Concussions and the 21st century

As I have mentioned in previous blog posts, today we expect there to be a pharmaceutical solution for every medical condition imaginable. Though this mentality doesn’t transfer to concussions. When I think of concussions I normally think of the phrases “walk it off” or “you should take a break”. It’s a weird thought that someday after getting a good whack to the head to be told, “Hey you don’t look so good, go take some __blank__ medication”.
Today we are starting to see many different administrations bringing the concussion issue to the front of their concerns. High schools, colleges, and professional sport organizations all have to decide where they sit on the issue. Do teams take out their fan favorites and risk losing, just to possibly save them some brain cells down the line?
In the eyes of sports organizations in perfect world an athlete could get a concussion, take a pill, and be right back on the field with no worries of consequences. So how close are we to this “perfect world”. To answer this question we need to look where current research stands. Luckily I found an article (1) that was published only 6 months ago that deals with this exact issue.
PGI-02776 is a prodrug aimed at minimizing the effects of a concussion. When a concussion occurs many different processes are initiated. As you can see in the figure there are a few chemical imbalances that occur after getting hit, PGI-02776 is aimed at preventing the glutamate increase. One might think that Glutamate shouldn’t be a concern because its increase is the smallest, but it also must be kept in mind that Glutamate is also one of the most complicated. Glutamate has many different effects in the body and brain so keeping its concentration level is necessary for a good health.
So in any good scientific experiment it is a good first test to see if a drug is actually doing anything. When PGI-02776 was tested with a concussion the glutamate produced was 20% of what was seen with no drug. Which could be considered successful results. So what other results are seen? Researchers were interested in cognitive results of this drug, so they developed a maze for rats. With this maze the drugs affects on long-term and short-term memories could be tested.
There were three different groups of rats:

  • Rats with no Traumatic Brain Injury (TBI)
  • Rats with TBI given PGI-02776
  • Rats with TBI given placebo

As would be expected the group of rats with no TBI were able to finish the maze fastest and had the best rate of learning. Rats that had a TBI and were given a placebo finished the maze slowest and had the slowest rate of learning. Resulting in our PGI-02776 drugged rats doing better then non-medicated rats, yet still worse then the rats with no TBI, which is to be expected.
The 3 categories of rats were then put through a test of motor skills. This was done through a swim test. Interestingly enough the two groups that suffered a TBI did best in the swim test with the TBI + PGI-02776 group swimming the fastest. I don’t know what to make of this data and it seems neither did the research group, they didn’t touch on the subject after writing the results.
Take home messages?
It seems that there may be solutions to concussions in the future. But this research must also be taken with not a grain but a large chunk of salt, just because something works in rats doesn’t mean it will work in humans to the same extent. Also this research is really only focused on the positive outcomes it isn’t known what side effects with come from PGI-02776 in the human body.
(1) Feng, J.; Van, K. C.; Gurkoff, G. G.; Kopriva, C.; Olszewski, R. T.; Song, M.; Sun, S.; Xu, M.; Neale, J. H.; Yuen, P.; Lowe, D. A.; Zhou, J.; Lyeth, B. G. Post-injury administration of NAAG peptidase inhibitor prodrug, PGI-02776, in experimental TBI. Brain Res. 2011, 1395, 62-73.

What happens when you get knocked on the head?

One of the most current and serious health issues today is concussion. You hear about it everywhere from the 4th grade football game to the scene of a fender bender. One of the scariest things about concussion is that it manifests itself in so many different ways– what exactly constitutes a concussion? Does everyone who has a concussion go unconscious? How long until your injury will heal? These questions are nearly impossible to answer because you are dealing with different bodies and different injuries.


According to the CDC, 1.7 million people suffer from concussions each year.1 Furthermore, they are the cause of 1/3 of all injury-related deaths annually.1 Sports-related concussions are particularly alarming due to their prevalence among adolescents. Per year, it is estimated that 1.6-3.8 million sports related concussions occur in the U.S. to those between the ages of 5 and 18.2 Frighteningly, some hypothesize that at least one mild concussion occurs in every football game played in the U.S.2 While many know that concussions are serious brain injuries, most are still unaware of the biology and chemistry behind these injuries.

What happens?

When the brain goes through some mechanical impact, the first thing that occurs is the opening of K+ channels. Since the cell usually maintains a negative charge within the cell and a positive charge outside the cell, this forces Na+/K+ pumps, the ones which move Na+ out and K+ in, to work overtime.
These channels working overtime is bad news for the cell. The pump needs energy to run, so this forces the cell to try to produce more and more ATP through glycolysis. However, since the brain is always running at its max energy production, this just causes stress on the cell. Additionally, since blood flow decreases in the brain upon injury, the cell doesn’t have much glucose to use to make ATP. Lactate, the endproduct of glycolysis, accumulates in the cell causing swelling and other adverse effects.
Another issue which the mechanical force causes is excitatory neurotransmitter release. Glutamate, the most common excitatory neurotransmitter, binds to its receptors which cause increased Ca2+ levels in the cell. Since Ca2+ in the cell is necessary for neurotransmitter release, this causes further excitation and release of glutamate. Increased Ca2+ also impairs mitochondria, the major players in oxidative metabolism. Of course, this just adds to the decreased energy problem the cell has. Lastly, another imbalance occurs within the cell – lowered Mg2+ levels. This has widespread effects for the cell as Mg2+ is required for so many cellular functions. One of these is energy production.4
The basic story of concussion seems to be a blow to the head and a resulting imbalance of ions and excitation. This leaves your cell scrambling to put everything back in its proper place, which requires a lot of energy – in fact, more energy than the cell can provide in its injured state.  Hopefully someday we can find a better way to protect our brains from being knocked around so much, or possibly a chemical treatment to help the cell effectively restore its original balances.
4. Giza CC, Hovda DA. The neurometabolic cascade of concussion. Journal of Athletic Training 2001; 36(3): 228-235.

NHL Hockey Brains

This weeks’ topic deals with concussions. Brain injury has been a hot topic in national sports leagues as of late, and for good reason. The danger associated with high impact collisions however is what puts many sports fans in the seats. The following two clips are of two NHL hits. The first is a completely legal, clean hit.
Clean Hit
Recent years have shown a trend towards “safer” hockey. Implementation of mouth guards has been strongly enforced at all levels of the sport and in many states age which young athletes can start checking has raised. Part of this can be attributed to creating to the goal of creating a safer environment. Part of it can be contributed to a lack of fans in the NHL. The NHL created a game focused more on “free” skating, skills and ultimately higher scoring games to put more fans in the seats. Tighter crackdown on physical play has trickled down to collegiate and youth levels, creating a “safer” game.  Most normal hockey fans love hard, open ice hits like the one above. The fact that the player obviously suffered head trauma is unfortunate, but hockey is a physical sport. Injuries such as this are expected to happen, although they are much less likely than the one shown below.
One Punched
This clip is interesting for a couple of reasons. Most hockey injuries are caused “cheap”, illegal hits. Now this punch may have been illegal or penalized, but it was by no means cheap. Both players were squared up and looking each other in the face, expecting to get punched. The player, who was knocked out, Matt Cooke, exemplifies why most hockey injuries happen. Type his name into YouTube and you’ll see a list of videos of him sticking out his knee and blindsiding players. Not only is he unenjoyably to watch, except in clips like above, but he puts the players who actually do something exciting at risk. The point is that the rules and guidelines in the NHL regarding head injuries are safe. Yes, there likely could be improvement, but it is not the biggest issue which puts brains at risks. It is with the enforcement of these rules. Hockey is a high pace sport, accidents happen and not every blindside illegal hit is intentional. Players however who are continually associated with these “accidents” are the problem. Why are players like Matt Cooke still playing professional hockey?
Don Cherry Wearing A Normal Suite

Magnesium and Other Treatments for Speedy Concussion Recovery?

Contact sports, falls, car accident, etc.  can all lead to concussions. But what exactly is a concussion? Concussions are defined as a traumatic brain injury, or TBI, caused by a blow to the head that shakes the brain inside the skull.  There are varying levels of damage that can occur in the brain depending on the amount of impact from the initial injury. Since concussions are difficult to directly study in humans, the complete story of what happens to the brain during trauma is not fully understood.  So if we still don’t know the whole story how can we treat concussions and how do we know when a person, suffering from a concussion, is fully recovered?  Unfortunately at this point there is no perfectly accurate test that can determine how long the healing process should last after brain trauma. For now, depending on the degree of the injury, the healing process for the brain, on its own, can take anywhere from a few days to several months.  If the brain trauma is severe, internal bleeding and permanent brain damage can occur. All types of concussions and traumatic brain injuries should be treated by a doctor.

Image from:

I was curious to find out if there was some type of drug or other treatment that could speed up the healing process and help the brain repair itself, especially since many annual brain injuries are in young athletes who want to get back out on the field. After doing a bit of research, I found that there are very few drug treatments available to be used in the recovery process for concussions. According to the Mayo Clinic, brain rest is the best treatment for concussions. This even includes avoiding TV, video games, outdoor activities, and using computers. Eating a light diet and avoiding alcohol are advised as well. Also acetaminophen (e.g. Tylenol) is good to use for excessive headaches.
One interesting piece of information I came across was the possible use of magnesium sulfate as a treatment. It is still in the trial stages of testing; however this is an interesting treatment choice, because it just so happens that magnesium levels in the body is related to concussions. When a concussion occurs, magnesium levels in the brain drop for up to four days. Magnesium levels are important because many energy producing enzymes require magnesium to do their job.  If energy levels are low in the brain, the recovery process may take longer.  As of right now magnesium sulfate trials for magnesium sulfate have deemed the drug inappropriate for concussion treatment, because no significant impacts were found by administering the drug after a concussion occurred. Other magnesium supplements have also been a suggested form of treatment such as, magnesium glycinate and magnesium taurinate. However the effectiveness of these treatments still needs to be tested. There is still much more research to be done on concussions as a whole, but there is hope is finding new treatments to stave off permanent brain damage.
If you want more information on concussions; prevention, symptoms, and treatments please visit:
If you would like to read about magnesium sulfate and its efficacy please visit:

The New Standard of Helmet Testing

Are helmets designed to stop concussions? I think you would be surprised to find out that helmets are not designed specifically to reduce concussion risk. Helmets are actually only tested for their ability to stop skull fracture. In the paper that was read for this week, the neurometabolic cascade of concussions was discussed.   We particularly discussed the effects of concussions on the still developing brains of adolescents. Concussions are particularly bad for growing children, however, we still subject them to sports where they are most susceptible to concussions. I don’t think that taking away sports is the answer, but I do think that helmets specifically designed to reduce the risks of concussions are important. This leads to the question, how are helmets designed and tested?
NOCSAE, or the National Operating Committee on Standards for Athletic Equipment, is an organization that formed in 1969 to create helmet regulations and standards for helmet performance testing. These tests are designed to evaluate the helmet’s ability to protect against serious brain injury, but not necessarily concussions.
Recently, researchers at Virginia Tech designed their own test for evaluating helmets. This new test rates each helmet based on their ability to protect against concussions. Their results were quite shocking. The helmet used last year in the NFL, the VSR4, was second from the bottom in VT’s ratings. This is also the helmet often used by high schools and colleges around the US.
VT’s new test is a great step in the right direction for concussion protection and awareness. With this new data made public, hopefully helmet producers will focus more on safety rather than style.
Further reading
In-depth information on helmet testing procedures

Justin Morneau: Wimp or Victim?

Morneaus Concussion
If you’re  a rabid Twins fan like I am, you’ve probably seen this video many times. Justin Morneau’s slide in an attempt to break up a double play may have been successful, but the blow to his head resulted in a concussion just before the 2010 All Star Break in July. Voted in as the starting first baseman for the AL, he was unable to play in the game. He was unable to play the rest of the season. His level of play significantly decreased throughout the following season, and it was clear he was not the player he was a year before.
Has this concussion become a scapegoat for Morneau’s decline, while other factors are the actual contributors? Many Twins fans have displayed obvious frustration with his inability to play at his all-star capability, and some have questioned whether he is simply using the concussion as an excuse for his shoddy play. Or is it possible the concusion suffered in July 2010 was still affecting him over a year later? I am inclined to think the latter.
Before his famed baseball years, Justin Morneau played youth hockey, and has admitted to having several head injuries during that time. An article we’ve been reviewing in our Neurochemistry class talks about the mechanisms behind concussions. A large mechanical force upon the brain (such as a shortstop’s knee to your head) can cause the rapid release of the excitatory neurotransmitter glutamate. These neurotransmitters can bind to certain receptors in the brain causing potassium ions to leave the cell. In an attempt to alleviate these neurological changes, pumps in the brain work overtime to restore the brain to its normal state. This requires energy, leaving the brain in an energy crisis and causing hyperglycolisis, the break down of glucose to provide energy. Any further injury or mechanism that requires energy during this crisis could cause the brain further injury. However, this period of vulnerability can often be quite short. Pitcher Josh Beckett took a line drive to the head and experienced concussion symptoms the next day, and was cleared to pitch 8 days later. Unlike Morneau, Beckett did not have a rich history of concussions.
Why do the number of concussions have an effect on concussion symptom severity and duration? If they didn’t, Justin Morneau could have been back after a week or two. However, our article explained that repeated brain injury can result in longer lasting symptoms. After the initial period of hyperglycolysis, the brain goes into a reduced state of glucose metabolism to counter this disrepancy between energy supply and demand. The body may not be able to respond correctly to another injury during this time. Additionally, calcium ions can enter the cell and accumulate due to the receptor binding mentioned above. Accumulated calcium can lead to cellular death through various mechanisms. The brain is very vulnerable during this time. It is not necessary to receive another blow in the head for the condition to worsen; simple activity can aggravate the sensitive system. This period of vulnerability becomes longer and longer the more concussions you have, leaving the vulnerability and chance of re-injury higher for much longer. For example, Morneau returning to batting practice or fielding practice can be enough to restart concussion symptoms even without a blow or disturbance of the head.
Tests have been developed to test whether athletes are ready to return to play after a concussion. While the test is more or less a simple test of reaction time and motor ability, slight deviations from the athlete’s baseline (how well they performed on the test when healthy) may result in being held from play longer to ensure full recovery. As recent as September 2011, Morneau still did not pass this test, despite being closer than he has been over the past year. This indicates he is still suffering from some symptoms over 14 months later. Further, steps are being made in the MLB to prevent players from rushing back to play after head injuries. A 7-day disabled list was added this last season so teams could fill a roster spot during the player’s injury, making them less likely to push their athletes into returning before their full recovery.
Though the brain is able to show plasticity and resistance/recovery from injury, it is the most important area of our body to protect. Too much traumatic brain injury can lead to long lasting loss of function and even neurological diseases. It will be interesting to see whether Morneau will ever be able to recover from his latest concussion. How many concussions can you have before your brain simply can’t restore itself to normal function? With Morneau, only time will tell.

Opioid Withdrawal. . . Not a Fun Process.

This week, our class focused on an article that discussed the role of glutamate (an important neurotransmitter) in drug addiction. It emphasized opioid addiction and its effects on the brain. Abused opioid drugs include morphine, heroin, oxycodone, hydromorphone, and more. It is thought that 9% of the population may abuse opiates sometime during their life. The drugs can create physical dependence, tolerance, and withdrawal once the drug is removed. People who were given opioids in the hospital even exhibit withdrawal. Early symptoms of withdrawal include agitation, anxiety, muscle aches, insomnia, and sweating. Later symptoms include abdominal cramping, diarrhea, nausea, and vomiting. The symptoms are not life-threatening, but are uncomfortable and may encourage return to drug usage.
Withdrawal Treatments
Withdrawal treatments involve both support and medications. Some of the medications are used to treat symptoms individually. Clondidine, one of the most common medication, reduces anxiety, agitation, muscle aches, sweating, runny nose and cramping. Buprenorphine is an efficient medication that can also decease detox time. Methadone is another one that is used. However, methadone requires long-term administration with a decrease in dosage over time. Check out this website for more information and links to other aspects of drug addiction:
MK-801 and Naloxone
MK-801 and naloxone are common drugs used during opioid research. On one hand, MK-801 blocks withdrawal symptoms. On the other, naloxone is used to induce withdrawal. Both of these drugs were used in various studies cited in the paper. You might think that MK-801 has potential as a withdrawal treatment as it blocks the withdrawal symptoms. But its mechanism of action brings in some interesting side-effects. The molecule binds to the glutamate receptor NMDA, blocking it. The receptor cannot let ions through to continue a signal. This is good, right? It stops the glutamate signalling so it cannot start dopamine release. Thus there is no reward system encouraged by the opioid drugs. There is more to the story. The site to which MK-801 binds is the same as PCP and ketamine. It exhibits some of the same side-effects as these drugs, mainly schizophrenic-like symptoms. If that wasn’t bad enough, there are also cardiovascular side-effects and formation of brain lesions. And that, ladies and gentlemen, is why an effective withdrawal symptom-blocker is not used as a treatment.
Withdrawal will stop eventually, but the desire to return to the drug will remain. The reward system driven by dopamine release is strong. Opioids have been used for centuries, first in the form as poppy seeds then morphine, then heroin. Pain relief is important, so it is just as important to understand the addictive properties of the current forms we use.

MAPK: A Mechanism of Cancer

Cancer. That one word strikes fear into the hearts of Americans. Our own bodies grow uncontrollably, destroying us. People everywhere have been affected by it, whether the tumors feed off of them or their loved ones. Cancer can develop from environmental sources or genetically. Whatever the cause, malignant cells have the same characteristic: they divide and grow unrestrained. One pathway plays a key role in the development. This is the MAPK pathway, specifically starting with the protein Ras, leading to Erk. In addition to cancer, the Ras/MAPK and other MAPK pathways are also associated with Alzheimer’s disease, Parkinson’s disease, and Amyotrophic lateral sclerosis (Lou Gehrig’s disease).
Ras/MAPK Pathway in Brief
Ras is a protein that is activated by signals such as growth factors. Once activated, it can activate (which usually means phosphorylate) other proteins. For this blog post, I will focus on Ras activating Raf. Raf then activates MEK which then activates ERK. This protein will then activate several transcription factors (TF), which are molecules that encourage the turning of DNA into RNA (which can then be used to make proteins!). The majority of the TFs that ERK activates are those that encourage cellular division, growth, and migration. They also play a role in regulating cell death. With its signalling effects, the Ras/MAPK pathway plays a significant role in the development of cancerous tumors.
Role of Ras and Raf in Cancer
The genes that Ras comes from is actually a family of genes. The family includes H-Ras, K-Ras, and N-Ras. K-Ras has been found to be mutated in many types of human cancers. About 50% of colon cancer case displayed a mutation in K-Ras. Mutations in the protein right after Ras, Raf, are also present in cancer. B-Raf mutations are responsible for about 66% of melanomas, which are cancers in the skin. One of the most common mutations results in B-Raf being activated constantly. It then continuously activates the MEK. MEK’s action continues, which means MEK, ERK, and the TFs are activated as well, resulting in cellular growth that cannot be turned off.
Kind of scary, but there’s hope!
Malignant tumors exhibit uncontrolled cell growth and migration that results from genetic mutations. These mutations may have been inherited or caused by the environment. There are other oncogenes (genes that cause cancer) that are important in the development of cancer such as Rb and Myc. As we learn more about the mechanisms of cancer, we will be able to develop treatments to prevent unrestrained cell growth. A previous blog post discussed different treatment options that take advantage of our current knowledge.

Discovering Ambrosia

Extending one’s life has fascinated people for centuries. Eternal life appears consistently in mythology and religion: as ambrosia, a gift from the gods or a philosopher’s stone. Today, the average human lifespan is around 80 years. However, we are finding that more and more age-related illness, such as Alzheimer’s Disease and Parkinson’s Disease, along with cancers, are exhibited more frequently. Both of my grandmothers have age-related diseases (Alzheimer’s and PSP). The subject strikes at home for me. As such, the paper we discussed in class for Neurochemistry sparked my interest. It reviewed known mechanisms of aging and how a certain receptor, IGF1-R, may play an important role in aging of the brain and Alzheimer’s disease.
IGF1-R, Alzheimer’s, Ceramide, oh my!
IGF1-R stands for insulin-like growth factor 1 receptor. This is considered a tyrosine kinase receptor, one of the types of receptors found in the brain. These kinds of receptors usually bind to growth factors like insulin. The receptors, after binding to signal molecules, or ligands, can start a chain reaction of other signals within the cell. The signal pathways that IGF1-R activates are the PKB/Akt or Ras/MEK/ERK pathways, both important in cell growth and reproduction. The Akt pathway also encourages cell death. This plays a role in aging.
The signal from IGF1-R is thought to contribute to the switch in the presence of two different receptors: TrkA and p75 neurotrophin receptors. TrkA is exhibited more in younger animals, while p75 is shown in greater amounts in older animals. Somehow, the expression of these receptors switches; the mechanism has yet to be discovered. But it is this switch that is thought to contribute to the aging of cells and eventual development of Alzheimer’s.
p75 receptor signaling is associated with the production of ceramide, a lipid (fat). This lipid stabilizes the enzyme that breaks up the precursor molecule to the amyloid-beta. Amyloid-beta is a molecule that builds up to form the plaques that are characteristic of Alzheimer’s.
So, let’s review! IGF1-R can help cell growth, but also encourages cellular death. Somehow, it can lead the switch to p75, which will result in more ceramide. More ceramide means more enzyme; more enzyme leads to more plaques. The mechanism for Alzheimer’s is more complicated, and becomes more so everyday.
The Practical Applications of Roundworms
One thing that caught my attention is how we discovered the possible aging pathway. It was first found in roundworms. Mutations in the gene age-1 extended the roundworms’ lifespans. This gene in the worms codes for the protein PI3K which is also found in humans. Then IGF1-R was implicated  as important to aging when mutations that inactivated the gene product in the daf-2 gene resulted in a doubling of the maximum lifespan of the worms. daf-2 codes for the insulin/IGF1 receptor. These genes and proteins are essentially the same as those found in humans. Further research into the human pathway confirmed that IGF1-R affects those pathways. It is logical to conclude that human lifespan, much like the roundworm’s, could be extended with mutations in the genes that code for IGF1-R and PI3K. However, we would not be able to see results right away like in the roundworm.
The fact that this information was obtained from a roundworm, something that is completely different from humans, is amazing. A simple organism can represent the “more highly evolved” organisms.  All cells are connected at their roots. So next time you hear about research on roundworms, seahorses, or yeast, and think money and resources are being wasted, consider our continuing quest for life. Research is a necessity if we want to find our own ambrosia.

Tough Questions with Science: All the small things.

This week’s assignment is to explain why the public should care. Specifically, why they should care about the article we read which covers Alzheimer’s disease, Parkinson’s disease, Lou Gehrig’s disease, and Cancer. This sort of question sets off my teacher training. When setting up a lesson, teachers are challenged to give a rational on why a student should care about that issue. But, I don’t think there is much purpose in arguing the importance of specific diseases without first arguing why should the public care about the neurochemistry behind a disease.
As I trudge further into my schooling I am often reminded of the phrase “Innocence is bliss”. As a youth I would find myself in the doctor’s office for some kind of minor issue. Usually these sessions would consist of a Q & A session followed by the prescribing of some drug. To me it almost seemed implied that this one drug was the best and only solution to solve my problem. This theory was put to the test when I was prescribed drugs for my acne, (which on its own I find ridiculous). At the time I didn’t even care enough to want to fix it. And, as if it had no consequence, I was quickly prescribed an oral drug. I was now putting medicine into my body to solve a problem that wasn’t really a problem. Here comes the interesting part. The positive effects on my acne were negligible, but after about 14 days on the drug I started experiencing horrific stomach pains. These pains left me unable to eat food for almost 24 hours, all just to “cure” a little acne. Looking back it seems quite foolish to introduce my one and only body to some biologically foreign chemical to solve something so small.
This experience leads me to add a bit to the previous phrase, now I would say “Innocence is bliss, yet the informed make the best decisions”. Now don’t get me wrong, I love the idea of having doctors. I am comforted by the fact that I am surrounded by many experts in the human body whose job it is to protect my health. Yet nobody knows the exact workings of the body, everyday there are new discoveries to how we function. In neurochemistry, the focus is on molecular pathways. A chemical pathway is sort of a domino effect, one molecule interacts with another which interacts with another….. and so on.

This domino effect has pros and cons to the medical world. Think of the last domino being the one that triggers the disease. This means that there are multiple places that medicine can intervene before that final domino is toppled. The same goes for molecular pathways. Many times a medicine is targeted at a specific point in the pathway to stop the disease from being triggered. Sadly, the con must come in. It is my regret to inform you this example is an oversimplification. Fixing our molecular pathways isn’t as easy as reaching in and removing a “domino”, Instead some sort of chemical reaction must take place in your body, usually by chemicals inside of pills. Many times the problem is that these chemicals don’t only react with the “trouble pathways” but they also react with “normal pathways” and this is where side effects come into play.
So picking the right molecule to target without disrupting other pathways can be a complicated thing. From what we know from research right now it isn’t easy/possible to determine the best way to handle a disease. So the next time a doctor hands you a pill, hopefully you will be more interested in finding out exactly what you are putting into your one and only body.

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