Pleasure Response from Chocolate: You Can See it in the Eyes

The brain’s pleasure response to tasting food can be measured through the eyes using a common, low-cost ophthalmological tool, according to a study just published in the journal Obesity. If validated, this method could be useful for research and clinical applications in food addiction and obesity prevention.

Dr. Jennifer Nasser, an associate professor in the department of Nutrition Sciences in Drexel University’s College of Nursing and Health Professions, led the study testing the use of electroretinography (ERG) to indicate increases in the neurotransmitter dopamine in the retina.

Dopamine is associated with a variety of pleasure-related effects in the brain, including the expectation of reward. In the eye’s retina, dopamine is released when the optical nerve activates in response to light exposure.

Nasser and her colleagues found that electrical signals in the retina spiked high in response to a flash of light when a food stimulus (a small piece of chocolate brownie) was placed in participants’ mouths. The increase was as great as that seen when participants had received the stimulant drug methylphenidate to induce a strong dopamine response. These responses in the presence of food and drug stimuli were each significantly greater than the response to light when participants ingested a control substance, water.

“What makes this so exciting is that the eye’s dopamine system was considered separate from the rest of the brain’s dopamine system,” Nasser said. “So most people– and indeed many retinography experts told me this– would say that tasting a food that stimulates the brain’s dopamine system wouldn’t have an effect on the eye’s dopamine system.”

This study was a small-scale demonstration of the concept, with only nine participants. Most participants were overweight but none had eating disorders. All fasted for four hours before testing with the food stimulus.

If this technique is validated through additional and larger studies, Nasser said she and other researchers can use ERG for studies of food addiction and food science.

“My research takes a pharmacology approach to the brain’s response to food,” Nasser said. “Food is both a nutrient delivery system and a pleasure delivery system, and a ‘side effect’ is excess calories. I want to maximize the pleasure and nutritional value of food but minimize the side effects. We need more user-friendly tools to do that.”

The low cost and ease of performing electroretinography make it an appealing method, according to Nasser. The Medicare reimbursement cost for clinical use of ERG is about $150 per session, and each session generates 200 scans in just two minutes. Procedures to measure dopamine responses directly from the brain are more expensive and invasive. For example, PET scanning costs about $2,000 per session and takes more than an hour to generate a scan.

(Image: Scott Thornburg)

Researchers unravel genetics of dyslexia and language impairment

A new study of the genetic origins of dyslexia and other learning disabilities could allow for earlier diagnoses and more successful interventions, according to researchers at Yale School of Medicine. Many students now are not diagnosed until high school, at which point treatments are less effective.

The study is published online and in the July print issue of the American Journal of Human Genetics. Senior author Dr. Jeffrey R. Gruen, professor of pediatrics, genetics, and investigative medicine at Yale, and colleagues analyzed data from more than 10,000 children born in 1991-1992 who were part of the Avon Longitudinal Study of Parents and Children (ALSPAC) conducted by investigators at the University of Bristol in the United Kingdom.

Gruen and his team used the ALSPAC data to unravel the genetic components of reading and verbal language. In the process, they identified genetic variants that can predispose children to dyslexia and language impairment, increasing the likelihood of earlier diagnosis and more effective interventions.

Dyslexia and language impairment are common learning disabilities that make reading and verbal language skills difficult. Both disorders have a substantial genetic component, but despite years of study, determining the root cause had been difficult.

In previous studies, Gruen and his team found that dopamine-related genes ANKK1 and DRD2 are involved in language processing. In further non-genetic studies, they found that prenatal exposure to nicotine has a strong negative affect on both reading and language processing. They had also previously found that a gene called DCDC2 was linked to dyslexia.

In this new study, Gruen and colleagues looked deeper within the DCDC2 gene to pinpoint the specific parts of the gene that are responsible for dyslexia and language impairment. They found that some variants of a gene regulator called READ1 (regulatory element associated with dyslexia1) within the DCDC2 gene are associated with problems in reading performance while other variants are strongly associated with problems in verbal language performance.

Gruen said these variants interact with a second dyslexia risk gene called KIAA0319. “When you have risk variants in both READ1 and KIAA0319, it can have a multiplier effect on measures of reading, language, and IQ,” he said. “People who have these variants have a substantially increased likelihood of developing dyslexia or language impairment.”

“These findings are helping us to identify the pathways for fluent reading, the components of those pathways; and how they interact,” said Gruen. “We now hope to be able to offer a pre-symptomatic diagnostic panel, so we can identify children at risk before they get into trouble at school. Almost three-quarters of these children will be reading at grade level if they get early intervention, and we know that intervention can have a positive lasting effect.”

Beauty and the Brain: Electrical Stimulation of the Brain Makes You Perceive Faces as More Attractive

The researchers, led by scientists at the California Institute of Technology (Caltech), have used a well-known, noninvasive technique to electrically stimulate a specific region deep inside the brain previously thought to be inaccessible. The stimulation, the scientists say, caused volunteers to judge faces as more attractive than before their brains were stimulated.

Being able to effect such behavioral changes means that this electrical stimulation tool could be used to noninvasively manipulate deep regions of the brain—and, therefore, that it could serve as a new approach to study and treat a variety of deep-brain neuropsychiatric disorders, such as Parkinson’s disease and schizophrenia, the researchers say.

"This is very exciting because the primary means of inducing these kinds of deep-brain changes to date has been by administering drug treatments," says Vikram Chib, a postdoctoral scholar who led the study, which is being published in the June 11 issue of the journal Translational Psychiatry. “But the problem with drugs is that they’re not location-specific—they act on the entire brain.” Thus, drugs may carry unwanted side effects or, occasionally, won’t work for certain patients—who then may need invasive treatments involving the implantation of electrodes into the brain.

So Chib and his colleagues turned to a technique called transcranial direct-current stimulation (tDCS), which, Chib notes, is cheap, simple, and safe. In this method, an anode and a cathode are placed at two different locations on the scalp. A weak electrical current—which can be powered by a nine-volt battery—runs from the cathode, through the brain, and to the anode. The electrical current is a mere 2 milliamps—10,000 times less than the 20 amps typically available from wall sockets. “All you feel is a little bit of tingling, and some people don’t even feel that,” he says.

"There have been many studies employing tDCS to affect behavior or change local neural activity," says Shinsuke Shimojo, the Gertrude Baltimore Professor of Experimental Psychology and a coauthor of the paper. For example, the technique has been used to treat depression and to help stroke patients rehabilitate their motor skills. "However, to our knowledge, virtually none of the previous studies actually examined and correlated both behavior and neural activity," he says. These studies also targeted the surface areas of the brain—not much more than a centimeter deep—which were thought to be the physical limit of how far tDCS could reach, Chib adds.

The researchers hypothesized that they could exploit known neural connections and use tDCS to stimulate deeper regions of the brain. In particular, they wanted to access the ventral midbrain—the center of the brain’s reward-processing network, and about as deep as you can go. It is thought to be the source of dopamine, a chemical whose deficiency has been linked to many neuropsychiatric disorders.

The ventral midbrain is part of a neural circuit that includes the dorsolateral prefrontal cortex (DLPFC), which is located just above the temples, and the ventromedial prefrontal cortex (VMPFC), which is behind the forehead. Decreasing activity in the DLPFC boosts activity in the VMPFC, which in turn bumps up activity in the ventral midbrain. To manipulate the ventral midbrain, therefore, the researchers decided to try using tDCS to deactivate the DLPFC and activate the VMPFC.

To test their hypothesis, the researchers asked volunteers to judge the attractiveness of groups of faces both before and after the volunteers’ brains had been stimulated with tDCS. Judging facial attractiveness is one of the simplest, most primal tasks that can activate the brain’s reward network, and difficulty in evaluating faces and recognizing facial emotions is a common symptom of neuropsychiatric disorders. The study participants rated the faces while inside a functional magnetic resonance imaging (fMRI) scanner, which allowed the researchers to evaluate any changes in brain activity caused by the stimulation.

A total of 99 volunteers participated in the tDCS experiment and were divided into six stimulation groups. In the main stimulation group, composed of 19 subjects, the DLPFC was deactivated and the VMPFC activated with a stimulation configuration that the researchers theorized would ultimately activate the ventral midbrain. The other groups were used to test different stimulation configurations. For example, in one group, the placement of the cathode and anode were switched so that the DLPFC was activated and the VMPFC was deactivated—the opposite of the main group. Another was a “sham” group, in which the electrodes were placed on volunteers’ heads, but no current was run.

Those in the main group rated the faces presented after stimulation as more attractive than those they saw before stimulation. There were no differences in the ratings from the control groups. This change in ratings in the main group suggests that tDCS is indeed able to activate the ventral midbrain, and that the resulting changes in brain activity in this deep-brain region are associated with changes in the evaluation of attractiveness.

In addition, the fMRI scans revealed that tDCS strengthened the correlation between VMPFC activity and ventral midbrain activity. In other words, stimulation appeared to enhance the neural connectivity between the two brain areas. And for those who showed the strongest connectivity, tDCS led to the biggest change in attractiveness ratings. Taken together, the researchers say these results show that tDCS is causing those shifts in perception by manipulating the ventral midbrain via the DLPFC and VMPFC.

"The fact that we haven’t had a way to noninvasively manipulate a functional circuit in the brain has been a fundamental bottleneck in human behavioral neuroscience," Shimojo says. This new work, he adds, represents a big first step in removing that bottleneck.

Using tDCS to study and treat neuropsychiatric disorders hinges on the assumption that the technique directly influences dopamine production in the ventral midbrain, Chib explains. But because fMRI can’t directly measure dopamine, this study was unable to make that determination. The next step, then, is to use methods that can—such as positron emission tomography (PET) scans.

More work also needs to be done to see how tDCS may be used for treating disorders and to precisely determine the duration of the stimulation effects—as a rule of thumb, the influence of tDCS lasts for twice the exposure time, Chib says. Future studies will also be needed to see what other behaviors this tDCS method can influence. Ultimately, clinical tests will be needed for medical applications.

High Sugar Intake Linked to Low Dopamine Release in Insulin Resistant Patients

PET study led by Stony Brook Professor indicates that overeating and weight gain contributing to onset of diabetes could be related to a deficit in reward circuits in the brain

Using positron emission tomography (PET) imaging of the brain, researchers have identified a sweet spot that operates in a disorderly way when simple sugars are introduced to people with insulin resistance, a precursor to type 2 diabetes. For those who have the metabolic syndrome, a sugar drink resulted in a lower-than-normal release of the chemical dopamine in a major pleasure center of the brain. This chemical response may be indicative of a deficient reward system, which could potentially be setting the stage for insulin resistance. This research could revolutionize the medical community’s understanding of how food-reward signaling contributes to obesity, according to a study presented at the Society of Nuclear Medicine and Molecular Imaging’s 2013 Annual Meeting.

"Insulin resistance is a significant contributor to obesity and diabetes," said Gene-Jack Wang, MD, lead author of the study and Professor of Radiology at Stony Brook University and researcher at the U.S. Department of Energy’s Brookhaven National Laboratory in Upton, N.Y. "A better understanding of the cerebral mechanisms underlying abnormal eating behaviors with insulin resistance would help in the development of interventions to counteract the deterioration caused by overeating and subsequent obesity. We suggest that insulin resistance and its association with less dopamine release in a central brain reward region might promote overeating to compensate for this deficit."

An estimated one-third of Americans are obese, according to the U.S. Centers for Disease Control and Prevention. The American Diabetes Association estimates that about 26 million Americans are living with diabetes and another 79 million are thought to be prediabetic, including those with insulin resistance.

The tendency to overeat may be caused by a complex biochemical relationship, as evidenced by preliminary research with rodents. Dr. Wang’s research marks the first clinical study of its kind with human subjects.

"Animal studies indicated that increased insulin resistance precedes the lack of control associated with pathological overeating," said Wang. "They also showed that sugar ingestion releases dopamine in brain regions associated with reward. However, the central mechanism that contributes to insulin resistance, pathological eating and weight gain is unknown."

He continued, “In this study we were able to confirm an abnormal dopamine response to glucose ingestion in the nucleus accumbens, where much of the brain’s reward circuitry is located. This may be the link we have been looking for between insulin resistance and obesity. To test this, we gave a glucose drink to an insulin-sensitive control group and an insulin-resistant group of individuals and we compared the release of dopamine in the brain reward center using PET.”

In this study, a total of 19 participants-including 11 healthy controls and eight insulin-resistant subjects-consumed a glucose drink and, on a separate day, an artificially sweetened drink containing sucralose. After each drink, PET imaging with C-11 raclopride-which binds to dopamine receptors-was performed. Researchers mapped lit-up areas of the brain and then gauged striatal dopamine receptor availability (which is inversely related to the amount of natural dopamine present in the brain). These results were matched with an evaluation in which patients were asked to document their eating behavior to assess any abnormal patterns in their day-to-day lives. Results showed agreement in receptor availability between insulin-resistant and healthy controls after ingestion of sucralose. However, after patients drank the sugary glucose, those who were insulin-resistant and had signs of disorderly eating were found to have remarkably lower natural dopamine release in response to glucose ingestion when compared with the insulin-sensitive control subjects.

"This study could help develop interventions, i.e., medication and lifestyle modification, for early-stage insulin-resistant subjects to counteract the deterioration that leads to obesity and/or diabetes," said Wang. "The findings set a path for future clinical studies using molecular imaging methods to assess the link of peripheral hormones with brain neurotransmitter systems and their association with eating behaviors."

Why Music Makes Our Brain Sing

MUSIC is not tangible. You can’t eat it, drink it or mate with it. It doesn’t protect against the rain, wind or cold. It doesn’t vanquish predators or mend broken bones. And yet humans have always prized music — or well beyond prized, loved it.

In the modern age we spend great sums of money to attend concerts, download music files, play instruments and listen to our favorite artists whether we’re in a subway or salon. But even in Paleolithic times, people invested significant time and effort to create music, as the discovery of flutes carved from animal bones would suggest.

So why does this thingless “thing” — at its core, a mere sequence of sounds — hold such potentially enormous intrinsic value?

The quick and easy explanation is that music brings a unique pleasure to humans. Of course, that still leaves the question of why. But for that, neuroscience is starting to provide some answers.

More than a decade ago, our research team used brain imaging to show that music that people described as highly emotional engaged the reward system deep in their brains — activating subcortical nuclei known to be important in reward, motivation and emotion. Subsequently we found that listening to what might be called “peak emotional moments” in music — that moment when you feel a “chill” of pleasure to a musical passage — causes the release of the neurotransmitter dopamine, an essential signaling molecule in the brain.

When pleasurable music is heard, dopamine is released in the striatum — an ancient part of the brain found in other vertebrates as well — which is known to respond to naturally rewarding stimuli like food and sex and which is artificially targeted by drugs like cocaine and amphetamine.

But what may be most interesting here is when this neurotransmitter is released: not only when the music rises to a peak emotional moment, but also several seconds before, during what we might call the anticipation phase.

The idea that reward is partly related to anticipation (or the prediction of a desired outcome) has a long history in neuroscience. Making good predictions about the outcome of one’s actions would seem to be essential in the context of survival, after all. And dopamine neurons, both in humans and other animals, play a role in recording which of our predictions turn out to be correct.

To dig deeper into how music engages the brain’s reward system, we designed a study to mimic online music purchasing. Our goal was to determine what goes on in the brain when someone hears a new piece of music and decides he likes it enough to buy it.

We used music-recommendation programs to customize the selections to our listeners’ preferences, which turned out to be indie and electronic music, matching Montreal’s hip music scene. And we found that neural activity within the striatum — the reward-related structure — was directly proportional to the amount of money people were willing to spend.

But more interesting still was the cross talk between this structure and the auditory cortex, which also increased for songs that were ultimately purchased compared with those that were not.

Why the auditory cortex? Some 50 years ago, Wilder Penfield, the famed neurosurgeon and the founder of the Montreal Neurological Institute, reported that when neurosurgical patients received electrical stimulation to the auditory cortex while they were awake, they would sometimes report hearing music. Dr. Penfield’s observations, along with those of many others, suggest that musical information is likely to be represented in these brain regions.

The auditory cortex is also active when we imagine a tune: think of the first four notes of Beethoven’s Fifth Symphony — your cortex is abuzz! This ability allows us not only to experience music even when it’s physically absent, but also to invent new compositions and to reimagine how a piece might sound with a different tempo or instrumentation.

We also know that these areas of the brain encode the abstract relationships between sounds — for instance, the particular sound pattern that makes a major chord major, regardless of the key or instrument. Other studies show distinctive neural responses from similar regions when there is an unexpected break in a repetitive pattern of sounds, or in a chord progression. This is akin to what happens if you hear someone play a wrong note — easily noticeable even in an unfamiliar piece of music.

These cortical circuits allow us to make predictions about coming events on the basis of past events. They are thought to accumulate musical information over our lifetime, creating templates of the statistical regularities that are present in the music of our culture and enabling us to understand the music we hear in relation to our stored mental representations of the music we’ve heard.

So each act of listening to music may be thought of as both recapitulating the past and predicting the future. When we listen to music, these brain networks actively create expectations based on our stored knowledge.

Composers and performers intuitively understand this: they manipulate these prediction mechanisms to give us what we want — or to surprise us, perhaps even with something better.

In the cross talk between our cortical systems, which analyze patterns and yield expectations, and our ancient reward and motivational systems, may lie the answer to the question: does a particular piece of music move us?

When that answer is yes, there is little — in those moments of listening, at least — that we value more.

Longer Days Bring ‘Winter Blues’—For Rats, Not Humans

Most of us are familiar with the “winter blues,” the depression-like symptoms known as “seasonal affective disorder,” or SAD, that occurs when the shorter days of winter limit our exposure to natural light and make us more lethargic, irritable and anxious. But for rats it’s just the opposite.

Biologists at UC San Diego have found that rats experience more anxiety and depression when the days grow longer. More importantly, they discovered that the rat’s brain cells adopt a new chemical code when subjected to large changes in the day and night cycle, flipping a switch to allow an entirely different neurotransmitter to stimulate the same part of the brain.

Their surprising discovery, detailed in the April 26 issue of Science, demonstrates that the adult mammalian brain is much more malleable than was once thought by neurobiologists. Because rat brains are very similar to human brains, their finding also provides a greater insight into the behavioral changes in our brain linked to light reception. And it opens the door for new ways to treat brain disorders such as Parkinson’s, caused by the death of dopamine-generating cells in the brain.

The neuroscientists discovered that rats exposed for one week to 19 hours of darkness and five hours of light every day had more nerve cells making dopamine, which made them less stressed and anxious when measured using standardized behavioral tests. Meanwhile, rats exposed for a week with the reverse—19 hours of light and five hours of darkness—had more neurons synthesizing the neurotransmitter somatostatin, making them more stressed and anxious.

“We’re diurnal and rats are nocturnal,” said Nicholas Spitzer, a professor of biology at UC San Diego and director of the Kavli Institute for Brain and Mind. “So for a rat, it’s the longer days that produce stress, while for us it’s the longer nights that create stress.”

Because rats explore and search for food at night, while humans evolved as creatures who hunt and forage during the daylight hours, such differences in brain chemistry and behavior make sense. Evolutionary changes presumably favored humans who were more active gatherers of food during the longer days of summer and saved their energy during the shorter days of winter.

“Light is what wakes us up and if we feel depressed we go for a walk outside,” said Davide Dulcis, a research scientist in Spitzer’s laboratory and the first author of the study. “When it’s spring, I feel more motivation to do the things I like to do because the days are longer. But for the rat, it’s just the opposite. Because rats are nocturnal, they’re less stressed at night, which is good because that’s when they can spend more time foraging or eating.”

But how did our brains change when humans evolved millions of years ago from small nocturnal rodents to diurnal creatures to accommodate those behavioral changes?

“We think that somewhere in the brain there’s been a change,” said Spitzer. “Sometime in the evolution from rat to human there’s been an evolutionary adjustment of circuitry to allow switching of neurotransmitters in the opposite direction in response to the same exposure to a balance of light and dark.”

A study published earlier this month in the American Journal of Preventive Medicine found some correlation to the light-dark cycle in rats and stress in humans, at least when it comes to people searching on the internet for information in the winter versus the summer about mental illness. Using Google’s search data from 2006 to 2010, a team of researchers led by John Ayers of San Diego State University found that mental health searches on Google were, in general, 14 percent higher in the winter in the United States and 11 percent higher in the Australian winter.

“Now that we know that day length can switch transmitters and change behavior, there may be a connection,” said Spitzer.

In their rat experiments, the UC San Diego neuroscientists found that the switch in transmitter synthesis in the rat’s brain cells from dopamine to somatostatin or back again was not due to the growth of new neurons, but to the ability of the same neurons there to produce different neurotransmitters.

Rats exposed to 19 hours of darkness every 24 hours during the week showed higher numbers of dopamine neurons within their brains and were more likely, the researchers found, to explore the open end of an elevated maze, a behavioral test showing they were less anxious. These rats were also more willing to swim, another laboratory test that showed they were less stressed.

“Because rats are nocturnal animals, they like to explore during the night and dopamine is a key part of our and their reward system,” said Spitzer. “It’s part of what allows them to be confident and reduce anxiety.”

The researchers said they don’t know precisely how this neurotransmitter switch works. Nor do they know what proportion of light and darkness or stress triggers this switch in brain chemistry. “Is it 50-50? Or 80 percent light versus dark and 20 percent stress? We don’t know,” added Spitzer. “If we just stressed the animal and didn’t change their photoperiod, would that lead to changes in transmitter identity? We don’t know, but those are all doable experiments.”

But as they learn more about this trigger mechanism, they said one promising avenue for human application might be to use this neurotransmitter switch to deliver dopamine effectively to parts of the brain that no longer receive dopamine in Parkinson’s patients.

“We could switch to a parallel pathway to put dopamine where it’s needed with fewer side effects than pharmacological agents,” said Dulcis.

Researchers identify pathway that may protect against cocaine addiction

A study by researchers at the National Institutes of Health gives insight into changes in the reward circuitry of the brain that may provide resistance against cocaine addiction. Scientists found that strengthening signaling along a neural pathway that runs through the nucleus accumbens — a region of the brain involved in motivation, pleasure, and addiction — can reduce cocaine-seeking behavior in mice.

Research suggests that about 1 in 5 people who use cocaine will become addicted, but it remains unclear why certain people are more vulnerable to drug addiction than others.

“A key step in understanding addiction and advancing treatment is to identify the differences in brain connectivity between subjects that compulsively take cocaine and those who do not,” said Ken Warren, Ph.D., acting director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Researchers at NIAAA, part of NIH, conducted the study.

“Until now, most efforts have focused on finding traits associated with vulnerability to develop compulsive cocaine use. However, identifying mechanisms that promote resilience may prove to have more therapeutic value,” said the paper’s senior author, Veronica Alvarez, Ph.D., acting chief of the Section on Neuronal Structure in the NIAAA Laboratory for Integrative Neuroscience. The study is available on the Nature Neuroscience website ahead of print.

In the study, mice were conditioned to receive an intravenous dose of cocaine each time they poked their nose into a hole in their enclosure. Cocaine was then made unavailable for periods of time during the day. Some of the mice would stop seeking the drug once it was removed while others would obsessively continue to poke the hole in an effort to obtain the drug.

Mice that quickly stopped seeking the drug were found to have stronger connections along the indirect pathway — a neural tract that forms indirect projections into the midbrain and contains cells called medium spiny neurons expressing dopamine D2 receptors (D2-MSNs). A parallel pathway — known as the direct pathway — forms direct projections into the midbrain neurons and contains medium spiny neurons expressing D1 receptors (D1-MSNs). These two pathways are thought to work together in complementary but sometimes opposing ways to affect behavior.

"We were very surprised by the results of the study because we were originally looking for vulnerability factors for developing compulsive drug use,” said Dr. Alvarez. “Instead, we found changes that only happened in subjects that show a resilience to becoming compulsive drug users. Resilient mice had a strong inhibitory circuit that allowed them to exert better control over their drug intake."

To test this observation, researchers used lasers to activate individual neurons, and found that stimulating D2-MSNs in the nucleus accumbens decreased cocaine seeking in the mice. Blocking D2-MSN signaling with a chemical process increased motivation to obtain cocaine.

“This research advances our understanding of how the recruitment, activation and the interaction among brain circuits can either restrain or increase motivation to take drugs,” said David Shurtleff, Ph.D. acting deputy director of the National Institute on Drug Abuse.

Previous studies have shown that people with lower levels of dopamine D2 receptors in the striatum, a brain region associated with reward and working memory, are more likely to develop compulsive behaviors toward stimulant drugs.

Dopamine is a key neurotransmitter involved in reward-based learning and addiction. Cocaine disrupts communication between neurons at the synapse, the small junction between nerve cells, by blocking the reabsorption of dopamine into the transmitting neuron. As a result, dopamine continues to stimulate the receiving neuron, causing feelings of alertness and euphoria.

Taste of beer, without effect from alcohol, triggers dopamine release in the brain

The taste of beer, without any effect from alcohol itself, can trigger dopamine release in the brain, which is associated with drinking and other drugs of abuse, according to Indiana University School of Medicine researchers.

Using positron emission tomography (PET), the researchers tested 49 men with two scans, one in which they tasted beer, and the second in which they tasted Gatorade, looking for evidence of increased levels of dopamine, a brain neurotransmitter long associated with alcohol and other drugs of abuse. The scans showed significantly more dopamine activity following the taste of beer than the sports drink. Moreover, the effect was significantly greater among participants with a family history of alcoholism.

Results of the study were published online Monday by the journal Neuropsychopharmacology.

"We believe this is the first experiment in humans to show that the taste of an alcoholic drink alone, without any intoxicating effect from the alcohol, can elicit this dopamine activity in the brain’s reward centers," said David A. Kareken, Ph.D., professor of neurology at the IU School of Medicine and the deputy director of the Indiana Alcohol Research Center.

The stronger effect in participants with close alcoholic relatives suggests that the release of dopamine in response to such alcohol-related cues may be an inherited risk factor for alcoholism, said Dr. Kareken.

Research for several decades has linked dopamine to the consumption of various drugs of abuse, although researchers have differing interpretations of the neurotransmitter’s role. Sensory cues that are closely associated with drug intoxication (ranging from tastes and smells to the sight of a tavern) have long been known to spark cravings and induce treatment relapse in recovering alcoholics. Many neuroscientists believe that dopamine plays a critical role in such cravings.

The study participants received a very small amount of their preferred beer — 15 milliliters — over a 15-minute time period, enabling them to taste the beer without resulting in any detectable blood alcohol level or intoxicating effect.

Using a PET scanning compound that targets dopamine receptors in the brain, the researchers were able to assess changes in dopamine levels occurring after the participants tasted the liquids.

In addition to the PET scan results, participants reported an increased beer craving after tasting beer, without similar responses after tasting the sports drink — even though many thought the Gatorade actually tasted better, said Brandon G. Oberlin, Ph.D., post-doctoral fellow and first author of the paper.

(Image: iStockphoto)