Community/Disease/Health/Hot topics/Uncategorized

Struggling to Hold On: The ALS Story

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You’re Not YOU

Picture this: You are 29 years old, in shape, happily married, thinking of children, an avid baker, and enjoying playing the piano in the evenings as you sip your daily glass of red wine. Could life get any better?
Suddenly, one day you start to notice unusual, yet slight tremors in your fingers. You don’t think anything of it. But then those tremors get larger, more pronounced, enough to disrupt your usual evening piano recital and eject the glass of red wine from your hand. Welcome to the beginning of one of the most relentless and soul-robbing diseases today: Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig’s Disease.
Meet Kate, a classical pianist who is diagnosed with ALS and the star of the movie shown below, “You’re Not You.” Throughout the span of a few years, Kate experiences the progressive weakening and atrophy of her voluntary muscles that rob her of the life she loved to live. If you would like to experience the life of an ALS victim through the eyes of Hollywood drama, spend your Saturday afternoon sobbing and watching “You’re Not You.”

 

 What is ALS?

ALS is a fatal motor neuron disease that is characterized by the weakening and atrophy of both upper and lower motor neurons. Normally upper motor neurons in the brain function to send signals to facial and cranial muscles, as well as to lower motor neurons located in the brain stem and spinal cord. The lower motor neurons then send signals out to respective muscles and cause contraction of those muscles to aid in our voluntary movements, such as talking, swallowing, breathing, and walking.
 
 Figure 1. Depiction of a healthy motor neuron and an atrophied motor neuron seen in ALS.
Figure 2. General locations of the upper and lower motor systems in the body.

Trapped

Although all voluntary muscles are affected by ALS, the cognitive state of victims usually remains in tact. Some would argue that this makes ALS even more torturous for its victims to suffer through. This relentless disease almost always results in respiratory failure and death within a few short years (3-5 years) after initial diagnosis.

The ALS Brain

There are four interconnected pathways identified in the vicious cycle and progression of ALS that specifically affect both the upper and lower motor neurons of ALS victims. Researchers are currently unsure which part(s) of these four pathways is responsible for initiating this vicious cycle. These pathway outcomes ultimately lead to the associated symptoms of ALS:
1. SOD1 and Oxidative Stress
Many ALS cases involve mutations (genetically inherited or sporadic mutation) of the gene encoding the superoxide dismutase enzyme (SOD1). SOD1 functions as a cytosolic antioxidant enzyme, defending against reactive oxygen species (ROS) formed in cells during normal cellular metabolism. When the SOD1 gene is mutated, SOD1 enzyme is defective, which leads to a buildup of ROS in the brain and ultimately oxidative stress.  The oxidative stress overpowers cellular organelles and leads to organelle dysfunction. The cellular organelle dysfunction leads to defective cellular metabolism and protein production and a prolonging of cellular oxidative stress.
2. Protein Folding
An increase in oxidative stress leads to the aggregation of misfolded proteins, which overpowers the body’s natural autophagy system (responsible for cleaning up misfolded proteins and defective organelles) and renders it dysfunctional. This amplifies the buildup of misfolded proteins in cells.
3. RNA Dysfunction
When under stress, the cell halts translation via the formation of stress granules in the cytoplasm: globules of non-translating mRNA, ribosomal subunits, and translation initiation factors (think of wads of gum). During prolonged oxidative stress, however, permanent stress granules form that cause important molecules in RNA processing and protein production (FUS and TDP43) to aggregate and render them nonfunctional. The stress granules are similar to wads of gum that stick to anything they touch, including FUS and TDP43. The failure of FUS and TDP43 to carry out RNA processing leads to dysfunctional RNA processing and protein production. This further amplifies cellular oxidative stress.
 
Figure 3. The formation of permanent stress granules in the cytoplasm and consequent aggregation of TDP43 and FUS.
4. Metal Ion Homeostasis
An altered metabolism and increase in cellular levels of iron and copper lead to an increase in cellular ROS. This increases the oxidative stress in the body, amplifying the dysfunctional RNA processing mentioned before, and ultimately protein degradation within the cells.
 

The Future of ALS

Currently, there is no cure for this horrible, life-altering disease.  However, there are multiple therapeutic options (physical therapy, occupational therapy, rehabilitation) to help ALS victims. There are also standard pharmaceuticals administered for pain relief and to aid in prolonging life, such as edaravone. Riluzole is a drug that has been shown to prolong the life of an ALS victim 2-3 months without treating symptoms of the disease.
The future of ALS lies in the hands of scientific researchers and the study of brains of ALS victims to develop a better understanding of the disease’s actions. Further pathways of the disease need to be identified in order to find potential therapeutic targets that may lead to the cure of ALS or a greater prolonging of life of ALS victims.
 
If you would like to learn more about the physiology of ALS, please visit:
http://www.sciencedirect.com/science/article/pii/S0304394016302877?via%3Dihub
Images From:
https://kin450-neurophysiology.wikispaces.com/ALS+II
https://www.slideshare.net/santhurao/physiology-859392
http://jcb.rupress.org/content/201/3/361

Community/Disease/Health

What We Don’t Know About ALS

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It all starts out with muscle weakness in either the hands or the feet, and slowly progresses to slurred speech, stumbling, bad posture. These are just some of the early symptoms of ALS and they only get worse as the disease progresses. Which, in most cases, is a relatively fast progression. In most cases of ALS, the individual diagnosed will generally pass away from the disease within 3 years. However, there are cases of people that live 13 or 14 years, maybe even more with the disease but as sad as it is, these are rare cases.

Forms of ALS

There are two different forms of ALS, the first form is sporadic ALS.
Sporadic ALS makes up roughly 90% of all cases and is defined as a random onset of the disease. There is not a genetic factor to this form, meaning it is not passed down from family member to family member. However, family members of those diagnosed with sporadic ALS are at an increased risk of being diagnosed themselves, this is still a relatively low risk.
The second form of ALS is familial.
Familial ALS is just as it sounds. The genetic form, meaning it is passed down from family member to family member. This makes up only 10 % of all cases. Within this 10% there is roughly a 25-40% chance ALS is caused by a mutation on the C9orf72 gene. This gene mutation is also associated with atrophy in the frontal lobe of the brain, which is linked to frontal lobe dementia. This form of dementia could possibly be associated with the cognitive declines that go along with ALS.

So What is Causing ALS?

There are two main ideas about the cause of ALS, however it is unknown which one comes first in the pathway.
It is believed that oxidative stress within the brain leads to RNA dysfunction, which is linked to the onset of ALS. It is also believed that RNA dysfunction leads to oxidative stress which then leads to the onset of ALS. This is like a vicious cycle because we don’t know what causes what. Does RNA dysfunction cause oxidative stress or does oxidative stress cause RNA dysfunction? We are also unsure of what is causing either of them to occur in the first place, which is what science is trying to figure out.
It IS known that the proteins TDP43 and FUS are spliced away from the nucleus and aggregate in the cytoplasm. They are then localized and trapped within stress granules, and this is somehow leading to the onset of ALS.

What leads to what? This is an artstract that depicts the confusion of whether RNA dysfunction leads to oxidative stress, or if oxidative stress leads to RNA dysfunction. 

Sources:

https://www.webmd.com/brain/understanding-als-symptoms#1
https://moodle.cord.edu/pluginfile.php/625305/mod_resource/content/0/ox%20stress%20and%20mito%20damage%20in%20ALS%202016.pdf
 

Uncategorized

ALS, It’s More Than the Ice Bucket Challenge

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Remember a few years back when the ice bucket challenge was a big thing? Everyone was doing it and the challenge went viral. Next thing I know my antisocial media mother is doing it too. She decided to create a Facebook just so she can get a bucket of ice cold water dumped on her.  She didn’t do it just because all her friends were doing it or to be cool (maybe?). She did it to spread awareness about a rear and fetal disease called ALS. At first I didn’t know what ALS was or why it was taking over the world. But as time passed, I became aware of the disease and how prevalent it was.
So what is ALS?
Amyotrophic lateral sclerosis or ALS is a fetal motor neuron disease that brings upon degradation of upper and lower motor neurons. The disease attacks the motor neurons which reach from the brain to the spinal cord and from the spinal cord to the muscles throughout the body. The progressive degeneration of the motor neurons in ALS eventually leads to their demise.

Types of ALS
There are two types of ALS.
Sporadic, which is the most common, affects about 90 to 95 percent of all cases and anyone might get at any time.
Familial, which accounts for 5 to 10 percent of all cases. Familial is inheritable which means a certain mutated gene may be passed on within family members, in those families, there is a 50% chance each offspring will inherit the gene mutation and may develop the disease.

Signs and symptoms of ALS
In the beginning symptoms and signs might be overlooked, they include.

  • muscle weakness or muscle atrophy (weakness in the arms and legs first)
  • trouble swallowing or breathing
  • cramping

As the disease progress the signs and symptoms become severe and widely noticeable. These may vary from person to person.

  • Lose in mobility, speech and swallowing
  • Cognitive declaim

Sensory nerves and the autonomic nervous system are generally unaffected, meaning the majority of people with ALS maintain hearing, sight, touch, smell, and taste.
What causes ALS?
Scientists have yet to pinpoint what exactly causes the disease but recent research has provided some understanding of what might be going on.  A recent study has shown that oxidative stress, mitochondrial damage and protein aggregation might be the problem.

  • Oxidative stress and mitochondrial damage cause RNA dysmetabolism
  • RNA dysmetabolism causes oxidative stress and mitochondrial damage
  • Accumulation of misfolded proteins, which can lead to the imbalance of the protein degradation pathway.
  • Iron homeostasis, high levels of iron lead to oxidative stress increase.

Is there a cure?
There is no known cure for ALS but certain studies have shown that the drug Riluzole a glutamate blocker slows the progression of ALS in some people. Also therapy in improving breathing and swallowing has been shown to improve daily living conditions of people with ALS. In addition, people with ALS may experience a better quality of life in living with the disease by participating in support groups and attending an ALS Association Certified Treatment Center of Excellence or a Recognized Treatment Center.
https://www.youtube.com/watch?v=JNZcC_3YLuo
for more information please visit the ALS Association website at  http://www.alsa.org/about-als/what-is-als.html?referrer=https://www.google.com/

Community/Disease/Health

ALS: Bringing Awareness to This Neurodegenerative Disease

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Background Information on ALS


Amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, is a debilitating disease that can often be difficult to diagnose. ALS can mimic, or appear to be, many of debilitating diseases, and all of these must be ruled out before this diagnosis is handed out. Many of the diseases that could present like ALS have treatments, and possibly cures; ALS does not. The degeneration of upper and lower motor neurons is a characteristic of this disease, and due to the long diagnostic time, many patients are already in the late stage of this disease, and will likely die of respiratory failure in only a few years. ALS is most commonly thought of as a musculodegenerative disease, but there can also be cognitive declines as well.
Two forms of ALS are familial ALS (fALS) or sporadic ALS (sALS). sALS is much more common, but fALS is usually due to inherited genetic risk factors. This disease is thought to be partially caused from an accumulation of iron in the body. This will lead to increased amounts of reactive oxidative species (ROS), which will go into stress granules. The body will then attempt to get rid of the ROS, and thus will develop oxidative stress, which will lead to mitochondrial damage and/or RNA dysmetabolism. This will then lead to problems forming correct proteins, and cellular function, especially in large neurons, is impaired.

Treatments

As there is currently no cure for ALS, the goals of treatment are slowing the progress of the disease and/or reducing pain due to symptoms.

  • Medications
    • Riluzole: appears to slow disease’s progress, acts by reducing glutamate levels (stop brain from developing glutamate excitotoxicity, which damages neurons)
    • Edaravone: was just approved this year, shows a reduced decline in daily functioning
    • Other pain relief medications for treating the symptoms
  • Therapies
    • Physical therapy: address pain, walking, mobility, bracing, and equipment; practice low-impact exercises
    • Breathing care: breathing devices if needed
    • Occupational therapy: help to find ways to remain independent, modify home for accessibility
    • Speech therapy: adaptive techniques to make speech more clear
    • Nutritional support: eating foods that are easier to swallow, eventually may need a feeding tube
    • Psychological and social support: financial help, insurance, getting equipment, emotional support

The Ice Bucket Challenge

One way ALS has gained attention as well as some funding was through the ice bucket challenge. This was a trend in which social media was utilized to raise awareness and funds for ALS through individuals doing their own challenge and then nominating others to do one as well. A timeline of this challenge can be found here. What started as a small gesture done by one man was able to race through the world due to the power of social media. Supporting those with ALS, as well as bringing awareness into communities is imperative in the fight against ALS.

Community/Disease/Spirituality

ALS – Finding Hope

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This past week the Fargo-Moorhead community lost an angel to a disease that continually seems to rip away our hope and block any light at the end of the tunnel. This one, like many diseases does not discriminate against who it takes. ALS, amyotrophic lateral sclerosis, is considered a debilitating and imprisoning disease with no cure. Little hope is found in those words. Therefore, we ask: What can we do as a community, as people who love each other, to help those who suffer from ALS, along with their families? What good can we bring of such hurt?
First, let’s begin with a brief overview of the disease from a biological standpoint to better understand its complexity.
ALS is a fatal disease that is commonly associated with the degeneration of upper and lower motor neurons, or the cells that allow our muscles to move. It can be a genetic disease, running in families, or randomly occurring. In the body of someone affected by ALS, there are essentially three things that are going wrong and leading to the disease.
The first thing going wrong is oxidative stress and RNA dysmetabolism, both of which are a part of a cycle that essentially leads to magnifying each other. Oxidative stress is a result of natural metabolic pathways that are working in overdrive and their products accumulate. These oxidative products cause damage to the cell and other cellular changes that are detrimental to normal function. In ALS, oxidative stress causes RNA-binding proteins TDP43 and FUS to delocalize from their neutral location and aggregate in the cell. This then hinders the proteins’ ability to function properly and metabolize RNA. Oxidative stress also allows for the production and release of stress granules which allow for the activation of “stress genes” and are characteristic of ALS neurodegeneration.
When RNA is unable to be properly metabolized, proteins such as FUS and TDP43 can create a negative impact on natural oxidative stress protections. This is the fatal cell cycle that continues to occur in ALS patients.
The second malfunction is protein folding. All the oxidative stress occurring in the cells leads to mutated proteins which aggregate and trap helper proteins that act to remove malfunctioning proteins. The cell is then unable to respond to the damage occurring, so it naturally performs autophagy which is to eat or destroy itself.
The third component that is failing in ALS is metal homeostasis. In patients suffering from ALS, there is an unusual metabolism of iron and copper which leads to an increase in both. This then leads to oxidative stress, which was previously discussed, which causes overall protein degradation or cell death.
As you can see, ALS is incredibly complex and gene specific in its effects. There is no clear pathway but rather a culmination of many pathways working in tandem. Because much of the biological pathway of ALS is still unclear, more research is required. As of now, the only treatment options available treat solely the symptoms. Therefore, the more we can learn, even at a small scale, can help add to the knowledge of specialized treatment options.
So, what does all this complexity and uncertainty mean to us and to our community?
It means there is much work and awareness that needs to be done. It means we come together as a community and lift each other up in kindness. It means we turn to faith for hope and we rely on the love of our faith to radiate and bring meaning to people’s lives. Finally, it means we do not turn our back on those suffering but be friends and be of service to our community’s needs.
Right now, it feels like there is no hope. However, with faith, kindness, love and many more hours of hard work and research, there can be immense hope.
“But those who hope in the Lord will renew their strength. They will soar on wings like eagles; they will run and not grow weary, they will walk and not be faint.” Isaiah 40:31.
https://www.ncbi.nlm.nih.gov/pubmed/27150074

Disease

How Does ALS Progress?

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To understand ALS, one needs to understand how the motor neurons in the brain are divided. The brain has different types of neurons, sensory (for example, detecting touch), and motor neurons (responsible for causing muscle contractions). The motor neurons are the one’s effected by ALS, there are two regions that we will be focusing on, the upper and lower motor neurons.
 
The upper motor neurons are in the brain and they extend into the lower motor neurons. The lower motor neurons are in the spinal cord going directly to the muscle tissue.
 Continue reading →

Uncategorized

Potential Key Players in ALS Disease: Better Targets for the Future Treatments

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Lou Gehrig’s disease is also called ALS. It is a motor neuron disease that impairs the physical activities in the life of the patients with ALS.
 
ALS begins with muscles weakness, stiffness, softness, tightness, or spastic. The patients with ALS feels fatigue, poor balance, slurred words, weak grip, or tripping. These symptoms may be so subtle they occur before diagnosis. The next stage of ALS presents with more widespread symptoms from above, paralyzed muscle groups, deformed and rigid joints, weakness in swallowing, unable to drive, weakness in breathing when lying down, and bouts of inappropriate laughing or crying. The final stage of ALS presents with most all voluntary muscles paralyzed such as speech, eating, drinking, limited ability to move air into and out of lungs (breathing) and poor respiration leads to fatigue, scattered thoughts, headaches, and pneumonia. In the last stage, the patient with ALS have a high risk of death.
 
Image result for als
 
Unfortunately, the diagnosis process of ALS usually takes 2 to 3 years, implying that the patients are usually at the late stage when they find out that they have ALS. The treatments are also limited. The treatments do not target to the specific area in the growth of ALS. Instead, they just try to slow down the progression of ALS disease.
 
In a current study, the oxidative stress, the mitochondrial damage and the RNA dysfunction are the important mechanisms contributing to the initiation and progression of ALS:
The mutant Fuse in Sarcoma (FUS) and TAR-DNA binding protein (TDP43) protein tend to aggregate and trap within the cytoplasm, leading to the impairment transcription and growth of motor neuron. This creates more oxidative stress in the cell. The autophagy and protein degradation, such as SOD1 and UPR, help to keep the oxidative stress at the normal level. When they are unable to resolve the oxidative stress in a timely manner, they shift their function to destroy the cells. Apoptosis is now the goal.
 
The key players in ALS disease:

  1. Fuse in Sarcoma (FUS) is essential in the nucleus and cytoplasm. In the nucleus, it is a transcription factor, a pre-mRNA splicing, and bringing other transcription factors together to initiate the transcription process. In the cytosol, FUS has less functions, so small amount of FUS is present in cytoplasm. FUS importantly acts as a mRNA transporter, bringing mRNA out of the nucleus. When FUS is mutated, it tends to aggregate and accumulate in the cytosol, leading to the inability for mRNA to be spliced properly, less miRNA produced, transcription issues, lack of mRNA transport to the dendrites in the cell that require it and destabilization of important mRNA.
  2. TAR-DNA binding protein (TDP43) is a DNA/RNA binding protein. It has the similar functions like FUS. It plays an important role in transcription and translation process. It also involves in stress granule response under condition of stress.
  3. SOD1 is a mainly cytosolic antioxidant enzyme that convert superoxide (O2–) into hydrogen peroxide (H2O2). Its important function in the complex defense against reactive oxygen species that are produced by the cell during normal cellular metabolism. Mutation SOD1 increase protein and lipid oxidation, making the metabolism work more and producing more ROS. In addition, mutant SOD1 sometimes runs in reverse, catalyzing the conversion of H2O2 into O2–, and worse, allows the nascent O2– to react with nitric oxide (NO) to yield peroxynitrite (ONOO–). Peroxynitrite intitate the oxidative stress in the cell and ultimately leading to motor neuron death.
  4. Oxidative stress may also lead the formation of unfolded protein. Unfolded Protein Response (UPR) is a cells response to restore normal function of the cells, breakdown of the misfolded proteins and increasing the production of chaperones in protein folding.

 
More studies are needed to understand in depth the mechanism of ALS disease to come up with the better treatments as well as improving the diagnosis process that is able to diagnose at the early stage in order to suppress effectively the growth of ALS.
 

Disease/Health

Steady Support in the Face of Deterioration: Supporting Those With ALS

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Amyotrophic Lateral Sclerosis (ALS)

Many neurodegenerative diseases are a devastating diagnosis for patients and ALS is no exception. ALS is a motor neuron disease in which the upper and lower motor neurons die. ALS is fatal usually due to respiratory failure within a few years of diagnosis, but some cases can progress less quickly. With such a variable prognosis length, it can be difficult for those diagnosed with ALS to feel like they can make plans for the future. With such a bleak diagnosis it can be easy to get discouraged, so how can friends, family, and neighbors best support someone with ALS?

Spreading Awareness & Education

One way to support those with ALS is to simply spread awareness and educate others about ALS. A very popular and effective way to spread awareness is through a fun activity or event in the community. An example of this is Relay for Life and how that event helps to raise awareness and educate others about cancer. Fun activities are even more effective at spreading awareness when they tie in social media, like the ice bucket challenge for ALS. The ice bucket challenge definitely got the word out about ALS and even raised some money, but it may not have been as effective at educating others on the topic.

Offering Support

Another way to show support is to actually offer support to the family of those with ALS. Families are usually responsible for caring for their family member that has been diagnosed with ALS once the disease has progressed enough to have motor disabilities. If the family themselves cannot care for the ALS patient, they may need to hire a nurse and that can get expensive. Offering to come help out even once a week to do laundry or other household chores, put them to bed a couple nights out of the week, or bringing meals in would be a huge gesture to any family that has a member with ALS.

Understanding all Options

As a friend or family member of someone with ALS, another important thing to be mindful of is all the options surrounding treatment for ALS. Most of the treatments around today are aimed at slowing the progression and alleviating symptoms. The supportive treatments are there to help the person live a comfortable remainder of their life as much as possible. When the disease begins to progress faster, it can be hard as someone close to the ALS patient to watch them deteriorate and suffer. The treatments may be simply prolonging the inevitable and even though it may not seem like a viable option, letting nature take its course may be the preferred option of the ALS patient. It can be hard as those close to the patient want to hold onto them as long as possible and be able to say they tried everything. However, if the person has lived a full life and is at peace with where they are it’s best to support and understand their wishes.
Sometimes once a person receives an ALS diagnosis they begin trying to live life to the fullest before their disease progresses too far for them to be able to function well independently. In some ways this is just as an important time to support the ALS patient as points are further in the progression.

For more on the science behind ALS: http://www.sciencedirect.com/science/article/pii/S0304394016302877?via%3Dihub
Feature image: https://alsnewstoday.com/
Ice Bucket Challenge image: http://bigthink.com/ideafeed/what-the-als-ice-bucket-challenge-tells-us-about-successful-viral-marketing
Paper Dolls image: http://namidupage.org/resources/support-groups/
Bucket List image: http://theolemissyearbook.com/bucket-list/

Community/Health/Hot topics/Uncategorized

Possibilities of Medical Marijuana

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Featured Image by Author
Medical marijuana has become one the most controversial debates. You’re either for it or against it, with very few people falling somewhere in the middle. But why exactly has this drug caught researchers, as well as health professionals’ interest? It all starts with the many therapeutic effects that is has the body, especially in the brain. Medical marijuana has shown to be effective in treating disorders such as anxiety and epilepsy. It also promotes apoptosis (cell death) in tumor cells, making it a promising treatment for cancers.
 

How does it work?

Our bodies have a system known as the endocannabinoid system, which upon activation, is associated with many of the therapeutic effects seen with marijuana usage. In the brain, this system occurs between two neurons that are connected. One neuron will send out signals to the other to produce and release molecules, known as endocannabinoids. When these molecules are released, they can go and bind to a receptor that is located on the first neuron. This will ultimately lead to the first neuron being shut down. Many of the disorders that marijuana is being used to treat, have overactive neurons and so they need to be shut off, essentially. Marijuana contains its own cannabinoids, such as THC, that can bind to the same receptor that the endocannabinoids bind to. Thus, it can shut off those over active neurons, just like the endocannabinoids that our bodies naturally produce.
 

What’s The Problem?

Even though medical marijuana can produce therapeutic effects, there are still some kinks that need to be worked out. The main one is THC, which is the most common cannabinoid in the drug. This molecule is not only responsible for the therapeutic effects, but also the high marijuana gives. However, there are other cannabinoids in the marijuana plant that can produce the same effects as THC, but without the high. These may be the most promising and may be what allows for medical marijuana to move forward.

Community/Health/Hot topics

Marijuana: Recreational Advocacy Sabotages Support for Medicinal Research

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The taboo topic of marijuana is splitting America at state lines. While the drug is illegal on a federal level, Individual states are taking opposing stances on its legalization in regards its use, psychoactivity, and possession incrimination.
 
I would venture to say that the debate of recreational v. medicinal use is actually stigmatizing marijuana research, making it difficult to find funding and fully understand its benefits or risks. While the public is so concerned with WHO should be able to legally utilize marijuana, we must rather educate ourselves on HOW marijuana has so many diverse effects.
 

How it works

Marijuana is a very complex plant with over 400 chemicals, 15% of which make up the active ingredients that are cannabinoid-based. Cannabidiol, Cannabinol, and THC are the among the most popular cannabinoids in marijuana, as they are responsible for both the psychotropic and medically beneficial effects of the drug.
 
So how does these work in our brain? Well, our brain actually has a system in which we make and use our own cannabinoids, called endocannabinoids (eCB). Two common forms of eCBs are anandamide (AEA) and 2-arachidonoylglycerol (2-AG), which are made and released in the brain.
 
These molecules bind to cannabinoid receptors (cB1 receptors) and can hold a number functions. For example, one function includes its inhibitory effects. When the eCB is released, transports back up to the pre-synaptic neuron, and shuts down the pathway and causes its pain-relieving, or analgesic, effects.
 

The medicinal benefit of marijuana use

THC and Cannabinol have psychotropic effects that are responsible for the user ‘high,’ but Cannabidiol does not. Not only does it lack the ‘high,’ but it also has many therapeutic benefits found in preclinical trials. These include anti-seisure, anti-inflammatory, anti-psychotic, analgesic, and neuroprotective properties.
 
If researchers were able to isolate this ingredient, the medical use of the altered marijuana would then run through the same FDA testing for approval as any other legal medication. However, research and funding is needed to get marijuana to this point in the process.
 

The recreational harm of marijuana use

Marijuana on our streets today is not the same marijuana baby boomers were smoking in the 1970’s. In the 1990’s, marijuana had about 3.1% THC content- marijuana tested in 2014 had 6.1% THC, almost doubling in the past 20 years.
 
Not only are growers increasing levels of THC content to induce a more effective high, they are developing new ways of administering the drug. They have now created cannabis oil extracts, which are inhaled and contain an astonishing 50-70% THC.
 
With increasing levels of THC, one must also consider its propensity for addiction. It’s a common sentiment that marijuana is not ‘that’ addictive, which does hold some truth when compared to hard drugs like cocaine and methamphetamine.
 
30% of marijuana users develop marijuana use disorder, in which they feel dependency and withdrawal symptoms, but subside after 2 weeks of their last use. If withdrawal symptoms continue, it is considered an addiction and develops in 9% of marijuana users. As THC content increases, so does their risk for developing an addiction.
 

So who should use?

THC and other psychotropic ingredients in marijuana increases its potential for abuse and decreases one’s cognitive judgement. These negative components are not grounds for consideration of legalizing recreational use of marijuana.
 
However, that it not to say that marijuana doesn’t have a potential benefit to our society. By isolating the beneficial components without the negative side effects, we can be one step closer to legalizing medical marijuana. Being an educated member of society and advocating for continued research on this topic will collectively empower us to improve patient outcomes.

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