The SAM-e Story: Stop Depression Now

The SAM-e Story: Stop Depression Now

JoAnn Guest

Jun 09, 2006 17:24 PDT

 

 

http://www.willner.com/article.aspx?artid=181

 

A chapter from the book Stop Depression Now, by Richard Brown, M.D.,

Teodoro Bottiglieri, Ph.D., and Carol Colman, published by Putnam

Sons 1999.

 

When people start taking SAM-e for the first time, two things

usually,happen

Within days, their mood begins to lift and they have an

increased sense of wellbeing. But that's not all. They also report

something quite unique to SAM-e. They consistently say that they

actually feel more energetic and healthier. That's quite a change

from

what you generally hear from a patient starting an antidepressant.

 

Unlike other antidepressants, SAM-e is made from substances normally

found in the human body—methionine and adenosine triphosphate (or

ATP).

Methionine is an essential amino acid, a building block of protein.

Found in high-protein foods such as fish and eggs methionine is

alsomade in small amounts by our cells, but not in enough quantity to

meetthe body's needs.

 

Good nutrition is key to maintaining adequate methionine levels.

Here's

why. Two key B vitamins, B12 and folic acid, are required for the

production of methionine. In fact, a deficiency in either one of

these

vitamins can result in depression and problems in mental function,

especially among older people. Much of Terry's research has centered

on

the role of these B vitamins in depression in general and in the

production of SAM-e in particular. As we will explain later, the two

are

inextricably linked, and the SAM-e story cannot be told without

including these vitamins.

 

ATP is a high-powered fuel that is produced by the cells to provide

energy to run the body. It is present in almost every cell and

provides

the juice to run all of the body's machinery. There is plenty of it

to

go around.

 

The product of this marriage of methionine and ATP is SAM-e, a

molecule

essential to many aspects of human health. But SAM-e levels are not

evenly distributed among all humans. Blood levels of SAM-e are seven

times higher in children than in adults.

Men have slightly higherlevels

of SAM-e than women do, probably because a considerable amount of

SAM-e is

produced and consumed in muscle tissue, which is more abundant in

men. Levels of SAM-e are notably lower among depressed people of any

age.

 

SAM-e deficiencies are also common in people with neurological

problems

such as Alzheimer's disease, Parkinson's disease, and HIV

complications

that can lead to dementia. Terry, who, as noted in Chapter 1, did

his

Ph.D. on SAM-e in 1982, was one of the first scientists to study

this

remarkable molecule in connection with the central nervous system

and,

more specifically, its role in regulating mood and mental function.

Recently, Terry discovered that levels of SAM-e are lower in the

cerebrospinal fluid of people with neurological complications like

depression due to severe vitamin B12 or folate deficiency. Low

levels of

SAM-e in cerebrospinal. fluid, as we have seen, indicates an

inadequate

amount in the brain. Clearly, these are compelling reasons not to

let

your SAM-e levels fall below normal.

 

SAM-e Turns On Key Reactions

 

SAM-e's key role in a process called the methylation cycle makes it

absolutely essential for human health. Methylation, a term for a

basic

yet critical chemical reaction in the body, is the passing of what

is

known in chemistry as a methyl group-one carbon and three hydrogen

atoms-from one molecule to another. Methylation is as vital to human

life as breathing. It is an " on-off `switch that activates more than

a

hundred different processes in the body, from producing important

neurotransmitters that allow brain cells to communicate, to

preserving

bone health, to protecting against heart disease. Methylation

activity

declines as we age, resulting in a slowdown of these vital

activities,

which many scientists suspect may contribute to the aging process as

well as to the onset of many diseases. There is also compelling

evidence

that a slowdown in methylation or a genetic tendency to

undermethylate

may be a key factor in depression for many. There are different

kinds of

SAMe/methylation reactions that trigger biological responses

throughout

the body. These reactions are the " greatest hits " of metabolism.

They

are what make us alive. When you review the list below, you will see

why

SAM-e is so fundamental to life that we could not exist without it.

 

DNA METHYLATION. There is nothing more fundamental to human life

than

DNA. It's the genetic " software " which runs the cells and contains

the

genetic code for every living thing. When SAM-e reacts with DNA by

donating a methyl group, it allows our genes to spring into action.

It's

like hitting the " on " switch on a computer; DNA methylation is the

operating system of the body, helping it to regulate important

processes

such as cellular growth and repair, production of immune cells to

fight

disease, wound healing, and reproduction. The undermethylation of

DNA is

believed to be a causal factor in cancer, because it could hamper

the

body's ability to repair damaged cells before they turn cancerous.

 

PROTEIN METHYLATION. Proteins form the basic structures of many key

components of the human body, including muscles, tissues, organs,

and

even hormones. The methylation of protein is critical for cell

growth

and repair. Sluggish protein methylation can trigger a downward

spiral

that can have a devastating impact on the body and mind, leading to

deterioration of key organ systems, including the heart and brain.

Protein methylation undoubtedly plays a major role in the onset of

depression. It is involved in the activation of receptors, special

sites

on cell membranes which bind with other molecules to stimulate a

response-in other words, the body's basic communication system. As

discussed in the last chapter, this is especially true of the brain,

where sluggish protein metabolism can pitch someone into depression.

Studies show that SAMe supplementation can stimulate protein

methylation, which not only boosts levels of the key

neurotransmitters

but increases the number of receptors.

 

PHOSPHOLIPID METHYLATION. Cell membranes are composed of fatlike

substances called phospholipids. In order to get into the cell,

substances must first pass through the cell membrane. As we age,

cell

membranes can become rigid, making it difficult for vital substances

to

move in and out. SAM-e is important for phospholipid methylation,

which

helps maintain the flexibility of the cell membrane, keeping it more

youthful. Through methylation, SAM-e also boosts the production of

phosphatidylserine, a phospholipid important for both mood and

memory.

 

Its role in the methylation cycle places SAM-e at the heart of many

lifesaving functions. But the SAM-e story doesn't stop here. SAM-e

is

also essential for another critical process, called trans-

sulfuration,

which produces a key chemical, glutathione.

 

SAM-e Boosts Glutathione

 

Many of you have heard of antioxidants, a group of compounds

produced by

the body and also found in many different foods, primarily fruits,

vegetables, legumes, and whole grains. Some well-known vitamins like

C,

E, and beta carotene are, in fact, antioxidants. As noted in Chapter

1,

antioxidants protect us from damage caused by highly reactive

compounds

called free radicals. The human body requires oxygen for its basic

chemical functioning, for metabolism, for energy. Everything we do

requires energy, both conscious activities like walking and

automatic

body functions like our heartbeat and breathing. Oxygen is the fuel

that

drives energy production and makes life possible, but it leaves

behind a

potentially dangerous by-productthe unstable oxygen molecules called

free radicals. Free radicals are fine up to a point-in fact, without

them, we couldn't live. If allowed to accumulate, however, they can

cause a great deal of mischief. They can attack DNA, possibly

initiating

cancer. They can attack fat molecules in the blood, causing them to

oxidize and form plaque, thereby clogging the arteries. They can

target

cells in key areas of the brain and may be a factor in brain aging.

 

The body has a defense system that controls free radicals, and

glutathione-known as the " master antioxidant " -is at its heart. You

cannot obtain glutathione through diet; it must be produced by the

cells. So crucial is it to the body that living a long, healthy life

requires making a constant supply. Below is a review of just a few

of

the lifesaving functions that glutathione performs in the body. It

could

not perform any of these tasks without SAM-e

 

DETOXIFIES THE LIVER. There is a huge amount of glutathione in the

liver, which also contains the body's heaviest concentration of SAM-

e.

The liver has many crucial jobs, including the production of bile,

but

its most important role is the detoxification of drugs (including

the

tricyclic antidepressants), alcohol, and poisons that are ingested

in

food, such as insecticides, or produced by the body through normal

metabolism. When glutathione encounters toxic compounds in the

liver, it

attaches itself to them, making them more water-soluble. This allows

the

toxins to be flushed out through the kidneys. Liver damage occurs

when

the liver is so overwhelmed by toxins that it cannot produce enough

cleansing glutathione. As I will discuss in Chapter 11 ( " Getting

Healthy

with SAM-e " ), SAMe has been used as an effective treatment for liver

disease, especially alcohol-induced liver damage.

 

PROTECTS DNA. Glutathione protects DNA from damage by free radicals,

which can contribute to diseases such as cancer and premature aging.

 

BOOSTS THE IMMUNE SYSTEM. glutathione is also important for a

well-functioning immune system, the body's defense against disease.

Interestingly, several studies have documented a link between

depression

and weakened immune function. Although it has never been studied,

the

decline in immunity seen in depression could be related to a

scarcity of

glutathione caused by a deficiency in SAM-e.

 

REDUCES INFLAMMATION. Another vital function of glutathione is the

role

it plays in the reduction of inflammation, which is the primary

cause of

discomfort in osteoarthritis, a condition caused by the wearing down

of

the cartilage (the protective covering on bones). As noted, SAM-e is

also a highly effective treatment for osteoarthritis, which could be

due

in part to its glutathione-boosting effect. (For more information on

SAM-e and arthritis, see Chapter 11, " Getting Healthy with SAM-e. " )

 

Without SAM-e, the body could not make adequate amounts of

glutathione.

In the process called transsulfuration, SAM-e helps produce the

precursor to glutathione, the amino acid cysteine. Cysteine combines

with two other amino acids, glutamic acid and glycine, to form the

precious glutathione. Although glutathione is sold as a supplement,

there is controversy about whether it can be used by the body in

that

form. Many scientists believe it breaks down in the stomach before

it

can reach the bloodstream. Therefore, one of the few effective ways

to

boost glutathione is to take supplemental SAM-e.

 

In addition to its ability to boost glutathione, SAM-e is also

essential

for the production of another type of compound found in the body

called

polyamines. The polyamines spermidine and spermine are involved in

cell

growth and cell differentiation. They also have an antiinflammatory

effect.

 

Although SAM-e performs hundreds of roles in the body, its ability

to

boost glutathionine is one of its most important. But there is still

more to report on the incredible SAM-e story.

 

The SAM-e/Homocysteine Connection

 

Recently, an amino acid called homocysteine has gained notoriety as

a

recognized risk factor for heart disease, stroke, and even some

forms of

cancer. What isn't widely known is SAM-e's key role in helping to

control homocysteine.

 

Homocysteine is produced by every cell in the body as a normal part

of

the methylation cycle. Like free radicals, homocysteine can actually

be

useful in small amounts, but if allowed to accumulate, it can be

terribly dangerous. Folic acid and Vitamin B12 can reduce

homocysteine

by converting it to methionine, the building block of SAM-e. SAM-e,

in

turn, helps remove homocysteine by increasing the activity of an

enzyme

(cystathione-beta-synthetase) that converts this potentially harmful

amino acid into the beneficial glutathione.

 

Here's another reason to keep your SAM-e levels high. Low SAM-e

levels

often go hand in hand with high homocysteine. Even slightly elevated

levels of homocysteine are believed to increase the risk of heart

disease and other problems:

 

•Homocysteine is toxic to the endothelial cells that line blood

vessels.

Damaged endothelial cells may lead to the formation of plaque in the

arteries, causing heart attack and stroke.

 

•Homocysteine may increase the risk of blood clots.

 

•The Stroke Prevention in Young Women Study revealed that young

women

with levels of homocysteine in the top tenth percentile had nearly

triple the risk of stroke-a risk comparable to that of smoking a

pack of

cigarettes daily.

 

High levels of homocysteine and a low intake of B vitamins are now

believed to be risk factors in several other diseases, including

reproductive cancers in women and cancers of the colon. More

recently,

they have been shown to be risk factors for Alzheimer's dementia.

 

There is also a link between high levels of homocysteine, low levels

of

SAM-e, and depression. Terry's research found low levels of folate

and

SAM-e in the red blood cells and spinal fluid of depressed patients.

This was associated with high levels of serum homocysteine. Terry

suspects that elevated levels of homocysteine as well as the

deficiencies in these key B vitamins may hamper methylation, which

could

explain their destructive effects on the body and mind.

 

The homocysteine connection in both heart disease and depression

raises

some intriguing questions. As noted in Chapter 2, people with

depression

are at greater risk of developing heart disease, just as people who

have

heart disease are at risk for depression. In fact, about twenty

percent

of all heart patients receive a diagnosis of major depression, and

as

many as one third will have a major depression within one year after

their heart attacks. Until recently, the depression associated with

heart disease has been dismissed as that which often accompanies any

chronic illness. After all, being sick is very stressful and stress

is a

key trigger for depression; chronic illness is hardly a happy event.

However, recent studies show that about half of all patients with

heart

attacks have had bouts of depression prior to the onset of heart

disease. Could treating your depression early in life by taking SAM-

e

prevent heart disease from striking down the road? Although this

question has never been studied, we believe it is possible that

early

intervention could make a difference.

 

This complicated set of chemical reactions means that SAM-e works on

many different systems of the body. As a result, it has been used as

a

treatment for many different and seemingly unrelated medical

problems,

including osteoarthritis, liver disease, and fibromyalgia.

 

SAM-e may help protect the brain against agerelated destruction of

the

cells responsible for mood, memory, and learning. As Terry noted in

a

recent study published in Nutrition Reviews (Vol. 54, No. 12), SAM-e

has

been shown to be reduced in the cerebrospinal fluid of patients with

Alzheimer's dementia, which suggests that methylation in the brain

may

be important for some forms of dementia. Currently, I am

investigating

the use of SAM-e as a treatment for Parkinson's disease. (For more

information, see Chapter 11, " Getting Healthy with SAM-e " .)

 

The fact that SAM-e is involved in so many different life processes

has

made it the subject of intense scientific scrutiny. In fact, as

noted in

Chapter 1, SAM-e has been the subject of thousands of scientific

studies, making it the only natural substance to have been so

thoroughly

researched in both Europe and the United States. In addition to

numerous

laboratory studies exploring the biochemistry of SAM-e, there have

been

thirty-nine published clinical studies on the use of SAM-e to

control

depression. While thirty-nine clinical studies may not seem like a

lot,

it's actually more than most prescription drugs can boast when they

go

on the market!

 

•Close to 1,400 patients have participated in carefully controlled

clinical trials on depression alone.

 

•In several studies directly comparing SAM-e to standard tricyclic

medications, SAM-e did as well as or better than these drugs,

without

the side effects.

 

•Most of these studies involved severely depressed patients who

often

did not respond to other antidepressants, but nevertheless did

surprisingly well on SAM-e.

 

•SAM-e has an excellent safety record. It has undergone rigorous

testing

and is approved as a prescription drug in Italy, Germany, Spain, and

Russia.

 

But what about in the real world? Well, there are hundreds of

thousands

of patients around the world taking SAM-e for depression. As you

know,

it outsells Prozac in Italy. SAM-e's worldwide reputation is

excellent,

and I have had amazing results with hundreds of patients taking it

in my

practice.

 

SAM-e's remarkable antidepressant properties were discovered

somewhat

serendipitously. Although SAM-e was first identified in 1953, it was

not

until 197 3 that researchers tested it as a treatment for

schizophrenia,

a disease many believe stems from a glitch in the methylation cycle.

While SAM-e did not help to control the symptoms of schizophrenia,

researchers were intrigued by one interesting finding. Unexpectedly,

the

schizophrenic patients treated with SAM-e became less depressed.

Since

then, scores of studies have investigated SAM-e's role as an

antidepressant, and the results have been quite extraordinary.

 

We're not entirely sure yet how it works, but we do know this: Long-

term

treatment with SAM-e in animals has been shown to increase brain

concentrations of norepinephrine, dopamine, and serotonin. Studies

in

humans have shown similar results. In one study reported in the

journal

The Lancet, Terry showed that depressed patients treated with SAM-e

over

a fourteenday period had a significant increase in cerebrospinal

fluid

concentrations of a key metabolite that is used as a marker for

serotonin levels in the brain. Other researchers have also found

that

when depressed people are treated with SAM-e, their cerebrospinal

fluid

levels of the marker for dopamine increase too. The exact way in

which

SAMe does this remains unclear, but an increase in these two markers

is

often associated with antidepressant effect.

 

Study after study has confirmed that SAM-e excels when tested

against a

placebo, an important way to test the efficacy of any

antidepressant.

You may wonder why it is considered important that a drug outperform

a

placebo, or sugar pill. It may surprise you to learn that at least

thirty percent of the effect of any antidepressant-for the first few

weeks-is attributed to the so-called placebo effect. In other words,

if

you believe that a drug will work, it will. Even though the placebo

effect wears off within a few weeks, it does underscore the power

the

mind can hold over the body. Therefore, in order to be certain that

a

drug and not the placebo effect has brought about a good response,

the

drug must consistently outperform a placebo by a substantial margin.

When matched against a placebo, SAM-e wins hands down.

 

SAM-e not only outperforms a placebo but can hold its own among

other

antidepressants. Numerous studies have confirmed that when tested

against several of the tricyclic antidepressants, SAM-e does as

well, or

nearly as well, with virtually no side effects. Also, since with SAM-

e

few patients drop out because of side effects or delay in onset of

action, more people have a chance to respond to it.

 

Here are some of the research highlights that have advanced our

understanding of SAM-e. We've only chosen a few of the many that

have

been done. (For a more complete list of studies, see the

bibliography on

page 245.)

 

THE FIRST SUCCESS. The first double-blind, placebocontrolled study

of

SAM-e was conducted in 197 3 in Verona, Italy. (Neither the

researcher

nor the patients knew who was taking SAM-e and who was taking the

placebo.) Such double-blind, placebo-controlled studies are the gold

standard of medical research. The study involved thirty depressed

patients ill enough to be in psychiatric hospitals. Twenty of them

were

given SAMe for up to fifteen days; the remainder were given a

placebo.

Based on the Hamilton Rating Scale, the most respected professional

index of depression, researchers reported that one hundred percent

of

the patientsevery single one of them-showed improvement in depressed

mood while taking SAM-e. Only thirty percent of patients taking the

placebo improved. In the researchers' own words, " SAM-e acts

favorably

and significantly on specific depressive symptoms (depressed mood,

work,

and interests; suicidal tendencies) which, in a high percentage of

patients, were greatly improved. " In particular, researchers

marveled

over how fast SAM-e worked. " The rapid action of the drug should be

stressed since in some cases almost all of the symptoms had

disappeared

after 4 days of treatment, and in general, after 6 or 7 days ... No

untoward side effects were observed in the patients to whom SAM-e

was

administered. " (Journal of Psychiatry Research, 1976, Vol. 13.)

 

SAM-E WINS OVER ANOTHER ANTIDEPRESSANT. Researchers from the

University

of California's Irvine Medical Center studied eighteen patients

suffering from major depression. Nine of the patients were given a

twoweek course of imipramine, a widely used tricyclic

antidepressant.

The other nine were given SAM-e for the same length of time. By the

end

of the fourteenth day, fully two-thirds of the SAM-e patients had

shown

a significant improvement in depressive symptoms. Only twenty-two

percent of the imipramine patients had the same relief. " It

appears, "

concluded the researchers, " that S-adenosylmethionine is a rapid and

effective treatment for major depression and has few side effects. "

Noting that SAM-e worked faster than imipramine, the researchers

added,

" This characteristic of the drug may be a considerable advantage,

considering the known risk of suicide during the early phase of

treatment with tricyclic antidepressants. " In other words, because

it

works so quickly, in some cases SAM-e could make the difference

between

life and death. (American Journal of

Psychiatry, " SAdenosylmethionine

Treatment of Depression: A Controlled Clinical Trial, " September

1988,

145:9.)

 

 

 

SAM-E AT MASS GENERAL. Researchers at Harvard University's

affiliated

Massachusetts General Hospital studied the effect of SAM-e on twenty

patients, nine of whom had been classified as treatment-resistant

because they did not improve on other antidepressants. The patients

were

given oral doses of SAM-e for up to six weeks. Researchers

noted, " The

group as a whole significantly improved with oral SAM-e. " Of the

eleven

patients who were not treatment-resistant, seven showed a full

antidepressant response on the Hamilton Rating Scale (an improvement

of

fifty percent or better). Two others showed major improvement but

did

not achieve a full response. Even more surprising, two of the nine

treatment-resistant patients showed a full antidepressant response.

Considering that very little works with treatment-resistant

patients-people for whom standard antidepressants have been

ineffectivethis is an excellent result. What makes SAM-e's

performance

even more significant is the fact that not one patient dropped out

of

the study because of side effects. (Acta Psychiatry

Scandanavica, " The

Antidepressant Potential of Oral S-Adenosyl-lMethionine, " 1990:81,

432-36.)

 

MAJOR STUDY'S EXCELLENT RESULTS. A major multicenter study evaluated

SAM-e in 195 outpatients in Italy. The subjects were given daily

400mg

injections of SAM-e for fifteen days. At the end of the study, 163

patients were evaluated (the rest were excluded either for lack of

compliance or because it was determined that they did not meet the

criteria to participate in the study in the first place). The senior

researcher, Dr. Maurizio Fava of the Depression Research Center of

Harvard's Massachusetts General Hospital, and his Italian

coresearchers

reported that depressive symptoms were significantly reduced after

seven

days for more than half of the patients who completed the study. In

fact, ninety patients showed more than a fifty percent improvement

on

standard assessment tests. This is considered an excellent result.

No

severe side effects were reported, an encouraging and unusual

finding

for such a large study involving an antidepressant. (Journal of

Psychiatry Research, 1995:56, 295-97.)

 

DESIPRAMINE OUTPERFORMED BY SAM-E! In 1994, a research team headed

by

Kate M. Bell at the University of California, Irvine Medical Center

compared SAM-e with desipramine, a tricyclic antidepressant. Twenty-

six

patients were involved in a double-blind study comparing oral SAM-e

with

oral desipramine. At the end of four weeks, sixty-two percent of the

patients taking SAM-e and fifty percent of the patients taking

desipramine showed significant improvement.

 

The researchers also investigated whether there was a correlation

between blood levels of SAM-e and mood. One interesting finding:

Regardless of which drug they took, patients showing a fifty percent

improvement or better in the Hamilton Rating Scale score-which is

considered a full response, an excellent result-had a significant

increase in blood plasma levels of SAM-e. As the researchers

noted, " We

found a significant relationship between change in plasma SAM-e

concentration and clinical improvement.... In summary, the

significant

correlation between plasma SAM-e levels and the degrees of clinical

improvement regardless of the type of treatment suggests that SAM-e

might play an important role in regulating mood. "

 

THE CHRONICALLY ILL HELPED BY SAM-E. As noted earlier, depression

and

illness often go hand in hand. But many people who are ill cannot

tolerate antidepressants, or may experience particularly bad side

effects from drug interactions. As the researchers in this study

noted,

in some cases, as with some forms of heart disease, antidepressants

may

make the chronic illness worse. " The 20 cardiovascular patients in

our

study were regarded as high-risk subjects because developing

depression

may cause suicidal ideation with further deterioration of quality of

life. Tricyclics and monoamine oxidase ... inhibitors may be

detrimental

to cardiac patients because of their toxic cardiovascular side

effects. "

It's a catch-22: Treating severe depression may not only hurt the

quality of life but also be life-threatening, yet treating with

standard

antidepressants may bring about the same result. For these people,

SAM-e

may be the treatment of choice. Forty-eight patients with major

depression and concurrent serious illnesses were given up to 800mg

of

SAM-e daily. The results as described by the researchers were

excellent:

" Response of patients treated with SAM-e was quite rapid and many

were

still improving at the end of the 28-day trial. " As noted, patients

not

only improved quickly on SAM-e, but did not experience any untoward

side

effects that could worsen their preexisting medical problems.

(Current

Therapeutic Research, June 1994, Vol. 5 5, No. 6.)

 

A MAJOR REVIEW OF THE STUDIES. A metaanalysis, a major review of the

published clinical studies on SAM-e, published in Acta Scandinavica

Neurologica in 1994 assessed the efficacy of SAM-e in the treatment

of

depression. What makes this study so important is that all of the

clinical trials of SAM-e published between 1973 and 1992 were

analyzed.

In eleven studies, SAM-e was tested against a placebo. In fourteen

studies, SAM-e was tested against a standard prescription

antidepressant. In another thirteen studies known as open studies,

SAM-e

was given to depressed patients without testing it against either a

placebo or an antidepressant. The patients were monitored to assess

improvement. In every study involving placebos, SAM-e was found to

be

more effective than the placebo. In fact, the author of the study

notes

that SAM-e does better on the placebo test than most other

prescription

antidepressants! In every study involving prescription drugs, SAM-e

was

found to be as effective as tricyclic antidepressants. In the open

studies, patients also showed significant improvement. The review

study

concluded, " In summary, this meta-analysis shows that the efficacy

of

SAM-e in treating depressive syndromes and disorders is superior to

that

of placebo and is comparable to that of standard tricyclic

antidepressants. Since SAM-e is a naturally occurring compound with

relatively few side-effects, its antidepressant effect makes it a

potentially important tool in the armamentarium of the modern

psychopharmacologist. "

 

TWO MULTICENTER STUDIES. In a 1997 review article published in

Expert

Opinion in Investigational Drugs, Terry outlined SAM-e's potential

as a

treatment for psychiatric and neurological disorders. He reported on

two

as yet unpublished clinical trials on SAM-e conducted at several

research centers in Europe involving 197 severely depressed patients

(based on the Hamilton Rating Scale). In the first study, involving

seventy-five patients, SAM-e was tested against a placebo. Both

compounds were given intravenously. Patients taking SAM-e had an

average

improvement rate of 40.8 percent compared to patients taking the

placebo, who improved by only 27.6 percent. Considering how severely

ill

these patients were, this is an excellent result.

 

In the second study, SAM-e went head-to-head with clomipramine,

perhaps

the strongest drug in the antidepressant arsenal. Although

clomipramine

is highly effective, recovery often comes at the cost of terrible

side

effects. In fact, many patients simply won't stay on the drug. In

the

trial, 122 patients were given either SAM-e or clomipramine

intravenously for three weeks. Patients taking SAM-e had an average

improvement rate of 36.5 percent compared to 48.8 percent for the

patients on clomipramine Even though SAM-e did not outperform

clomipramine it did bring about a major improvement in these

severely

depressed patients, and it achieved this good result with virtually

no

side effects. As Terry noted in his review, " The drugrelated adverse

events and dropouts for adverse events were significantly lower in

SAM-e

than in clomipramine. " In other words, many patients did not

continue to

take clomipramine because they could not tolerate the side effects.

If

the dropouts had been factored into the final result as

nonresponders,

clomipramine would not have fared as well.

 

From these studies, it's apparent that although SAM-e may be a

powerful

antidepressant, it works gently in the body. SAM-e can hold its own

among even the strongest of the prescription drugs, yet it does not

have any of the onerous side effects...

 

 

 

The preceeding was one chapter from the book, Stop Depression Now,

byR.Brown, M.D., T. Bottiglieri, Ph.D., and C. Colman, Putnam Sons,

1999.

 

This book is available at Willner Chemists.

_________________

 

 

JoAnn Guest

mrsjo-

www.geocities.com/mrsjoguest/Diets