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PTSD and Disordered Eating - Food Addiction as Self-Medication

Posttraumatic Stress Disorder and Disordered Eating:
Food Addiction as Self-Medication
Timothy D. Brewerton, M.D., DFAPA
In this issue of the Journal of Women’s Health Hirth et al.
report important new data that confirm links between
posttraumatic stress disorder (PTSD) symptoms and eating
disordered behaviors. Furthermore, they extend those links
with PTSD to the ingestion of sugary sodas and fast foods, a
finding that persists despite race or ethnicity, marital status,
education, income level, and body mass index (BMI). Al-
though PTSD and its symptoms have previously been asso-
ciated with bingeing or purging behaviors or both, as well as
smoking cigarettes,
this is the first study to demonstrate a
connection between PTSD (and, hence, traumatic experiences)
and the frequency of ingesting particular types of foods, for
example, sugary sodas and fast foods.
An emerging body of evidence over the last few years has
characterized highly palatable foods, such as those found in
fast food restaurants, as potentially addictive and acting very
much like licit and illicit substances of abuse in the brain.
Specifically, high concentrations of refined sugar, fat, salt, and
caffeine are common components of fast food menus, and it
has been posited that all these foodstuffs have addictive
The results of the Hirth et al. article
have important and
far-reaching implications. For one, their data help to elucidate
the underlying mechanisms and behavioral pathways of how
trauma and subsequent PTSD eventually lead to an increased
chance of developing one or more of the leading causes of
death in the United States.
In addition to an array of medical
disorders, it is well established that PTSD is associated with
significantly higher rates of substance use disorders, other
comorbid psychiatric disorders, and a variety of self-
destructive and impulsive behaviors, including suicide.
These data also suggest that the ingestion, and especially
overingestion, of fatty or sugary energy sources may be just
another strategy that traumatized individuals use to numb
themselves from their unpleasant feeling states and memo-
ries. In essence, certain foods can act just like other substances
that alter brain chemistry and, hence, consciousness. Much
work in the neurosciences has been done to establish the
neurochemical mechanisms underlying these phenomena.
Using food to self-medicate dysphoric states is by no means
a new idea. For some time now, many people who have
struggled with compulsive overeating have identified their
problem as a food addiction. In 1956, Randolph
first de-
scribed the phenomenon of food addiction and linked it with
addictive drinking. Overeaters Anonymous (OA), which was
founded in 1960, defined compulsive overeating as a pro-
gressive, addictive illness and focused on refined sugar as the
addicting agent, a conclusion that is no longer so far-fetched.
In addition, those with overt eating disorders have described
using food to self-medicate as well as being addicted to
bingeing or purging behaviors.
Not only do these behaviors
often become habitual methods of affect regulation, but eating
foods with high hedonic value can quickly, inexpensively,
and legally offer a modicum of comfort and relief, however
transiently, and only more problems ensue.
During the last several years, mainstream science has be-
gun to accept the notion that certain foods can act like other
addicting substances in the brain, despite having other pe-
ripheral metabolic effects that substances of abuse do not
necessarily have.
It has been shown in both animal and
human experiments that food intake and drug use both cause
dopamine release in parts of the brain that mediate pleasure
and emotion. Furthermore, the degree of dopamine release
correlates with the sense of subjective reward or experience of
pleasure from both food and drug use. Similar patterns of
brain activation as seen on functional magnetic resonance
imaging (MRI) in response to food and drug cues have also
been found. Other studies demonstrate that food can stimu-
late the opiate system and that there are striking similarities in
use and withdrawal patterns of sugar and of classic drugs of
abuse. In addition, there often appear to be reciprocal rela-
tionships among food and other substances, in that people
may gain weight when they stop smoking or drinking. Taken
together, these observations support the conclusion that food
and classic addictive substances compete for the same brain
pathways and may serve the same purposes psychologically.
This reorientation toward entertaining the concept of food
addiction has been a result of the fact that at least one third of
people in the United States are obese, and the mortality and
morbidity associated with obesity have become a major focus
throughout medicine and public health. Even though the re-
sults of the study by Hirth et al.
did not find that women with
PTSD symptoms had higher BMIs than those women without
such symptoms, these data are relevant to an increase in
the understanding of the current obesity epidemic. Other
investigators have reported that obese patients have high rates
of trauma and PTSD.
That women with PTSD symptom-
atology were engaged in more strategies to lose weight, for
Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, South Carolina.
Volume 20, Number 8, 2011
ªMary Ann Liebert, Inc.
DOI: 10.1089/jwh.2011.3050
example, dieting, vomiting, and smoking behaviors, may have
counteracted the inevitable weight gain that a steady diet of
fast foods would incur. More importantly, these women were
young, averaging 20.8 years of age, and the effects of chronic,
excessive intake may not have had time to manifest.
In summary, the argument that certain foods can be ad-
dicting to certain people, especially traumatized people, is
very compelling. As with other addictions, when individuals
are exposed to, for example, alcohol, nicotine, illicit drugs of
abuse, or gambling, a certain subset of these people will be
highly attracted to these substances or behaviors and will
continue to use or do them to the point of becoming addicted,
whereas others will not. There are a number of risk factors,
some recognized and some not, that may determine if some-
one will go on to develop an addiction to food or to any
substance or behavior. Some of these risk factors are genetic.
For example, people with reduced dopamine type 2 receptor
availability have a predisposition toward obesity and sub-
stance dependence. Other risk factors are environmental, for
example, a prior history of physical, sexual, or emotional
abuse or interpersonal violence. In addition, given what we
have learned about gene and environment interactions, many
genetic disorders will be manifested only when the environ-
mental triggers are present.
These data contribute further evidence to the validity of the
self-medication hypothesis of PTSD. Victims of interpersonal
violence may not only resort to eating disordered behaviors
and smoking to alleviate psychic pain but also preferentially
select highly palatable foods containing high concentrations
of sugar, fat, salt, or caffeine, sometimes to the point of ad-
diction, in an attempt to dampen arousal and facilitate
numbing and avoidance, symptoms specific to PTSD.
Future directions of this work might be to replicate these
findings in other and perhaps older samples of women with
and without PTSD and to extend these studies to include men
and children. Traumatic experiences are very common in
children, who are especially vulnerable to the complex neu-
rodevelopmental changes of early stress and addiction. Chil-
dren are also likely to be exposed to fast foods, which can
subsequently lead to use of such foods to self-medicate neg-
ative mood states. It has already been reported that food ad-
diction is a viable concept in children.
Disclosure Statement
The author has no conflicts of interest to report.
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Address correspondence to:
Timothy D. Brewerton, M.D., DFAPA
216 Scott Street
Mt. Pleasant, SC 29464
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