga can reduce depressive symptoms and induce remission (Table 2). The studies were generally small and of short duration, and depression severity and interventions varied widely. Most participants were young and relatively fit, raising questions about yoga’s applicability to older or less fit patients. Reporting of adverse events was limited, but no safety issues or adverse effects were identified.

Conclusion. Yoga has been studied primarily as an alternative treatment, but its physical health and group participation benefits and lack of side effects make it a suitable complementary treatment as well.

Clinical Point

Yoga’s positive effects suggest that exercise does not have to be aerobic to provide an antidepressant benefit

Exercise. Extensive literature has examined the relationship between exercise and depression. We identified 7 reviews published between 1993 and 2008 (Table 3). All supported positive effects of exercise except for patients age <20.>

  • 45% with supervised exercise

  • 40% with home-based exercise

  • 47% with sertraline, 50 to 200 mg/d

  • 31% with placebo.4


Table 2
5 RCTs of yoga’s effectiveness in treating depression

RCT

Interventions

Conclusion

Broota and Dhir, 1990

Yoga and PMR vs control

Yoga and PMR were more effective than control, with yoga more effective than PMR

Khumar et al, 1993

Shavasana yoga vs no intervention

College students with severe depression improved during and after yoga treatment

Janakiramaiah et al, 2000

SKY vs ECT vs imipramine

Reductions in BDI scores for all 3 groups; ECT > SKY or imipramine, SKY=imipramine

Rohini et al, 2000

Full SKY vs partial SKY

30 individuals with MDD improved with either therapy, but results were not statistically significant

Woolery, 2004

Iyengar yoga vs wait list

28 mildly depressed individuals benefitted from yoga, as measured by BDI scores at midpoint and throughout treatment

BDI: Beck Depression Inventory; ECT: electroconvulsive therapy; MDD: major depressive disorder; PMR: progressive muscle relaxation; RCT: randomized controlled trial; SKY: Sudarshan Kriya yoga

Source:
Broota A, Dhir R. Efficacy of two relaxation techniques in depression. Journal of Personality and Clinical Studies. 1990;6(1):83-90.
Khumar SS, Kaur P, Kaur S. Effectiveness of Shavasana on depression among university students. Indian J Clin Psychol. 1993;20(2):82-87.
Janakiramaiah N, Gangadhar BN, Naga Venkatesha Murthy PJ, et al. Antidepressant efficacy of Sudarshan Kriya yoga (SKY) in melancholia: a randomized comparison with electroconvulsive therapy (ECT) and imipramine. J Affect Disord. 2000;57(1-3):255-259.
Rohini V, Pandey RS, Janakiramaiah N, et al. A comparative study of full and partial Sudarshan Kriya yoga (SKY) in major depressive disorder. NIMHANS Journal. 2000;18(1):53-57.
Woolery A, Myers H, Sternlieb B, et al. A yoga intervention for young adults with elevated symptoms of depression. Altern Ther Health Med. 2004;10(2):60-63.


Table 3
Evidence of the antidepressant effect of exercise

Literature review

Methodology

Conclusion

Byrne and Byrne, 1993

13 studies, clinical samples, measured changes in depressed mood

90% of studies reported beneficial effects, especially in clinical populations

Scully et al, 1998

4 literature reviews, 1 monograph, 1 study

Positive relationship of physical activity and depression in healthy and clinical samples, increased over time

Lawlor and Hopker, 2001

14 RCTs from 1966 to 1999 with depression as an outcome

Significant methodologic weaknesses, but exercise effect > no treatment and=cognitive therapy

Dunn et al, 2001

Examined dose effect in 37 studies; subjects diagnosed with depressive disorders, mild-to-moderate symptoms, and no medical comorbidity

Only level B and C evidence; positive effects with exercise from light to heavy intensity; aerobic=nonaerobic; improvement may or may not be related to improved fitness

Brosse et al, 2002

12 RCTs from 1979 to 1999

Significant methodologic limitations, but authors concluded evidence supports a positive effect of exercise in healthy and clinical populations

Larun et al, 2006

4 RCTs in children and youth age <20

Exercise effect same as no intervention, low-intensity relaxation, or psychosocial intervention

Barbour et al, 2007

2 meta-analyses, 1 RCT, 2 studies

Positive effect; high-energy was optimal dose; aerobic=nonaerobic; improvement may or may not be related to improved fitness

RCT: randomized controlled trial

Source:
Byrne AE, Byrne DG. The effect of exercise on depression, anxiety and other mood states: A review. J Psychosom Res. 1993;37(6):565-574.
Scully D, Kremer J, Meade MM, et al. Physical exercise and psychological well being: a critical review. Br J Sports Med. 1998;32(2):111-120.
Lawlor DA, Hopker SW. The effectiveness of exercise as an intervention in the management of depression: systematic review and meta-regression analysis of randomised controlled trials. BMJ. 2001;322(7289):763-767.
Dunn AL, Trivedi MH, O’Neal HA. Physical activity dose-response effects on outcomes of depression and anxiety. Med Sci Sports Exerc. 2001;33(6):S587.
Brosse AL, Sheets ES, Lett HS, et al. Exercise and the treatment of clinical depression in adults: recent findings and future directions. Sports Med. 2002;32(12):741-760.
Larun L, Nordheim LV, Ekeland E, et al. Exercise in prevention and treatment of anxiety and depression among children and young people. Cochrane Database Syst Rev. 2006;3:CD004691.
Barbour KA, Edenfield TM, Blumenthal JA. Exercise as a treatment for depression and other psychiatric disorders: a review. J Cardiopulm Rehabil Prev. 2007;27(6):359-367.

Conclusion. Evidence supports exercise for short-term treatment of mild or moderate depression in adults. Studies tend to be small and brief, to enroll young physically -sound patients, and to include little follow-up. Studies of subjects age <20>

At least 2 studies suggest that high-energy exercise and aerobic or resistance training provide greater reductions in depressive symptoms than exercises such as walking.5,6 Yoga’s positive effects suggest, however, that an aerobic effect is not necessary for an antidepressant benefit.

Exercise has not been adequately tested as a complementary treatment but likely is safe for most psychiatric patients. Perspiration and dehydration might alter therapeutic blood levels of lithium or other medications. Advise patients to drink water before, during, and after exercise and to avoid outdoor exercise in extreme temperatures. More vigorous monitoring might be indicated in specific cases.

Tailor exercise programs to individual needs, considering the patient’s age and health status. Refer a patient with a known heart problem or increased cardiovascular risk to his or her physician for selective exercise testing.

Bibliotherapy—reading self-help books, usually about cognitive-behavioral approaches to depressive disorders—has been relatively well studied. A recent meta-analysis examined 29 studies with pre-post designs. Group differences in the 17 controlled studies yielded a large effect size of 0.77. Participants who read the materials benefitted similarly whether they met in groups or applied the information on their own. Older adults tended to be less depressed at baseline and made smaller treatment gains.7

Clinical Point

Self-administered CBT learned from reading books has been shown to be an effective treatment for mild-to-moderate depression

A study of 31 patients age >60 with mild-to-moderate depression8 compared 16 sessions of professionally administered cognitive-behavioral therapy (CBT) with self-administered cognitive therapy learned from reading a book.9 Both groups showed greater improvement in depressive symptoms compared with a control group. Subjects in the CBT group did somewhat better during the trial, but at 3-month follow-up most patients in both treatment groups no longer met diagnostic criteria for MDD.

Conclusion. Evidence supports bibliotherapy as an effective treatment for mild-to-moderate depression. No convincing data support its use as a complementary treatment, but it poses virtually no risk.

St. John’s wort (Hypericum perforatum) has been extensively studied for depressive disorders, with 29 RCTs in a meta-analysis of MDD trials through July 2008.10 Another meta-analysis compared St. John’s wort with selective serotonin reuptake inhibitors (SSRIs) in 13 studies through June 2008.11 These and most RCTs have found St. John’s wort significantly more effective than placebo in reducing depressive symptoms.

Data selected from double-blind RCTs totaling 217 patients with mild depression [Hamilton Depression Rating Scale (HDRS) scores <20]>12 Studies routinely show that treating MDD with St. John’s wort is comparable to using tricyclic or SSRI antidepressants.

Side effects with St. John’s wort generally are no different than with placebo and significantly less than with comparison treatments. Even so, using St. John’s wort instead of SSRIs for MDD remains controversial.

Studies vs SSRIs. Many of the favorable St. John’s wort trials were conducted in Europe, particularly in Germany. Two large RCTs conducted in the United States reported that the St. John’s wort standardized extract LI-160 was not more effective than placebo, but neither could be clearly interpreted as negative for St. John’s wort:

  • In an 8-week trial, St. John’s wort and placebo groups improved significantly but at unusually low rates. The remission rate with St. John’s wort was small but significantly higher than with placebo.13

  • A study sponsored by the National Institute of Mental Health compared St. John’s wort, 900 to 1,500 mg/d; sertraline, 50 to 100 mg/d; and placebo in 340 adults with MDD. No positive effects were found for St. John’s wort or sertraline.14

Side effects. St. John’s wort can affect blood levels of circulating medications metabolized by the cytochrome P450 liver enzyme system, including tricyclic antidepressants. Case studies have reported pregnancy from oral contraceptive failure, skin rashes, headache, and mania with St. John’s wort use. Although these reports are disturbing, St. John’s wort’s side effects when compared with SSRIs have been less frequent (40% vs 49%) and milder (clinical trial dropout rate 2% vs 7%).11

Conclusion. Standardized extracts of St. John’s wort—particularly WS5570, 300 mg tid, and ZE117, 250 mg bid—appear to be effective treatments, especially for mild-to-moderate MDD. Because St. John’s wort is available without prescription and can interact with SSRIs or other antidepressants:

  • care is required for its complementary use

  • it is important to ask if patients are using St. John’s wort on their own.

St. John’s wort is used as a first-line depression treatment in Europe, but U.S. physicians may be less familiar with its potential interactions with other medications. We recommend that you consider St. John’s wort:

Clinical Point

Consider St. John’s wort for first-line use only when you can adequately gauge its effects on your patient’s other medications

  • for first-line use only when you can adequately gauge its effects on your patient’s other medications

  • especially for depressed patients who cannot tolerate SSRIs.

SAMe is a metabolite involved in bio-synthesis of norepinephrine, serotonin, and dopamine.15 SAMe salts (such as 1,4-butanedisulfonate) are used as an over-the-counter supplement for depression treatment. Dozens of RCTs show SAMe has greater efficacy than placebo and positive effects comparable to those of standard antidepressants. In a meta-analysis of 28 RCTs by the Agency for Healthcare Quality and Research, SAMe produced significantly greater symptom improvement compared with placebo.16

SAMe has become a popular alternative treatment for depression since its introduction to the United States in the late 1990s, but it has been studied in only 2 U.S. open trials. One showed SAMe to be very effective in reducing depressive symptoms in patients with HIV/AIDS.17 The other found a 50% response rate and 43% remission rate with adjunctive SAMe, 800 to 1,600 mg/d for 6 weeks, in 30 adults with MDD who failed to respond adequately to SSRIs or the serotonin-norepinephrine reuptake inhibitor (SNRI) venlafaxine. The most common side effects were gastrointestinal (GI) symptoms and headaches.18 This open trial led to an ongoing National Institutes of Health-sponsored RCT on the safety and efficacy of SAMe for patients with treatment-resistant depression.

Conclusion. SAMe appears to have a faster onset of antidepressant effect than standard SSRIs or SNRIs and a favorable side-effect profile, which make the lack of rigorous trials in the United States striking. We recommend that you consider SAMe:

Clinical Point

SAMe could be useful as a complementary treatment to speed the onset of antidepressant effects

  • as an adjunct in patients with incomplete response to standard treatments

  • as a complementary treatment to speed onset of antidepressant effects.

Polyunsaturated fatty acids (PUFAs), usually from fish oils, have long been popular nutritional supplements because of their beneficial effects on cholesterol and cardiovascular health. Omega-3 and omega-6 fatty acids are the most common PUFAs. The omega-3 PUFAs include eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).

Four meta-analyses independently looked at largely the same dozen RCTs through 2006 and found that 1 to 2 grams daily of omega-3 PUFAs was significantly more effective at reducing depressive symptoms than placebo.1922 Other data suggest that omega-3 PUFAs can induce depression remission in depressed Parkinson’s disease patients23 and depressed pregnant women.24 Since 2006, however, findings have been inconsistent. Several trials have found PUFAs no more effective than placebo.2527

An 8-week double-blind study compared EPA, 1 gram daily; fluoxetine, 20 mg/d; or both agents in 60 outpatients with MDD. Response rates—as measured by ≥50% reduction in baseline HDRS scores—were 50% with fluoxetine, 56% with EPA, and 81% with combination therapy.28

Clinical Point

Although PUFAs’ therapeutic effects remain unclear, they appear safe to use as adjuncts if standard treatment is not satisfactory

Conclusion. Questions remain about dosing, ratio of EPA to DHA, patient selection, and baseline blood levels of PUFAs compared with response. PUFAs have a benign side-effect profile, with occasional reports of diarrhea or GI upset. Although their therapeutic effects are being clarified, PUFAs appear safe to recommend as an adjunct treatment if standard care is not satisfactory.

Insufficient evidence

L-tryptophan. It seems reasonable to expect a serotonin precursor to increase serotonin in the CNS and improve depressive symptoms. Of 111 trials on L-tryptophan for depression, however, only 2 met the quality criteria for inclusion in a recent meta-analysis.29 Combining the 2 trials showed L-tryptophan alone and in combination with a tricyclic antidepressant was more effective than placebo for treating depressive disorders in adults.

Conclusion. Very little research continues to test L-tryptophan as a viable CAM for depressive disorder. Its serious side effect of eosinophilia-myalgia syndrome makes clinical use of this agent unlikely.

Acupuncture. Numerous small studies with questionable controls, different needling placements, and poor allocation concealment and blinding limit the ability to draw conclusions about acupuncture for treating depression (Table 4). A recent meta-analysis by Wang et al30 added 2 Chinese trials not included in an earlier review31 and found acupuncture significantly reduced depressive symptoms. No consistent differences were detected in response or remission rates, however.

Conclusion. Evidence is methodologically weak, and the use of acupuncture as an alternative or complementary treatment of depression is questionable.


Table 4
Acupuncture: Insufficient evidence of antidepressant effect

Literature review

Methodology

Conclusion

Mukaino et al, 2005

Systematic review of 7 RCTs including 509 patients; compared either manual or electroacupuncture with any control procedure

Inconsistent evidence of manual acupuncture’s effectiveness vs sham; electroacupuncture’s effect may be similar to that of antidepressant medication and merits further study

Leo and Ligot, 2007

Systematic review of 9 RCTs, 5 considered low quality; some focused on very specific populations (ie, hospitalized stroke patients or pregnant depressed patients)

Evidence inconclusive because of study designs and methodologies

Smith and Hay, 2005

Meta-analysis of 7 trials including 517 adults with mild-to-moderate depression; 5 trials (409 participants) compared acupuncture with medication; 2 trials compared acupuncture with wait list or sham acupuncture

No difference between acupuncture and medication; study quality too poor to support acupuncture’s efficacy

Wang et al, 2008

Meta-analysis of 8 small RCTs totalling 477 subjects (256 received active acupuncture, remainder received sham acupuncture); sham acupuncture design, number of acupuncture sessions, and duration varied among studies

Significant reduction in HRSD or BDI scores for acupuncture vs sham, but no significant effect of acupuncture on response or remission rates

BDI: Beck Depression Inventory; HRSD: Hamilton Rating Scale for Depression; RCT: randomized controlled trial

Source:
Mukaino Y, Park J, White A, et al. The effectiveness of acupuncture for depression—a systematic review of randomised controlled trials. Acupunct Med. 2005;23(2):70-76.
Leo RJ, Ligot JS Jr. A systematic review of randomized controlled trials of acupuncture in the treatment of depression. J Affect Disord. 2007;97(1-3):13-22.
Smith CA, Hay PPJ. Acupuncture for depression. Cochrane Database Syst Rev. 2005;(2):CD004046.
Wang H, Qi H, Wang BS, et al. Is acupuncture beneficial in depression? A meta-analysis of 8 randomized controlled trials. J Affect Disord. 2008;111(2-3):125-134.

Related resources

Drug brand names

    Fluoxetine • Prozac
    Imipramine • Tofranil
    Lithium • Eskalith, Lithobid
    Sertraline • Zoloft
    Venlafaxine • Effexor

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

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