Friday, September 17, 2010

Eleviv – What to Expect?

If you’re reading this blog, then it’s likely that you have already heard of Eleviv – the natural dietary supplement for improving “Vigor” from Xango. If this is your first exposure to Eleviv, then you may be wondering what exactly “Vigor” refers to – or if you’ve been using Eleviv for a period of time, you may be wondering how to best explain Eleviv to people you may want to share it with.

As the formulator of Eleviv, the way that I typically describe the product to people is that it is the BEST and ONLY dietary supplement that I know of for significantly improving psychological Vigor in people with stress. I then tell them that researchers define “Vigor” as “a 3-tiered sustained mood state characterized by physical energy, mental acuity, and emotional well-being.”

As such, Vigor is a true measure of wellness because it encompasses much more than simply feeling “energetic” or being in a “good mood” or having a “sharp” mind. People with high Vigor scores are those “can-do” individuals who feel like getting things done – they’re motivated – they have a certain “momentum” in their daily lives – and for lots of people, “Vigor” is a state that they have not experienced in many years.Feelings of low Vigor are common in our modern stress-filled world. Millions of us succumb to chronic stress and end up feeling “tired, stressed and depressed” because of specific metabolic imbalances (specifically, disruptions in hormones like cortisol and testosterone, and neurotransmitters like dopamine and norepinephrine) that lead to feelings of reduced Vigor.

When hormones like cortisol and testosterone are out of balance – we lack physical energy, so we often feel constantly fatigued and depressed. When neurotransmitters like dopamine and norepinephrine are out of balance – we lack mental energy, so we often feel unfocused and irritable. When we restore balance between our hormones and neurotransmitters, we also restore our feelings of physical and mental energy (the combination of which is what we refer to as Vigor) – and Eleviv is a novel and effective approach to doing just that.

Can You Restore Vigor?

Yes! However, very few people outside of the research community have ever even heard of “Vigor” or have any idea that you can achieve it naturally by restoring metabolic balance (the balance between hormones and enzymes and neurotransmitters that have become disrupted by chronic stress).We can attempt to temporarily “reduce” fatigue with an energy drink or other stimulant, but that approach does not restore Vigor. Instead, energy drinks and related options are inadequate solutions because they do not address the underlying cause of low Vigor (metabolic imbalance). In fact, not only do energy drinks not restore Vigor, they are more likely to increase tension and anxiety (two other indications of “mood state” that we can measure in our studies). True Vigor goes much beyond what most people associate with energy/fatigue—it really gets to the heart of how people want to feel.

Improving Vigor (Restoring Metabolic Balance)

Over the past 6 years, our group has conducted a series of human clinical studies in “stressed” volunteers, as short as 1-week and as long as 12 weeks, where we have been able to significantly improve Vigor by 25-30% (following a restoration of metabolic balance). This means that although chronic stress disrupts metabolic balance, we now know that restoring metabolic balance helps to improve feelings of Vigor quickly (within 1 week) and that those changes persist for months thereafter – indicating a unique and lasting improvement in overall well-being that is far superior to the fleeting and temporary effects of energy drinks and related products.

Typically, we will see very rapid improvements in indices of mental energy following a rebalancing of neurotransmitters (which tend to respond faster to metabolic interventions) – followed soon thereafter by improvements in physical energy as hormone balance is restored (which takes longer depending on the degree and duration of stress that the individual has been exposed to).

I feel very strongly—in fact, I am certain—that once you understand the relationship between modern stressors, your metabolic balance, and its effects on your long-term health, you will be motivated to do something about getting your metabolism back into balance.The bottom line is that living in the twenty-first century brings with it a certain amount of unavoidable stress—and with that stress comes a certain degree of disrupted metabolism. It is how we deal with that stress and what we do to control those hormone levels that can make all the difference when it comes to our long-term health and how we feel on a daily basis.

Shawn M Talbott, Ph.D. is the author of “Vigor - 7 Days to Unlimited Energy, Focus, and Well-Being” (

Sunday, August 29, 2010

Vigor paper published in Progress in Nutrition Journal

Lots of people have been asking me about the new manuscript on Vigor published in the peer-reviewed scientific journal, Progress in Nutrition (Volume 12 - April 2010). The title of the paper is, “Ancient wisdom meets modern ailment – traditional Asian medicine improves psychological Vigor in stressed subjects.”

As you can see from the title, “Ancient wisdom meets modern ailment” - the general idea of the publication is to highlight the fact that ancient practitioners of traditional medicine used natural approaches to solving health problems - and that we can use that ancient wisdom about herbs and nutrients to counteract some of today’s most debilitating conditions (such as chronic stress, Burnout, low mood, fatigue, mental fog, and many others).

The scientific journal, Progress in Nutrition, is a peer-reviewed journal from an Italian publisher that specializes in producing “proceedings” from scientific meetings. I was asked to submit this one on Vigor after delivering an invited presentation on “Traditional Medicine as Modern Dietary Supplements” that I gave at a scientific conference in Hong Kong.

This issue of the Progress in Nutrition journal features the proceedings from the 4th International Symposium on Functional Foods entitled, “New Horizons in Chinese Medicines & Health Foods” that took place at the Hong Kong Polytechnic University (sort of like China’s version of MIT) on October 29-30, 2009.

It was interesting to participate in the Symposium with a broad range of Western scientists and Eastern herbalists. Just as I was speaking about the Western concept of “Vigor” – other scientists were speaking about the Eastern concept of Qi (“life force” – pronounced “Chee”) – and we were both speaking about the SAME concept and using some of the SAME natural approaches to restore Vigor/Qi in the face of various types of stress.

In my presentation and in the Progress in Nutrition manuscript, I outlined some of the early studies on the herbal formula that would eventually become Eleviv – so you will see the very same blend of Eurycoma, Citrus peel, and Green tea noted in the Methods section of the paper.

The text of the summary/abstract appears below. A PDF of the publication can be downloaded (for free) and a color reprint of the Progress in Nutrition article can be purchased in the “Vigor Media” section of

If you’re looking for more information about psychological Vigor, my new book entitled, “Vigor – 7 days to Unlimited Energy, Focus, and Well-Being” (400 pages, including dozens of individual experiences) is available at (all profits to support Operation Smile charity).

I hope you enjoy the manuscript and I hope you will share it with others so that more of us can enjoy the high state of Vigor that we all want.

Summary/Abstract (Progress in Nutrition, Volume 12 (April 2010)

Background: Chronic stress plays a major role in the pathophysiology of many disease states, particularly psychological disorders including depression, chronic fatigue syndrome, anxiety, fibromyalgia, and burnout. These stress-related changes in psychology may be due to both endocrine and behavioral factors – and may be mediated or attenuated by lifestyle factors including diet, exercise, and dietary supplements. Vigor is defined as a 3-tiered sustained mood-state that is characterized by (1) physical energy, (2) mental acuity, and (3) cognitive liveliness. Vigor can also be described as the opposite of “Burnout” (physical fatigue, mental exhaustion, and cognitive weariness). Objective: Our objective was to assess changes in Vigor, Mood State, and Metabolic Hormone Profile (cortisol and testosterone balance) in response to a modest lifestyle intervention including a dietary supplement based on traditional Asian medicine and including Eurycoma longifolia root, Citrus sinensis peel, and Camellia sinensis leaf – each of which is used in traditional Asian medicine to improve “life force” and well-being in fatigued individuals. Methods: We report on 82 subjects – all displaying moderate levels of psychological stress. We measured endocrine parameters [salivary cortisol to testosterone, (C:T) ratio)], and Global Mood State (MOOD) and related subscales: Vigor (V), Fatigue (F), and Depression (D), using the Profile of Mood States (POMS) psychological survey before and after the supplementation intervention. Subjects followed a supplementation periods of either 8-weeks or 12-weeks. Each intervention included recommendations to follow a balanced diet, moderate exercise, and daily supplementation. Results: Compared to pre-supplementation values, post-supplementation measurements indicated significant changes for C:T ratio (-15-19%), MOOD (+20-22%), Vigor (+27-29%), Fatigue (-41-48%), and Depression (-40-52%). Conclusion: These data indicate that factors that are typically disrupted during periods of chronic stress (metabolic hormone profile and psychological mood state) may be positively and significantly impacted by modest changes in diet, exercise and supplementation patterns that mirror those commonly used in traditional Asian medicine.

Saturday, August 28, 2010

Anti-Aging Nutrients?

We get a lot of questions at about supplements for “anti-aging” benefits. Here is a short bit of correspondence that I had with a journalist writing a story on “anti-aging nutrients” - hope you find it interesting...

Hi Wxxx - hope you are well...

Here are some comments for your article on anti-aging supplements, please let me know if you need any further details...

I have written a book focused on aging of the skin - which highlighted the 4 areas (“pillars”) of biochemistry that must be balanced to slow the effects of aging ( - which are:

1. Oxidation (caused by free radicals and controlled by antioxidant nutrients such as vitamins C/E, thiols, carotenoids, and flavonoids)

-Flavonoids in particular are potent antioxidant nutrients because their chemical structure provides multiple active sites to help fight numerous free radicals simultaneously - great dietary sources are tea (catchins), apples (quercetin), berries (anthocyanidin), and citrus (PMFs).

2. Inflammation (caused by an imbalance between inflammatory/antiinflammatory eicosanoids and cytokines and controlled by antiinflammatory types of fatty acids, turmeric, xanthones, etc)

-Eating more fatty fish or supplementing with fish oil provides an antiinflammatory dose of omega-3 fatty acids that can help reset your inflammatory balance. Other good sources of antiinflammatory nutrients are flax seed (omega-3), mangosteen (xanthones), and turmeric (curcumin). 

3. Blood sugar (too much glucose in the blood will “age” tissues prematurely by a process called glycation - so you want to keep blood sugar from getting too high - or fluctuating too much)

-Eating “whole” grains and limiting refined carbs helps control sugar fluctuations, as does combining any carbs with balanced amounts of protein/fat/fiber. Specific nutrients for controlling blood sugar include flavonoids, gymnema, bitter melon, PMFs, and many others.

4. Stress hormones (too much cortisol exposure leads to increased blood sugar and increased inflammation - so controlling cortisol also controls inflammation and blood sugar).

-Any type of stress, but especially the low-grade chronic stress that most of us experience on a daily basis from work, traffic, deadlines, bills, etc tends to result in cortisol overexposure (as well as a drop in testosterone - in women as well as men) and thus lead to fatigue and depression. That same cortisol overexposure also interferes with blood sugar control and with inflammation/oxidation - so getting a handle on stress and on stress hormones is essential for good health. Some nutrients that help rebalance stress hormone exposure include theanine, eurycoma, citrus PMFs, and green tea.

These are just a few suggestions - but I’m happy to expand on them in greater detail if you still need info for your article - just let me know...

All best,



Shawn M. Talbott, Ph.D.

Nutritional Biochemist and Author

NEW BOOK - “Vigor - 7 Days to Unlimited Energy, Focus, and Well-Being” (


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-Killer at Large - an award-winning documentary exploring the causes and solutions underlying the American obesity epidemic  (

-The Health Professionals Guide to Dietary Supplements (Lippincott, Williams & Wilkens) -

-Cortisol Control and the Beauty Connection - The All-Natural Inside-Out Approach to Reversing Wrinkles, Preventing Acne, And Improving Skin Tone (Hunter House) -

-Natural Solutions for Pain-Free Living (Chronicle Publishers - Currant Books)

-The Cortisol Connection - Why Stress Makes You Fat and Ruins Your Health (Hunter House) -

-The Cortisol Connection Diet - The Breakthrough Program to Control Stress and Lose Weight (Hunter House) -

-A Guide to Understanding Dietary Supplements - an Outstanding Academic Text of 2004 (Haworth Press) -

Thursday, July 29, 2010

How do you stay in shape after 40?

I am VERY often asked by friends and colleagues the simple question of “how to stay in shape” given the demands of work, family, travel, and all the rest...

It’s a tough question to answer because it doesn’t help very much to tell someone to “eat right and exercise” - because everyone knows that - it is more the “HOW” of what exactly do DO that gets in our way.

I just answered an email from an old college buddy (not that he or I are actually “old” - so let’s just get that straight right up front)...He asked, “Let me know what you suggest for a 45-year old trying to keep the “glory days” from ending on the roads and the ice rink.

Here is my reply:

John - Here is a quick type of circuit workout that I rely on, especially when low on time and when traveling...They are intense enough to make a difference in your fitness and quick/easy enough to do anywhere and not represent an “obstacle” based on time or equipment constraints.

For eating, I use this approach (myself and in several research studies) that I call the “Helping Hand” (I also write about this in more detail at - it is pretty self-explanatory based on the graphic below and enables you to “count calories” without really counting - pretty much every meal you would create using the Helping Hand ends up at about 400-600 calories. Do this at breakfast, lunch, and dinner and you average out to about 1,500 calories per day (eat a 4th time if you’re exercising that day).

Hope these help - and let me know if you have any questions...


Cal Circuit

Exercises = 8

Work Time = 24min (3 sets)

Warmup – 2min

Cool-down/Stretch – 2min

Rest = 1min between sets 1 & 2 (2min total)



WarmupJumping Jacks (whole body warmup)

Set 1 – 45 seconds ON / 15 seconds OFF

            1min H2O break

Set 2 – 50 seconds ON / 10 seconds OFF

            1min H2O break

Set 3 – 55 seconds ON / 5 seconds OFF

Cool down / Stretch


1.     Sit Jacks (abs)

2.     Bent-over Rows – 60# bar (back)

3.     Jumpies (legs)

4.     Pushups (chest)

5.     Squats – 60# bar (legs)

6.     Upright Rows – 60# bar (shoulders)

7.     Burpies (whole body)

8.     Curls – 60# bar (arms)

Hope that helps a few people - Thanks for reading,



Shawn M. Talbott, Ph.D.

Nutritional Biochemist and Author

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Thursday, May 20, 2010

SAMe (S-adenosyl-L-methionine)

SAMe is a substance naturally found in many of our body’s tissues and it is made up of the amino acid methionine (a sulfur containing amino acid) combined with adenosine. SAMe is used in a number of the body’s processes that require sulfur, especially the methylation reactions. There have been many favorable clinical studies on SAMe that indicate its potential as a therapy for osteoarthritis, depression and liver disease. SAMe’s general mechanism of action as a supplement is as a methyl donor for methylation reactions in our body’s natural processes. A deficiency of SAMe could be caused by a deficiency in the cofactors of its production, such as methionine, choline, and B vitamins. A defect in methylation may also cause a deficiency in SAMe. Overall, SAMe has been found to have anti-inflammatory, analgesic and anti-depressive effects.
One theory on depression and other neuropsychiatric disorders is that they are caused by a defect in our biochemical methylation process. Low levels of folate (used in methylation reactions) and serotonin have been linked to lower levels SAMe in depressed patients, and in clinical studies, the supplementation of SAMe has been shown to have an anti-depressant effect that also increases serotonin levels. The National Institute on Alcohol Abuse and Alcoholism and the Office of Dietary Supplements sponsored a conference examining the possible role of SAMe in treating alcoholic liver disease. Since oxidant stress is known to play a major role in the development of liver disease, and SAMe is involved in the manufacture of important liver antioxidant compounds (glutathione), it is being studied for its role in treatment of alcoholic liver disease. SAMe’s potential for osteoarthritis is based on its ability to support a higher production of proteoglycans, a substance that makes up cartilage.
SAMe seems to be a relatively safe and effective way of correcting our biochemical methylation process, what may be a route of cause for depression, osteoarthritis, liver disease, and other conditions. However, more clinical studies are needed for understanding exactly what kinds of depression SAMe works best for, more about its specific risks and therapeutic side effects, and its potential for other disease processes before it is an accepted treatment method for these and other conditions.
Scientific Support
A review of the published literature (from 1966 to 2001) on SAMe found that the majority of the clinical evidence for its use has been conducted on various depressive disorders, osteoarthritis, and fibromyalgia, and sample sizes and the dose used has varied widely. Several reviews and meta-analysis have been published all concluding that SAMe was better than placebo in treating depression, and equally as effective as the standard tricyclic antidepressants. However, the authors pointed out that even though SAMe seems well tolerated with most side effects being presented as gastrointestinal complaints, it may have the potential risk of psychiatric and cardiovascular adverse side effects. They concluded that until the side effects are more thoroughly researched, people should not be consuming it in an unmonitored fashion, and healthcare providers should be aware of the need for more research into the potential for adverse events (Fetrow and Avila, 2001; Bressa, 1994).
SAMe was tested in depressive patients and compared to imipramine in two multicenter studies. In one study (involving 143 patients over 6 weeks), 1600 mg of SAMe was given orally daily, and in the second study (involving 138 patients over 4 weeks) 400 mg of SAMe was given intramuscularly, and in both studies the SAMe treatment was compared (in 138 patients over 6 weeks) to the effects of 150 mg of imipramine given orally each day in a double-blind manner. The assessment measures were the Hamilton Depression Rating Scale (HAM-D) and the Clinical Global Impression at the endpoint. The authors stated that SAMe is the most important methyl donor in the central nervous system, and they concluded that both treatments of SAMe was as effective as 150 mg imipramine daily orally, but that SAMe was associated with significantly fewer adverse events (Delle Chiaie et al., 2002).
In one pilot study involving 13 depressed patients with Parkinson’s disease, for which no other previously tried antidepressant agents were effective (and were with intolerable side effects), SAMe was administered in doses of 800 to 3600 mg daily for 10 weeks. Ten of the eleven patients that completed the study showed at least a 50% improvement in the HAM-D score. One patient did not improve, and two dropped out due to increased anxiety. The only side effects noted in the others were mild nausea (in one patient) and mild and transient diarrhea (in two others). The authors concluded that this preliminary trial showed that SAMe is well tolerated and may be a safe alternative to current antidepressant agents used in Parkinson’s patients (DiRocco et al., 2000).
In an open, multi-center study involving 195 patients, 400 mg of SAMe was given parentally for 15 days. Depressive symptoms were found to decrease after days 7 and 15 of treatment with no serious adverse events reported. The authors concluded that further double-blind studies are need to confirm the findings that SAMe is not only a safe and effective anti-depressant, but that it is fast-acting, and could be a possible method for reducing the delay in antidepressant response (Fava et al., 1995).
The anti-depressive effect of SAMe was compared to desipramine in a double-blind randomized clinical study involving 26 patients. In the SAMe group, 62% showed significant improvement compared to 50% in the desipramine group. Regardless of the treatment group, the plasma SAMe concentration was shown to have been significantly improved in all patients that showed a 50% decrease in their HAM-D assessment. The authors concluded that this ladder finding showed that SAMe played a major role in regulating mood (Bell et al.,1994).
Another study examined the effect of SAMe in depressed postmenopausal women in a 30 day double-blind, placebo-controlled randomized design. Eighty women who were diagnosed with DSM-III-R major depressive disorder or dysthymia 6-36 months subsequent to menopause (either natural or through hysterectomy) were given 1,600 mg daily SAMe or placebo. A significant improvement was found in depressive symptoms compared to placebo starting day 10 of the study, and side effects were mild and transient (Salmaggi et al., 1993).
In an effort to study the effect of speeding up the onset of action of the antidepressant imipramine, SAMe was given to 40 patients in a double-blind manner alongside imipramine at 150 mg daily. The SAMe was administered at 200 mg daily intramuscularly. SAMe was concluded to effectively increase the onset of antidepressive action of imipramine (Berlanga et al., 1992).
In one earlier study, SAMe was administered both orally and intravenously and levels of SAMe were found to significantly rise in the cerebrospinal fluid, indicating that it crossed the blood-brain barrier. The authors also pointed out that SAMe levels were low in a group of Alzheimer’s patients, and that this suggested a problem in methylation in the disease that the possible use of SAMe as treatment (Bottiglieri et al., 1990).
A meta-analysis of randomized controlled clinical trials was conducted on the use of SAMe compared to nonsteroidal anti-inflammatory drugs (NSAIDs) for osteoarthritis. SAMe was found to be as effective as NSAIDs as reducing pain and functional limitation of osteoarthritis but without the side effects associated with NSAIDs (Soeken et al., 2002).
In another meta-analysis of the use of SAMe in osteoarthritis, all randomized clinical trials on SAMe and oxaceprol were reviewed for their efficacy in osteoarthritis. Assessments of clinical trials were based mostly on pain scores and pain and function scores. Because there were only a few trials that had a mixture of results, the authors cautioned that the results of the meta-analysis had to be interpreted very carefully, but that overall there was not enough evidence to recommend using SAMe and oxaceprol for the treatment of osteoarthritis, but that there was a comparable effect of them to NSAIDs (Witte et al., 2002).
SAMe was tested in a bicentric, randomized, double-blind, placebo-controlled study on its effectiveness for treatment on 81 patients with osteoarthritis. After a 7-day washout period, patients were administered either 400 mg boluses of SAMe i.v. for 5 days followed by 200 mg three times daily for 23 days or a matching placebo regimen. The major outcome measures were the Stanford Health Assessment Questionnaire disability and pain scales, and supplemental visual analog scales for rest and walking pain. In one center, where the patients tended to have a milder baseline of osteoarthritis, the SAMe showed a significantly greater effect in reducing overall pain and resting pain than placebo. In the other center, the baseline osteoarthritis was much more severe, and there was no difference between treatment groups in outcome measures. The authors concluded SAMe to be beneficial to the treatment of osteoarthritis in some patients, and that intravenous loading of SAMe may be an more effective strategy to beginning oral treatment (Bradley et al., 1994).
In one study of SAMe for fibromyalgia, 34 patients were given 600 mg i.v. or placebo for 10 days in a double blind cross-over trial. The primary outcome measure was the tender point change between the treatment groups, and there was no significant difference between the two found, even though there was a trend towards the SAMe group showing significantly improved measures of perception of pain (Volkmann et al., 1997).
In another study on fibromyalgia treatment using SAMe, 800 mg of SAMe was administered orally daily or placebo for 6 weeks in a double-blind, placebo controlled study. The outcome parameters measured that showed improvement vs. placebo were clinical disease activity, subjective symptoms (visual analog scale) of pain experienced during the last week, fatigue, and morning stiffness, and mood parameters evaluated by the Face Scale. Parameters for which there was no improvement found were tender point score, isokinetic muscle strength, and mood evaluated by Beck Depression Inventory. The authors noted that there were no differences in side effects between treatment and placebo groups, and concluded SAMe to be beneficial to primary fibromyalgia (Jacobsen et al., 1991).
Liver Disease
A review of clinical and preclinical science on SAMe was performed in order to give relevance to new findings of the role of SAMe in liver growth, differentiation and injury. Through genome sequence analysis, it was revealed that all organisms make SAMe, and a large percentage of all genes are SAMe dependent methyltransferases. Since most methylation reactions occur in the liver and a large percentage of methionine metabolism occurs in the liver, the authors contended that the liver is essential in the regulation of blood methionine. They added that SAMe is not only an intermediate in methionine catabolism, but that it is a control switch that works intracellularly to regulate liver regeneration, differentiation and protection (Mato et al., 2002).
A systematic review of the clinical studies on the use of SAMe in alcoholic liver disease was performed. Once the clinical studies were compiled, the methodology of each one was assessed using the components of quality and the Jadad-score. In the review, there were 8 placebo-controlled randomized clinical trials found, and of these, only one of them (involving 123 patients) used the adequate methodology and reported with clarity on mortality and liver transplantation. The authors found no significant effect of SAMe on mortality, liver related mortality, liver transplantation or liver complications, and therefore did not recommend it for alcoholic liver disease outside clinical trials (Rambaldi and Gluud, 2001; Mato et al. 1999).
SAMe was tested in a randomized placebo-controlled study involving 32 women with intrahepatic cholestasis of pregnancy. The study groups were divided into those who were treated with (a) ursodeoxycholic acid, (b) SAMe, (c) both drugs, or (d) a placebo. The authors found the combination treatment, group (c) to be significantly more effective than placebo or than either drug alone (groups a, b or d) (Nicastri et al., 1998).
In another study comparing SAMe treatment to ursodeoxycholic acid for intrahepatic cholestasis of pregnancy, 20 women were treated with either SAMe (1000 mg/day i.m.) or ursodeoxycholic acid (450 mg/day) from the last trimester of pregnancy until time of delivery. Ursodeoxycholic acid was shown to be more effective at treating pruritus and total bile acids than SAMe, and was recommended for further testing in this indication (Floreani et al., 1996). Earlier studies on the use of SAMe for intrahepatic cholestasis of pregnancy have likewise given mixed results (Ribalta et al., 1991; Frezza et al.,
Parkinson’s Disease
See DiRocco et al., 2000 in the section above on Depression.
Safety / Dosage
Experimental studies have found that SAMe does not cause the same side effects as other non-steroidal anti-inflammatory agents, such as aspirin, on the gastric irritation, or by interfering with blood clotting mechanisms, or inhibition of prostaglandins. In clinical studies the side effects noted have been mostly mild and transient, especially gastrointestinal discomfort.
SAMe appears to be well absorbed through intravenous and intramuscular routes, and through oral administration if an enteric-coated capsule is used. In clinical studies, the amounts taken ranged from 600 to 1,600 mg a day for osteoarthritis. For depression, higher amounts of SAMe are recommended, starting with a high dosage of 1,600 mg daily (divided into two or four doses per day) for two to three weeks, and then to reduce the dosage to a maintenance level depending on the individuals’ depressive symptoms (such as 800 mg or 400 mg daily). Preclinical studies suggest that SAMe functions when folate and vitamin B12 levels are normal (not low) (Grazi and Costa, 1999).
1.Bell KM, Potkin SG, Carreon D, Plon L. S-adenosylmethionine blood levels in major depression: changes with drug treatment. Acta Neurol Scand Suppl. 1994;154:15-8.
2.Berlanga C, Ortega-Soto HA, Ontiveros M, Senties H. Efficacy of S-adenosyl-L-methionine in speeding the onset of action of imipramine. Psychiatry Res. 1992 Dec;44(3):257-62.
3.Bottiglieri T, Godfrey P, Flynn T, Carney MW, Toone BK, Reynolds EH. Cerebrospinal fluid S-adenosylmethionine in depression and dementia: effects of treatment with parenteral and oral S-adenosylmethionine. J Neurol Neurosurg Psychiatry. 1990 Dec;53(12):1096-8.
4.Bradley JD, Flusser D, Katz BP, Schumacher HR Jr, Brandt KD, Chambers MA, Zonay LJ. A randomized, double blind, placebo controlled trial of intravenous loading with S-adenosylmethionine (SAM) followed by oral SAM therapy in patients with knee osteoarthritis. J Rheumatol. 1994 May;21(5):905-11.
5.Bressa GM. S-adenosyl-l-methionine (SAMe) as antidepressant: meta-analysis of clinical studies. Acta Neurol Scand Suppl. 1994;154:7-14.
6.Delle Chiaie R, Pancheri P, Scapicchio P. Efficacy and tolerability of oral and intramuscular S-adenosyl-L-methionine 1,4-butanedisulfonate (SAMe) in the treatment of major depression: comparison with imipramine in 2 multicenter studies. Am J Clin Nutr. 2002 Nov;76(5):1172S-6S.
7.Di Rocco A, Rogers JD, Brown R, Werner P, Bottiglieri T. S-Adenosyl-Methionine improves depression in patients with Parkinson's disease in an open-label clinical trial. Mov Disord. 2000 Nov;15(6):1225-9.
8.Jacobsen S, Danneskiold-Samsoe B, Andersen RB. Oral S-adenosylmethionine in primary fibromyalgia. Double-blind clinical evaluation. Scand J Rheumatol. 1991;20(4):294-302.
9.Fava M, Giannelli A, Rapisarda V, Patralia A, Guaraldi GP. Rapidity of onset of the antidepressant effect of parenteral S-adenosyl-L-methionine. Psychiatry Res. 1995 Apr 28;56(3):295-7.
10.Fetrow CW, Avila JR. Efficacy of the dietary supplement. S-adenosyl-L-methionine. Ann Pharmacother. 2001 Nov;35(11):1414-25.
11.Floreani A, Paternoster D, Melis A, Grella PV. S-adenosylmethionine versus ursodeoxycholic acid in the treatment of intrahepatic cholestasis of pregnancy: preliminary results of a controlled trial. Eur J Obstet Gynecol Reprod Biol. 1996 Aug;67(2):109-13.
12.Grazi, S. and Costa, M. The European Arthritis and Depression Breakthrough: SAMe. 1999. Prima Health: Rocklin, CA. 248 pp.
13.Mato JM, Camara J, Fernandez de Paz J, Caballeria L, Coll S, Caballero A, Garcia-Buey L, Beltran J, Benita V, Caballeria J, Sola R, Moreno-Otero R, Barrao F, Martin-Duce A, Correa JA, Pares A, Barrao E, Garcia-Magaz I, Puerta JL, Moreno J, Boissard G, Ortiz P, Rodes J. S-adenosylmethionine in alcoholic liver cirrhosis: a randomized, placebo-controlled, double-blind, multicenter clinical trial J Hepatol. 1999 Jun;30(6):1081-9.
14.Mato JM, Corrales FJ, Lu SC, Avila MA. S-Adenosylmethionine: a control switch that regulates liver function. FASEB J. 2002 Jan;16(1):15-26.
15.Nicastri PL, Diaferia A, Tartagni M, Loizzi P, Fanelli M. A randomised placebo-controlled trial of ursodeoxycholic acid and S-adenosylmethionine in the treatment of intrahepatic cholestasis of pregnancy. Br J Obstet Gynaecol. 1998 Nov;105(11):1205-7.
16.Rambaldi A, Gluud C. S-adenosyl-L-methionine for alcoholic liver diseases. Cochrane Database Syst Rev. 2001;(4):CD002235.
17.Ribalta J, Reyes H, Gonzalez MC, Iglesias J, Arrese M, Poniachik J, Molina C, Segovia N. S-adenosyl-L-methionine in the treatment of patients with intrahepatic cholestasis of pregnancy: a randomized, double-blind, placebo-controlled study with negative results. Hepatology. 1991 Jun;13(6):1084-9.
18.Salmaggi P, Bressa GM, Nicchia G, Coniglio M, La Greca P, Le Grazie C. Double-blind, placebo-controlled study of S-adenosyl-L-methionine in depressed postmenopausal women. Psychother Psychosom. 1993;59(1):34-40.
19.Soeken KL, Lee WL, Bausell RB, Agelli M, Berman BM. Safety and efficacy of S-adenosylmethionine (SAMe) for osteoarthritis. J Fam Pract. 2002 May;51(5):425-30.
20.Volkmann H, Norregaard J, Jacobsen S, Danneskiold-Samsoe B, Knoke G, Nehrdich D. Double-blind, placebo-controlled cross-over study of intravenous S-adenosyl-L-methionine in patients with fibromyalgia. Scand J Rheumatol. 1997;26(3):206-11.
21.Witte S, Lasek R, Victor N. Meta-analysis of the efficacy of adenosylmethionine and oxaceprol in the treatment of osteoarthritis. Orthopade. 2002 Nov;31(11):1058-65.
EDITOR'S NOTE: This monograph can be found in The Health Professional's Guide to Dietary Supplements (Lippincott, Williams & Wilkins) by Shawn M. Talbott, PhD and Kerry Hughes, MS.

St. John's Wort

St. John’s wort (Hypericum perforatum), also called Klamath weed, is a five-petaled yellow flower, which is especially plentiful in Northern California and Southern Oregon. The “St. John’s” name comes from the red color of the extract (from squeezed buds and flowers), which was associated with the blood of St. John the Baptist and the fact that the herb typically flowers around the time of the feast of St. John. St. John’s wort has been used for centuries for everything from a “protector against evil spirits” (depression) and for wound healing to its most common present-day use as an antidepressant. The active ingredients in St. John’s wort extract are unknown, but extracts standardized to contain napthodianthrone compounds such as hypericin and pseudohypericin along with phloroglucinols such as hyperforin and adhyperforin are known to be effective in alleviating mild to moderate depressive symptoms.
As an antidepressant, St. John’s wort has been shown to inhibit an enzyme (catechol-O-methyltransferase) which degrades certain neurotransmitters such as dopamine. It has also been shown to inhibit serotonin re-uptake in the brain, and to reduce expression of interleukin-6 and gamma-amino butyric acid (GABA) uptake. Each of these actions can contribute to alleviating depression by slowing the recycling of neurotransmitters needed for maintaining emotional balance. As an anti-viral agent, St. John’s wort has been reputed to inhibit replication of several viruses, including the Herpes simplex, HIV, and the virus that causes mononucleosis, but its use as a dietary supplement for treating viral infections is generally not supported.
St. John's wort appears to be helpful in about 50-60% of cases of mild to moderate depression – but as with prescription antidepressants, the full effect takes about 4-6 weeks to develop. It is important to note that St. John's wort should never be used for the treatment of severe depression (feelings of suicide, extreme inability to cope with daily life, severe anxiety, or extreme fatigue) – and physician-directed drug therapy may mean the difference between life and death.
That said, St. John’s wort is sold in a variety of forms, including tea, drops, tablets, and capsules. In tablet or capsule form, standardized St. John’s wort extracts, (300-900mg/day) represent a relatively safe and effective dietary supplement for those with mild to moderate depression, anxiety, or seasonal affective disorder.
Scientific Support
Several clinical studies have been conducted to determine the efficacy of St. John’s wort for those with mild to moderate depression. In one review of 23 randomized trials (15 placebo-controlled and 8 drug comparisons) including nearly 2,000 patients with mild or moderate depressive disorders, extracts of St. John’s wort were nearly 3 times more effective than placebo, and were comparable to prescription anti-depressants and with fewer side effects (Gaster & Holroyd 2000). Across the studies, fewer than 1% of those taking St. John’s wort dropped out of the study, compared with a drop-out rate of 3% taking a prescription anti-depressant. Perhaps the most encouraging results were that in contrast to the high percentage of side effects in those taking prescription anti-depressants (52.8%), only 19.8% of those taking St. John’s wort experienced any adverse effects (Linde et al. 1996). Other well-controlled studies comparing the St. John’s wort extract LI 160 (from Lichtwer Pharma) to prescription anti-depressants such as Prozac (fluoxetine), sertraline (Zoloft), paroxetine (Paxil), imipramine, amitriptyline and maprotiline have all found St. John’s wort to be comparable in effectiveness, but superior to prescription drugs with regard to tolerability. Overall, more than a dozen double-blind placebo-controlled studies have been conducted (mostly small studies) with the majority supporting the case for the effectiveness of St. John's wort in alleviating mild to moderate depression (Hansgen et al. 1994; Harrer et al. 1994; Philipp et al. 1999.
In the one recent study in the literature that explored the use of St. John’s wort as a retroviral agent for use in HIV-infected patients (Woelk et al. 1994), over half of the patients discontinued treatment early because of severe cutaneous phototoxicity (skin sensitivity to sunlight exposure). Of those who remained in the study, there were no significant changes in virologic markers. It should be noted that HIV-positive patients should NOT use St. John’s wort without specific advise and consultation of their personal physician, as the herb has been shown to almost completely inactivate the effects of certain antiviral medications (indinavir and other protease inhibitors).
St. John’s wort is quite safe in terms of observed side effects, the most common of which are typically mild gastrointestinal upset, mild allergic reactions (skin rash), tiredness and insomnia/restlessness. There have been no published reports of serious adverse side effects from taking the herb alone and animal studies with large doses of St. John’s wort have not shown any serious problems. The most commonly studied adverse effect of St. John’s wort is its ability to cause photosensitivity, especially in fair-skinned individuals. This condition is reversible upon discontinuation of the herb. Thus, special care should be taken to avoid ultraviolet light, or to frequently apply sunscreen and wear sunglasses (due to an increased risk of cataracts) when it is necessary to be outside. Other side effects include gastrointestinal symptoms, dizziness, confusion and tiredness, and tend to be equivalent in incidence to placebo.
Scientific studies conducted in vitro (test tube studies) have shown St. John’s wort to be mutagenic and toxic to sperm, suggesting that it should not be taken when trying to become pregnant. On the other hand, St. John’s wort has also been shown to interfere with the action of certain oral contraceptives (birth control pills). St. John’s wort is not recommended for children, or for women who are pregnant or lactating.
Although direct side effects from consuming St. John’s wort appear to be quite rare, several recent reports have raised the possibility that the herb may interact with and decrease the effectiveness of various medications, including HIV drugs (protease inhibitors), immunosuppressants (such as cyclosporin for organ transplants), digoxin (for congestive heart failure), blood thinners (Coumadin/warfarin), chemotherapy drugs, (olanzapine/clozapine) and asthma medications (theophylline). If you are currently taking any of these, or other prescription medications, DO NOT begin taking OR discontinue taking St. John’s wort without first consulting your personal physician (abrupt withdrawal of the herb could increase blood levels of various medications, which could be dangerous in certain cases).
The recommended dosage for St. John’s wort is 900mg per day (300mg taken 3 times per day) of an extract of the flowers and leaves standardized to contain 0.3% hypericin in a complex of other natural compounds, or 3-5% hyperforin (the main constituent which is thought to inhibit neurotransmitter re-uptake). Minimal treatment time is 4-6 weeks. St. John’s wort is sold in the U.S. only as an herbal supplement, although it is marketed as a drug in Germany for the treatment of mild depression and anxiety.
1.Cott JM, Fugh-Berman A. Is St. John's wort (Hypericum perforatum) an effective antidepressant? J Nerv Ment Dis. 1998 Aug;186(8):500-1.
2.Firenzuoli F, Luigi G. Safety of Hypericum perforatum. J Altern Complement Med. 1999 Oct;5(5):397-8
3.Fugh-Berman A, Cott JM. Dietary supplements and natural products as psychotherapeutic agents. Psychosom Med. 1999 Sep-Oct;61(5):712-28.
4.Gaster B, Holroyd J. St John's wort for depression: a systematic review. Arch Intern Med. 2000 Jan 24;160(2):152-6.
5.Hansgen KD, Vesper J, Ploch M. Multicenter double-blind study examining the antidepressant effectiveness of the hypericum extract LI 160. J Geriatr Psychiatry Neurol. 1994 Oct;7 Suppl 1:S15-8.
6.Harrer G, Hubner WD, Podzuweit H. Effectiveness and tolerance of the hypericum extract LI 160 compared to maprotiline: a multicenter double-blind study. J Geriatr Psychiatry Neurol. 1994 Oct;7 Suppl 1:S24-8.
7.Holsboer-Trachsler E, Vanoni C. Clinical efficacy and tolerance of the hypericum special extract LI 160 in depressive disorders--a drug monitoring study. Schweiz Rundsch Med Prax. 1999 Sep 9;88(37):1475-80.
8.Hubner WD, Lande S, Podzuweit H. Hypericum treatment of mild depressions with somatic symptoms. J Geriatr Psychiatry Neurol. 1994 Oct;7 Suppl 1:S12-4.
9.Jobst KA, McIntyre M, St George D, Whitelegg M. Safety of St John's wort. Lancet. 2000 Feb 12;355(9203):575
10.Johne A, Brockmoller J, Bauer S, Maurer A, Langheinrich M, Roots I. Pharmacokinetic interaction of digoxin with an herbal extract from St John's wort (Hypericum perforatum). Clin Pharmacol Ther. 1999 Oct;66(4):338-45.
11.Kasper S. Treatment of seasonal affective disorder (SAD) with hypericum extract. Pharmacopsychiatry. 1997 Sep;30 Suppl 2:89-93.
12.Laakmann G, Schule C, Baghai T, Kieser M. St. John's wort in mild to moderate depression: the relevance of hyperforin for the clinical efficacy. Pharmacopsychiatry. 1998 Jun;31 Suppl 1:54-9.
13.Linde K, Ramirez G, Mulrow CD, Pauls A, Weidenhammer W, Melchart D. St John's wort for depression--an overview and meta-analysis of randomised clinical trials. BMJ. 1996 Aug 3;313(7052):253-8.
14.Martinez B, Kasper S, Ruhrmann S, Moller HJ. Hypericum in the treatment of seasonal affective disorders. J Geriatr Psychiatry Neurol. 1994 Oct;7 Suppl 1:S29-33.
15.Miller AL. St. John's Wort (Hypericum perforatum): clinical effects on depression and other conditions. Altern Med Rev. 1998 Feb;3(1):18-26.
16.Philipp M, Kohnen R, Hiller KO. Hypericum extract versus imipramine or placebo in patients with moderate depression: randomised multicentre study of treatment for eight weeks. BMJ. 1999 Dec 11;319(7224):1534-8.
17.Sommer H, Harrer G. Placebo-controlled double-blind study examining the effectiveness of an hypericum preparation in 105 mildly depressed patients. J Geriatr Psychiatry Neurol. 1994 Oct;7 Suppl 1:S9-11.
18.Stevinson C, Ernst E. Hypericum for depression. An update of the clinical evidence. Eur Neuropsychopharmacol. 1999 Dec;9(6):501-5.
19.Volz HP, Laux P. Potential treatment for subthreshold and mild depression: a comparison of St. John's wort extracts and fluoxetine. Compr Psychiatry. 2000 Mar-Apr;41(2 Suppl 1):133-7.
20.Vorbach EU, Arnoldt KH, Hubner WD. Efficacy and tolerability of St. John's wort extract LI 160 versus imipramine in patients with severe depressive episodes according to ICD-10. Pharmacopsychiatry. 1997 Sep;30 Suppl 2:81-5.
21.Vorbach EU, Hubner WD, Arnoldt KH. Effectiveness and tolerance of the hypericum extract LI 160 in comparison with imipramine: randomized double-blind study with 135 outpatients. J Geriatr Psychiatry Neurol. 1994 Oct;7 Suppl 1:S19-23.
22.Wheatley D. LI 160, an extract of St. John's wort, versus amitriptyline in mildly to moderately depressed outpatients--a controlled 6-week clinical trial. Pharmacopsychiatry. 1997 Sep;30 Suppl 2:77-80.
23.Williams JW Jr, Mulrow CD, Chiquette E, Noel PH, Aguilar C, Cornell J. A systematic review of newer pharmacotherapies for depression in adults: evidence report summary. Ann Intern Med. 2000 May 2;132(9):743-56.
24.Woelk H, Burkard G, Grunwald J. Benefits and risks of the hypericum extract LI 160: drug monitoring study with 3250 patients. J Geriatr Psychiatry Neurol. 1994 Oct;7 Suppl 1:S34-8.
EDITOR'S NOTE: This monograph can be found in The Health Professional's Guide to Dietary Supplements (Lippincott, Williams & Wilkins) by Shawn M. Talbott, PhD and Kerry Hughes, MS.


Valerian (Valeriana officinalis or Valerianae radix) has been used as a medicinal anti-anxiety herb and sleep aid since the days of the Romans. The dried roots of the plant are used in teas, tinctures and in capsule/tablet forms. The fresh root has no distinctive odor, however, over time hydrolysis of compounds present in the volatile oil produce isovaleric acid, which has an offensive odor (akin to sweaty socks). Traditionally valerian was used to treat migraine headache, anxiety, fatigue, and seizures and many traditional Chinese remedies include valerian for treatment of numbness due to rheumatic conditions, colds, menstrual difficulties, bruises and wound healing. Currently, valerian may be used orally for the treatment of insomnia, restlessness, sleeping disorders with anxiety, mood disorders, muscle and joint pain, menstrual cramps and menopausal symptoms. It is unclear which of the numerous compounds is the true “active” – but the combination of compounds appears to work together in the brain to produce an overall effect similar to the action of prescription tranquilizers such as Valium and Halcion.
As a mild tranquilizer and sleep aid, valerian may be an effective herb for dealing with temporary feelings of anxiety, nervousness or insomnia. The effects of valerian are generally quite mild when compared to prescription products and synthetic OTC products and generally do not result in “morning after hangover” effects experienced with certain sleep aids.
Scientific Support
Valerian taken before bedtime appears to reduce the amount of time that it takes to fall asleep (sleep latency). It is unknown, however, whether the quality of the sleep is affected by valerian consumption. Valerian is generally regarded as a mild tranquilizer and has been deemed safe by the German Commission E for treating “restlessness and sleeping disorders brought on by nervous conditions” (Donath et al. 2000). The medicinal portion of the valerian plant is the root and most of the pharmacological effects of valerian root have been attributed to valepotriate and volatile oil constituents, specifically monoterpenes and sesquiterpenes. However, it is hypothesized that multiple constituents are responsible for its therapeutic effects rather than to a single active compound. Valepotriate constituents are believed to have sedative-hypnotic and spasmolytic effects, while the sesquiterpenes, valerenic acid and kessyl glycol have been shown to cause sedation in animals (Houghton 1999). Another mechanism of action is likely to involve valerenic acid’s ability to inhibit the enzyme system responsible for the central catabolism of GABA, increasing GABA concentrations and decreasing CNS activity (Houghton 1999).
Several studies have examined the effects of valerian on sleep. In one placebo-controlled crossover study with 128 participants, 400mg of valerian extract (plus hops) reduced sleep latency and improved sleep quality compared with placebo (Leathwood et al. 1982). Analysis of the results suggested that valerian had an increased effect with participants that described themselves as “poor” or “irregular” sleepers. Another trial evaluated the effectiveness of 450-900mg of valerian on healthy volunteers between the ages of 21 and 44 (Kuhlmann et al. 1999). Sleep quality was measured using a questionnaire, night-time motor activity recordings, and spectral analysis of the sleep EEG. Both doses elicited mild hypnotic effects and improved sleep quality. Other studies of valerian supplementation have shown improvements in slow-wave (deeper stage) sleep, compared with placebo and equivalence of 600mg valerian with 10mg oxazepam for indices of overall sleep quality (Vonderheid-Guth et al. 2000). In terms of anxiolytic effects, several studies have shown 100-300mg of valerian root extract to be more effective than placebo and as effective as 20mg propranolol on measures of social stress, somatic arousal, anxiety, and emotional tension (Kuhnen & Oswald 1988).
Occasional reports of headaches and mild nausea are documented, but habituation or dependency is unlikely when used as directed. Valerian should be avoided by pregnant and lactating women and should not be consumed by children. Individuals currently taking sedative drugs or antidepressant medications should be advised by their personal physician before taking valerian. Do not take valerian in conjunction with alcohol or other tranquilizers and do not consume for more than two weeks.
Because the activity and strength of valerian preparations can vary significantly from one product to the next, it is recommended to select a standardized product (0.5-1.0% valerenic acids) whenever possible and to follow the directions on the particular product. As a general guideline, approximately 200-900mg of a standardized extract can be taken 30-60 minutes before bed (as a sleep aid) or as needed as a mild tranquilizer.
1.Assemi, Mitra Pharm D. Herbs Affecting the Central Nervous System: Gingko, Kava, St. John’s Wort, and Valerian. Clinical Obstetrics and Gynecology 2001; 44(4): 824-835.
2.Balderer G, Borbely AA. Effect of valerian on human sleep. Psychopharmacology (Berl). 1985;87(4):406-9.
3.Cauffield JS, Forbes HJ. Dietary supplements used in the treatment of depression, anxiety, and sleep disorders. Lippincotts Prim Care Pract. 1999 May-Jun;3(3):290-304.
4.Donath F, Quispe S, Diefenbach K, Maurer A, Fietze I, Roots I. Critical evaluation of the effect of valerian extract on sleep structure and sleep quality. Pharmacopsychiatry. 2000 Mar;33(2):47-53.
5.Heiligenstein E, Guenther G. Over-the-counter psychotropics: a review of melatonin, St John's wort, valerian, and kava-kava. J Am Coll Health. 1998 May;46(6):271-6.
6.Houghton PJ. The scientific basis for the reputed activity of Valerian. J Pharm Pharmacol. 1999 May;51(5):505-12.
7.Kammerer E. Phytogenic sedatives-hypnotics--does a combination of valerian and hops have a value in the modern drug repertoire? Z Arztl Fortbild (Jena). 1993 Apr 12;87(5):401-6.
8.Kirkwood CK. Management of insomnia. J Am Pharm Assoc (Wash). 1999 Sep-Oct;39(5):688-96.
9.Kohnen R, Oswald WD. The effects of valerian, propranolol, and their combination on activation, performance, and mood of healthy volunteers under social stress conditions. Pharmacopsychiatry. 1988 Nov;21(6):447-8.
10.Kuhlmann J, Berger W, Podzuweit H, Schmidt U. The influence of valerian treatment on "reaction time, alertness and concentration" in volunteers. Pharmacopsychiatry. 1999 Nov;32(6):235-41.
11.Leathwood PD, Chauffard F, Heck E, Munoz-Box R. Aqueous extract of valerian root (Valeriana officinalis L.) improves sleep quality in man. Pharmacol Biochem Behav. 1982 Jul;17(1):65-71.
12.Leathwood PD, Chauffard F. Aqueous extract of valerian reduces latency to fall asleep in man. Planta Med. 1985 Apr;(2):144-8.
13.Plushner SL. Valerian: Valeriana officinalis. Am J Health Syst Pharm. 2000 Feb 15;57(4):328, 333, 335.
14.Schulz H, Stolz C, Muller J. The effect of valerian extract on sleep polygraphy in poor sleepers: a pilot study. Pharmacopsychiatry. 1994 Jul;27(4):147-51.
15.Vonderheid-Guth B, Todorova A, Brattstrom A, Dimpfel W. Pharmacodynamic effects of valerian and hops extract combination (Ze 91019) on the quantitative-topographical EEG in healthy volunteers. Eur J Med Res. 2000 Apr 19;5(4):139-44.
16.Willey LB, Mady SP, Cobaugh DJ, Wax PM. Valerian overdose: a case report. Vet Hum Toxicol. 1995 Aug;37(4):364-5.
17.Wong AH, Smith M, Boon HS. Herbal remedies in psychiatric practice. Arch Gen Psychiatry. 1998 Nov;55(11):1033-44.
EDITOR'S NOTE: This monograph can be found in The Health Professional's Guide to Dietary Supplements (Lippincott, Williams & Wilkins) by Shawn M. Talbott, PhD and Kerry Hughes, MS.