July 3, 2012 |
An alternative to the old talking cure is expanding the knowledge base
of psychotherapy as we recognize the role that exercise, nutrition,
spirituality, mind-body approaches, and lifestyle can play in enhancing
our clinical effectiveness. Epidemic depression is occurring at a time
when the field of mental health appears very robust. There are more
mental health professionals treating more people than ever before in
history: psychiatrists, clinical psychologists, licensed social workers,
counselors, and therapists of all kinds.
We have a powerful
“therapeutic arsenal” of drugs to make us happier, calmer, and saner.
When I leaf through the pharmaceutical ads that take up so much space in
psychiatric journals, I get the feeling that we should all be in great
emotional health. Depression and anxiety should be as fully conquered as
smallpox and polio. But more of us than ever are discontented and not
experiencing optimum emotional well-being. What is wrong with this
picture? Why is the vast enterprise of professional mental health unable
to help us feel better?
I want you to consider the possibility that the basic assumptions of
mainstream psychiatric medicine are obsolete and no longer serve us
well. Those assumptions constitute the biomedical model of mental health
and dominate the whole field.
In 1977, the journal
Science published a provocative article
titled “The Need for a New Medical Model: A Challenge for Biomedicine.” I
consider it a landmark in medical philosophy and the intellectual
foundation of today’s integrative medicine. The author, George L. Engel,
M.D., was a professor of psychiatry at the University of Rochester (New
York) School of Medicine. Determined to overcome the limiting influence
of Cartesian dualism, which assigns mind and body to separate realms,
Engel envisioned medical students of the future learning that health and
illness result from an interaction of biological, psychological,
social, and behavioral factors, not from biological factors alone. He
fathered the field of psychosomatic medicine and devoted much of his
career to broadening our understanding of disease. He was particularly
interested in mental health.
George Engel died in 1999 with his vision largely unrealized. In fact,
the field of psychosomatic medicine ran out of steam sometime before his
death and was never able to challenge the ascendancy of biological
medicine.
“Biology Explains All” was in full swing when I was a student at
Harvard Medical School in the late 1960s. At that time, I was taught
that just four diseases were psychosomatic: peptic ulcer, rheumatoid
arthritis, bronchial asthma, and ulcerative colitis. Four out of the
entire catalog of diseases is not a lot, but at least for those four,
doctors conceded that mental/emotional factors played a role. Peptic
ulcer was knocked off the list in the early 1980s when a bacterial
infection (
Helicobacter pylori) was identified as the “real”
cause of ulcers, now treatable with antibiotics. Investigation of
biological factors associated with the three remaining conditions has
led to more powerful drug treatments for them and greatly lessened
interest in attending to any psychological, social, or behavioral
factors that might be involved.
Rheumatologists today, for example, are
most enthusiastic about a new class of immunosuppressive drugs called
TNF-α blockers, which often appear to put rheumatoid arthritis and
ulcerative colitis into full remission. Never mind that these drugs can
be highly toxic and are very expensive; once doctors prescribe them for
these conditions, they no longer see the point of addressing emotional
or lifestyle factors of the patients who have them.
Although George Engel’s efforts in psychosomatic medicine were ahead of
their time, their relevance today is great, and I advise all health
professionals, especially mental health professionals, to read his 1977
paper in
Science. I will summarize his “challenge for
biomedicine” here, because it exposes the great limitations of the
conceptual model that now dominates medicine in general and psychiatric
medicine in particular. That model often fails to help doctors maintain
and heal our physical bodies, and it has greatly hindered our
understanding of and ability to manage the epidemic of depression and
other mood disorders that plague our society. It does not point the way
to contentment, comfort, serenity, and resilience, nor does it show us
how to attain optimum emotional well-being.
Models are belief systems—sets of assumptions and explanations we
construct to make sense of our experience. In Engel’s words, “The more
socially disruptive or individually upsetting the phenomenon, the more
pressing the need of humans to devise explanatory systems.” Disease is a
very upsetting phenomenon, and humans throughout history have come up
with a variety of belief systems to explain it, from the wrath of the
gods to possession by spirits to disharmony with the forces of nature.
The dominant model of disease in our time is biomedical, built on a
foundation of molecular biology. As Engel explains, “It assumes disease
to be fully accounted for by deviations from the norm of measurable
biological (somatic) variables. It leaves no room within its framework
for the social, psychological, and behavioral dimensions of illness. The
biomedical model not only requires that disease be dealt with as an
entity independent of social behavior, it also demands that behavioral
aberrations be explained on the basis of disordered somatic (biochemical
or neurophysiological) processes. Thus the biomedical model embraces
both reductionism, the philosophic view that complex phenomena are
ultimately derived from a single primary principle, and mind-body
dualism.”
Engel goes on to say, “The biomedical model has . . . become a cultural
imperative, its limitations easily overlooked. In brief, it has now
acquired the status of a
dogma. . . . Biological dogma requires
that all disease, including ‘mental’ disease, be conceptualized in
terms of derangement of underlying physical mechanisms.” He proposed an
alternative: a
biopsychosocial model of health and illness.
There is no question that over the past century, biomedicine has
advanced our knowledge of human biology, but the real test of a
scientific model—the measure of its superiority to an alternative belief
system—is whether or not it increases our ability to describe, predict,
and control natural phenomena. In my books about health and healing, I
have written a great deal about how strict application of the biomedical
model has actually made it harder for us to understand and manage
common diseases. For instance, I have pointed out that it fails to
account for the fact that many people infected with
H. pylori
never develop peptic ulcers or have any symptoms at all. They coexist
with it in a balanced way. Clearly, factors other than the simple
presence of that germ play a role in peptic ulcer disease, including the
strength or weakness of host defenses, of an individual’s resistance.
One of those defenses is stomach acid, whose production is influenced by
the autonomic (involuntary) nervous system and through it by emotions.
In the fight-or-flight response, the sympathetic division of the
autonomic nervous system shuts down gastrointestinal function, which is
unnecessary in an emergency, in order to divert energy and blood flow to
muscles. That includes turning off the production of acid in the
stomach. In chronic anxiety and stress, the sympathetic nerves are
constantly overactive, and therefore there is constantly less acid in
the stomach to keep potentially invasive germs from causing tissue
damage. To say that
H. pylori infection is strongly correlated
with peptic ulcer disease is accurate. To say that it is the sole cause
of ulcers ignores the complexity of causation and the possible influence
of emotions.
In 1980, the American Psychiatric Association radically revised the
Diagnostic and Statistical Manual–III (DSM-III)
to be in accord with the biomedical model. As a consequence, the role
of psychiatrists went from being facilitators of insight in patients to
being dispensers of drugs to modify brain chemistry. Although some
psychiatrists still rely on talk therapy, of all medical specialties,
the profession as a whole is the most dominated and, to my mind, hobbled
by blind faith in biomedicine. Psychiatrists were easily seduced
because of a collective inferiority complex with regard to their place
in the medical hierarchy. Still referred to as witch doctors and shrinks
(from headshrinkers), they themselves have a history of questioning
whether they are real doctors and whether they need the same basic
medical training as cardiologists and surgeons. With the spectacular
rise of biomedicine, their discomfort increased, and, not wanting to be
left behind, they looked for ways to be even more biologically correct
than their colleagues in other specialties. They saw their ticket to
acceptance in the new and rapidly developing field of
psychopharmacology—the study of the effect of drugs on mental and
emotional disorders.
In 1921, Otto Loewi (1873–1961), a German pharmacologist, demonstrated
that nerve cells (neurons) communicate by releasing chemicals. Prior to
that time, neuroscientists thought nervous communication was electrical.
Among the many important breakthroughs that followed from Loewi’s work
were the identification of neurotransmitters and the discovery of
receptors on cell surfaces that bind them. Neurotransmitters are
chemicals made within the body, stored in tiny sacs clustered within a
neuron and released into the synapse, the gap between the neuron and a
target cell, which might be another neuron (the postsynaptic neuron) or a
muscle or glandular cell. The released molecules then bind to
receptors—specialized proteins on the surface membrane of the target
cell—causing changes in that cell, making it more or less likely to
produce an electrical signal (in the case of a neuron), to contract (in
the case of a muscle), or to secrete a hormone (in the case of a
glandular cell). Later, the neurotransmitters can separate from their
receptors and be taken up by presynaptic cells for reuse or be broken
down by enzymes into inactive metabolites. Neuroscientists have now
compiled long lists of neurotransmitters, described their actions, and
identified many types and subtypes of receptors.
Three of the most studied neurotransmitters are norepinephrine,
dopamine, and serotonin, all very relevant to the subject at hand
because they influence our moods and emotions. For example, dopamine is
involved in what is known as the reward system of the brain; drugs that
affect it can alter our experience of pleasure. Cocaine is such a drug.
It blocks reuptake of dopamine back into the presynaptic neuron,
effectively increasing its action at the synapse to produce an intense
pleasurable response. With prolonged use of cocaine, postsynaptic
neurons become less responsive to dopamine, leading to depression and
dependence on the drug to relieve it. The dopamine hypothesis of
schizophrenia attributes psychosis to overactivity of this
neurotransmitter. Norepinephrine regulates both reward and arousal.
Disturbances in that neurotransmitter system are associated with anxiety
disorders. And serotonin affects our moods and sleep.
The most widely used psychiatric drugs today influence the production
and effects of these major neurotransmitters. Psychopharmacologists made
their first big breakthrough in the 1950s from work with
antihistamines, used to quell allergic symptoms. Although antihistamines
are best known for blocking the effects of the compound responsible for
certain immune responses, they also affect the brain, often making
people groggy, sleepy, and depressed. By tinkering with these molecules,
chemists produced a new class of psychoactive drugs—the
phenothiazines—that blocked dopamine transmission. Thorazine and other
phenothiazines were successfully marketed as major tranquilizers and
antipsychotics and quickly revolutionized the treatment of
schizophrenia. Psychiatrists hailed them as magical compounds that cured
psychosis, while critics argued that they simply made psychotic people
groggy, sedated, and easier to manage, even as outpatients. Energized by
this achievement, psychopharmacologists then turned their attention to
depression. Over the past sixty years, they have come up with a number
of drugs to treat it.
The efforts of psychopharmacologists give us an opportunity to evaluate
the usefulness of the biomedical model in psychiatry. In practice,
psychiatric medicine today is synonymous with psychopharmacology. The
credo of that field is “There is no twisted thought without a twisted
molecule.” (The words of the American neurophysiologist Ralph Gerard,
1900–1974). The biomedical model explains depression as the result of a
chemical imbalance in the brain, specifically of neurotransmitters
affecting our moods. How well does that explanation enable us to
describe, predict, and control depressive illness? In other words, just
how effective are the antidepressant drugs that psychopharmacologists
have developed, that the big pharmaceutical companies sell such
quantities of, and that so many people today take? The answer, I’m
afraid, is not very.
The first antidepressant drug was discovered serendipitously in 1952.
Iproniazid, an antimicrobial agent being studied as a possible treatment
for tuberculosis, was found to affect mood, making even terminally ill
patients cheerful and optimistic. Investigation of a possible mechanism
for this unexpected psychoactivity revealed that the drug blocked
enzymatic breakdown of all three major neurotransmitters:
norepinephrine, dopamine, and serotonin.
Pharmaceutical chemists then
looked for other drugs with this action and soon after produced a
different class of antidepressant drugs by modifying the phenothiazine
tranquilizers. These became known as tricyclic antidepressants, of which
amitriptyline was the prototype; Merck pharmaceutical company gave it
the brand name Elavil. In 1961, the FDA approved Elavil for the
treatment of major depression, and it quickly became a bestselling drug.
The tricyclics appeared to work by blocking presynaptic reuptake of
norepinephrine and serotonin without affecting dopamine.
Because all of the early antidepressants had unpleasant side effects
and serious potential interactions with other drugs and medications,
pharmaceutical chemists continued their search for better ones with more
specific action. But what specific action should it be? Some thought
deficiency of norepinephrine was the biochemical cause of depression.
Others argued for a serotonin hypothesis of depression and looked for
compounds to prevent its breakdown or reuptake. The proponents of the
serotonin hypothesis would win the day; their big discovery came in the
1970s, again, interestingly enough, as a result of work with an
antihistamine.
Very likely you have taken Benadryl (diphenhydramine) at some point in
your life. It is one of the oldest and most widely used antihistamines,
the first such drug to be approved by the FDA for prescription use, in
1946. Benadryl is so sedating that it is now sold over the counter as a
sleep aid. In the 1960s, this tried-and-true drug was found to have an
action independent of its effect on histamine: it selectively inhibited
the reuptake of serotonin. By modifying this molecule, scientists at Eli
Lilly and Company in the 1970s came up with the first safe and
effective selective serotonin reuptake inhibitor, fluoxetine, much
better known by its brand name Prozac. The rest is history. Today the
accepted biomedical explanation of depression is that it results from a
deficiency of serotonin at synapses in key areas of the brain;
therefore, boosting the activity of this neurotransmitter with drugs
that block its reuptake will treat or cure the problem.
It’s a good bet that thirty years ago, not one American in a thousand
had heard of this neurotransmitter—or any neurotransmitters, for that
matter. Today, when you Google
serotonin, about 11 million results appear, and Amazon sells nearly three thousand books with the word in the title (including
The Serotonin Solution: The Potent Brain Chemical That Can Help You Stop Bingeing, Lose Weight, and Feel Great).
“Serotonin” is the name of a professional wrestling team and an album
by the British rockers The Mystery Jets. You can even proclaim your
autumn blues to friends by way of a greeting card that reads, “The
leaves and my serotonin levels are falling.” A once-obscure
neurochemical has become pop-culture currency, and increasing levels of
this feel-good compound has turned into a public obsession.
None of this just happened on its own. In order to sell antidepressant
medications, drug manufacturers launched a relentless worldwide
marketing and public-relations campaign promoting serotonin as the
distilled biochemical essence of happiness. The message was that
selective serotonin reuptake inhibitors—SSRIs—increase synaptic levels
of serotonin in the brain by slowing its rate of reabsorption by
presynaptic neurons, ending depression. Psychiatrists and other
physicians got the technical version of this message, while consumers
got a simplified one, often reduced to the rallying cry “Boost
serotonin!”
The only problem is that it probably isn’t true.
Like the dopamine hypothesis of schizophrenia and other attempts to
attribute complex mental phenomena to simplistic biochemical causes, the
serotonin hypothesis of depression is shaky at best. Several studies
have established that lowering serotonin levels does
not
negatively impact mood. In fact, a new pharmaceutical known as
tianeptine—sold in France and other European countries under the trade
name Coaxil—has been shown to be as effective as Prozac. Tianeptine
works by
lowering synaptic serotonin. As psychology professor Irving Kirsch of the University of Hull in England told
Newsweek,
“If depression can be equally affected by drugs that increase serotonin
and by drugs that decrease it, it’s hard to imagine how the benefits
can be due to their chemical activity.”
It is, indeed, especially as evidence accumulates that, in most cases,
SSRIs work no better than placebos to boost mood. The first such
analysis, published in 1998, looked at thirty-eight
manufacturer-sponsored studies that included more than three thousand
depressed patients. It found negligible differences in improvement
between those on the drugs and those on dummy pills. At least 75 percent
of the benefit from this class of antidepressants seemed to be a
placebo effect. This finding has since been confirmed by other research.
To say that biomedically minded physicians have been reluctant to
accept this finding or modify their prescribing habits as a result would
be a great understatement. Both professional and popular media have
tried to play down the significance of this new research and in some
cases have misreported the findings. In April 2002, the
Journal of the American Medical Association (JAMA)
published the results of a large randomized controlled study sponsored
by the National Institutes of Health to evaluate a popular herbal
treatment for depression, St. John’s wort (
Hypericum perforatum).
Its effect was compared with that of the widely prescribed SSRI Zoloft
(sertraline) and a placebo in 340 patients with major depressive
disorder. The conclusion that made front-page news around the world was
that St. John’s wort worked no better than the placebo at relieving
depression. Television news shows featured reporters in health-food
stores pointing to St. John’s wort products and advising consumers not
to waste their money on natural remedies whose supposed benefits were
nothing more than old wives’ tales.
Never mind that St. John’s wort is not indicated for the treatment of
major depression, making the point of the study questionable. The
finding from this well-designed trial that should have made front-page
news was that Zoloft also worked no better than the placebo. In fact,
the placebo treatment was acually more effective in these very depressed
patients than either Zoloft or St. John’s wort!
Irving Kirsch summarized the growing body of evidence against SSRIs in his 2010 book,
The Emperor’s New Drugs: Exploding the Antidepressant Myth,
which I recommend. In response, proponents of the drugs and the
serotonin hypothesis retreated to a more defensible position: SSRIs may
owe much of their apparent benefit to patients’ belief in them, they
admit, but they still have a real biochemical effect that makes them
useful in the treatment of severe depression. Unfortunately for those
proponents, the most recent analysis, published in the January 6, 2010,
issue of
JAMA, rates the real biochemical effect of SSRIs as
nonexistent to negligible even in most cases of severe depression. Only
in patients with very severe symptoms can researchers detect a
statistically significant drug benefit compared with that of a placebo.
About 13 percent of people with depression have very severe symptoms.
One of the authors of the
JAMA paper, Steven D. Hollon, Ph.D.,
of Vanderbilt University, has said, “Most people [with depression] don’t
need an active drug. For a lot of folks, you’re going to do as well on a
sugar pill or on conversations with your physicians as you will on
medication. It doesn’t matter what you do; it’s just that you’re doing
something.”
I would argue that the dismal performance of Prozac, Zoloft, Paxil, and
other antidepressant drugs relative to placebos not only leaves the
serotonin hypothesis of depression without a leg to stand on but also
exposes the failure of the biomedical model to further our understanding
of and ability to manage emotional disorders. I firmly believe that the
nature of depression will never be revealed solely in studies of brain
biochemistry that are isolated from the rest of human experience. Like
coronary heart disease, depression is a multifactorial health problem,
rooted in complex interactions of biological, psychological, and social
variables, best understood and managed through a broader biopsychosocial
model of the sort proposed by George Engel.
Loneliness, for example, is a powerful predictor of depression.
Numerous studies show that people with few intimate social contacts are
more likely to be depressed than those who enjoy a rich network of
friends and family.
Reductionists might argue that being part of a
social group boosts serotonin, but I am confident that there is
something in a successful social life that transcends any effect on
brain biochemistry, at least insofar as we currently understand that
biochemistry. In other words, a happy family life probably raises
serotonin in some people, lowers it in others, and leaves it unaffected
in still others. Yet it makes them all more comfortable, serene, and
relatively immune to mood disorders through a body-mind-social
interaction that can’t be reduced to its constituent parts.
The New Model
I have written about possible causes of epidemic depression in our
society, among them such lifestyle factors as diets high in processed
foods, lack of physical activity, social isolation resulting from
affluence, and altered brain activity from information overload. In its
narrow focus on molecular biology, the biomedical model fails to capture
any of this, and practitioners under its spell cannot give depressed
patients the advice they need to address the complex causes of their
problems. All they can do is dispense drugs that for the majority of
patients might as well be sugar pills.
In an effort to give mental health professionals more and better
options, I convened the first national conference on integrative mental
health in March 2010. Together with Victoria Maizes, M.D., executive
director of the Arizona Center for Integrative Medicine, I invited
psychiatrists, psychologists, social workers, and other health
professionals to attend a three-day event in Phoenix to “learn how to
treat their patients within a new paradigm of integrative mental health
care that utilizes scientifically proven alternative methods in
combination with drugs and traditional therapy to address patients’
physical, psychological, and spiritual needs.” The use of the word
spiritual
here is significant; it expands George Engel’s concept to include yet
another dimension of human life, one often overlooked in medicine.
Adding it creates a biopsychosocialspiritual model. For convenience, I
prefer the term
integrative to describe this new way of thinking about health and illness in general and mental health in particular.
Dr. Maizes and I invited leading practitioners and researchers to share
their experience and findings with attendees. We planned for an
audience of three hundred, but, in a time of great economic recession,
the conference sold out six weeks in advance with a total of seven
hundred registrants. If we had had a larger venue, we could have doubled
that number, so great was the interest in the topic—evidence, I think,
that professionals are even more fed up than patients with the dead end
that the drug-only approach represents.
On the closing day of the conference, I spoke about the failure of the
biomedical model and the great advantages of the new integrative model
of mental health. I quoted Albert Einstein on the subject of conceptual
models:
“Creating a new theory is not like destroying an old barn and erecting a
skyscraper in its place. It is rather like climbing a mountain, gaining
new and wider views, discovering unexpected connections between our
starting point and its rich environment. But the point from which we
started still exists and can be seen, although it appears smaller and
forms a tiny part of our broad view gained by the mastery of the
obstacles on our adventurous way up.”
The new integrative model of mental health does not ignore brain
biochemistry. It takes into account correlations between imbalances in
neurotransmitters and mood disorders. Nor does it reject
psychopharmacology. Integrative treatment plans for depression,
particularly for severe depression, may well include medication, but my
colleagues and I prefer to try other methods first and to use
antidepressant drugs for short-term management of crises rather than
rely on them as long-term solutions. One of the invited speakers, a
noted expert on psychopharmacology, gave an optimistic presentation on
psychiatric drugs of the future, drugs that will have more specific,
better-targeted actions. People listened to his lecture with interest
but showed much greater enthusiasm for talks on the critical importance
of dietary omega-3 fatty acids to optimum emotional health and the
latest neuroscientific evidence for the benefits of meditation, among
others.
To say that the psychiatrists, psychologists, and other mental health
professionals in attendance appreciated this larger perspective fails to
convey their excitement. One told me that she had been waiting years
for such a conference. Another said he would take the information he
received and use it to change standards of practice in a large group of
mental health care facilities in his state. Many expressed interest in
seeking formal training in integrative mental health, training that I
and my colleagues at the University of Arizona hope to provide.
Presentations that particularly interested me concerned
neuroplasticity, the potential of the brain and nervous system to change
and adapt. The speakers were neuroscientists influenced by Buddhist
psychology and the teachings of the Dalai Lama. Using such new
techniques as PET scans and functional MRIs, which make it possible to
visualize living brains, they have been able to show that individuals
trained in meditation have different brain activity from those without
such training, and they respond differently to situations that would
cause most of us to lose our emotional equilibrium. The broader
implication of this research is that changes in the mind can cause
changes in both the function and structure of the brain, a fact that
cannot be explained by the biomedical model and that suggests many more
options for taking charge of our emotional well-being.
In retrospect, seeing human beings as nothing more than the sum of
biochemical interactions was probably a necessary stage of medical
evolution. Medical systems of the past lacked the technology to study
the biological underpinnings of human health with rigor and precision.
Now we have that technology, and we’ve used it well to gain invaluable
insights about our physical bodies. But it is impossible to restore or
promote human health unless we begin with a complete definition of a
human being. An incomplete definition will always result in incomplete
diagnoses and less-than-optimal treatments.
So now is the time to ascend the mountain and see the biomedical model
as one part of our broadening view. Our health or lack of it is the
result of biochemical interactions and genetics, dietary choices,
exercise patterns, sleep habits, hopes, fears, families, friends, jobs,
hobbies, cultures, ecosystems, and more. Chemical imbalances in the
brain may well correlate with depression, anxiety, and other emotional
states but the arrows of cause and effect can point in both directions.
Optimizing emotional wellness, by improving attention, changing
destructive patterns of thinking, and finding contentment within, can
also optimize brain chemistry, correcting any deficiencies in
neurotransmitters.
George Engel showed us the path upward more than thirty years ago. Now, I am happy to say, we are starting to follow it.
Andrew Weil, M.D., is a world-renowned
leader and pioneer in the field of integrative medicine, a healing
oriented approach to health care which encompasses body, mind, and
spirit.
