Regarding the Orthomolecular Approach

Travel back to the days when nutrients were the focus of a brave few medical professionals who believed that inflammation was a key factor in mental health, along with nutrient depletion.
These were the Orthomolecular Pioneers of the 1950s.

" Is depression a kind of allergic reaction?

A growing number of scientists are suggesting that depression is a result of inflammation caused by the body’s immune system

by Caroline Williams

Barely a week goes by without a celebrity “opening up” about their “battle with depression”. This, apparently, is a brave thing to do because, despite all efforts to get rid of the stigma around depression, it is still seen as some kind of mental and emotional weakness.
But what if was nothing of the sort? What if it was a physical illness that just happens to make people feel pretty lousy? Would that make it less of a big deal to admit to? Could it even put a final nail in the coffin of the idea that depression is all in the mind?
According to a growing number of scientists, this is exactly how we should be thinking about the condition. George Slavich, a clinical psychologist at the University of California in Los Angeles, has spent years studying depression, and has come to the conclusion that it has as much to do with the body as the mind. “I don’t even talk about it as a psychiatric condition any more,” he says. “It does involve psychology, but it also involves equal parts of biology and physical health.”
The basis of this new view is blindingly obvious once it is pointed out: everyone feels miserable when they are ill. That feeling of being too tired, bored and fed up to move off the sofa and get on with life is known among psychologists as sickness behaviour. It happens for a good reason, helping us avoid doing more damage or spreading an infection any further.
It also looks a lot like depression. So if people with depression show classic sickness behaviour and sick people feel a lot like people with depression – might there be a common cause that accounts for both?
The answer to that seems to be yes, and the best candidate so far is inflammation – a part of the immune system that acts as a burglar alarm to close wounds and call other parts of the immune system into action. A family of proteins called cytokines sets off inflammation in the body, and switches the brain into sickness mode.
Both cytokines and inflammation have been shown to rocket during depressive episodes, and – in people with bipolar – to drop off in periods of remission. Healthy people can also be temporarily put into a depressed, anxious state when given a vaccine that causes a spike in inflammation. Brain imaging studies of people injected with a typhoid vaccine found that this might be down to changes in the parts of the brain that process reward and punishment.

Advertisement

There are other clues, too: people with inflammatory diseases such as rheumatoid arthritis tend to suffer more than average with depression; cancer patients given a drug called interferon alpha, which boosts their inflammatory response to help fight the cancer, often become depressed as a side-effect.
As evidence like this continues to stack up, it’s not surprising that some people have shifted their attention to what might be causing the inflammation in the first place. Turhan Canli of Stony Brook University in New York thinks infections are the most likely culprit, and even goes as far as to say that we should rebrand depression as an infectious – but not contagious – disease.
Others aren’t willing to go that far, not least because infection is not the only way to set off inflammation. A diet rich in trans fats and sugar has been shown to promote inflammation, while a healthy one full of fruit, veg and oily fish helps keep it at bay. Obesity is another risk factor, probably because body fat, particularly around the belly, stores large quantities of cytokines.
Add this to the fact that stress, particularly the kind that follows social rejection or loneliness, also causes inflammation, and it starts to look as if depression is a kind of allergy to modern life – which might explain its spiralling prevalence all over the world as we increasingly eat, sloth and isolate ourselves into a state of chronic inflammation.
If that’s the case, prevention is probably the place to start. It’s not a great idea to turn off inflammation entirely, because we need it to fend off infections, says Slavich, but “lowering levels of systemic inflammation to manageable levels is a good goal to have”.
The good news is that the few clinical trials done so far have found that adding anti-inflammatory medicines to antidepressants not only improves symptoms, it also increases the proportion of people who respond to treatment, although more trials will be needed to confirm this. There is also some evidence that omega 3 and curcumin, an extract of the spice turmeric, might have similar effects. Both are available over the counter and might be worth a try, although as an add-on to any prescribed treatment – there’s definitely not enough evidence to use them as a replacement.
In between five to 10 years, says Carmine Pariante, a psychiatrist at Kings College London, there may be a blood test that can measure inflammation in people with depression so that they can be treated accordingly. Researchers have already come up with a simple finger-prick test that reliably measures inflammation markers in a single drop of blood.
And as for the stigma – could it really be killed off by shifting the blame from the mind to the body? Time will tell. This is not the first time that depression has been linked to a physical phenomenon, after all. A recent survey found that despite wider awareness of the theory that “chemical imbalances” in the brain cause depression, this has done nothing to reduce stigma; in fact, it seemed to make matters worse.
This time, though, the target is not any kind of brain or mind-based weakness but a basic feature of everyone’s body that could strike anyone down given the right – or wrong – turn of events. And if that doesn’t inspire a greater sympathy and understanding, then nothing will.
• This article was amended on 4 January 2015. It originally stated that curcumin was an extract of cumin. This has now been corrected." SOURCE

The Better Benefits of Nutrition

As the new DSM manual, used to establish insurance billing guidelines for the most part, is under development it seems likely that nutritional care for mental health and addiction disorder will most likely continue to be ignored. 

It is unfortunate that this researcher did not continue research utilizing nutritional therapy to see how improved nutrition supports mood and health.

Usually sweet cravings are indicative of deficiency in B vitamins and in many cases, protein as well.

At CHI we think it is better to treat nutritionally than rely on carcinogenic-benzene-fluoride containing antidepressants.

Sweet tooth 'hints at depression'

While most children like sweets, those with an extra-sweet tooth may be depressed or at higher risk of future alcohol problems, researchers say.
The US team report in the journal Addiction that certain children are especially drawn to very sweet tastes.
These were children who had a close relative with an alcohol problem or who themselves had symptoms of depression.
But it is unclear if the preference for the very sweet is down to genuine chemical differences or upbringing.

The researchers say sweet taste and alcohol trigger many of the same reward circuits in the brain.

“ It may be that even higher levels of sweetness are needed to make depressed children feel better ”
Lead researcher Julie Mennella

Lead author Julie Mennella said: "We know that sweet taste is rewarding to all kids and makes them feel good.
"In addition, certain groups of children may be especially attracted to the intense sweetness due to their underlying biology."
Experts say alcoholics tend to have a sweet tooth.
But the link is less clear in children. Other US researchers have shown that a preference for the sweetest drinks was found in the ones undergoing growth spurts.
In the latest study, the scientists at the Monell Chemical Senses Center asked 300 children aged five to 12, of whom half had a family member with alcohol dependency, to taste five sweet water drinks containing different amounts of sugar.
The children were asked to say which tasted the best and were also asked questions to check for depressive symptoms.
A quarter had symptoms that the researchers believed suggested they might be depressed.
Sweet tooth
Liking for intense sweetness was greatest in the 37 children who had both a family history of alcoholism and reported depressive symptoms.

“ The taste difference may be explained by differences like parental control over sweet consumption ”
Taste expert Professor Tim Jacob

These children preferred the drink containing the most sugar - 24% sucrose, which is equivalent to about 14 teaspoons of sugar in a cup of water and more than twice the level of sweetness in a typical cola.
This was a third more intense than the sweetness level preferred by the other children.
The researchers then decided to test whether the children's taste difference had any impact on their reaction to pain or discomfort - past studies have suggested sweets may help act as analgesics as well as mood lifters.
They found non-depressed children were able to tolerate keeping their hands in very cold water for longer if they had a sugar hit.
However, the extra sugar did nothing to the depressed children's pain threshold.
Cardiff University's Professor Tim Jacob, an expert in smell and taste, said the findings were interesting, but that it was hard to make firm conclusions or generalisations from one study alone.
He said the findings could be down to brain chemistry, but might also be explained by behaviour and upbringing.
"While it is true that sweet things activate reward circuits in the brain, the problem is that sweets and sugar are addictive, because the activation of these reward circuits causes opioid release, and with time more is needed to achieve the same effect.
"But the taste difference may be explained by differences like parental control over sweet consumption."

Story from BBC NEWS: http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/8506758.stm
Published: 2010/02/10 © BBC MMX

Therapy Better than Drugs

Now with the specter of universal health care looming upon us with the Daschle/Clinton/Obama clique at hand, I believe we need to be vigilant.

For those of you who recall Hillary's first attempt to force universal coverage for the masses, to the exclusion of her governmental cronies, the Clinton's were pushing for drugs only (such as Prozac) with no therapy.

Of course those of us who have seen the fall out from Prozac and similar fluoride based SSRI drugs, we now have the zombie generation performing homicide and suicide as the fallout.

And of course Big Insurance is sitting on the side lines until after January 20 to get the same handouts as Big Pharma has received over the last eight years.

Obama just doesn't get it when it comes to health care, todays drugs and insurance.

Depression Treatment: Mindfulness-based Cognitive Therapy As Effective As Anti-depressant Medication, Study Suggests

ScienceDaily (2008-12-02) -- Research shows for the first time that a group-based psychological treatment, Mindfulness Based Cognitive Therapy, could be a viable alternative to prescription drugs for people suffering from long-term depression. In this study, MBCT proved as effective as maintenance anti-depressants in preventing a relapse and more effective in enhancing peoples' quality of life. The study also showed MBCT to be as cost-effective as prescription drugs in helping people with a history of depression stay well in the longer-term. ... > read full article

No Difference in Psych Drugs for Depression

SSRI group of anti-depressant pharmaceuticals have been problematic ever since Prozac was introduced some decades ago. The list of side effects and untoward behavior related to fluoride containing drugs also creates other concerns.

If it all boils down to looking at the issues of side effects, cost and response then I would suggest that better evaluation of the person's state of general health, especially endocrine health, and nutritional status be addressed before prescribing any of these drugs.

For example, I learned that a friend was taking Chantix in an effort to stop smoking. My knowledge of this person's situation is that he was smoking to cover up a deep seated emotionally painful life event.

After he started on Chantix, and while he was taking endocrine system altering drugs for prostate cancer, he became depressed.

He was just written an Rx for Lexapro, however, no effort was taken to evaluate his history and symptoms or look at drug side effects and related issues.

I can't quite get the current ethic to overlook this basic health care function, but perhaps it is why I gave up on my work in mainstream medicine 15 years ago after I was attacked by a young girl taking Zoloft, and seriously injured.

Internist Group Finds No Efficacy Difference Among Modern Antidepressants
By John Gever, Senior Editor, MedPage Today
Published: November 17, 2008

Practice Guidelines


PHILADELPHIA, Nov. 17 -- Second-generation antidepressants all have similar efficacy, so physicians should base their medication choices for depressed patients on side effects, cost, and patient response, according to a new practice guideline from the American College of Physicians.

Clinicians should also begin monitoring patients for adverse effects and clinical response within one to two weeks of starting antidepressant therapy, recommended Amir Qaseem, M.D., Ph.D., M.H.A., of the American College of Physicians, and the other authors of the guideline, published in the Nov. 18 issue of Annals of Internal Medicine.

"The current evidence did not show any clinically significant differences between efficacy, effectiveness, or quality of life between various second-generation antidepressants," said Dr. Qaseem.
Action Points

* Explain to interested patients that a treatment guideline from the American College of Physicians recommends that second-generation antidepressant choices be made on the basis of side effects, cost, and patient preference, since efficacy of these drugs is equivalent.

* Explain that individual patient factors should always guide treatment decisions.

* Note that the guidelines do not address use of older medications that are still available and may be appropriate for some patients.

The findings do not differ markedly from the American Psychiatric Association's current practice guideline on major depressive disorder, last updated in 2005.

"The effectiveness of antidepressant medications is generally comparable between classes and within classes of medications," according to the APA guideline. "Therefore, the initial selection of an antidepressant medication will largely be based on the anticipated side effects, the safety or tolerability of these side effects for individual patients, patient preference, quantity and quality of clinical trial data regarding the medication, and its cost."

The ACP's recommendations were based on a review of more than 200 published studies of a dozen antidepressants, conducted by a separate group of researchers led by Gerald Gartlehner, M.D., of Danube University in Krems, Austria.

Drugs covered in the review included:

* Fluoxetine (Prozac)
* Sertraline (Zoloft)
* Paroxetine (Paxil)
* Bupropion (Wellbutrin)
* Citolapram (Celexa)
* Escitolapram (Lexapro)
* Duloxetine (Cymbalta)
* Fluvoxamine (Luvox)
* Mirtazapine (Remeron)
* Trazodone (Desyrel)
* Nefazodone (Serzone)
* Venlafaxine (Effexor)

The guideline also calls for physicians to modify treatment if patients fail to respond adequately within six to eight weeks.

Drugs that show adequate symptom relief should be maintained for four to nine months after a major depressive episode, or longer in the case of recurrent episodes.

The review and guidelines do not address more traditional medications such as tricyclic antidepressants and monoamine oxidase inhibitors.

Dr. Qaseem and colleagues said these agents are no longer in common use because newer drugs have similar effectiveness with less toxicity.

Among the newer drugs, the review disclosed no efficacy differences among patient subgroups defined by age, sex, race-ethnicity, or comorbid conditions.

A few studies identified certain agents as better than others in patients with other neuropsychiatric symptoms besides depression, such as insomnia or anxiety. But these studies were mostly not of the highest quality, and others found little or no difference.

Those findings stand in contrast to the APA's depression guideline, which suggests that some subgroups may benefit more than others from particular agents, although with no specifics.

The ACP review found relatively few clear differences between second-generation drugs in side effects.

"Most of the second-generation antidepressants had similar adverse events, with some differences in the incidence of specific adverse events," according to the guideline authors.

Nausea and vomiting were more common with venlafaxine than with other agents, they noted, whereas sertraline appeared especially prone to cause diarrhea.

Weight gain was more frequent with mirtazapine and paroxetine, and drowsiness was relatively common with trazodone compared with several other drugs.

Sexual adverse effects were another area where drugs have different profiles.

For example, bupropion was less likely to have sexual adverse effects than fluoxetine and sertraline, whereas paroxetine had relatively high rates.

The ACP review found little difference between agents in suicidality, although non-fatal suicide attempts appeared to be more common with SSRIs (citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline, and venlafaxine) than with other drug classes.

Few data were available on other severe adverse effects such as seizures, cardiovascular problems, liver toxicity, hyponatremia, or serotonergic abnormalities, the researchers said.

The guideline graded the evidence and recommendations by using the American College of Physicians clinical practice guidelines grading system.

All four recommendations were considered to be strong with moderate quality evidence.

The American College of Physicians funded the review underlying the recommendations.

Authors of the guideline reported relationships with Atlantic Philanthropies, Novo Nordisk, Boehringer Ingelheim, Sanofi Pasteur, and Endo.

Authors of the literature review reported relationships with GlaxoSmithKline, Pfizer, Wyeth-Ayerst, Shire Pharmaceutical, Phillips Lytle, Bristol-Myers Squibb, Novartis, Robert Wood Johnson Foundation, and M-3 Corporation.

Primary source: Annals of Internal Medicine
Source reference: Qaseem A, et al "Using second-generation antidepressants to treat depressive disorders: a clinical practice guideline from the American College of Physicians" Ann Intern Med 2008; 149: 725-33.

Additional source: Annals of Internal Medicine
Source reference: Gartlehner G, et al "Comparative benefits and harms of second-generation antidepressants: background paper for the American College of Physicians" Ann Intern Med 2008; 149: 734-50.

And as an additional consideration, it has been suggested that more than 85% of physicians are unaware that Serotonin Syndrome even exists.

How Common or Significant Is Serotonin Syndrome?

Joel Lamoure, RPh, BSP, FASCP
Medscape Pharmacists. 11/10/2008 ©2008 Medscape

Question
We are seeing more patients who are taking multiple antidepressants of different classes. All drug interaction programs cite drug-drug interactions leading to the potentially severe toxicity known as serotonin syndrome. Just how common and clinically significant is serotonin syndrome?

Response from Joel Lamoure, RPh, BSP, FASCP
Assistant Professor, Department of Psychiatry, University of Western Ontario, London, Ontario, Canada; Mental Health Pharmacist, London Health Sciences Centre, London, Ontario, Canada

The Toxic Exposure Surveillance System reviewed cases from office-based practices, inpatient settings, and emergency departments and found that during 2004, selective serotonin reuptake inhibitors (SSRIs) caused significant toxic effects in 8187 persons, leading to 103 deaths.[1] The true incidence of serotonin syndrome and associated morbidity are likely to be much greater. This syndrome may be underdiagnosed given the fact that SSRIs are not the only contributing class of agents. Moreover, it has been suggested that more than 85% of physicians are unaware that the syndrome even exists.[2]

Serotonin syndrome is a condition caused most often by the concurrent use of 2 or more agents that enhance synaptic serotonin levels.[3] A triad of clinical changes -- cognitive, neuromuscular, and autonomic -- characterizes this syndrome. Specific changes may include confusion, delirium, agitation, restlessness, muscular spasms, hyperpyrexia, diaphoresis, tachycardia, blood pressure fluctuations, mydriasis, nausea, or diarrhea.[4,5] Symptoms often develop within 2 hours of the increase in the synaptic level of serotonin.[6] The clinician must be proactive to identify the early symptoms, such as cognitive changes, when they occur.

Confusion about symptoms may be responsible for the difficulty in assessing the actual incidence of serotonin syndrome.[2] Agitation, a cardinal symptom of serotonin syndrome, is clinically similar to activation, an adverse effect associated with SSRI use.[7]

Polypharmacy is pandemic, and the incidence of serotonin syndrome may be on the rise. Both drug factors and patient factors can contribute to the toxicity of SSRIs in some individuals. A wide range of medications can increase serotonin levels in the body. When these agents are combined, the risk of serotonin syndrome increases. Drug classes implicated include anti-migraine agents (eg, triptans); antidepressants (eg, SSRIs, serotonin-norepinephrine reuptake inhibitors, buspirone, tricyclic antidepressants, monoamine oxidase inhibitors); antipsychotics; anticonvulsants; anti-Parkinsonian agents; analgesics (eg, meperidine, tramadol); over-the-counter products (eg, medications containing dextromethorphan); herbal products (eg, St. John's Wort); and antibiotics (eg, linezolid).[6,8-14]

Concurrent use of medications that interact with serotonergic drugs through the inhibition of the cytochrome P450 pathway can also contribute to serotonin syndrome.[15] For example, extra caution should be observed if a patient is taking an SSRI in addition to a cytochrome P450 2D6 (CYP2D6) inhibitor because SSRIs are extensively hepatically metabolized by this isozyme.

Susceptibility to the serotonin syndrome can also be conferred by patient factors, such as the capacity to metabolize certain drugs. One of the key enzymes related to adverse drug reactions, the CYP2D6 system, has a high degree of genetic polymorphism.[16] An example of this was reported in a study of 4 elderly patients who ostensibly developed serotonin syndrome as a result of an interaction between tramadol and mirtazapine.[17] The patients had auditory and visual hallucinations, myoclonus, hypertension, and changes in behavior. Tramadol may be subject to genetic polymorphism; about 7% of whites are poor metabolizers of CYP2D6.[18,19] Consequently, these patients would have higher serum levels of tramadol and be at increased risk for serotonin syndrome when a second serotonergic agent is added.[18]

Although rare in monotherapy, serotonin syndrome is more prevalent with polypharmacy, even across medication classes. When a computer flags this interaction, the clinician should consider the whole patient: What medications has the patient taken previously? What adverse reactions have previously been experienced? When making an evidence-based recommendation, it is essential to apply the therapeutic thought process and carry out a sound risk-benefit assessment. Awareness of serotonin syndrome and education about its effects are vital. All of these factors must be considered, lest all the "holes in the Swiss cheese line up" and the patient comes to harm.[20]

The author acknowledges Jessica Stovel, pharmacist, and Katherine Bateman, pharmacy resident at London Health Sciences Centre, for their research and contributions to this article.

References
Watson WA, Litovitz TL, Rodgers GC, et al. 2004 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. 2005;23:589-666. Abstract
Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med. 2005;352:1112-1120. Abstract
Dunkley EJ, Isbister GK, Sibbritt D, Dawson AH, Whyte IM. The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity. Q J Med. 2003;96:635-642.
Lane R, Baldwin D. Selective serotonin reuptake inhibitor-induced serotonin syndrome: review. J Clin Psychopharmacol. 1997;17:208-221. Abstract
Isbister GK, Bowe SJ, Dawson A, Whyte IM. Relative toxicity of selective serotonin reuptake inhibitors (SSRIs) in overdose. J Toxicol Clin Toxicol. 2004;42:277-285. Abstract
Turner EH, Loftis JM, Blackwell AD. Serotonin a la carte: supplementation with the serotonin precursor 5-hydroxytryptophan. Pharmacol Ther. 2006;109:325-338. Abstract
Vorstman J, Lahuis B, Buitelaar JK. SSRIs associated with behavioral activation and suicidal ideation. (letter) J Am Acad Child Adolesc Psychiatry. 2001; 40:1364-1365.
Mills K. Serotonin syndrome. A clinical update. Crit Care Clin. 1997;13:763-783. Abstract
Mitchell, PB. Drug interactions of clinical significance with selective serotonin reuptake inhibitors. Drug Sa.f 1997;17:390-406.
Egberts AC, ter Borgh J, Brodie-Meijer CC. Serotonin syndrome attributed to tramadol addition to paroxetine therapy. Int Clin Psychopharmacol. 1997;12:181-182. Abstract
Manos G. Possible serotonin syndrome associated with buspirone added to fluoxetine. Ann Pharmacother. 2000;34: 871-874. Abstract
Sclar DA , Robison LM , Skaer TL. Concomitant triptan and SSRI or SNRI use: a risk for serotonin syndrome. Headache. 2008;48:126-129. Abstract
Lavery S, Ravi H, McDaniel WW, Pushkin YR. Linezolid and serotonin syndrome. Psychosomatics. 2001;42:432-434. Abstract
Gardner DM, Lynd LD. Sumatriptan contraindications and the serotonin syndrome. Ann Pharmacother. 1998;32:33-38. Abstract
Looper KJ. Potential medical and surgical complications of serotonergic antidepressant medications. Psychosomatics. 2007;48:1-19. Abstract
Ingelman-Sundberg M, Genetic polymorphisms of cytochrome P450 2D6 (CYP2D6): clinical consequences, evolutionary aspects and functional diversity. Pharmacogenomics J. 2005;5: 6–13.
Gnanadesigan N, Espinoza RT, Smith R, Israel M, Reuben DB. Interaction of serotonergic antidepressants and opiod analgesics: Is serotonin syndrome going undetected? J Am Med Dir Assoc. 2005;6:265-269.
Gan SH, Ismail R, Wan Adnan WA, Wan Z. Correlation of tramadol pharmacokinetics and CYP2D6*10 genotype in Malaysian subjects. J Pharm Biomed Anal. 2002;30:189-195. Abstract
Enggaard TP, Poulsen L, Arendt-Nielsen L, Brosen K, Ossig J, Sindrup SH. The analgesic effect of tramadol after intravenous injection in healthy volunteers in relation to CYP2D6. Anesth Analg. 2006;102:146-150. Abstract
Reason J. Human error: models and management. BMJ. 2000;320:768-770. Abstract

Suggested Readings: Evans RW. The FDA alert on serotonin syndrome with combined use of SSRIs or SNRIs and triptans: an analysis of the 29 case reports. Medscape General Medicine. 2007;9:48. Available at: http://www.medscape.com/viewarticle/561741 Accessed October 31, 2008.

St. John's Wort treats major depression

Over many years of clinical and educational work in the areas of medicine and natural health care I have seen very good results from using properly prepared extracts of St. John's Wort. This has been in contrast to so many so-called studies about this herb in an effort to downplay effectiveness.

In 2003 I wrote on this issue.

In 2005 I reported on this issue.

And for those of us who now, in the northern hemisphere, are heading into the darker, colder months, I mention St. John's Wort (SJW) in this article from 2004.

Amidst all the work that has shown SJW to be effective for depression and mood elevation among its other benefits I was subjected to a substantial amount of verbal attacks for my position from psychologists and others in mainstream medicine who have a vested interest in promoting drugs, while denigrating natural therapies.

Needless to say, SJW is not fluoride based like the majority of SSRI anti-depressants and it has few if any of the serious side effects similar to these pharmaceuticals. The herb did not push tryptophan out of favor either.

Additionally SJW is a nervous system nutritive and it acts as a very potent form of natural interferon which reinforces its anti-viral benefits.

For excellent quality spagyrically prepared SJW extract please contact us.

St. John's Wort effective for depression
Tue Oct 7, 2008

The herbal remedy St. John's Wort effectively treats symptoms of major depression, an analysis of previous studies found on Wednesday.

St. John's Wort extracts tested in the different trials were better than placebos and as effective as standard antidepressants with fewer side effects, the researchers reported in the Cochrane review, a journal that analyses medical and scientific studies.

"The studies came from a variety of countries, tested several different St. John's Wort extracts, and mostly included patients suffering from mild to moderately severe symptoms," Klaus Linde of the Center for Complementary Medicine in Munich, Germany wrote.

The herb works in a similar way to some prescription antidepressants by increasing the brain chemical serotonin, involved in controlling mood.

The Cochrane review analyzed 29 studies that together included 5,489 men and women with symptoms of major depression and compared the remedy's effectiveness with placebos and standard treatments.

The researchers found that St. John's Wort extracts were not only effective but that fewer people taking them dropped out of the trials due to adverse side effects.

They also noted that results were more favorable in German-speaking countries where doctors often prescribe the remedy and cautioned against using the remedy without medical advice because the extracts can affect other drugs' work.

In Germany such herbal treatments are also more controlled for content, unlike in many other markets where the quality and content of herbal products may vary considerably.

"Using a St. John's Wort extract might be justified, but products on the market vary considerably, so these results only apply to the preparations tested," Linde said.

Depression is a leading cause of suicide and affects about 121 million people worldwide, according to the World Health Organization. Standard treatments include Prozac, which U.S. drugmaker Eli Lilly and Co introduced in 1987.

The treatment, which belongs to a class of compounds called selective serotonin reuptake inhibitors (SSRIs), is now off patent and widely available generically as fluoxetine.

(Reporting by Michael Kahn; Editing by Maggie Fox)
Copyright © 2008 Reuters Limited.