Nearly one in five Americans have been diagnosed with some form of anxiety disorder. These range from panic attacks and post-traumatic stress disorder to social phobias and obsessive-compulsive disorders.
Anti-anxiety
drugs or antidepressants can curb symptoms that interfere with
day-to-day life. And these drugs are big business. In 2013, Americans
filled 48 million prescriptions for the benzodiazepine drug alprazolam
(Xanax). Patients also picked up 27 million prescriptions for sertraline
(Zoloft), an antidepressant drug that also helps some people with
anxiety.
Yet, while many
people do find relief in these drugs, they don’t work for everyone.
Benzodiazepines can interfere with normal thinking and induce
drowsiness. They also can be highly addictive, so doctors are reluctant
to prescribe them for people with a history of substance abuse. Zoloft
and other selective serotonin reuptake inhibitors (SSRIs) also don’t
work for everyone. They can cause nausea, jitters, insomnia, suicidal
thoughts, and loss of libido.
However, researchers are teasing out another option for reducing anxiety. When stress kicks in, so would this experimental drug.
“By targeting specific enzymes,” said neuroscientist J. Megan Gray, “we can minimize side effects.”
Researchers
from Calgary to Southern California are investigating the inner
struggle between one brain chemical that keeps stress in check and
another that is part of the body’s fight or flight response. Many of
these investigators talked about their latest findings during the
November 2014 Society for Neuroscience conference in Washington, D.C.
The
brains of humans and some animals naturally synthesize
endocannabinoids, molecules that help regulate functions including
appetite, mood and response to stress. An ample supply of
endocannabinoids keeps anxiety under control, and this is the function
that Gray and her colleagues at the Hotchkiss Brain Institute at the
University of Calgary want to boost.
When something stressful
happens — a deadline approaches or travel plans go awry — the fight or
flight response floods the brain with corticotropin-releasing hormone
(CRH). It degrades endocannabinoids and turns anxiety on. That’s like
releasing the parking brake when a car is parked on a hill. The new drug
would boost the level of endocannabinoids in the brain, creating a
buffer against CRH’s action.
Endocannabinoids and the active
compounds in marijuana both bind to the same brain receptors, which is
why some people self-medicate by smoking marijuana.
“Often, if you
go to a medical marijuana place and tell them you have anxiety, they’ll
give you marijuana,” said James Lim, a neuroscientist at the University
of California-Irvine. The problem is that cannabis also contains many
other chemicals, including harmful tars, that complicate the reaction.
If researchers can design an endocannabinoid-boosting compound that is
simpler, said Gray, “we can better understand what people are exposing
themselves to.”
Previously, researchers assumed that the stress
“parking brake” system acted the same in everyone. But new research
during the November conference points to a different model — that some
people’s brains synthesize more endocannabinoids than others, and that
people with higher levels can handle more stress.
Researchers have
long known that some people can take more metaphorical heat than
others. “Some kids can undergo a lot of traumatic events in early life
and turn out just fine,” said University of Michigan researcher Pam
Maras. “Some undergo relatively minor things and turn out to have severe
anxiety and depression.”
Numerous
researcher teams are using rat models to try to understand how stress
responses can be manipulated, and they reported their findings at the
conference.
In separate experiments, Gray and Lim tinkered with
endocannabinoid levels in rats. Both found that rats with higher levels
acted less anxious after being exposed to stress. Lim made part of a
maze scary by tainting it with the scent of a fox’s feces. Rats with
more stress-braking power would explore the tainted regions of the maze.
More timid rats avoided it for as long as seven days after the scent
was laid down.
Two other research groups, working independently in
Ohio and Colorado, manipulated CRH levels in different ways but arrived
at complementary results.
At Kent State University,
neuroscientist Lee Gilman blocked CRH receptors in mice, shutting out
the stress-inducing peptide and enabling them to approach other,
unfamiliar mice.
At the University of Colorado-Boulder,
Christopher Lowery is interested in how the brain responds to repeated
social defeat. For example, what happens when a child is repeatedly
bullied? He mimicked this by putting a male rat into the home cage of
another male rat, where the newcomer would be forced to surrender to the
more dominant native. In his study, rats that faced social defeat over
and over produced more CRH each time, and were more quickly immobilized
by fear during later encounters.
However, as Lim and Gilman both
observed, some animals can put the brake on anxiety longer than others.
Clinicians know this is true for humans; what the laboratory scientists
are probing is when and how those differences manifest in the brain.
Michigan
researcher Pam Maras sees evidence that these differences begin early
in development. Her more nervous rats began displaying excessive anxiety
as early as 11 days after birth, which corresponds to the fifth week of
life for an infant. Animals that did not manifest anxiety at that point
grew up to be more resilient to stress, though Maras can’t say why.
“We
don’t have an answer for that right now,” said Maras. “It’s exciting
sometimes when you don’t have an answer, because that means that there’s
more to do.”
Some people are probably born more vulnerable to
anxiety disorders than others. And although they might benefit greatly
from a medication that puts a brake on runaway anxiety, scientists have a
lot to learn before such a drug will be ready for clinical use.
Source: http://psychcentral.com/blog/archives/2015/01/15/new-research-into-anxiety-disorders/
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