Cobbers on the Brain – Page 124 – Student Commentary on the Neurological Sciences

ALS: A Brief Background & Why It…Sucks.

Posted on November 22, 2016 by / 0 Comment

ALS, or amyotrophic lateral sclerosis, is a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord.
After discussing our weekly article in our Neurochemistry class on ALS, I found this to be one of the most interesting but also quite saddening neurological diseases. I want to first lay out general facts that are important to ALS but also what the disease does to you overtime.
ALS, as stated above, is a fatal motor neuron disease where the average person with the disease only makes it a few years due to respiratory failure. Nerve cells start to die and degrade and cause sclerosis or essentially hardening in the spinal cord leading to muscle atrophy or failed muscle movements.
Most people with this disease have it because it being sporadic, but about 10% of people genetically inherit the disease. You can test for it genetically then if that’s the case. The disease is a painless progress, but things that start giving evidence that you may have it include: tripping, dropping things, abnormal fatigue in appendages, slurred speech, muscle cramps, and weirdly enough, uncontrollable periods of laughter or crying. Regarding respiratory failure, people with ALS typically receive assistance in breathing with a permeant ventilator due to respiratory muscles like the diaphragm.
Currently, there is one main drug that inhibits glutamate release which is called Riluzole. It works to assist breathing but does not help everyone that takes it. The drug extends ALS patients lives by a few months. Besides that, treatment for ALS typically is just weakening the side effects like reducing muscle cramps or fatigue—There is no cure for this disease.
Yeah, I would have to say so far from what I said, ALS sucks. All diseases suck, but I would argue this is one the worst. First, you get all this muscle weakness and you start to need assistance from others around you to do normal things. Getting through that hoop is plenty, but throwing on top that you only will live on average a few years after diagnosis? Knowing there is no cure?
Yeah all neurological diseases have NO cure. Some of those diseases eat away at you mentally and you forget maybe who your significant other is, like seen in types of dementia This motor neuron disease isn’t targeting you mentally but only physically. So, you start as a grape and end as a raisin, but indirectly I would argue you are being affected mentally. YOU are aware of everything. You see yourself deteriorate, you see yourself slowly become less and less social because you communicate less. You watch your family and friends help you, help you so far until the decision is life or death. There’s that point where you can’t even blink or move, but inside your head your thoughts and ideas fly—do you get to choose what happens next?

Disease

Treatment of ALS With Stem Cells

Posted on November 21, 2016 by / 0 Comment

At the moment, a diagnosis of amyotropic lateral sclerosis (ALS), or Lou Gherig’s disease, is an incurable neurodegenerative disease that targets motor neurons in the central nervous system, mainly the primary motor cortex, brainstem, and spinal cord. There are currently only drugs that will slow the progression of ALS, but one of the most effective drugs, riluzole, only prolongs a patient’s life by about two months. Researchers are trying to develop more drugs that are more effective because the only other techniques for helping patients with ALS are physical therapy and psychological support, which are not the “treatments” that patients expect when they are diagnosed with a deadly disease.
Some researchers think that it is time for something a little bit more radical to be used as a treatment for ALS. Researchers at places such as the Mayo clinic are working on stem cell therapy as a potential treatment for this disease.

This research study is still underway at Mayo, but other groups have published the results of their initial research studies and surgical trials. A group based out of Italy performed a stem cell trial that consisted of them injecting human fetal stem cells, from natural in utero death, into the anterior horns of the spinal cord of more than 200 patients.

This study was phase one of their trials, though, so it was more focused on testing the safety of the procedures.The group mainly tested the effects of the surgeries to see if there would be any unexpected complications that resulted from the injection of highly concentrated stem cells into the spinal cord, and they found none. They monitored patients for up to 18 months after their surgeries to ensure that there were no complications resulting from the stem cells.
The group also carried out evaluations of all of the patients before and after undergoing surgery to gather preliminary results for the research. From their article, “Clinical progression was assessed using the ALS-FRS-R, Ashworth Spasticity Scale and the Medical Research Council (MRC) scale of 34 muscle groups of the upper and lower limbs and FVC. At each examination a clinical psychologist also evaluated the patients. Profile of Mood State (POMS) and SEIQoL-DW questionnaires were provided to patients to assess the mood state and the quality of life.”
From their assessments of the patients, they concluded that there was no increase of disease progression due to the treatment, and three patients showed improvement based on the scores form the ALS-FRS-R mentioned above.
There are other research trials underway, and hopefully no groups encounter too much resistance from groups opposing stem cell research. This group is carrying out research that should eliminate ethical concerns because of the nature of the stem cells collected and it was approved by an ethics committee, and other groups are following their lead. Although a treatment for ALS using stem cells is far from being developed, the potential is there and I am optimistic.

Disease/Health

ALS Mutations

Posted on November 21, 2016 by / 0 Comment

Many of the neurodegenerative diseases have new information coming out on it. Amyotrophic Lateral Sclerosis (ALS) is one of the diseases that people are aware due to its relation with Stephen Hawking, but are not familiar with the symptoms or cause of ALS. ALS symptoms can vary between people, but it is a gradual, painless onset of muscle weakness because it affects the motor neurons within the spinal cord. Initial symptoms can include tripping, dropping items, fatigue, and slurred speech.
Genetic mutations along with environmental factors can be seen as the cause of ALS. The cause of ALS can be sporadic (non-familial) which accounts for 90% of ALS patients or familial which accounts for 5-10% of ALS patients. A common theory is that sporadic mutation when paired with an environmental factor, can cause ALS. Of the familial ALS patients, around 60% have a genetic mutation. Most frequently heard of is the SOD1 mutation which has caught a lot of attention. However, there are other mutations that individuals should be aware of that have been linked to ALS such as FUS, TDP43, and C9orf72.
SOD1
The SOD1 mutation is responsible for 15-20% of familial cases in the world. SOD1 is an enzyme typically localized to the cytoplasm, nucleus, lysosomes, and mitochondria. It is involved in the body by attaching to copper or zinc and breaking down toxic superoxide radicals. It then forms ribonucleoprotein complexes in the brain and spinal cord. Within familial ALS, around 200 mutations in the gene have been linked. Most of the mutations result in an amino acid change within the protein of the enzyme. Mutations cause SOD1 aggregates to form in the cytoplasm and ribonucleoprotein complexes are not able to form which reduces the half-life.
FUS
The FUS mutation is responsible for around 5% of cases. The FUS protein regulates transcription by binding to DNA, prevents genetic damage by repairing DNA mistakes, and is involved in alternative splicing, processing, and transporting of mRNA to other cell structures to become a mature protein. Mutations involving this gene are found in ALS, Ewing sarcoma, and cancers (AML). Within ALS, the FUS gene can have around 85 mutations occur. The mutations usually affect building blocks in FUS protein, DNA binding, mRNA processing and transporting. This results in FUS protein and mRNA being trapped within the cell creating aggregates and stress granules. The picture below shows how the mutations can affect RNA metabolism.

TDP43
The TDP43, also referred to as TARDBP, mutation is responsible for around 5% of cases. TDP43 is a RNA-binding protein and found in very small concentrations in the cytoplasm of healthy individuals. Some of the functions of this protein are similar to the FUS protein above, including transcription and splicing of mRNA. However, TDP43 aggregates are found in the brain tissue of post-mortem ALS patients which lead to it being studied for ALS. Oxidative stress and mutations lead to more of this protein being moved into the cytoplasm and causing stress granules. There are nearly 30 mutations, the majority occurring in the C-terminal (shown in the picture below), that have been connected to ALS. The picture above shows how the mutations can affect RNA metabolism.

C9orf72
The C90orf72 mutation is responsible for 30-40% of familial cases in the US and Europe. C9orf71 is a protein found in neurons of the cerebral cortex and motor neurons of the brain and spinal cord. It is thought to play a role in the production and transportation of RNA and production of proteins. ALS occurs when a segment of the gene is largely repeated. It is not known if the repeat causes abnormal function.

Community/Disease/Health

Will ALS Be Treatable in the Future?

Posted on November 21, 2016 by / 0 Comment

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder which affects motor neurons in the brain and spinal cord, resulting in reduced muscle function. Most individuals are diagnosed with the disease between the ages of 40-70, the average age being 55. There are cases where individuals can be diagnosed at an early age, such as in their 20’s or 30’s. The majority of people who are diagnosed are given between 3-5 years to live, but there have been cases such as Stephen Hawking who has lived with the disease for 53 years. The degeneration of the neurons in the central nervous system (CNS) eventually results in lack of movement resulting in death from the inability to contract the diaphragm to breath.
Treatment for ALS is scarce. In fact, there is not a cure, but rather one drug called Riluzole that is used to slow the disease down. Riluzole acts byinhibiting the release of glutamate in the brain, which is the primary neuroexcititory compound in the CNS. The drug has a neuroprotective effect, which can result in an increase in life-expectancy for those diagnosed with ALS. But, there are side effects that come along with the drug such as fatigue, constipation, and spasticity. There are few other options for treatment, such as physical therapy and/or psychological support, but these are not “fixes” for the disease. These options may be recommended by a physician in order to make the individual more comfortable as the disease progresses.
Since the only treatment option available only slows the disease down, new treatment options would open the door to better lives for those diagnosed with ALS. Research is currently being conducted to find a new drug for ALS, but how much longer will it take scientists to find the “magic” treatment? The mechanisms that are involved in ALS progression are mitochondria disfunction, apoptosis, neurotoxicity from glutamate, inflammation, etc. These are all possible targets to research in order to develop a new treatment for ALS. Due to the heterogeneity of the disease, individuals who are diagnosed would most likely benefit from multiple forms of treatments. With so many possible starting points for treatments, how can scientists decide which is the best point to start from?
With so many different options for research, the possibility for a cure or better treatment is on the horizon for ALS patients. Research takes time, especially when it involves the development of new drugs, so the best thing to do is to wait and hope. With all of the technology available for medical research, I have no doubt that a new treatment will be available for patients with ALS sooner rather than later.

Disease

The Ambivalence of ALS

Posted on November 20, 2016 by / 0 Comment

Stephen Hawking was born on January 8th, 1942 in Oxford, England. He has used his education in physics, mathematics, and cosmology to study the basic laws which govern the universe. One of his most significant contributions to science was the conjecture that the universe has not boundary in imaginary time, which implies that the universe began completely according to the laws of science. As a result, Hawking has received many awards, medals and prizes for his academic work.
Stephen Hawking was diagnosed with Amyotrophic Lateral Sclerosis (ALS) when he was 21. According to the ALS Association (ALSA), ALS is a progressive neurodegenerative disease that affects motor neurons in the brain and spinal cord. Motor neurons stretch from the brain to the spinal cord and from the spinal cord to all the body’s muscles.

The gradual degeneration of the motor neurons in ALS eventually leads to their death, which restricts voluntary muscle action.
ALSA reports that the initial symptoms of ALS can vary between people, and the onset of the disease is quite gradual. Some possible symptoms include:

Progressive muscle weakness
Tripping
Dropping things
Abnormal fatigue of arms and/or legs
Slurred speech
Muscle cramps and twitches

The muscle weakness and paralysis can eventually affect the breathing muscles, leading to respiratory failure. The average survival time with ALS is 3 to 5 years.
In a class discussion, we addressed the difficult topic of what one would do if their family member was close to dying due to ALS. At this point, the degenerating breathing muscles can

Is it worth the emotional and financial burden to keep a loved one with ALS alive by permanent ventilatory support?
At what point would an individual with ALS, keenly cognizant of the damage from ALS to his or her body, wish to end their life?
Should physician assisted suicide be considered as an option for ALS patients?

We never came to a consensus. At the end of the day, it might be a better use of one’s time to devote herself to researching such a destructive disease, in hopes of developing an effective cure or preventative treatment.
According to a review study by Bozzo, Mirra, and Carri (2016, there are 3 mechanisms that cause ALS and seem to function cyclically:

Oxidative Stress
Mitochondrial Damage
RNA Dysmetabolism

Oxidative stress is a disturbance in the balance between reactive oxygen species and antioxidant defenses. It is characterized by protein aggregation in the cytosol by extra or permanent Stress Granules (SGs). SGs form under oxidative stress to quickly modulate gene expression.
Mitochondria show damage early in the neurodegeneration process of ALS. In fact, changes in the mitochondria can be detected before physical symptoms in ALS patients.
RNA dysmetabolism is caused by the delocalization of FUS and TDP43 from the nucleus into the cytosol. Aggregation, alternative splicing, and misfolding of these proteins are involved in RNA dysmetabolism.
Ultimately, ALS seems to be characterized by this vicious cycle of pathogenic mechanisms.
Currently, riluzole is the only drug approved to treat ALS. It helps decrease the progression of ALS, and it has helped increase the life expectancy of people with ALS. However, this drug does not work on everyone.
Stephen Hawking has managed to live 53 with a slow-progressing form of ALS. Being wheelchair-bound and reliant on a computerized voice system for communication has not held him back from remaining close with his family, continuing research endeavors, and traveling to give public lectures.
Yet, some are not this lucky, and the aggressive development of their ALS continues to limit their daily life until the very ability to live no longer exists.

Uncategorized

Medicinal Marijuana Isn’t Federally Legal—Let’s Fix That

Posted on November 15, 2016 by / 0 Comment

According to narconon.org, marijuana has been used since ancient times; the Chinese first described it in a medical reference dated back to 2737 B.C. Marijuana to them had noticeable intoxicating effects, but they saw it as a medicine for rheumatism, gout, malaria, and oddly enough, absent-mindedness. Marijuana arrived in America in the late 1800’s where some medicines in the era contained marijuana, but most were of opium or cocaine. The U.S. Federal Bureau of Narcotics saw marijuana as a “gateway” drug in the 1930’s and the Controlled Substance Act of 1970 termed marijuana along with heroin and LSD as a Schedule 1 drug. Coming directly from the DEA,” Schedule I drugs, substances, or chemicals are defined as drugs with no currently accepted medical use and a high potential for abuse. Some examples of Schedule I drugs are: heroin, lysergic acid diethylamide (LSD), marijuana (cannabis), 3,4-methylenedioxymethamphetamine (ecstasy), methaqualone, and peyote.
That’s just a glimpse and highlights that I believe are important to marijuana’s history. The key statement mentioned was that marijuana is a schedule one drug. This makes research very difficult to occur and for the FDA to consider marijuana as a true medicine, it needs carefully conducted clinical trials of hundreds to thousands of human subjects to determine its benefits and risks. Supposedly, research has yet to prove that.
However, emerging research is being done on chemicals in the cannabis plant other than the main active ingredient which is THC. CBDs or cannabinoids are like THC but many/most all do not give the “high” you receive from THC. There are over 100 of these CBDs in the plant and research has been able to reproduce cannabis plants with little to no THC in them only CBDs. CBDs have gained a large popularity due to his help in treating certain diseases like epilepsy, multiple sclerosis, HIV/AIDS, Alzheimer’s disease, inflammation, pain, substance use disorders, and mental disorders.
With that overwhelming list only growing, how could someone vote against medical marijuana? As a society, we have accepted swallowing synthetically made pills of assortments of compounds to treat certain diseases or symptoms. Many of the pills today mimic something the body does naturally just as marijuana cannabinoids are naturally in the brain. Two endogenous cannabinoids, AEA and 2-AG are naturally produced in the human body, and medical marijuana helps work towards activating pathways that these natural endocannabinoids do on their own. Medication many times than not is simply to help either increase or decrease the amount of some molecule or compound which leads to a cascade of events relieving the symptoms. If you or someone you know has any of those diseases or conditions, you should be all for medical marijuana, as its going to be the leading medicine across all pharmaceuticals in the next couple decades.

Community/Health/Hot topics

High Driving – Is It Really That Bad?

Posted on November 15, 2016 by / 0 Comment

If you do a quick Internet search on this topic, the answers are mixed. However, after doing some digging, it seems to be pretty clear.
Marijuana is known to decrease cognition, motor skills, and problem solving in users. So, why wouldn’t this be bad for driving?
Well, according to the National Highway Traffic Safety Administration, there is “no significant increased crash risk attributable to cannabis after controlling for drivers’ age, gender, race, and presence of alcohol.”
So what does this mean? It means that after you remove factors like age, gender, race, and presence of alcohol, driving high has no link to crashing. But, my question is, how can you remove factors like age and presence of alcohol and still make that conclusion?
It is no secret that younger people are more likely to use marijuana, and that they are typically poorer drivers than older people. Additionally, using marijuana and alcohol together is not uncommon. So how can we say that driving high is okay when it has only been studied without regard to age or alcohol use, but it is not isolated from these factors in real life?
In addition to this information, drugabuse.gov states that, “studies have found a direct relationship between blood THC concentration and impaired driving ability.” So, even though the National Highway Traffic Safety Administration found “no significant increased crash risk,” it does not mean that high driving is at all safe.
Finally, a Drug and Alcohol Independence Study showed that people with a blood-THC content of 13 micrograms/liter “had the same level of impairment as someone with a blood-alcohol content of 0.08%.” Additionally, “Smoking a joint typically raises a person’s THC levels to about 20 micrograms per liter.”

So, now we know that high driving is bad. What is law enforcement currently doing about it?
Enforcement is currently determined on a state-by-state basis. Some states have consequences for have any amount of THC or its metabolites in your system, while some have a threshold like 5 micrograms/liter.
They test impairment by using field sobriety tests, identical to what is used for alcohol sobriety. Additionally, they can do blood and urine tests to measure levels of THC or its metabolites in the driver.
These tests are a problem though, because blood and urine THC levels are unreliable. People who chronically use marijuana have constantly higher levels of THC in their system, and the metabolites can stick around for a really long time. This renders these means of measuring marijuana impairment to be inaccurate.
So what’s my point, after all of this? In light of recent legalizations of both medical and recreational marijuana, I think that this will become an increasingly important issue. This information makes me question: are we really eady to legalize this drug if we don’t have laws and accurate measurements in place for penalizing its misuse on the road?

Disease/Health

Socially Unacceptable, Yet Highly Effective: The Tale of Medical Marijuana

Posted on November 15, 2016 by / 0 Comment

Marijuana, or Cannabis, is one of the most widely used illicit drugs in countries throughout the world. THC, the psychoactive element found in recreational (and some medical) marijuana is responsible for giving a user the “high” effect.
How does it work?
While it was long thought that the psychotropic effects of THC resulted from interference with membrane fluidity, it has now been found that cannabinoid activity is highly selective and there are actually specific cannabinoid receptors (CBRs – CB1 and CB2) and their associated ligands that THC binds to. This causes an intracellular signaling cascade resulting in the typical associated effects of marijuana.
Endocannabinoid System
Intrigued by the discovery of CBRs, researchers speculated that an endogenous cannabinoid-like substance might exist.
This is exactly what they found. In fact, our body produces two main endogenous cannabinoids: 2 – arachidonoylglycerol (2-AG) and anandamide (AEA).
Even more interesting, is that natural and synthetic cannabinoids, physiologically and pharmacologically, were found to have similar properties to AEA and 2-AG, such as analgesia, motor depression, catalepsy, hypothermia, reduced emesis, etc.
These compounds, AEA and 2-AG, are produced by the body as needed and can serve vital biological functions. Quite obviously, they do not produce the same “high” effect as synthetic or natural cannabinoids.
Medical vs. Recreational Marijuana
It is quite evident that the functions of 2-AG and AEA are physiologically critical. Pain relief, anti-epileptic, reduced vomiting – these all seem like good functions to have. And it has been proven that synthetic and natural cannabinoids, such as marijuana, have many of these same effects.
So why are we so resistant to the idea of medical marijuana?
I know this is not the case for everyone, but many individuals I have spoken to are hesitant when it comes to the idea of medical marijuana. The fact is, many of these individuals are uninformed. I too fell into that category at one point.
The distinction must be made that the use of medical marijuana is not just “patient’s stitting around, getting high to feel better.” Silly as that image may seem, that is what many people think. And this associated stigma can keep us from bringing to the medical forefront a highly effective medicine – yes, marijuana as medicine.
That fact is that medical marijuana, if prescribed and use properly, is not meant to cause any “high” at all. In fact, most patients that use marijuana medically don’t want the high. If they are taking this medicine morning, noon and night, or even once a day, they don’t want to get “high” every time they do. Imagine getting “high” whenever you took your daily vitamin, or a Tylenol. Though that may sound appealing to some, to many it is a nightmare. As such, doctors are very particular in the amounts they prescribe to their patients.
Additionally, pharmacists or dispensaries are very particular in the making of the drug. Most medical marijuana has a fundamentally different composition than recreational marijuana. THC levels are drastically decreased, and cannabidiol (CBD) levels (a compound of cannabis with some of the greatest medical properties, but no psychoactive effect) are elevated.
THC and CBD work in accordance to the entourage effect. When THC is present, CBD functions at a greater level and vice versa. This is taken into account when medical marijuana is produced. Some prescriptions have high CBD and zero THC, however, these are not very successful as the entourage effect is lacking.
In some serious cases, such as to treat chronic pain or epilepsy, both THC and CBD levels remain high in order to allow the CBD to function at its maximum potential.
Most prescriptions of medical marijuana, however, will have elevated levels of CBD and miniscule levels of THC. In this manner, the CBD function is promoted, but no ingested amount of the prescription would ever have a “high” effect.
What can we do to decrease this stigma?
Perhaps changing the name to something less likely to ruffle feathers would be a significant enough action. Perhaps not. I believe what is most important is becoming educated on this subject and advocating it to those who are uninformed.
Although it is rare with medical marijuana, getting “high”, is merely a side effect to a drug with many critical functions. It is not the end goal of its use. There are many other currently used drugs with side effects far and beyond more dangerous. We must look at this drug in the light of all it has to offer, and it order to do so, must rid it of its stigma.

Health/Hot topics

If Yes to Marijuana, Why Not LSD? How About Ecstasy? Ketamine? Cocaine? Mushrooms?

Posted on November 15, 2016 by / 0 Comment

These illicit drugs have been shown to have medicinal properties, too, so why aren’t we voting to legalize them?
Because that isn’t how the system should work. Since when does the general population, with little to no knowledge on the scientific research, get to vote on whether or not a new drug should be legal and used in medicine?
It is mind-boggling to me that we have been allowing these votes to take place in recent elections. I understand that research has shown that the active ingredients in marijuana, such as delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD), have been shown to be beneficial in treating certain disorders, but I don’t understand why all of a sudden we can bypass the system that is in place to keep us safe from the harmful effects of drugs.
These same compounds have also been linked to long-term brain problems, psychotic symptoms, lung problems, and heart problems, but people aren’t discussing the problems with marijuana. Ultimately, this is because they aren’t truly known yet.
The FDA has not determined that marijuana is a safe and effective drug. It has not been put through the proper human trials to be declared so, and it might not be for a long time. There has not been a significant number of long-term studies that can draw reasonable and consistent conclusions based on the results.
There are two main reasons that I believe we are going about legalizing marijuana incorrectly. I think we are jumping the gun and there is no reason that this should have ever come to popular vote.
We have moved very quickly when it comes to legalizing marijuana, and I hope it does not bite us in the butt. It is unlikely that we have a repeat of something like the tragedy surrounding the use of thalidomide, but I don’t think there is enough consensus within the scientific community and backing by the research to support the recreational or medicinal use of marijuana.
In addition, there is a reason that the general population does not vote on things related to medicine and science. The general population does not have the knowledge base or research to support what they are voting for. Maybe we should vote on vaccines in a few years and see where that gets us. Fifteen percent of people don’t believe vaccines are safe, that number is growing, according to statistics released by the CDC, only 35% of the population in some states get vaccinated for certain diseases. If we leave what drugs we should and shouldn’t take up to popular vote, why not the prevention of disease with vaccines? As a future health care professional, I think that is a scary thought.
I want to be clear and say that I am not saying I am against marijuana, I’m just arguing that we are going about legalizing it in the wrong way. Marijuana should go through the proper channels just like any other drug, and we, as the general population, should not be voting on what should or shouldn’t be used in medicine. Further research should have been done before the scientific community, its research, and the FDA determined marijuana to be safe and effective for medicinal and recreational use, but it is too late for that now. I guess we will just have to keep our fingers crossed and hope that the current and future research has good news.

Community/Disease/Health

Should Cannabis Be Schedule I?

Posted on November 14, 2016 by / 0 Comment

In 1970, cannabis was placed as a schedule I drug under the Controlled Substance Act (CSA). Schedule I substances are defined by the DEA as drugs without an accepted medical use, high abuse potential, and potential of severe psychological or physical dependence. Since cannabis was denoted a schedule I in 1970, there has been controversy on whether cannabis should be a schedule II. Schedule II substances have a high abuse potential and a potential of psychological or physical dependence (DEA, 2015).
The main differences between Schedule I and II are the severity of the potential danger and the potential medical use of the substance. In order to do clinical research for potential medical uses of cannabis, the researcher must have a DEA license and approval from the FDA. As a schedule I drug, cannabis is difficult for researchers to obtain. To obtain the substance, the researcher has to go through the National Institute on Drug Abuse (NIDA). These steps a researcher has to go through to obtain and research a schedule I drug tend to be problematic and limiting the amount of studies conducted within the United States. Therefore, most studies have been done on tetrahydrocannabinol (THC), a component of cannabis, and cannabinoids.
There are more than 60 compounds in cannabis. THC is the most studied of the components and is psychoactive. It can be ingested or inhaled and is commonly thought of as the “high” component of cannabis. THC works by binding to cannabinoid receptors, the most prominent receptor found within the body. Another compound is cannabidiol (CBD) which is non-psychoactive and is thought to contain the medicinal effects of cannabis. THC and CBD work synergistically enhancing their effects, known as the Entourage Effect. This explains that both, THC and CBD, need to be present for medical benefits, however, THC can be at a much lower concentration for medical marijuana (cannabis).

Cannabis has several studies from other countries that support medical use. The American Academy of Neurology supports the use of cannabinoids for multiple sclerosis (MS). Evidence supports improvements in spasticity and reduction of central pain in MS. The US National Cancer Institute suggests evidence of cannabis use for cancer-related pain and vomiting (antiemetic). Other possible areas of treatment are with HIV neuropathy, depression, and neurodegenerative disorders. There are presumed disadvantages of cannabis. These include anxiety, dysphoria, euphoria, hallucinations, paranoia, acute memory impairment and reduced cognitive function. Smoking cannabis is thought to have an effect on the increase in airway diseases, risk of schizophrenia, and oropharyngeal cancers.
In the US, there has been 28 states and DC to legalize medical marijuana, including Minnesota. Other states have legalized the use of the non-psychoactive extract called CBD. There are 7 states and the District of Columbia which have legalized the recreational use of marijuana. Nearly half of US citizens have used cannabis once in their life. A common misconception is lowering cannabis to a schedule II drug will increase the likelihood of it being used recreationally, but I believe it should be lowered for the use of research on further potential medical uses and long-term effects of cannabis. The United States has moved forward with medical uses for cannabis, but it continues to be a schedule one. Researchers have difficulty accessing it, yet it has been legalized in many states. Questions about the long-term effects are prevalent in the US, but we must rely on other countries to continue the research. Many people here in the US have access to cannabis for health benefits, but researchers struggle to gain access to it to understand the mechanism, long-term use effect, or how else it may be used.