Cobbers on the Brain – Page 63 – Student Commentary on the Neurological Sciences

Concussion: CBD as a Potential Treatment?

Posted on October 27, 2020 by / 0 Comment

Concussions, AKA mild traumatic brain injuries (mTBIs), can be frustrating to deal with. This is because they can cause many side effects including: headaches, confusion, nausea, depression, amnesia, trouble sleeping, and difficulty with concentration and learning. Although the symptoms usually disappear after a few weeks, as the brain heals, during the concussion one must put their life on hold. This is because the only current treatment for concussions is getting plenty of physical and mental rest. Along with over-the-counter medications, to make the person comfortable and alleviate headaches. This leads to the question, are there other medications that could be taken to help after a concussion?

In The Brain

First, it is important to understand what is happening in the brain when someone gets a concussion. When the brain gets shook around in the skull there can be injuries to axons which is a part of a neuron. Neurons are cells that send signals to one another which allows us to function. The axons could be bent, broken, or dead due to impact. The impact causes a leaky membrane on the neuron. This causes ions like calcium and sodium to come into the axon, allowing the neuron to become imbalanced and depolarized. Depolarization is important because when a neuron becomes depolarized it has more positive ions, which makes the neuron altogether more positive. A positively charged neuron wants to signal to other neurons.

After depolarization, the living, damaged neurons will then over signal causing glutamate release. Glutamate is a neurotransmitter that travels to other neurons making them fire. All of this firing causing a lot of activity to happen in the brain. The brain knows that the ions are not balanced, so it will use a lot of sodium, potassium, and ATP to try to balance out these ions and get the voltage back to normal. Burning ATP provides energy to the brain. This will then induce hyperglycolosis and metabolic uncoupling which contributes to behavior issues one might experience during a concussion.

Following, the burning of ATP forms lactate. Since the brain is burning a lot of ATP, there is lactate accumulation and calcium storing in the mitochondria. The mitochondria normally makes ATP. Calcium blocks the mitochondria from making ATP levels from returning to normal. Further, all this stress happening in the brain causes hypometabolism. Hypometabolism happens because the brain is using all this energy to balance ions, it isn’t able to use the energy to transport other things correctly. Calcium that is not stored in the mitochondria activates protease which is a protein that starts destroying other proteins, which then leads to apoptosis, AKA cell death. This whole process and the ions can get restored and fixed within roughly 10 days with proper treatment, but it is very easy to obtain other concussions during the healing process. If one gets a second concussion, the healing process takes much longer and there might be further long-term damage to the brain.

CBD Vs. THC?

Before explaining CBD as a treatment for concussions, it is important to note where it comes from and clear up any misconceptions that there might be about it. Cannabidiol (CBD) is a chemical found in the plant commonly known as marijuana or hemp. There are over 80 chemicals identified in this plant. One of which is the psychoactive chemical known as delta-9-tetrahydrocannabinol (THC). Like other chemicals in hemp, CBD can be extracted from hemp with little to no trace amounts of THC. Therefore, CBD does not get you high.

CBD as a Treatment?

In one study, researchers induced a concussion in male mice. After the concussion, the mice were placed in a comfortable environment during the experiment. Meanwhile, the mice were given oral CBD treatment. After 14 and 60 days there were 7 tests performed. Some of the tests showed CBD significantly improved symptoms in mice. The 7 tests included: Allodynia Test, Rotarod Test, Open Field Test, Resident-Intruder Test, Three Chambers Sociability Test, Tail Suspension Test and Microdialysis Test.

These were the results:

Allodynia Test-
- CBD treatment showed signs of reduced pain in mice.
Open Field Test-
- CBD treatment showed little significant changes in mice, but CBD did decrease “reckless behavior” shown by less rearing.
Resident-intruder test-
- CBD treatment significantly decreased aggressive behavior in mice.
Tail suspension Test-
- CBD treatment decreased depression like behavior, shown by decreased immobility in mice.
Microdialysis Test-
- CBD treatment administered prior to 60 days after trauma, normalized glutamate and D-Aspartate levels in the brain of mice.
Rotarod Test-
- CBD treatment showed no significant difference in motor coordination impairment in mice.
Three Chambers Sociability Test-
- CBD treatment showed no significant changes in social interaction in mice.

The data from this study shows promising results for CBD as a treatment for concussions. This being said, further research must be done to understand the full effects CBD has in concussions and on the body. For information about CBD as a treatment for other illnesses and side effects CBD might cause go to: https://www.medicalnewstoday.com/articles/cbd-oil-effects#side-effects

References

https://www.webmd.com/vitamins/ai/ingredientmono-1439/cannabidiol-cbd

https://www.frontiersin.org/articles/10.3389/fphar.2019.00352/full

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Concussion – Just an annoyance?

Posted on October 26, 2020 by / 0 Comment

Concussion is typically thought of as simply a hindrance to doing “normal” stuff, whether that be schoolwork, or getting back out onto the field, as most concussions happen through athletic means. But are the ramifications of a concussion just to feel a little dizzy and disoriented for a bit? Research into postcussed individuals suggests otherwise, as post concussion depression has been found to be a prevalent after-effect.

When people generally think of concussion, their first thought is typically not in relation to other mental disorders such as depression, but it should be. One study found that at least 35% of individuals that experience a traumatic brain injury (TBI) develop depression. This means that at least a third of people who get a concussion develop depressive symptoms afterward, which is quite a dramatic number. Another fact that was found is equally concerning: one study found that after only a mild traumatic brain injury, there was a 15% chance that the person developed major depression. This is the lightest and least serious type of brain injury (which you can get simply by hitting your head slightly too hard) and the worst, most serious type of depression, occurring in more than 1 in 7 people who experience a concussion. This is significant not only because of the depression part, but because this points to concussion as being more than purely “an annoyance”. In fact, the total prevalence across all severities of TBIs for major depression is 14-29%. In other words, up to a third of people who experience a concussion develop the clinically-worst type of depression.

This prevalence for depression isn’t universal however, there are certain people who develop more depressive symptoms than others post-concussion. Some risk factors are: being an older age when starting your first sport, having a history of substance abuse, and lower levels of education. Something that was found is that the severity of the TBI didn’t consistently lead to higher rates of depression, but losing consciousness was related to risk for developing major depression among mTBI patients. Some more demographic information reveals that ethnicities other than white experience greater post-concussion symptoms, and IQ has a negative correlation with such symptoms as well. These results are more speculative as to why they would be the case, but this highlights the need for greater concussion protocol and faculty in lower-socioeconomic areas, which unfortunately, by definition, have less access to such resources.

Figuring out why these results are the case has the ability to help numerous concussion victims recover with more vigor and not have to deal with bouts of depression while trying to recover. Neurologically speaking, one culprit could be the “differential patterns of calcium flux” that can occur postconcussion, which could be leading to less brain-derived neurotrophic factor (BDNF), leading to depression. BDNF is essential for cell proliferation and so without adequate amounts of it, cell levels and signalling may be messed up enough to contribute to startling equilibrium and causing depressive symptoms. The article also states that BDNF is directly associated with NMDA receptor alteration, which concussion causes as well. Another factor that would seemingly lead to higher depressive symptoms post-concussion would be increased GABA levels and signalling, as that has been found to increase related to depression. This however, is not the case with concussion, as GABA levels have been observed to fall in post-concussed individuals.

With the rates of depressive symptoms among concussed individuals being more than 1 in 3 people, more research should be done to figure out some of the mechanisms for bringing this number down. Preventing concussions in the first place would be the best option, but preventing post-concussion depression is also an important step in making things better for everyone who experiences this sort of thing, especially athletes. To loop back to my normal point, concussion is more than just an annoyance to be blown off as a headache, and more guidance should be brought into schools of all levels and education on the subject should continue so that everybody involved understands how to respond and properly help the individual heal.

Health

Ring Ring, Concussion Calling

Posted on October 25, 2020 by / 0 Comment

Your phone starts to ring, and you wonder who could be calling at this odd time of day. You pick up your phone, only to see that your concussion is calling. Debating whether to just send it to voicemail (it’s a pesky caller!), you ultimately decide you will hear out what it has to say. So, what does your concussion have to say to you?!

I’m hurting!

Your concussion begins the conversation by telling you that your brain is struggling, in more ways than one. It’s pretty common knowledge that concussions need a good amount of time to fully heal, but you might not know what exactly is going wrong.

When that blow to your head first strikes, the membranes within the brain’s axons get leaky, letting substances in and out that would normally be more tightly regulated. Because of this, sodium and calcium ions rush into the cell, leading to depolarization of the membrane. When the cell depolarizes, it is much more likely to fire an action potential. When the ion movement is going awry, the sodium-potassium ATPase works in overdrive to try to restore the normal concentrations. Here’s the kicker, though: the ATPase requires an immense amount of energy, so kicking it into overdrive means that we have an energy crisis—too much ADP and too little ATP.

The leaky membrane also means that the cell will face altered neurotransmission, specifically releasing WAY too much glutamate as a result of depolarization and wanting to fire. Another important issue is that the axons are suffering from injury as well, meaning that they are not functioning properly. While they may not die altogether, the injury can be so severe that the damage is beyond repair and the axon may never function properly again. The last point your concussion tells you is that the cells may start to die off. These aforementioned problems may lead to activation of proteases, which are enzymes that will destroy other proteins and ultimately lead to apoptosis: cell death.

After hearing all of that, you start to feel bad for your concussion! You thought it was just a nuisance, but you’re now realizing that it’s no wonder it is taking a long time to recover, there’s so many issues happening!

Take care of me!

After your concussion has told you some of the scary things happening at the molecular level in your brain, it moves on to tell you how to best recover, saying don’t spend time on your phone!

It may be common knowledge, but phone use is heavily discouraged when recovering from a concussion, as it can significantly prolong recovery time. In a study of 335 concussion patients, it was concluded that those with higher mental stimulation (from electronics, for example) needed on average double the time required to make a full recovery. Not something to mess around with! Think about it: with all of the issues mentioned previously, you do not want to be overstimulating your brain! The main takeaway here is that recovery time is largely dependent on a patient’s ability to avoid excessive mental stimulation.

But… do you need to halt phone use altogether?!

Use your phone wisely!

While it is known that phone use can prolong recovery times, there may be constructive ways to incorporate phone use into recovery. A mobile phone app called SuperBetter, used in conjunction with standard medical care, was demonstrated to improve outcomes and optimism for concussed teenagers. The app essentially functions as a gamified symptoms journal, where concussed individual reports symptoms and feelings, then the app turns those inputs into a game-like version of their feelings. This can help avoid social isolation associated with concussion recovery, especially since concussion patients are urged not to do anything that may be detrimental to their recovery. Within the app, users could form a network around their symptom log and comment and interact with other users’ posts, generating a cohesiveness between patients that may be looking for some more interaction when able. The main takeaway here is that, while you shouldn’t be overstimulating your brain and harming recovery, you can use what little screen time you have in a positive manner, leading to a more efficient recovery.

With that, your concussion decides it has said enough. You hang up the phone, in awe at how much you didn’t know about what’s going on in your brain, and how you can best help it recover. Maybe now you’ll give your concussion more credit.

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Got Myelin?

Posted on October 25, 2020 by / 0 Comment

Does your head hurt? Do you have a headache or sore neck? Are you sensitive to light and/or sound? These are just a few of the basic questions one gets asked while trying to make a diagnosis that lacks a more accurate way of assessment: a concussion. Otherwise known as a TBI (traumatic brain injury), it is something that most probably worry about getting after suffering a blow to the head or may be the reason altogether as to why parents steer their children towards a sport/activity with minimal contact. What exactly happens inside of the brain when it is suddenly thrown around, concussion or not? This will be explored below, as well as a term that may not regularly be incorporated with TBIs: myelin. Let’s keep reading!

A Journey Inside the Brain

Oh no! Your high school quarterback has just been diagnosed with a concussion from the football game last night. Thinking back to just seconds after he was hit from behind, let’s examine what occurred microscopically inside of his brain as a result. The sudden movement inside his skull most likely started out with neurons becoming “leaky”, or more permeable for ions to flow in/out of the cell. For TBIs, there is an extreme influx of calcium and sodium ions with an efflux of potassium ions.

This sets off a series of reactions, starting with glutamate being released from these neurons and the cell uses up much of the ATP it has stored inside. This shortage results in the cell needing to generate more ATP to maintain other crucial reactions within the cell which creates a state known as hyperglycolysis. The lack of oxygen entering the body compared to the amounts being consumed intracellularly results in an unfavorable side product being formed with ATP (lactate) and extra calcium getting stored in the mitochondria. Shrinking and running out of options, these cells quickly realize that they are now only doing more harm than benefit and decide to turn to apoptosis: programmed cell death.

And to think- all of this is happening before he even stands back up from getting tackled.

Good Old Myelin

So now you probably are still curious about the cliffhanger I left you with from the beginning about this “myelin” stuff and how that plays a role in the brain and TBIs. Myelin is what wraps around the axons of neurons not only to help propagate action potentials, but also towards generating plasticity and cognitive abilities in the brain. Damage to these areas can result in a slower processing speed due to signal disruptions. Interestingly, humans are born with a pretty unmyelinated central nervous system, and so myelination is not something that is present until after our first couple years, which after still continues to contribute towards thickening the protective layers around individual axons in the ever-maturing brain. Different areas of the brain develop myelinated axons at different speeds, making it a very unfortunate scenario when an individual may develop a TBI in a place that is just underdeveloped compared to the rest.

Takeaway message: Younger individuals have less myelination in their brain and a more flexible set of axons, but this results in a higher vulnerability for damage to occur, therefore this ultimately leads to cellular dysfunction and/or apoptosis.

Looking Ahead

Sadly, rest is the current go-to “antidote”, as there remains no over-the-counter medication that can be prescribed for individuals suffering from TBIs. Future advancements that are being developed with the growth of technology and science give optimism for things such as biomarkers to be not-so-much of a distant thought or conversation to be had.

Source of image: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4479139/

Community/Health/Hot topics

Concussion and Aggression: “Infuriating” Side Effects

Posted on October 24, 2020 by / 0 Comment

Concussions, also known as mild traumatic brain injuries (mTBIs), often have unpleasant side effects: headaches, nausea, confusion, amnesia, trouble sleeping, and difficulty with concentration and learning. Most of the items on that formidable list tend to dissipate in a matter of weeks as the brain heals and starts to go back to normal. However, months or even years following the mTBI, a significant proportion of people begin to show other symptoms: permanent emotional symptoms ranging from increased levels of anger and aggression to complete personality changes. How can a concussion change your personality—and what does it even do to your brain in the first place? To answer those questions, let’s take a closer look at the neurochemistry.

What happens to the brain after mTBI?

The changes described in the following list take place in neurons, which are brain cells that send signals to one another to let us think. Neurons are shaped a bit like an oak tree. Signals come into branches at the ‘top’ of the tree, travel down the neuron’s axon, which would be the tree’s trunk, and go out through the roots to the next neuron. The signal that comes into the branches is a neurotransmitter chemical. The neurotransmitter either tells a neuron to fire (which means to be activated and pass the signal on to the next neuron, which passes it to the next, and so on), or not to fire. If a neurotransmitter tells a neuron to fire, molecules that have positive or negative electric charges cross the cell membrane (a thin membrane like a water balloon that lets molecules go in and out) and change the voltage of the entire neuron. Becoming more and more positively charged makes a neuron want to fire and keeps a signal going.

Phew, lots of neuroscience there—but it’s important background information to understand concussions! Keep that treelike structure and the way neurons fire based on voltage in mind while we look at a basic version of the cascade of molecular effects following a blow to the head.

Neurons are physically damaged from the impact. The damaged axon (remember the tree trunk from earlier?) has a harder time carrying signals and might even stop working entirely.
The cell membrane, also damaged from the impact, becomes leaky to ions (molecules that have an electric charge). Lots of positively charged ions like calcium and sodium leak into the neuron.
With this positive charge, the neuron is activated and wants to fire. To fire, the neuron releases a neurotransmitter called glutamate which travels to more neurons and makes them fire, causing a lot of activity in the brain.
The neuron knows that it has too much positive charge, so it spends lots of energy (in the form of ATP molecules) pumping those positive ions back out of the cell trying to get back to its normal voltage.
The byproduct of burning ATP at such a high level is lactate, which starts to build up in the brain.
All of the extra calcium (which is still leaking into the cell) is stored in a part of the cell called the mitochondria that normally makes ATP. This blocks the mitochondria’s function and prevents ATP levels from returning to normal.
The calcium that isn’t stored in the mitochondria can activate a protein called protease that starts destroying other proteins and leads to apoptosis—cell death.

This altered function lasts roughly ten days following mTBI, directly causing the harmful symptoms of concussions. The ions flowing into neurons cause headaches. The damaged axons cause cognitive difficulty, making it harder to think, remember things, or react quickly. Steps 1-6 above slowly go back to normal as the brain heals, cell membranes are repaired, and neurotransmitter levels begin to return to normal. The headaches, ‘foggy brain’, and other symptoms mentioned above go away in most mTBI patients as days or weeks pass.

However, step 7, cell death, is irreversible. This protease-caused cell death leads to the permanent emotional symptoms that we see in some mTBI patients: anger, aggression, and personality change.

How often do emotional side effects occur, and what do they mean?

28.4% of people who suffer mTBI report an increase in aggression, whether physical or verbal. However, unlike cognitive changes discussed above, these side effects don’t tend to get better on their own, and the emotional changes show up after months or even years have passed since the mTBI. Late onset and irreversibility are signs that emotional side effects are caused by the final ‘cell death’ step of the cascade we looked at earlier.

Some have theorized that since mTBI can cause increased aggression, people who sustain repeated head injuries (like professional athletes) are at a high risk of developing violent behavior. People frequently cite statistics like highly publicized levels of domestic violence among professional football players. However, this correlation has not been sufficiently studied to implicate mTBI as the cause; it is likely that people who are successful at professional sports may have higher baseline levels of psychological factors like aggression and risk-taking, or that an unknown third variable exists. It’s also difficult to pinpoint causation on mTBI when these symptoms develop unpredictably months or years after the injury.

Beyond increases in aggression, some report in themselves or loved ones who have experienced mTBI a complete personality change. Janet Cromer, a college professor, writes about having to completely re-form her relationship with her husband after he sustained an mTBI and began to experience angry outbursts that he had never displayed previously.

Is there any way to avoid permanent emotional side effects from mTBI?

Since mTBI symptoms vary case-by-case, it is difficult to predict if emotional side effects will arise. One extremely important preventative measure is avoiding a second head injury while still in the vulnerable ten-day period after the mTBI. Sustaining a second injury while still recovering from the first has been shown to put much more strain on the healing brain and increase unpleasant symptoms. Resting both physically and mentally during the vulnerable period can also reduce the strain on your brain and give a chance to return the molecular cascade we looked at back to normal.

Disease/Health

The Surprising Connection Between Traumatic Brain Injury (TBI) and the Menstrual Cycle

Posted on October 24, 2020 by / 0 Comment

How is Traumatic Brain Injury Classified?

Traumatic Brain Injury (TBI) occurs when there is a sudden injury to the head, such as a concussion, resulting in damage to the brain. This damage can range from producing mild and temporary consequences to severe and long-lasting effects that can potentially permanently reduce various cognitive functions.
When a concussion occurs, there are a myriad of physiological consequences that ensue within the brain, leading to headaches, impaired cognition, and other common symptoms that are often associated with this form of injury. The cellular mechanisms and structures affected by the impact include the increased flux of various key ions, energy deprivation, cell death, and damage to neurons that results in a lack of neuronal communication throughout the brain. The duration of these impairments can range from acute to chronic, as numerous factors, including recovery time and repeated trauma, dictate the course of the injury.

The Hypothalamus and the Pituitary Gland

The two main players involved within the relationship between TBI and the menstrual cycle are undeniably the brain regions of the hypothalamus and the pituitary gland. A vital role of the hypothalamus and pituitary gland is to control the functioning and regularity of the menstrual cycle. The hypothalamus triggers the pituitary gland to synthesize and release specific hormones that prompt the ovaries to make estrogen and progesterone. Estrogen and progesterone will then prepare the endometrium for pregnancy until fertilization occurs. If fertilization does not occur, estrogen and progesterone levels decrease, resulting in the shedding of the endometrium, otherwise known as menstruation.
Since the pituitary gland and hypothalamus are located in the inferior aspect of the brain and unprotected by layers of brain tissue, these brain structures are at greater risk of damage from trauma from when an injury to the brain does indeed occur.
Injury to this region of the brain often results in hypopituitarism, a phenomenon in which the pituitary gland is unable to properly synthesize and release the necessary hormones for adequate bodily functioning. In a study with 1,000 TBI patients, hypopituitarism occurred in 27.5% of the cases. This finding demonstrates the high probability of endocrine malfunctioning following TBIs as a result of damage to the pituitary gland and consequent hypopituitarism.

Now What is the Relationship Between TBI and the Menstrual Cycle?

One of the most notable effects of endocrine disruption is the impact on the routine pattern of the menstrual cycle. Both irregularities in the menstrual cycle and amenorrhea (absence of menstruation) have been shown to be a primary consequence of damage to the pituitary gland from TBI. This damage results in the hypopituitarism state mentioned above, in which there is a lack of sufficient estrogen and progesterone that can sustain a normal, regular menstrual cycle.
This finding is strengthened by the fact that a common consequence of pituitary gland tumors in women is the symptom of amenorrhea.
Other key findings:
- Research has shown a correlation between the duration of amenorrhea and severity of brain injury, as more severe TBIs result in a longer period of amenorrhea and vice versa.
- Many women who have experienced one or more TBIs report a greater intensity of menstrual cramps during menstruation following the injury.

Looking Ahead

As novel guidelines and options for treatment continue to advance within the realm of TBIs, the consequences of endocrine disturbances as a result of brain damage, including amenorrhea and menstrual cycle irregularities, should be further recognized and researched.

Disease/Health/Hot topics

What’s the best way to understand Addiction..?

Posted on October 16, 2020 by / 0 Comment

What’s the best way to understand Addiction?

Although virtually everyone either has struggled or knows someone who has struggled with addiction, actually defining what addiction is can be tricky. To hopefully clear some things up, I will briefly contrast two competing definitions of addition: the dominant disease model and an alternative developmental cascade model. I argue that the developmental cascade model is a more compelling model because it more closely aligns with contemporary neuroscience (re: neuroplasticity) and offers less stigma/more agency for those struggling with addiction.

What is the disease model of addiction?

The National Institute on Drug Abuse defines addiction as a “chronic, relapsing brain disorder characterized by compulsive drug seeking and use despite adverse consequences”. The following sentence talks about how similar addiction is to other diseases, like heart disease…but does the brain science support this view?

Most researchers and medical professionals take the disease definition at face value, arguing that it is more accurate and helpful than unscientific views of addiction which portrayed addicts as “weak-willed” or “immoral”. The disease model of addiction also focuses on pharmaceutical treatments to solve addiction, much like cancer or heart disease. However, not everyone agrees with this view on addiction.

A close look at the disease model of addiction shows that it largely rests on two pillars, 1) There are distinct, significant changes in the brain associated with addiction, and 2) these changes are pathological because they can be extremely harmful to the drug-addicted individual.

What happens in the brain (The disease model interpretation)?

All drugs of abuse ultimately produce the same effect: they increase the amount of dopamine that flows from the VTA to the nucleus accumbuns (the reward circuit). Repeated use of these drugs can lead to changes in which the size and strength of synapses, how genes are regulated, and reduced connections between the reward circuit and other parts of the brain, like the pre-frontal cortex. Over time these neurological changes become stable, the act of drug-seeking changes from impulsive to compulsive, and harmful consequences occur more frequently and more severely.

Clearly, there are long-lasting changes in the brain involved with addiction, and these changes can be extremely harmful/deadly to those suffering from addiction, but does that make it a disease?

Why is the disease model wrong?

First, to the claim that addiction changes the brain. Yes, addiction absolutely changes the brain, but here’s the thing—so does literally everything we do! Change is the constant of the brain. Neuroplasticity, neural change through experience, is foundational for learning, without a changeable brain you couldn’t read this post!

How the brain changes in substance use disorders (alcohol, heroin, other typical “drugs”) are very similar to brain changes in behavioral addictions (gambling, internet, sex, binge-eating, etc) where there is no molecular drug that crosses the blood-brain-barrier to “hijack” our reward system.

Even more shocking is how human behaviors most people think are “healthy”, like falling in love, also produce significant changes in the reward system! At the molecular level, the types of cellular/molecular changes (cellular memory) at play in addiction are also seen in non-problematic behaviors/habits. In other words, when someone says addiction changes the brain, they’re not necessarily saying a whole lot because everything changes the brain.

Secondly, just because the consequences of addiction can be incredibly harmful, both to the individual and to those around them, does not make addiction a disease. Bullying, domestic violence, and racism are all deeply harmful and destructive human traits, but they’re learned behaviors, not diseases.

What all these examples hopefully show is that a different mechanism might be at play in addiction. Just because something changes the brain in no way necessarily means that change is caused by a disease.

What could be a more accurate picture of addiction?

In contrast, the learned behavior/developmental cascade model of addiction defines addiction as “motivated repetition that leads to deep learning”. The concept of “desire” comes in handy here. Desire, the longing feeling(s) of wanting something, is how the brain motivates us to repeatedly pursue goals. Dopamine is a key neurotransmitter involved in focusing attention on what to desire, regardless of the type of reward (food, euphoria, comfort, etc). As desirability increases so does the amount of VTA-nucleus accumbuns dopamine signaling. Therefore, addiction can be seen as a difference in degree, not kind, compared to gambling, falling in love, or cheering on a favorite sports team.

To be clear, rejecting the disease model does not mean reverting back to the moral failing model. Instead, by focusing on neuroplasticity the habit model provides agency for those afflicted by addiction and avoids stigmatizing them with either helplessness or shame. Most people recover from addiction, and surprisingly most recovered addicts do so without traditional treatment. Another blow to the disease model (I don’t think most cancer patients spontaneously recover), this fact shows that providing resources and support for addicts to change in their own time might be a more effective way to help.

Redefining addiction as a deeply learned behavior does not mean the addict is at fault, or that they just need to “get over it”. Addiction changes the brain. What we do have is the power to influence how our own brains change, given the right tools and a supportive environment. Since addiction is learned via neuroplasticity, the same way brains learn everything, and since addiction is maintained by reduced neuroplasticity, recovery can focus on returning that neuroplasticity the toolbox is the same! Helping people (re)discover interests beyond their specific addiction and educating them on neuroplasticity might be fruitful ways to help addicts who are ready to grow out of addiction. What is needed is empathy and support, not shame or stigma.

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Internet addiction and personality disorders

Posted on October 15, 2020 by / 0 Comment

The internet is a wondrous thing that we have at our disposal, to be able to search up and connect with anyone or anything on the planet. One of its downsides is that internet/social media use can have the ability to act neurologically similar to gambling, which can have an addictive quality to it. With gambling, pulling a slot lever is an action taken that will be rewarded, but only maybe. This ambiguity is what makes it appealing psychologically, where the reward can come at any moment, with any pull of the lever, but you need to actually pull the lever in the first place to get the reward. Pulling the lever usually comes to some detriment: in the case of gambling, a loss of money, and with video games, a loss of money or time. The synonymous action here would be having a really good performance within a video game, or getting more likes on your latest post on insta compared to your last one. These are both results that are unpredictable in some sense, as they are out of your control, but start with you taking action. They come with the reward of feeling good, but there could always be more of it, there could always be something better with how the result ends up. And thus the addictive nature is there, where maybe you didn’t have the best performance (or had a good game or post but still could do better) and so you’ll just try again in order to get that rush of feeling good, or chasing the high, as drug users call it.

Classical substance abuse disorder patients have many physiological and behavioral signals that tend to characterize the disorder. Many of these same links were found with what several researchers have phrased, “internet abuse”, or “internet usage disorder”. For instance, participants that have internet abuse behaviors had higher impulsivity, or in other words, a lower response inhibition. They had a more difficult time inhibiting a natural response to wanting to play a game or browse social media. These participants also had a heightened activation of brain regions that deal with reward response. The responses seen through MRI were positively correlated with self-reported urges to game. The correlation here to drug addicts would be that not only are the same brain regions activated, but these urges are similar to drug users experiencing cravings, which are neurological in nature but manifest to influence behaviors. Another way in which this addictive quality can be seen with chemical changes in the brain is through looking at the dopaminergic system. In drug addicts, the binding capacity for dopamine receptors is diminished, which means that drug users need more of that drug (or higher doses) to feel the same amount of high as they have before. This is also referred to as tolerance. This reduced dopamine capacity was also found in internet abuse participants. In participants that were identified as having gaming related addictions, their binding potential (or ability to feel good while playing their game) was diminished in ways that rivaled an injection of amphetamines, a highly addictive (and psychoactively responsive) drug.

Now that we’ve established that the internet, and specifically certain parts of it, can have the same properties as a substance abuse disorder (or drug addiction), another interesting correlation has been discovered in relation to personality disorders. Drug addiction has been found to positively correlate with a number of personality disorders, such as Antisocial PD and Borderline PD. An observation with both of these PD’s is that they contain the symptom of impulsivity, which as noted above, is present in drug addiction as well. It was found that internet addicts were found to have higher rates of PDs as well, with most of the correlations found in women, like with Borderline, Narcissistic, Avoidant, and Dependant PD, and in men, Narcissistic PD. The main question then that comes up amid these findings is: Does addiction simply correlate with personality disorders (due to behavioral tendencies), or does one cause the other, or do they both have similar neurological bases for developing and so then arise together? Some researchers theorize that substance use disorders and Cluster B PDs may share neurobiological, cognitive, and environmental risk factors that contribute to their individual and joint manifestations. This information cautions even more against obsessive internet use then, as there are even more cognitive abnormalities that can arise. But from this information as well it can be discerned that the environment is also at play to develop both of these, and that personality disorders and internet or substance abuse may arise together. To restate the beginning of this blog, the internet is a wonderful tool, but should be used as such.

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The Consequences of Addiction: A Neurochemical and Behavioral Story

Posted on October 14, 2020 by / 0 Comment

How do you picture addiction? Based off their personal experiences and knowledge people have an innate ability to paint their own image of addiction. For some it could be an alcoholic family member or friend who can’t seem to shake the habit. Personally when I think addiction baseball players who always seem to have some chewing tobacco in their bottom lip comes to mind. For others they think of tragedy, such as an overdose which has been running rampant in recent years. The prevalence and dire consequences of addiction has led to an abundance of research in recent years. While addiction looks different on the outside, some very distinct and fascinating neurochemical processes are taking place inside the brain manifesting in addictive behaviors that cause chaos for both addicts and the people who love them.

Neurochemical Mechanisms

In the brain addiction manifests itself one apparent pathway. Dopaminergic neurons (DA) stretching from the Ventral Tegmental Area of the Midbrain to the Nucleus accumbens (NAc=brain reward center) have been identified as a primary neural circuit in addiction. Every time you have a “feel good” feeling it is most likely there has just been a dump of dopamine into your nucleus accumbens. You got an A on a test? You get a shot of DA. You’re starving and you finally eat food after not having anything all day? Another shot of DA. Now let’s say you shoot up cocaine and have been for a while…well you just earned yourself a massive amount of dopamine into your NAc. You have just caused your body to release so much dopamine some very real, and a little scary, changes in your brain are about to take place.

Neurochemically speaking, there are several changes that are now going to take place. The synapses, or area where your brain communicates with other brain cells, can both increase and decrease in size in response to chronic drug use. Long term depression (LTD) occurs immediately in response to drug use as the synapse size decreases to the high concentration of chemical messengers. Over time this synapse increases (Long Term Potentiation) without the drug and can almost be thought of with the metaphor of synapse getting bigger and “craving” the drug.

Behavioral Learning

These neurochemical changes have behavioral manifestations. Your body becomes accustomed to taking drugs in certain situations, whether that be with people, places, or even in the presence of certain objects. As your body encounters these items a physiological response can take shape in the body. If you always do drugs in your car, every time you go to your car you might feel cravings, or maybe even start to feel your heart being faster. Your car has now become a conditioned stimulus that elicits a conditioned fear response that increases the likelihood that you will begin to take the drug.

The neurochemical and behavioral consequences of addiction are numerous, and one could spend a lifetime studying them. Perhaps the moral of the story is your brain changes in several ways with taking drugs, and the changes that take place are most likely not going to be pleasant.

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Gateway Drugs: Psychology or Physiology

Posted on October 13, 2020 by / 0 Comment

As most people know, a gateway drug is a drug that may lead to the use of other, possibly more addictive drugs down the road. What many incorrectly assume however, is that a gateway drug is simply of behavioral consequence. Of course, it makes sense in a vacuum. A person drinks, then maybe they try smoking a cigarette, then possibly they are more likely to move into illicit substances as they progress. While this is not untrue, it only paints part of the picture. The physiological changes that occur during the use of “gateway drugs” also can play a huge role in the progression of, and addiction to, these substances. These two parts of the picture added into the role that environments and genetics play in the occurrence of substance use and abuse, give us a clearer idea of the causation behind addiction.

Nicotine

Studies on nicotine have given us tangible evidence of the changes a “gateway drug” can make in the brain. Early research has shown that FosB expression levels in the brains reward centers can be linked to cocaine addiction. A study of mice published in 2011 compared FosB expression in mice under various treatment methods. The experimental group was treated with Nicotine for 7 days, while the control group was not. The findings showed a 61% increase in FosB expression over the control group. As a stimulant, which is also addictive, this adds up. However, when both groups were then treated with cocaine, the experimental (nicotine) group had an additional 74% increase in FosB expression over the control (cocaine only) group. The “priming” by nicotine of the receptors also responsible for cocaine is what is believe to cause this effect. Further, cocaine is known to affect the expression of FosB via altering chromatin structure, typically near the FosB promoter. What was found is that nicotine causes accelerated acetylation of histones H3 and H4. Cocaine was only responsible for increases in acetylation in H4. It is believed that this hyper-expression/acetylation is due to the nicotine acting as an HDAC (histone deacetylase) inhibitor. When HDAC was inhibited, and cocaine administered, there was again a 71% increase in FosB expression, consistent with the previous study done with nicotine and cocaine.

Marijuana

The research on marijuana as a gateway drug in a physiological sense is still ongoing. In rodents, early exposure to cannabinoids resulted in a change in the dopamine receptors in the brains reward centers later in the brain. This finding is concurrent with the studies of people who began marijuana use at a young age and later developed substance-related problems. Another fact which puts marijuana into the gateway drug category, is that animal experiments have shown that THC has a similar ability to nicotine to “prime” the brain. This priming leads to an enhanced response when the body is exposed or subjected to a new drug. While much of the argument surrounding marijuana is circumstantial, there are certainly some parellels to the effect of nicotine on the brain’s reward center.

Other Possibilities

While these substances are shown to have a correlation, and there is a physiological change to back it, it is vital to remember the other possibilities involved. The impacts of environments, and genetics cannot be overlooked. It is well-known that addiction, and addictive behaviors are a largely heritable genetic predisposition, not just a behavioral phenomenon. Some people are environmentally more likely to engage in drug use, and some are genetically more likely to develop an addiction of some sort. The next phase of this research can hopefully expand into a human model. Comparing the brain activity and expression of an addiction-predisposed individual to a person who likely has no predisposition could give the gateway drug hypothesis verity. Or it could show that while a gateway drug “primes” the brain’s reward centers, it does it completely differently in varying types of people. While there may be no definitive answer yet, there is certainly a consequential future in researching this conversation.