This between behavioral addictions like BED and PG and

This study compares the opioid and
dopamine function between the two behavioral addiction phenotypes of
pathological gambling (PG) and binge eating disorder (BED). The purpose of the
study is to see if these findings can indicate if someone can be predisposed to
these addictive behaviors through genetics. The researchers also hoped to gain
a better fundamental understanding of the biological effects these behavioral
addictions in an effort to advance the research for possible drug treatments
similar to those provided to people with drug addictions. For this study, BED
is defined as the fast paced consumption of copious quantities of calories in rapid
succession and an overall lack of self control.

               In terms of their striatal post-synaptic D2
receptor availability and dopamine responses to pharmacological challenges,
both PG and BED respond differently than typical substance use disorders.
Researchers are still trying to gain better knowledge of the role
neurotransmitters play in behavioral addictions and their effectiveness in treatment.
Lisdexamfetamine is a prodrug of dextroamphetamine and is the first FDA
approved drug to treat BDE. The drug works by increasing the user’s dopamine by
blocking dopamine reuptake transporters. This shows a clear and discernable
link between behavioral addictions like BED and PG and the body’s use of
dopamine. It also increases the need for a better understanding of how
presynaptic dopamine functions in relation to BED. Depression symptoms are also
commonly associated with both PG and BED and anti-depressants have been used to
successfully treat BED in the past. Rodent studies also suggest that the opioid
system is linked to reward and craving components especially pertaining to BED.

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              With
all of this in mind, the researchers decided the best way to obtain their
desired dated was to observe the mu-opioid receptors and dopamine
neurotransmitters of a population using high resolution carfentanil (C) and
fluorodopa (F) brain PET scans to easily and directly compare the brains of BED
and PG subjects. Their original hypothesis stated that addicted brains might
present with lowered levels of dopamine and raised mu-opioid receptor binding.
They came to this conclusion based on the observation of the data of subjects
with substance abuse disorders. In order to test this hypothesis, sixty-seven
subjects were monitored with medical consultations, simple blood screenings,
and urine drug test. Following this, thirteen of the original participants were
eliminated from the study because of prior commitments, while four did not meet
the criteria for PG or BED. Five more were excluded due to conflicting
comorbidity issues and six were dismissed for undisclosed reasons. In the end,
thirty-nine subjects were used in the study. The groups were broken up into
seventeen healthy control (HC) subjects, fifteen PG subjects, and seven BED
subjects. The diagnoses for PG and BED were confirmed with a structured
clinical interview. Researchers ensured that no subjects were actively
utilizing drugs proven to interact with the opioid or dopamine systems.

              All
participants were restricted from tabacco use eight hours before the scan, from
drinking coffee or tea 12 hours before the scan, and from consuming alcohol 48
hours prior to scanning. Food consumption remained normal for the patients
before, during, and after the scanning process. To reduce the possibility of
interference from the effects of arousal on tracer bindings, the subjects were
forbidden to sleep during C imaging. At this point, one participant was unable
to complete the study because of a scanner malfunction, and three participants became
unavailable for F analysis scans. Those that remained in the study were given
brain scans with a PET-MRI scanner. PET scans were conducted uniformly through
the day at fixed intervals with C scans between 0900-1000 hours, and F scans at
between 1430-1530 hours. For four subjects, the PET scans had to be rescheduled
for separate days for undisclosed reasons. The patients were each were scanned
for a duration of 51 minutes for their C scans and 90 minutes for their F
scans. The C scans were comprised of 13 frames each while the F scans contained
twenty-two frames. Each subject was fitted was an individually shaped
thermoplastic mask during their scans to help minimize possible physical disturbances
and any disturbances were documented and adjusted for in the results.

              With
this study, researchers found that patients with BED had lower carfentanil BPNP than anyone else in many
areas of the brain, including the nucleus accumbens, the thalamus, the
hippocampus, the posterior cingulate gyrus, the thalamus, the frontal pole, the
lateral of the orbitofrontal cortex, and several more. The hippocampus was the
brain region in which researchers observed the largest decreases in BED
compares with PG patients. In the prefrontal cortex, binge eaters had 30% lower
C binding than pathological gamblers. BED patients also had lower Ki than the HC group and the PG
patients in the nucleus accumbens. Researchers determined that any other group
comparisons were insignificant.  

              The
researchers found that BED usually presents as inhibited mu-opioid receptor function
and poor dopamine production in the basal ganglia. This is in comparison to the
PG population which was linked to a decrease in available mu-opioid receptor in
the limbic lobe. This discovery has critical significance in the understanding addictive
behavior and may lead to more effective treatment options. They also found that
their hypothesis had been proven wrong and, rather than higher mu-opioid
receptor activity for both PG and BED patients, the decreased availability of
mu-opioid receptors, especially in binge eaters, are almost completely opposite
to similar tests run on drug addicted patients. It is thought that this
observation could exemplify variations in mu-opioid receptor regulation or internal
opioid release due to foreign substances or incentive motivation. Overall,
these findings have possible significance pertaining to the future of addiction
treatment through mu-opioid antagonists.

              This
study was incredibly easy to follow and did a wonderful job explaining the
science behind the mechanisms of research in a way made reading the article
much less frustrating. The study itself was simple in its methods and clear in
its objectives. The researchers were also able to create a replicable and causal
experiment that has major implications in the future of addiction treatment.
They did a good job isolating and eliminating confounding variables in subjects
with comorbidity or medicinal conflictions. The researchers comment on the fact
that their population of binge eating patients was smaller than they would have
liked and that the results of this group therefore need further replication
studies. They also note that BED were afflicted longer than PG subjects, which
could have skewed results. I would have liked for the authors to have expanded
further on the possible applications of their research beyond just the
statement that it has possible positive implications in the treatment of
behavioral addictions.

              This
research can have enormous real-world applications. It obviously expands our
understanding of neurotransmitters and the opioid system as it relates to some
behavioral addictions. Having the data to be able to compare the dopamine
responses between biological and behavioral addictions is crucial to
understanding the physiological differences between the two categories. The
ultimate trajectory is to use these differences to develop more effective
treatments for behavioral addictions as they are far less understood. These
findings also have the goal of getting closer to understanding what makes a
person more genetically predisposed to addiction. All of this adds up to
research that can be monumental in the mounting fight against behavioral
addictions like pathological gambling and binge eating disorders as well as
drug addictions like the current opioid crisis.

 

 

References

Majuri,
J., Joutsa, J., Johansson, J., Voon, V., Alakurtti, K., Parkkola, R., & …
Kaasinen, V. (2017). Dopamine and opioid neurotransmission in behavioral addictions:
A comparative PET study in pathological gambling and binge eating.
Neuropsychopharmacology, 42(5), 1169-1177. doi:10.1038/npp.2016.265