Adaptive Behavior & PTSD Treatments

Adaptive behavior is described to be a behavior that allows an individual to cope with PTSD within their environment. It is also used to help with phobias, depression, and anxiety.

Adaptive behavior helps individuals reflect on their ability to meet the demands of everyday life such as:

  • relationships
  • safety
  • eating and drinking
  • working
  • financial management
  • cleaning self and environment

(5)
PTSD treatments and therapies (4)


There are many forms of treatments and therapies for PTSD. I have listed some methods of treatment along with short descriptions. These are categorized by treatments that are supported and proved to be effective and treatments that are still being studied for their effectiveness, benefits, and safety

Supported Treatments & Therapies:

Cognitive Behavior Therapy (CBT): a type of psychotherapy that is effective for both long and short-term results. It focuses on identifying, understanding, and changing thinking and behavioral patterns. The individual has to actively engage inside and outside the appointments. Methods used include:

  • exposure therapy
  • cognitive restructuring

Presented Centered Therapy (PCT): this is a non-trauma-focused treatment that delves into the current issues of the individual rather than processing the trauma. The counselor discusses psycho-education about the impact of trauma on the individual’s life and teaches problem-solving strategies to deal with current life stressors. (1)

Trauma-Sensitive Yoga: yoga that has gentle movements and less hands-on adjustment. There is an emphasis on choices and freedom to perform the actions and feel their emotions. I can see this being helpful for individuals who have experienced any type of abuse as they did not have control of that element in their life.

Acupuncture: This has been practiced for hundreds of years. Individuals who have experienced acupuncture report feeling less stress and anxiety afterward.

Virtual Reality Exposure: helps the individuals approach the trauma with less fear. They work to become desensitized to the impact of the trauma. The individual will feel a sense of disconnect with the trauma to do the event being played on screens and unable to harm them compared to in person. This allows gradual exposure to the traumatic situation. A patient who was not identified within the article stated: “You go over the story over and over again. I got so bored with my own story that it no longer elicited a reaction.”

Aromatherapy: lavender, chamomile, basil, frankincense for anxiety and PTSD

Nature Exposure: Individuals who sit in nature report feelings of calm, happiness, hope, and aliveness. It has been observed that this experience reduces blood pressure, heart rate, muscle tension, and the production of stress hormones

Music therapy: actively listening to or performing music

Emotional Support Animals

Hypnosis

(4)


Treatments & Therapies being Studied:

Ketamine infusion: Eskatamine is administered with very low doses to decrease side effects. One infusion treatment for approximately 40 mins can lead to a decrease in PTSD symptoms quickly. The individual will undergo multiple sessions over a few weeks. Esketamine is an NMDA receptor antagonist used to treat adults with treatment-resistant depression. It comes as a nasal spray and can help reduce suicidal and depressive symptoms (2)

MDMA-assisted therapy: The individual will consume ecstasy and work to alter the traumatic memories to become less traumatic as they process the event.

Eye Movement Desensitization and Reprocessing (EMDR): a type of psychotherapy that involves processing trauma-related memories, thoughts, and feelings. The individual will pay attention to either a sound or a back-and-forth movement while thinking about the trauma memory. There are mixed research results to whether the repeated exposure to the trauma or distraction of the sounds and/or eye movements help.

(3) (4)

Resources:

  1. https://www.ptsd.va.gov/publications/rq_docs/V29N4.pdf
  2. https://www.webmd.com/anxiety-panic/guide/anxiety-disorders
  3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2966959/#S1
  4. https://www.verywellmind.com/ptsd-treatment-2797659
  5. https://dictionary.apa.org/adaptive-behavior

 

What is Anxiety: Causes, Symptoms, Treatments

What is Anxiety?

Anxiety is a normal, occasional experience in every human life course. There is even good stress/ anxiety that can help us, versus the bad stress that makes us feel unable to accomplish tasks. When people begin to experience intense, persistent worry and fear over everyday situations is when anxiety disorders are diagnosed, and nearly 30 percent of adults at some point in their life are diagnosed. Feelings of anxiety and panic can begin to interfere with the daily activities of life and can begin to feel debilitating. Let us look at what happens inside of us in times of stress. First, the sympathetic nervous system (SNS) is activated. The SNS is responsible for our fight or flight response. This causes a cascade of events, which can also be followed in the image, of both hormonal and physiological that occur after the SNS is activated. The amygdala is responsible for processing fear and arousal, along with emotional stimuli to determine the actions that are necessary to happen next. If needed, the amygdala sends a signal to the hypothalamus regarding the stress. The hypothalamus activates the SNS, and the adrenal glands release stress hormones (like epinephrine). This results in the physical symptoms of anxiety, such as increased heart rate and others which can be seen in the symptoms section below. While the body continues to perceive a threat, the hypothalamus activates the hypothalamic pituitary adrenal axis (HPA axis). Cortisol is then released from the adrenal cortex and allows the body to be alert during a threat. Also, cortisol’s mechanisms are able to provide energy to the body. Now we will look at causes of anxiety, other symptoms of anxiety, and some possible treatments. We can also look more closely at glucocorticoids levels, as they are believed to be linked to generalized anxiety disorders and PTSD.

Causes of Anxiety: view image on the right

  • Genetics
  • Traumatic life events; death of a loved one
  • Nature and nurture; parenting styles and childhood
  • Stressful life events; financial stress, school or work stress
  • Medication side effects
  • Medical causes; heart disease, chronic pain 
  • Illegal recreational drugs; cocaine

Glucocorticoids:

  • Glucocorticoids; hormones that produce effects to respond to stress.
  • The main glucocorticoid stress steroid is cortisol, and it is synthesized in the adrenal cortex
  • Glucocorticoids are needed for creating the of memories associated with the stress 
  • Glucocorticoids respond to the adrenocorticotropic hormone and stimulates gluconeogenesis to provide energy for “flight or fight”

Symptoms of Anxiety:

  • Feeling a sense of danger or panic; difficulty controlling worry
  • Feeling nervous and tense; to the point of avoiding things/ events that could lead to triggering anxiety
  • Increased heart rate
  • Increased breathing
  • Inability to be still and calm 
  • Trouble concentrating on things and trouble sleeping
  • GI problems

Treatments of Anxiety:

  • Without medications:
    • Exercise/ meditation
    • Healthy diet; along with avoiding alcohol and drugs
    • Healthy sleeping habits
  • With medications/ therapy: 
    • Anti-anxiety medications, antidepressants are also sometimes used to treat anxiety disorders
    • Benzodiazepines (sedatives) for short term use
    • Cognitive  behavioral therapy
    • Exposure therapy
    • Music therapy

Sources:

Martin, E. I., Ressler, K. J., Binder, E., & Nemeroff, C. B. (2009). The neurobiology of anxiety disorders: brain imaging, genetics, and psychoneuroendocrinology. The Psychiatric clinics of North America32(3), 549–575. https://doi.org/10.1016/j.psc.2009.05.004

Thau L, Gandhi J, Sharma S. Physiology, Cortisol. [Updated 2021 Sep 6]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538239/ 

https://www.webmd.com/anxiety-panic/guide/causes-anxiety

https://www.mayoclinic.org/diseases-conditions/anxiety/diagnosis-treatment/drc-20350967

 

Schizophrenia vs. Multiple Personalities: How the film industry feeds our confusion

Whether we like it or not, the film industry has always had a significant influence on the representation, as well as our understanding of mental illness. With the popularity of Hollywood comes both, positive and many negative consequences.

Movies, such as Split are said to have done more harm than good in trying to show and destigmatize personality disorders. Split, while tackling dissociative identity disorder (DID), has been officially categorized under “schizophrenia movies” by Google. Another example that is categorized under the same genre and adding to the confusion is the movie Shutter Island, in which some might argue it is DID that is being represented, or even Delusional Disorder rather than Schizophrenia. It seems as though movies that show DID are commonly mistaken for showing schizophrenia. As one might imagine, mislabeling and miscathegorizing movies is quite problematic for various reasons, the most important one being that they are two completely different mental disorders. How? – you might say, so let’s look at them now.

 

Schizophrenia

Dissociative Identity Disorder (DID)

Differences ·   part of schizophrenia spectrum disorders (DSM-5)

·   hallucinations, catatonia, disorganization, psychotic symptoms

·   acute psychotic episodes

·   research focused on biological factors

·   treatment: focus on antipsychotics

·   largely genetical illness

·   late onset

·   part of dissociative disorders (DSM-5)

·   disruptions in functions of consciousness, memory, identity, or perception

·   chronic episodes

·   fragmentation of the identity, multiple fragments can exist side by side

·   research focused on life experiences

·   treatment: focus on psychotherapy

·   amnesia, derealization, identity confusion, identity alteration

·   early onset

Similarities

·   pathological dissociation (although higher in DID) and absorption, imaginative involvement

·   high co-occurrence

·   environment and personality can influence symptoms

·   role of trauma in development

·   depersonalization, delusions

 

What may be the cause of schizophrenia?

As indicated in the table, one of the major differences is that DID is mostly associated with traumatic life experiences, while schizophrenia is mainly associated with genetic factors. Given the significant focus of research on the biological background of this disorder, we are able to suggest some explanations as well as offer pharmacological treatment.

The above visual is showing a cell signaling pathway, the Wnt/B-catenin pathway, which plays an important role in early development. Dopamine is a key regulator of this signaling cascade, and in the event of increased levels it can lead to abnormally high levels of GSK3 and B-catenin, resulting in the overall inhibition of the pathway. This inhibition results in low levels of TCF/LEF, which are transcription factors at the end point of the Wnt signaling cascade, and are involved in growth. Schizophrenic patients presented with higher than normal levels of dopamine, and researchers thus have concluded that the disruption of this signaling pathway may result in the development of schizophrenia.

 

So, what now?

While there is no cure for schizophrenia at this time, doctors are able to offer various treatment options.

  1. Psychosocial Interventions
    • Therapy
      • Individual and/or family therapy are amongst the options, as well as something called an electroconvulsive therapy.
    • Skills training
      • Behavioral skills training (BST) is a method frequently used by many applied behavior analysts in order to teach skills one might be lacking due to mental illness(es).
  1. Pharmacological treatment
    • Antipsychotics
      • First and second-generation antipsychotics are targeting dopamine in the signaling pathway.
    • Lithium
      • This medication is targeting Akt and GSK3 (both of which that were mentioned above) to regulate the overall Wnt signaling pathway.

 

Links and/or images:

https://pubmed.ncbi.nlm.nih.gov/23379509/

https://www.mayoclinic.org/diseases-conditions/schizophrenia/diagnosis-treatment/drc-20354449

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5216848/

 

Understanding Gateway Drugs

Gateway Drugs: Nipping Drug Use in the Bud - blueFire

An Overview of Addiction

Drug addiction, also known as substance use disorder, is the inability to control impulses regarding drug-seeking and drug-using behavior. Addiction can result from knowingly overindulging in a substance, from being administered drugs in a clinical setting that are inherently addictive, and everywhere in between. Regardless of the cause of these behaviors, the brain is affected in a very similar way. Some drugs are addictive by their very nature, such as nicotine or opiates, and some are not addictive but the repeated administration can result in a dependency, leading to the same addictive outcome.

What are Gateway Drugs?

Gateway drugs are drugs that encourage the user to experiment with stronger, more dangerous drugs; not by the way of “I smoke cigarettes so now I want to try heroin” but by the way that these drugs are so addictive that they make the brain more susceptible to becoming addicted to new substances. This is best explained by the gateway-drug effect, which explains that the repeated use of particular psychoactive drugs increases the chance of using and becoming addicted to other substances, usually stronger and more dangerous, by altering neural connectivity throughout the brain (particularly the nucleus accumbens (NAc) and ventral tegmental area (VTA)). Some of these drugs include tobacco, alcohol, and marijuana, but the list is difficult to completely define.

Animal Models of Multi-Drug Addiction

While the gateway-drug effect has been shown in humans, it has been the most easily studied in animal models. Studies show that repeated THC injections in mice increase the self-administration of morphine, heroin, and nicotine. Nicotine addiction in mice was found to increase cocaine consumption and drug-seeking behavior compared to non-addicted mice. Alcohol was found to increase drug-seeking behaviors for cocaine and decreased the average time needed to become addicted to the substance. In all of these experiments, profound changes were seen in the reward regions of the brain in very similar ways, regardless of drug class.

Neurophysiology of Drug Addiction

The Brain on Drugs: From Reward to Addiction - ScienceDirect

Figure 1 – Reward, Plasticity, and Behaviors associated with Chronic Drug Use

Drugs become addictive largely by their effects on dopamine signaling in the NAc and VTA, which play overarching roles in reward, motivation, and addictive behaviors due to the large deposits of dopaminergic neurons in these areas. In the context of gateway drugs, even a single administration of a substance can increase dopamine release in the NAc and VTA, which can have immediate, long-term effects on both the affected neuron and synapse (Figure 1). Figure 1 shows that repeated drug exposure increases DA activity and encourages AMPA receptor migration to the post-synaptic domain and decreases NMDA receptor density, which ultimately increases long-term potentiation (LTP). By having a very high amount of AMPA receptors on the postsynaptic cell, it is much more sensitive to excitation, which strengthens the connections between the two neurons.

Conclusions

Ultimately, this explains that repeated drug use strengthens the connections between neurons in the NAc and VTA which makes it very difficult to stop the use of an addictive drug. Gateway drugs do exactly this. By becoming addicted to this small collection of substances, the brain can be altered for years, even permanently, encouraging the use of stronger, dangerous drugs. This is not to say that smoking marijuana or having a cocktail now and then will lead to drug addiction, but it is important to understand the risks of chronic use.

Sources

  1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898681/
  2. https://www.mayoclinic.org/diseases-conditions/drug-addiction/symptoms-causes/syc-20365112
  3. https://www.sciencedirect.com/science/article/pii/S0092867415009629
  4. https://bluefirewilderness.com/blog/gateway-drugs-nipping-drug-use-in-the-bud/

Behavioral Addictions: An Unseen Danger

What does an addiction mean to you? Does it represent a drug addict hanging out on the street? How about a dangerous man robbing a pharmacy for more pain killers? What if I told you that addiction can be so much more than that? What if I told you that cousin Joe who goes shopping 5 times a week is an addict? What if I told you that your nephew Jenny playing video games for 3 hours a day makes her a very young addict? These addictions are more closely related to a drug addiction than we knew before, below are some more examples of these behavioral addictions, or process addictions

Figure 1: Many, but not all types of behavioral addictions. Source

What Does Addiction Look Like in the Brain?

Part of the problem with addiction is that many people still consider it a choice, or a moral failing to become addicted to something. Recent research has instead found that many people possess both a natural inclination to addiction as well as irreparable chemical damage following an addiction. The idea of being naturally drawn to addictive substances is not new, but until recently it was never understood just how much the susceptibility of a brain can change from person to person. The answer to this lies in the concept of dopamine and how much a brain can tolerate, which is highly variable. Dopamine is a chemical receptor that regulates how your body processes various stimuli such as drugs or in our case an outside stimulus. Normal dopamine signaling encourages your body to engage with a stimulus in order to hit the “appropriate level” of dopamine, for example if you are hungry your body will signal to get more food to hit that dopamine threshold and to keep you alive. Addictions abuse that cycle by adding in a strong stimulus that requires increasing and dangerous amounts of intake in order to reach the dopamine thresholds that make your brain feel normal. People have different levels of dopamine that feels normal, hence the potential for some becoming addicted much easier than others. In the past this was called an addictive personality, but we now know it is related to these dopamine levels more than anything people can control. Below are some physical signs and symptoms of addictions, especially behavioral. More on risks and dopamine

Figure 2: Signs and symptoms of behavioral addictions. Source

Why Are Behavioral Addictions Dangerous?

While addictions are universally regarded as bad, behavioral addictions are not treated as seriously as chemical addictions in many scenarios. This occurs for a number of reasons, but it often boils down to either treating it as harmless or downplaying the severity of the addiction. The former can be seen in many addictions that aren’t gambling, such as a boss not helping their employee with a work addiction or a mother dismissing their child’s video game addiction. The latter comes from the idea that addiction must require a chemical input, which has been proven to be false. New studies have found that a chemical called Delta FosB is misused in the brain the same way from a chemical addiction and a behavioral addiction. This link is still new, but the damage these addictions have already caused and will continue to cause is entirely preventable with new information and treatment. These addictions can be treated similarly to normal addictions; with things such as therapy, counseling, and medication, but too often they are written off until it is far too late. The sooner these behavioral addictions are treated more urgently, the better the chances become of overcoming these troublesome connections to surprisingly dangerous everyday activities. More on Delta FosB

 

Source for Feature Image

 

Cocaine

Cocaine is one of, if not, the most prolific drug of the last 50 years. It is extracted from the leaves of cocoa plants by multiple acid base and other redox reactions. Cocaine was originally synthesized in the year of 1859 by the chemist Albert Neiman. However recently, its wide spread recreational use wasn’t popularized until the 1970’s in America. While it was a part of American culture in the early 20th century it wasn’t widely available until Columbian drug cartels began shipping massive amounts. With over 70 billion dollars of cocaine on the street there are approximately 20 million users across the world.

How does Cocaine work?

In the short-term cocaine works by inhibiting the reuptake of dopamine specifically in the Nucleus accumbens of the brain. This is the region of the brain that regulates our reward feelings. When we are hungry and eat, or are thirsty and drink, the sense of relief and reward on3 experiences is caused by dopaminergic cells flooding the nucleus accumbens with dopamine. This good feeling makes us want to eat and drink again, keeping us alive. The artificial accumulation of dopamine in this region of the brain gives us an exaggerated feeling of reward and drives us to need cocaine in the same way we need food. In fact, when mice are given the option of cocaine or food many will choose cocaine to and past the point of starving to death.

Personal Artwork

Cocaine and Addiction

Dopamine however has a relatively short life in the synapses of the brain’s neurons, giving a high that rarely last longer than a few hours. The long-term addiction affects must be explained by another mechanism in the brain. Addiction and its affects are caused by changes in the expression of certain genes. One particular transcription factor cocaine influence is ΔFosB. “Researchers believe ΔFosB may constitute an important molecular “switch” in the transition from drug abuse to addiction.” ΔFosB lasts for up to 8 weeks before it breaks down causing it to accumulate in repeated cocaine use. Mice with increased levels of ΔFosB have shown addictive behaviors even when not exposed to a drug. However, addiction lasts much longer than 8 weeks, research shows ΔFosB is still to blame.

How does ΔFosB work?

Chronic cocaine exposure causes nerve cells in the nucleus accumbens to extend and sprout new offshoots on their dendrites. This growth is caused by an accumulation of the transcription factor ΔFosB. These dendrite growths cause the nucleus acccumbens to pick up more signaling from other parts of the brain which may explain the very long-lived behavioral changes associated with addiction. “For example, enhanced inputs from the hippocampus and amygdala could be responsible for the intense craving that occurs when drug-associated memories are stimulated.”

This picture shows dendrite growth in different mouse brains with long term exposure to a variable. Saline shows baseline growth and cocaine is shown in comparison. Cocaine paired with ΔFosB inhibitors (G9a and JUND) show very little extra dendrite growth. Saline with artificially elevated ΔFosB showed more dendrite growth then the baseline.

 

The Use of Naltrexone to Help Addiction Recovery 

Pre-knowledge before using naltrexone 

Naltrexone is an opioid antagonist that is not addictive and does not cause withdrawal symptoms with the use of stopping it. Naltrexone blocks the euphoric and sedative effects of opioid receptors and reduces opioid craving. Before starting Naltrexone, an individual needs to wait 7 days after their last use of short-acting opioids and 10-14 days for long-acting opioids and alcohol. Accidental or intentional ingestion of naltrexone in opioid dependent people will result in an acute block of opioid receptors and precipitate a severe opioid withdrawal reaction. Symptoms of withdrawal can appear after only five minutes following ingestion and may last up to 48 hours. 

How was naltrexone created?

Naloxone, the long-acting naltrexone is a MOR antagonist. It was first synthesized in 1963 by Endo Laboratories. Though the drug remained essentially dormant for several years, it attracted interest in 1972 when Congress passed the Drug Abuse Office and Treatment Act for the purpose of developing non-addictive treatments for heroin addiction. At that time, methadone, a long acting MOR agonist, was the only medication available for opioid addiction. It seemed to stop cravings yet not produce as significant of a “high” or cognitive inhibition of heroin. However, in some cases individuals did report having experienced some of these cravings.

How does naltrexone work? 

https://www.researchgate.net/figure/Mechanism-of-action-of-naltrexone-The-reversible-interaction-of-an-opioid-agonist-with_fig1_259961081

Repeated exposure to drugs of abuse can lead to an increase in delta FosB levels that persist for a long time after the cessation of drug treatment. To give a little background, research has found that the transcription factor of delta FosB is a mechanism that drugs of abuse produce changes within the brain the contribute to the addiction phenotype. FosB transcription factors accumulate within the nucleus accumbens and dorsal striatum. These brain regions are heavily impacted by repeated drug abuse.  https://pubmed.ncbi.nlm.nih.gov/11572966/

Naltrexone attenuates ethanol consumption via antagonizing the down regulation of CaM kinase IV and the phosphorylation of CREB in the striatum region induced by forced ethanol exposure. Naloxone increases the firing of VTA dopamine neurons by inhibiting VTA GABAergic interneurons. It has been shown that μ opioid receptor agonists indirectly increase dopamine release in NAc and caudate putamen and that the induction of delts FosB by psychostimulants is mediated by D1 dopamine receptor pathway. Furthermore, naltrexone attenuates striatum dopamine levels, which are increased by systemic administration of ethanol. Therefore, naltrexone-induced attenuation of dopamine levels may contribute to its attenuation of FosB/delta FosB IR upregulation observed in current study. In summary, the present study demonstrates that chronic voluntary consumption of large quantities of ethanol induces FosB/delta FosB expression selectively in the subregions of the striatum and the prefrontal cortex, which is reversed by naltrexone treatment. https://www.pnas.org/content/85/14/5274.short. https://www.sciencedirect.com/science/article/pii/S0014299904002249

https://www.researchgate.net/figure/Representative-in-vitro-drug-release-profile-of-the-lead-formulation-of-extended-release_fig6_8157185

Figure 1. Representative in vitro drug release profile of the lead formulation of extended-release naltrexone.

A near linear in vitro release profile shows the extended release of naltrexone over one month trial that indicated the success rate after so many days once an individual has started taking naltrexone.

Clinical Review

More research needs to be conducted regarding the use of naltrexone as an antagonist in addiction recovery. The nature, severity, and duration of naltrexone induced acute opioid withdrawal varies greatly between people and the clinical course of events is unpredictable. With the trend for more addicts to be treated with naltrexone in the community, and the possibility that current addicts may see naltrexone as a misguided means to break the cycle of drug dependence, the potential exists for increasing numbers of similar presentations. Physicians involved in the emergency care of these patients must be aware of the dramatic clinical course of the ingestion of naltrexone in opioid misusers and be prepared to manage the complications. 

Addiction is a Difficult Road to Travel

Preconceptions of Addiction

What comes to your mind when you hear the word “addiction?” Maybe you think coffee—how you have to have it every morning to be able to function. Maybe you think of a loved one that has battled alcoholism for years. Or maybe you imagine a creepy old man lurking in a dark alley, wearing a trench coat and offering you a small bag of white powder. Personally, I tend to think of the latter example. The stereotypes associated with addictions, and the way media portrays this illness, tend to lend themselves to these types of images. However, addictions don’t relate only to drugs, and they don’t only affect people with drug history. In fact, I would be willing to bet that every single person on the planet has at least one addiction, though it isn’t necessarily dangerous. Addictions could include social media, food, or television. An addiction can be thought of something you want to stop doing, thinking, or taking, but find it nearly impossible to do so, despite the consequences. Is there something in your life that you think could be an addiction? Keep your “addiction” in mind as you read through the rest of this post. . . Relating an abstract idea to yourself helps you to understand it (or so I have been told).

Addicted to Science

The main brain pathway that has been studied in addiction is the reward pathway, primarily the areas of the ventral tegmentum (VTA) and the nucleus accumbens (NAc). An image of where these areas are located within the brain is shown below.[1]

Fig. 1. An image of the brain, depicting where the VTA and NAc are. Figure obtained from ResearchGate.Net.

There are two molecular components of the reward pathway that interact in drug addiction.

cAMP Response Element Binding Protein

cAMP response element binding proteins (CREB) are activated in the NAc during drug addiction. CREB is important in addiction because it contributes to the impaired reward pathway highlighted above. When CREB is activated, it produces a peptide (dynorphin) that suppresses dopamine transmission from the VTA (where dopamine is produced) to the NAc which is the reward center of the brain (reinforces an activity or feeling). I know that summary was really scientific and had a lot of acronyms, so I will do my best to break this down a little more. There is a protein in the brain that is activated in the brain’s reward center when an individual is addicted to something—CREB. This protein produces another protein that stops a neurotransmitter called dopamine from traveling from its production site to its destination. Think of the function of the CREB as placing a “road closed” sign in the brain. The road closed sign (dynorphin) stops the car (dopamine) from getting to its destination (NAc), which causes the driver (you) to be upset (no activation of reward center). This is a really simplistic way of describing the function of CREB, but I think it illustrates the central idea in a more relatable way.

Delta FosB

So, we just discussed the role of CREB in the brain where addiction is concerned, but CREB has a special relationship with another protein called Delta-FosB. This protein is the predominant Fos family protein that is expressed after repetitive drug exposure. The Delta-FosB protein’s function is essentially opposite to that of CREB—FosB increases sensitivity to the addictive stimulus and promotes a natural reward response. I don’t have a driving-related analogy for FosB, but you are welcome to add your own.  FosB and CREB have a really important interaction in the brain’s reward pathway. Dynorphin, as I previously discussed, suppresses dopamine transmission from the VTA to the NAc. However, when FosB is present, dynorphin is suppressed. To talk about it in terms of car analogies, FosB temporarily removes the “road closed” sign imposed by CREB.

The Two Frenemies and Their Role in Addiction

In this final section, I will try to sum up what I talked about in the previous sections then relate it to some characteristics of addiction, as well as the development of addiction, itself. CREB, as we previously discussed, puts a roadblock in the brain that prevents dopamine from activating the NAc which is responsible for giving the “high” feeling. Based on this information, drug tolerance (needing more of the drug to receive the same effect) is induced by the activation of CREB. FosB is responsible for temporarily removing this roadblock, thus allowing dopamine to travel to the NAc and trigger a “high.” I hope this illustrates how these two proteins are related to characteristics of addiction, but how do they relate to the development of addiction? Great question. Another characteristic of FosB is that it induces synaptic plasticity. Synaptic plasticity is the strengthening and/or growing connections in a neural pathway. This means that, when FosB is present due to repeated drug use, it is strengthening the pre-existing connections and creating new connections in the reward pathway which results in greater and faster activation of that pathway. Addiction occurs because you have taught your brain how to respond to the presence of a specific stimulus via positive reinforcement.

[1] https://www.researchgate.net/figure/1-The-dopaminergic-mesocorticolimbic-circuit-the-VTA-ventral-striatum-including-the_fig2_270788950

Drug Addiction

When you think of a person who is a drug addict or an alcoholic, some people would think of typical stereotypes of them such as having no control over themselves. However, just because they are an addict doesn’t mean that they have no self control. Some people do not know all of what goes on in a person’s body when they become addicted to drug stimulants or sedatives. I believe it is important to understand the chemical and physical side effects while the drugs are in your system and when they are out of your system during a period of withdrawal. 

One important piece of information about drug addiction is the changes in your body that can be caused by drugs. One such change is involved in epigenetics. Much of epigenetics is still unknown but it is defined as the changes or mutations on the outside structure of the DNA, specifically on the histones [1]. Histones are a group of proteins that the DNA wraps around to be condensed into chromatin and fit in the nucleus of a cell [2]. How much the DNA is condensed can be heavily influenced by the epigenetics of the histones. Two types of histone modifications are histone methylation, which causes the chromosomes to become more compressed and inhibit transcription, and histone acetylation, which causes the chromosomes to become loose and increase transcription [1]. More transcription means that the cell has more activity and more things that are being produced as opposed to no transcription with little activity in the cell. Drugs like cocaine and amphetamines can cause Histone acetylation because they act as stimulants [1]. This is but one change occurring on your body when you use drugs and it only gets worse the more you use them.  

Another important change is involved in affecting synaptic plasticity of the person and this is probably the most detrimental change on the body. Synaptic plasticity is when there is a change in structure shown in the synapses between the neurons causing a type communication between them that results in an overall action. Different types of drugs can influence the synapses by hijacking and impairing their behavior and elicit the release of dopamine, a reward drug to make somebody feel good [1]. The mechanism of synaptic plasticity with the release of Dopamine is shown in the figure below. This explains why people do drugs because in a way, we all know how it feels. Whether we get a good grade on an exam or win a competition, dopamine is released so you feel a surge of pleasure and satisfaction that we would all like to experience. That is why people do drugs, to get the same feeling. However, the more you use the drug, the more your body gets tolerant of it so in order to get the same feeling of pleasure, you need to increase the amount you take, which can cause drastic effects on your body, especially if you want to try to stop [3].

With these changes caused by epigenetics and synaptic plasticity, it can cause a person to depend on the drugs to a degree that when they stop using drugs, they experience a great deal of withdrawal. Withdrawal can cause very harming physical and mental effects such as depression, fatigue, nausea, sweating, vomiting, restlessness, and sleep deprivation [4]. This shows that just because somebody is continuing to use drugs, despite knowing the side effects, doesn’t mean that they do not want to stop or that they just don’t have enough self control. It is possible that they keep using drugs because of the painful withdrawal effects they go through afterwards. It is because of these effects we should be more mindful and thoughtful of what drug addicts go through to stop and get clean. 

  1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898681/
  2. https://www.nature.com/scitable/definition/histones-57/ 
  3. https://www.drugabuse.gov/publications/drugfacts/understanding-drug-use-addiction
  4. https://www.verywellmind.com/what-is-withdrawal-how-long-does-it-last-63036

 

Gambling, what could go wrong?

Overview

If you are anything like me, you don’t see the point in gambling. You see that you are risking a lot with minimal chance of winning big. Around 6-9% of young adults experience problems related to gambling. Gambling becomes an addiction once a person starts to compulsively gamble, even when it takes a toll on your life. Compulsive gambling is a serious condition that can destroy lives.

Artstract by Alex Braun

Symptoms

A person might be a compulsive gambler if they are preoccupied with how to get more gambling money, needing to gamble with increasing amounts to get the same thrill, try to cut back and are unsuccessful, or they gamble to escape problems in their life. Unlike most casual gamblers who stop when losing or set a loss limit, people with a compulsive gambling problem are compelled to keep playing to recover their money; a pattern that becomes increasingly destructive over time (Mayo Foundation et al., 2016).

https://inventa.com/en/news/article/642/can-gambling-and-casino-trademarks-be-protected-in-egypt

Biological similarities between substance abuse and compulsive gambling

Pathological gamblers generally have lower levels of norepinephrine than normal gamblers. Furthermore, norepinephrine is secreted under stress, arousal, or thrill, so pathological gamblers gamble to make up for their under dosage. It was also found during MRI and fMRIs that, “Monetary reward in a gambling-like experiment produces brain activation very similar to that observed in a cocaine addict receiving an infusion of cocaine (Jazaeri et al., 2012).

Comparison on prevalence of substance abuse and gambling disorder

Comparing substance abuse and compulsive gambling

Compulsive gambling is described as “persistent and recurrent maladaptive gambling behavior,” similar to the description for substance dependence and abuse (Jazaeri et al., 2012). One of the key components to categorize substance abuse is withdrawal. One of the criteria for compulsive gambling is a need to gamble with increasing amounts of money to achieve the desired excitement. This is an example of “tolerance” in gambling. Furthermore, substance abuse includes a persistent desire or unsuccessful efforts to cut down or control substance use. Similar in compulsive gambling, a person may desire to cut down on the amount they gamble, but may find themselves unsuccessful (Jazaeri et al., 2012).

 

Treatments

There are a few ways to treat compulsive gambling including, therapy, medications, and self-help groups. Therapy can include behavioral or cognitive therapy. Behavior therapy uses systematic exposure to the behavior you want to unlearn and teaches you skills to reduce your urge to gamble. Cognitive behavioral therapy focuses on identifying unhealthy, irrational and negative beliefs and replacing them with healthy, positive ones. For medications, antidepressants and mood stabilizers may help problems that often go along with compulsive gambling such as depression, OCD or ADHD. Narcotic antagonists, which are useful in treating substance abuse, may help treat compulsive gambling (Mayo Foundation et al., 2016).

 

Conclusion

Although I may not understand the desire some people may have to gamble, it is clear that this is a serious disorder that some people cannot control. It is important to recognize if someone you know might be a compulsive gambler so you can reach out to them and help. If you currently are like me and do not gamble, you should probably keep it that way.

 

 

Works cited

Jazaeri, S. A., & Habil, M. H. (2012). Reviewing two types of addiction − pathological gambling and substance use. Indian Journal of Psychological Medicine, 34(1), 5–11. https://doi.org/10.4103/0253-7176.96147

 

Mayo Foundation for Medical Education and Research. (2016, October 22). Compulsive gambling. Mayo Clinic. Retrieved from https://www.mayoclinic.org/diseases-conditions/compulsive-gambling/symptoms-causes/syc-20355178.

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