As a college student I often hear stories from friends and classmates that involve lots and lots of alcohol. Not one to drink, I didn’t really know much about alcohol and its effects, other than what kids are told in grade school. After doing some searching I found out that, not only was there a lot of information known, but that there was still a lot of research being done on the topic.
Some interesting statistics that I found include:
- Alcoholism is one of, if not the, most prominent neuro psychiatric disorders in society today.
- In 2010 the number of alcohol-induced deaths, excluding accidents and homicides, was 25,692.
- Around 35% of abuse victims report that offenders are under the influence of alcohol.
- Alcohol use is also associated with 2 out of 3 incidents of intimate partner violence.
- Alcohol is often a major factor in cases of child abuse and neglect and 10% of children in the US live with a parent that abuses alcohol
Statistics like these make me wonder why people drink alcohol. What is it about alcohol that leads us to consume it? Why do some people become dependent on it? It turns out that alcohol, like other drugs that humans tend to use and abuse, actually causes changes to our brains when it is used frequently enough and in large quantities.
The neurological pathway that leads to alcohol addiction is called the Reward or Pleasure pathway. This pathway involves multiple regions of the brain including the ventral tegmental area (VTA), the nucleus accumbens, and parts of the prefrontal cortex. Unlike other drugs alcohol does not directly affect the dopamine pathway, which is an integral part of the reward pathway. Instead it acts on GABAA receptors located on interneurons in the VTA. Ethanol binds to the GABAA receptors and cause GABAA gated chloride channels to open, and stay open longer than normal. This leads to the neurons becoming excitatory, and their interaction with the reward pathway causes an increase in dopaminergic activity in the VTA. The dopamine from the VTA interacts with the nucleus accumbens, activating the reward system there as well.
Over time the human brain can become used to this overabundance of dopamine and become dependent on alcohol activating the reward pathway. This leads to dependency on alcohol meaning that the person is now addicted to it. Because the brain has been changed by alcohol if its use is discontinued there can be some very nasty side effects. These side effects are called withdrawal symptoms and they can start as soon as two hours after an addicts last drink. They can be extremely severe. So severe in fact that, if not treated, they can lead to death.
There are two categories of withdrawal symptoms, psychological and physiological. Anxiety and confusion are two of the more mild psychological side effects while hallucinations fall on the more extreme end of the spectrum. Physiological symptoms include shaking, sweating, nausea, and vomiting. They can also include more serious symptoms like high fever, irregular heartbeat, and even seizures, all of which require immediate medical attention. The avoidance of these withdrawal symptoms are a reason that, along with the modification of the brain, keep people dependent on alcohol.
Over all I learned a lot about alcohol use and abuse. Some of what I learned was quite scary and all of it definitely makes me think twice about heading out to have a drink with friends.
More information can be found:
Boileau I., Assaad J.M., Pihl R.O., Benkelfat C., Leyton M., Diksic M., Tremblay R.E., Dagher A. Alcohol promotes dopamine release in the human nucleus accumbens. Synapse. 49(2003):226-31
Pestell, Katharine. “Alcohol Addiction.” Trends in Pharmacological Sciences 22.9 (2001): 448. Print.
Lishman, W. A. “Alcohol and the Brain.” The British Journal of Psychiatry 156.5 (1990): 635-44. Print.
Vengeliene, V., A. Bilbao, A. Molander, and R. Spanagel. “Neuropharmacology of Alcohol Addiction.” British Journal of Pharmacology 154.2 (2008): 299-315. Print.

Sleep Deprived?

As a graduating college student one has time to look back and reflect on many things. Although the intended goal of college is to nurture one’s thirst for knowledge, gain critical thinking skills, and to improve one’s connection to society, it inadvertently harms its students. Most college students at Colby College, are not just students, they are athletes, leaders, and general active members of society. On paper this ability to be well-rounded helps the people excel, but this active involvement also harms those people. There never seems to be enough time in the day for one to juggle academics, leadership positions, clubs, sports, and sleep all while trying to remain a social being.  Usually an aspect of one’s life has to take the back burner to excel in the other aspects, and sleep is usually placed in the back burner. The amount of college students who usually run on less than 6 hours of sleep is alarming. Some people go multiple days with only 2-3 hours of sleep.

Sleep, although often neglected, is vital to make sure proper neural cognition, and to regenerate cells/tissues/neurons. There is grand consensus that missing out on proper sleep, or attempting to train your body to work on limited amount of sleep is so negative for the body, especially the brain. Research has looked into the effects of sleep deprivation on motor cognition, memory, and speech, specifically the processing of language.

In the cerebral cortex the temporal lobe is the site associated with processing language, this was ascertained from verbal learning tests done while simultaneously observing the activity of the brain region using a functional magnetic resonance imaging scan(fMRI). It was shown that in sleep deprived people performing the visual test the temporal lobe was not active at all. But, in people who were severely sleep deprived are still able to do the verbal learning test to some degree. This allowed researchers to wonder how or why this occurs even though there is no activity within the temporal lobe. Using fMRI researchers were able to show that the parietal lobe in sleep deprived people were active in verbal learning tests to attempt to compensate for the inactive temporal speech regions. Because it is not the parietal lobe’s usual responsibility to deal with speech it, so it is not adept at it. The parietal lobe is adept at short-term memory, which can give evidence to support why sleep deprived people have better short term memory than their rested counterparts. The parietal lobe is more active in sleep deprived people.

When thinking of how sleep deprivation affects an person an important part is how the brain creates a sense of self, termed I-function. The prefrontal cortex has been linked in the connection to the I-function. In sleep deprived people the pre-frontal cortex is usually more active. The prefrontal cortex is regenerated in the first stages of sleep allowing people to feel refreshed after a quick nap.

“REM sleep stimulates areas of the brain used for learning and memory. When a person is taught a new skill his or her performance does not improve until he or she receives at least eight hours of sleep. An extended period of sleep ensures that the brain will be able to complete the full sleep cycle, including REM sleep. The necessity of sleep for learning could be due to the fact that sleep increases the production of proteins while reducing the rate at which they are broken down. Proteins are used to regenerate the neurons within the brain. Without them new synapses may not be able to be formed, thus limiting the amount of information a sleep-deprived person can maintain.” (S.L. 2008)

 Sleep deprivation over prolonged periods of time can also lead to death, because other parts of the body weakens along the brain. The immune system weakens the longer one goes without sleep, causing the number of white blood cells available to be decreased. Also, the amount of growth hormone produced by the body, and the body’s ability to metabolize sugar decreases.

Sleep deprivation has a great impact on our body, health, and well-being. Some of the damages caused by sleep deprivation may be long lasting, but even with that knowledge people every day push sleep aside as if it is not important. For college students it may seem sleep is not always one’s first priority, but it needs to be.


Gambling Addiction

Gambling is one of many addictions that plague our society and individuals within it. Like most addictions, compulsive gambling consumes and destroys lives. It is one of the more dangerous addictions because it is so accessible. It is promoted and perpetuated by the government and casinos across the country. Around 1-3% of Americans suffer from compulsive gambling and the negative consequences vary from person to person. For many compulsive gamblers, betting isn’t as much about money as it is about the excitement. Sustaining the thrill that gambling provides usually involves taking increasingly bigger risks and placing larger bets. Gambling addiction researchers propose that our brains have not been evolved to properly make decisions in todays society especially gambling decisions and therefore we consistently make errors in judgment, this is amplified in gambling addicts who cannot override their impulses to gamble and cannot properly make decisions that mediate risk and reward. Neuroimaging studies suggest similarities between behavioral and substance addictions. Gambling addiction has extremely similar effects in the brain as a drug addiction would. Here is a great quote from Dr. Alan Leshner, a prominent addiction researcher, applicable to any addiction, “Understanding that addiction is, at its core, a consequence of fundamental changes in brain function means that a major goal of treatment must be either to reverse or to compensate for those brain changes”. Gambling is a deadly combination of reinforcement. A near miss has the same kind of conditioning effect on behavior as a success. A near miss could produce some of the excitement of a win, i.e., secondary reinforcement. Therefore, the player is not constantly losing but constantly nearly winning. Failing to fulfill a goal (e.g., not winning on a slot machine) produces frustration, which energizes ongoing behavior. Subsequent wins then reinforce behavior. The frustration produced by nearly winning would induce a form of cognitive regret. The elimination of regret can be achieved by playing again, and this in turn encourages future play. The mechanisms that drive compulsive gambling are very powerful and can change one’s brain chemistry for a very long time. For more information on gambling and neuroscience start with this article:


Being Sick is No Fun!

I’m a person who loves to go skiing. Every Thursday, I wake up early to drive an hour and twenty minutes for a fun day on the slopes. Unfortunately, the road to the ski mountain is windy and bumpy…and consequently I spend nearly every Thursday morning stopped along the side of the road, car sick.

So what causes car-sickness, and how can I prevent it so I can enjoy my time skiing? Actually, there is no difference between the cause of car-sickness, sea-sickness, and air-sickness (from airplanes). All have the same symptoms of nausea/vomiting, headache, a general feeling of being unwell, paleness, and/or sweating. Motion is sensed by three different systems: the inner ear, which is responsible not only for hearing but also balance, the eyes, and the deep-tissue skin. The vestibular system plays a major role in balance and spatial orientation, which is located in the inner ear. For example, when we walk somewhere, all these systems are coordinated: the eyes see movement, the inner ear senses movement, and the body feels that it is walking.

The leading theory behind motion sickness is that it is a defense against neurotoxins. The part of the brain responsible for inducing vomiting when poisons are detected is called the area postrema. This part of the brain is also responsible for resolving conflicts between vision and balance. There are three types of motion sickness: when motion is felt but not seen, when motion is seen but not felt, and when both systems detect motion but they do not correspond. When these systems transmit conflicting information, the area postrema attempts to resolve the system through vomiting.

Let’s take sea-sickness as an example. Pretend you are on a boat with no windows. When the boat is moving, the inner ear senses motion, and transmits this information to the brain. The eyes, however, tells the brain that everything is still. The brain thus concludes that one system is hallucinating, and further concludes that this hallucination is due to ingesting poison. The brain responds by forcing the body to vomit, which would get rid of the (supposed) toxin.

So back to my car-sickness. My eyes mostly see the interior of the car, which is motionless, while the inner ear senses motion as the vehicle goes over those rotten bumps in the road or around curves. My eyes are telling my brain that I am not moving, but my ear is telling my brain that I am. This is why closing my eyes doesn’t help: my ears still sense movement. However, looking off into the distance can be helpful, because it allows my eyes to sense motion, which corresponds to my inner ear’s detection. This re-orients the inner sense of balance by providing visual information that transmits motion.

Fortunately, there are some treatments that can help with car-sickness. There are medications available that block signals from the vestibular system, which helps alleviate the conflicting information sent to the brain. Sitting in the front seat of a car can be helpful too, because the eyes then sense the movement of the car through the front windshield rather than the backs of the seats, which transmits signals to the brain that the body is stationary. Some people also use motion sickness bracelets, which claim to work by applying pressure to the “Nei-Kuan” acupressure point. There is no strong evidence behind these bands’ effectiveness, however.
vestibular system

Eat Your Broccoli—Choline in the Brain

There have been many studies investigating the ways that the brain develops and which supplements play essential roles in helping the brain grow and function at maximum capacity. One such nutrient is choline. Choline is a precursor to the neurotransmitter acetylcholine, which is important in memory and cognitive function in the brain. For this reason studies have been conducted on choline and its role in brain development areas involved in cognitive function and memory.

One study by (Zeisel, 2004) looked at choline as a dietary supplement. Researchers found that in utero (early development) rat offspring whose mothers received choline supplements had noticeable brain function change in the hippocampus resulting in increased lifelong memory enhancement. The rat offspring also displayed faster learning abilities and larger brain cells compared to normal diet rats. The researchers commented that changes in the brain were noticeable enough that they could distinguish between rats born in the control group, and those rats whose mothers had been given choline supplements during their pregnancy. Other related studies have made connections with prenatal choline supplements resulting in better learning in mice born with Down’s syndrome.

In a food questionnaire study, it was found that adults who reported eating a diet with choline high foods scored higher on memory tests. Individuals with reported higher intake of choline also were less likely to show white matter hyperintensity on brain scans suggesting that they have a decreased risk of dementia or stroke in the future. This study also factored in other supplement nutrients such as vitamins B6 and B12 and still came to the same conclusion about the positive benefits of choline on brain health.

In addition low levels of choline have shown increased likelihood neural tube defects in babies of women who have a deficiency of choline in their blood during prenatal periods. Low choline has also been connected to later development of Alzheimer’s and other brain problems due to ageing and degrading cells in the brain.

As a side note in connection to our discussions around schizophrenia, mothers who were given phosphatidylcholine (a supplemental precursor to choline) during their 2nd and 3rd trimesters of pregnancy had babies who were twice as likely to respond correctly to a clicking noise test used as an analytical test for “markers” of increased risk for developing schizophrenia (University of Colorado).

The overall conclusion is that the evidence seems to suggest choline has a beneficial effect on brain growth and development both during prenatal periods and as an adult and can increase memory and cognitive function. While some may claim that the increased growth and increase in memory is not unarguably significant, it still seems that choline plays an important role in preventing or at least slowing the “pathway toward mental decline” including dementia and Alzheimer’s.

As a medical application, some pharmaceutical companies are looking into drug development with phosphatidylcholine to prevent cognitive decline and regrow brain cells and neural connections. Furthermore, efforts have been made to use phosphatidylcholine, due to its role in building cell membranes, to protect the digestive tract and help treat gastrointestinal issues. Choline is naturally contained in several foods such as eggs, soybeans, liver, and broccoli. It is also available in supplement form.



Is it Possible to Inherit a Resistance to Cocaine?


     As to date, human genetic studies have shown that cocaine addiction is heritable. Shocking? Not really. When you think of a cocaine addict producing offspring, you’d assume that the offspring would be at high risk or rather, predisposed to using cocaine. We’ve thought for years that yes, addiction is heritable and tends to run in families. But what if it’s not? What if there was some type of protective effect that could be passed down to offspring from a paternal or maternal cocaine abuse? A study published in 2013 titled, Epigenetic Inheritance of a Cocaine Resistance Phenotype, suggested just that.

     The goal of this study was to examine the influence of paternal cocaine self- administration of cocaine reinforcement in offspring. What they did was allow male rats to self -administer cocaine for 60 days while the control group self -administered saline. All male rats were then mated with healthy female rats. The graph below shows the extent to which male and female offspring self administered cocaine when given the opportunity to take both low (0.5mg) and high ( 1.0mg) doses. What they found was not at all what they hypothesized. The male offspring of “cocsired” rats (fathers who self-administered cocaine) when given the opportunity to self-administer cocaine, self-administered a significant less amount of cocaine, regardless of dosage offered, than male offspring of “salsired” (fathers who self-administered saline) rats. There was no difference between female offspring in regards to self-administration of cocaine, regardless of whether their fathers were cocsired or salsired. Meaning that, female offspring whose fathers self-administered cocaine self-administered the same amount of cocaine as female offspring whose fathers self-administered saline.


    Brain derived neurotropic factor (BDNF) in the medial pre-frontal cortex is known to blunt the behavioral effects of cocaine. So essentially, with a larger expression BDNF one would be less likely to experience the rewarding effects of cocaine. So, in order to ensure that it was an increase in BDNF protein causing reduced administration of cocaine in cocsire rats, they administered a TrkB antagonist called ANA-12. The reason being is that BDNF signals primarily through TrkB receptors. So because the antagonist would inhibit BDNF from binding, we should see a reverse or increase in administration of cocaine, and this is what they found. What does this mean? BDNF expression in the medial pre-frontal cortex reduced cocaine administration in cocsired male offspring.


     Shocking? Yeah, I’d say so! This study suggests that exposure to cocaine in father rats might cause some kind of protective effect in their male offspring. Meaning, cocaine is interacting somehow in the fathers abusing cocaine, and in turn is causing some type of shielding effect in male offspring specifically. Though this research controlled for environmental factors and only studied the effect of cocaine without it’s interaction with other drugs, something impossible to do with humans, unlike human genetic studies, however, this study was not correlational. Something to think about.

Questions to think about:What is going on neurologically in the fathers abusing cocaine? And why is this protective effect sex specific?

Vassoler, F.M., White, S.L., Schmidt, H.D., Sadri-Vakili, G., and Pierce, R.C. (2013) Epigenetic Inheritance of a Cocaine Resistance Phenotype. Nat Neurosci.16(1): 42-47. doi:10.1038/nn.3280. 

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