Cobbers on the Brain – Page 182 – Student Commentary on the Neurological Sciences

Diseases Inhibited by Pharmaceutical Inhibitors

Posted on October 24, 2012 by / 0 Comment

We live in a society where drugs (pharmaceuticals) dominate the medical world. Are you clinically depressed? Try Lexapro or Cymbalta. Is your cholesterol too high? Maybe Lipitor or Zocor will work for you. But don’t forget that drugs rarely work in the body without unwanted side effects! Why is this? How do pharmaceuticals work?
The majority of pharmaceuticals work by acting on receptors that are found on the surface of cells or enzymes (which regulate the rate of chemical reactions). The receptors have a high specificity for a particular substance, similar to a lock and key. If a molecule (the key) does not fit the receptor (the lock), it will not bind to the receptor. When a drug mimics the action of an endogenous compound, it is called an agonist. Essentially, the drug is encouraging a certain physiological response to transpire. For example, when Drug A binds a receptor, it may initiate a cascade of events to occur (called a signaling pathway) that leads to the synthesis Protein A. On the contrary, when a drug blocks a physiological response from occurring, it is called an antagonist or an inhibitor. By binding a receptor, it blocks an agonist of the receptor from binding and prevents that response from occurring. Continuing with the previous example: when Drug B binds the receptor, it prevents Drug A from binding and Protein A is not synthesized within the cell. The number of ways pharmaceuticals are used in the body is extraordinary and continues to grow each day.
The MAPK, or mitogen-activated protein kinase, pathway is recognized for its role in certain neurodegenerative diseases as well as certain cancers. Specifically, MAPK is identified for its role in Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS).
Scientists have determined that the MAPK pathway can induce neuronal apoptosis, or neuronal suicide. In Alzheimer’s disease, these pathways are upregulated and cause increased phosphorylation of certain proteins and increased expression of specific secretases that are known to induce AD. Similarly, these pathways are also affected in Parkinson’s disease. The activation of the MAPK, p38 and JNK pathways leads to the death of dopaminergic neurons in the brain, which characterizes the symptoms seen in patients with PD. Furthermore, the activation of the same pathways listed above may also prompt motor neuron death. As these motor neurons die, patients with ALS experience muscle atrophy, paralysis, and eventually die from the symptoms of the disease.
Unrelated to neurodegenerative diseases, but altogether related to diseases associated with the MAPK (and other listed) pathways are certain cancers, such as colon cancer. Scientists have focused on the ERK pathway in the cancer story. As certain proteins in the ERK pathway are phosphorylated, they encourage cell proliferation and growth as well as cancer cell migration.
You might be wondering why these pathways exist in the body if they can lead to such diseases, but as with most things, the danger comes in too MUCH activation of the pathway and not the existence of the pathway itself. In fact, the body NEEDS mechanisms that lead to the death of neurons. Similarly, it is vital that the body is able to grow and divide its cells to replenish dying ones.
However, as patients with these diseases do have pathways that function properly in a variety of ways, scientists are left to find ways to counter-act the problems specific to the disease. In the cases of AD, PD, ALS, and cancers, scientists look to inhibitors (or antagonists), drugs that suppress the physiological responses that are activated more often than they should be and cause excessive cell death or excessive cell growth. Ultimately, the goal of the research is to understand the mechanisms associated with the diseases and then to find ways to inhibit these mechanisms with accurate specificity. As always, negative side effects exist. Influencing a pathway, whether by activating or suppressing it, almost always leads to unwanted side effects. Nonetheless, at some point the symptoms of the disease override the unwanted side effects and this is when we rely on pharmaceuticals to “solve” all of our problems.

Health

Isolating Cell Signalling

Posted on October 24, 2012 by / 0 Comment

Our topic this week was the MAPK pathways. Quite simply, the MAPK pathways are a series of signalling molecules that carry messages from outside sources into the cell’s nucleus. This signal is carried from a receptor on the surface of the cell activating a signalling molecule. After that signalling molecule is activated, a signal cascade occurs. That is to say that a series of molecules whose purpose is to activate the next molecule in a chain of events are all activated. This carries the signal to the nucleus where it can have diverse effects from killing the cell to making the cell divide.
One apparent problem with these pathways is that the same molecule can occur in several pathways that lead to very dissimilar results. One can only imagine how disastrous it would be to promote cell death whenever the cell was supposed to divide and vice versa. Within our cells, however, there is little to no crosstalk between the pathways in spite of the same molecules being used. The reason for this is that in many cases, the signalling molecules are bound to scaffold proteins that keep them localized in one area and direct their signal to specific other molecules.
Although scaffold proteins do not play an active role in carrying the cell signal, by coordinating which molecules receive it next and where in the cell that signal goes next, they are one of the most important parts. They are analogous to the designer who decides how an assembly line is to be set up: although the designer doesn’t actually put any of the pieces together, they in effect decide what is going to be made through their organization.

Disease/Health/Spirituality

Quality of Life and End of Life Decisions

Posted on October 24, 2012 by / 2 Comments

In a discussion of neurodegenerative diseases, especially those that appear as late-onset varieties, a question arises about prolonging life and improving quality of life. Amyotrophic Lateral Sclerosis (ALS), or Lou Gehrig’s disease, is a neurodegenerative disease involving the loss of motor neurons to the point of muscle atrophy. This results in weakness and an eventual loss of mobility in the extremities and the rest of the body. In advanced and severe cases, loss of these neurons in the chest region can cause difficulties in breathing well on one’s own, if at all (See the ALS Association website for more information about ALS: http://www.alsa.org). Medical technology of the last century has enabled our society to sustain the life of individuals long past what would have been their natural time of death. While less invasive methods can drastically improve quality of life and mobility by artificially taking on the body’s natural capacity to sustain life, more invasive methods require patients to become dependent and much less in control of their own life. At this point, life support merely delays the inevitable and may draw out the most physically and emotionally painful part of a person’s life. How long should life support be used and when is it acceptable to end another person’s life by terminating life support?
The issue of implementation and removal of life sustaining measures has and will continue to be a source of conflict in our society. The legal, medical definition of death in all fifty states includes the loss of cardiopulmonary functioning and/or the irreversible end of all brain functioning, including the brain stem; others may personally see death when there is the loss of higher brain functioning, such as those in a permanent vegetative state, or a loss of personhood (Munson 2012). Let us examine again the case of a patient with ALS whose chest muscles no longer function in breathing. If this patient is put on a ventilator, modern medicine has effectively circumvented medical definition of death number one: the loss of cardiopulmonary functioning. Once this happens, we may no longer rely on the cut and dry, legal, biological definition of death. Intervening in this way has propelled us to a much more ethically problematic situation.
I would like to avoid the ethics question altogether by posing a different question entirely: What is the purpose of implementing life-sustaining measures? I see these measures as a means of buying time when there normally would be none. They allow the time needed to repair injury or to alleviate the body from the strain of sustaining itself when weak, such as when a patient with ALS develops pneumonia. Often, these measures may result in a loss of dignity, may lead to a permanent need for medical care, drain the emotional stamina of friends and family as well as financial resources, and prolong life at the expense of quality of life. When damage is irreparable, these measures can be wasteful, unnecessary, and not being used for the purposes which they were intended. Of course, many people will disagree with me. I, myself, may disagree should I find myself faced with a loved one at a turning point between natural death and medically sustained life.
When making decisions regarding the end of life, keeping the lines of communication open becomes extremely important. While variable, the average life span after diagnosis of ALS is two to five years (http://www.alsa.org/about-als/facts-you-should-know.html). With this in mind, any treatment for advanced cases of ALS could and should be viewed as end of life decisions. Beliefs and wishes regarding medical treatment should not only be made clear to loved ones, but be recorded in a living will or durable power of attorney for health care. This will ensure that in the event of an imminent medical emergency, one’s wishes will be followed.

Disease/Health

MAPK: the Wrong Way?

Posted on October 24, 2012 by / 0 Comment

The more I read about neurochemical systems and associated diseases and disorders, the more I get a sense for how vast the problems and intricacies for treatment are and how much work there is to be done. Signaling systems are intertwined with other processes, proteins have multiple functions, and often there are multiple contributing factors to a disease, making targeting for disease treatment extremely difficult. As with any problem, there are many possible routes to solve these health problems, and one of the first steps is determining which routes are most effective and feasible.
Fairly recently, studies have determined the mitogen-activated protein kinase (MAPK) system as an integral contributor to neurodegenerative diseases such as Alzheimer’s (AD), Parkinson’s (PD), and Amyotrophic lateral sclerosis (ALS). The general layout of the MAPK has several steps: typically, stimuli activates a MAP4 kinase enzyme, the MAP4 kinase phosphorylates a MAP3 kinase, which in turn phosphorylates a MAP2 kinase, which in turn phosphorylates a MAP kinase, resulting in phosphorylation of various proteins including transcription factors, all ending in a cellular response. In short, there is a phosphorylation cascade with at least three enzyme intermediates before a protein is affected that induces a cellular response. The three most common MAPK pathways are called ERK, p38, and JNK.

Six steps? Really?? Just cut to the chase and make it one, already.

Alzheimer’s disease is characterized by β-amyloid plaques in the brain and neurofibrillary tangles leading to neuronal apoptosis (cell death). The MAPK system plays a role in AD in a few different ways. Oxidative stress provides conditions for JNK and p38 to be activated, which then directly or indirectly activate the β- and γ-secretases, leading to β-amyloid plaques and neuronal apoptosis. Also, kinases such as JNK, p38, and ERK mediate the phosphorylation of the protein tau, which results in neurofibrillary tangles and apoptosis. Lastly, the JNK and p38 pathways have been shown to directly induce neuronal apoptosis, contributing to AD pathogenesis.
The main characteristic of Parkinson’s disease is a loss of dopaminergic neurons. As opposed to that in AD, the role of MAPK in PD is seemingly a secondary factor for its pathogenesis. The primary factors in the development of PD involve a defective gene encoding a defective protein which then activates MAPK signaling. One mechanism starts with a defective α-synuclein protein which aggregates, activating MAPK signaling, resulting in inflammation and dopamine neuron death. Another mechanism involves the p38 pathway inducing the expression of the protein Bax which, along with α-synuclein aggregates, decreases mitochondrial viability and leads to dopaminergic apoptosis. Still another mechanism involves the JNK and p38 pathways; the defective, mutant proteins parkin and DJ-1 can activate the JNK and p38 pathways leading to dopaminergic apoptosis.
Amyotrophic lateral sclerosis is characterized by a selective loss of motor neurons. The primary cause for this is thought to be a mutation in the SOD1 gene and protein, causing activation of the JNK and p38 signaling pathways. Overactivation of p38 has been shown to correlate with motor neuron degeneration, directly relating the p38 pathway with ALS development.
In describing the roles of MAPK pathways in these neurodegenerative disorders, I glossed over a fair number of intermediate steps. Many intermediate steps do exist with these mechanisms, however, which generally means that altering one component may result in many unwanted side effects down the cascade; a bigger system means it’s more complex and a bigger pain in the neck, unfortunately. This makes me skeptical as to whether the MAPK system would really be effective as a target for treatment; it is involved in so many different processes and often can lead to both positive and negative cell responses, including cell growth as well as death. Instead of MAPK inhibitors, I would suggest gene therapy for some of the mutations involved in these diseases, or perhaps an increase in mitochondrial protection. Forgive me for the football reference, but if a team is doing poorly, they either have to beef up the offense to attack the opponent more effectively or strengthen their defense to deter the opponent’s advances. In this case, I’m wary of going on the offensive to destroy the MAPK system, so better protection may be a safer and more effective route since a lack of protection from oxidative stress is a widespread factor in neuronal cell death. As always, more time and research will tell!

A Jared for the mitochondria would cure EVERYTHING.

Uncategorized

A Hopeful Future for Alzheimer's Patients?

Posted on October 24, 2012 by / 4 Comments

This week, I would like to talk to you about Alzheimer’s disease, a serious disease that has been brought up on this blog before just a couple weeks ago. When we talked about it before, we brought up the topic of diabetes and how the malfunctions of insulin in a diabetic patient could lead to Alzheimer’s disease. This week I will talk about another pathway scientists believe may be a factor in the development of Alzheimer’s disease.
This week, we focus in on the MAPK pathway. This pathway is responsible for several operations within our extremely complex bodies, but we will be concerned with its effects on cell proliferation, growth, and death. The pathway works through a series of activating different proteins within the cell and when each protein is activated, it can go off onto its own path and either promote cell growth or cell death.
As you know already, Alzheimer’s is signified by a buildup of Aβ plaques and neurofibrillary tangles within the brain. But what is believed to be the cause of these buildups? Well, scientists believe that activation of these MAPK pathways through oxidative stress (a risk factor for Alzheimer’s) eventually lead to a certain protein or enzyme which promotes neuron destruction which will lead to Alzheimer’s. As you can imagine, the actual process is a lot more complex, but we’ll keep it simple here.
When we compare the two paths for Alzheimer’s we have covered thus far, we must ask ourselves, “Is one of these a better option than the others when looking into curing this disease? And if so, where would our money be better spent?” Personally, I think the MAPK pathway is a more important area of research than the diabetes. To me, the rate of diabetes in the country can be significantly lowered just by changing your lifestyle, which really isn’t too hard. It just involves eating a little healthier and going outside a little more. If everyone in the nation did this alone, I feel it would cut our diabetes in half and thus lower their risk for developing Alzheimer’s disease, therefore not worth our time to research. The MAPK pathway, however, is not something we can change as easily. The oxidative stress comes from our lifestyle and how stressful it is, but it is not as easy to change that as it is in the diabetes case. The MAPK pathway also has implications in many other diseases such as Parkinson’s disease, ALS, or even cancer, so research in that area could also prove to be crucial in several other diseases. The only problem with working on the MAPK pathways brings up is the fact that they DO control so much in our body, it is not a single pathway we can just stop. It is a nasty maze that hurts your eyes looking at the entire pathway (see image), but perhaps more research in the area would help overcome that obstacle.

As you can see, the MAPK pathway proves to be crucial in the development of Alzheimer’s disease and personally, I think money should be invested into researching this area more in hopes of a brighter future.

Uncategorized

Lou Gehrig’s Disease: How close to a cure are we?

Posted on October 24, 2012 by / 1 Comment

Prior to 1939, Lou Gehrig was on top of the world. He was coming off several great seasons leading the New York Yankees to World Series titles in 1936, 1937, and 1938. He was so good Time magazine wrote an article in 1936 described Lou Gehrig as “the games number 1 batsman” and someone who “takes boyish pride in banging a baseball as far and running around the bases as quickly, as possible”. However, Lou Gehrig’s career came to an abrupt end by the end of the 1939 season due to a sudden decrease in motor function. Lou Gehrig went to the Mayo Clinic in 1939 where he was diagnosed with amyotrophic lateral sclerosis (ALS), commonly called “Lou Gehrig’s disease” today.²
Today, 73 years after Lou Gehrig was diagnosed, the cause of ALS is still not completely understood. However, some progress is being made. In the research paper our class examined, scientists have identified a mutated gene encoding for an enzyme called SOD1. SOD1 is an enzyme responsible for stopping highly reactive molecules called free radicals from damaging important components in cells. However, in ALS this defective SOD1 enzyme doesn’t stop the free radicals. As a result the body initiates a biological pathway called the p38/MAPK pathway to kill the cell. This leads to the death of many types of cells such as the motor neurons causing ALS.
To better understand the effect of free radicals and the SOD1 enzymes in cells I have thought up a metaphor which may help. Imagine bringing your kids to a toy store. Now imagine your kids had the worst sugar and caffeine rush you have ever seen while you were in the toy store. They would probably be running all over the store, trying to play with every toy in sight and it is up to you to stop them from damaging anything. In essence, this is what is happening in our bodies. The SOD1 enzyme (you) are trying to control the free radicals (kids) from making a mess. Now imagine letting your sugar and caffeine crazed kids, and all other sugar and caffeine crazed kids in the store, wander around unsupervised. This would probably result in a scene similar to one found in the movie Cheaper by the Dozen and if it got too bad the store might have to close down to clean up. This is like what happens in the motor neurons in some ALS patients.
So what can be done to stop ALS? Is stopping the SOD1 gene from mutating the key to stopping motor neuron death in ALS? Unfortunately, it does not seem SOD1 is the key to stopping ALS. Mutation of the SOD1 gene is only responsible for approximately 10% of the ALS cases. The cause of ALS in the other 90% of cases is still unknown. Therefore, to successfully cure ALS additionally research is needed. This means for people like Lou Gehrig there is hope that one day we will cure amyotrophic lateral sclerosis, but it appears that this day may still be in the distant future.
Sources:
1) bleacherreport.com
2) http://en.wikipedia.org/wiki/Lou_Gehrig

Disease

A Light of Hope in Neurodegenerative Diseases

Posted on October 23, 2012 by / 0 Comment

Mitogen-activated protein kinase (MAPK) pathway is one of the most important cell signaling pathways in human brain. Many crucial cellular activities are controlled by the MAPK pathway including cell proliferation, differentiation, and apoptosis. Therefore, it is normally tightly regulated. In the paper we read for this week, the researchers discussed the pathological roles of different kinds of MAPK pathways (ERK, JNK and p38) play in human diseases, including the Alzheimer’s, Parkinson’s, and Amyotrophic lateral sclerosis (ALS). And hopefully by researching into these neurodegenerative diseases, we will be able to eventually find out treatments in order to provide these patients a better quality of life. While oxidative stress is commonly thought to be related to cell death that is associated with both Alzheimer’s and Parkinson’s disease, the risk factors for mutations that are linked to ALS still remain unclear and further investigations are required.
In Alzheimer’s, the reactive oxygen species such as hydroxyl radical, superoxide anion, and hydrogen peroxide cause the oxidative stress and trigger the JNK and p38 signaling pathways. And the activations of these two pathways often lead to cell apoptosis and the formations of senile plaques and neurofibrillary tangles which are generally found in the brains of Alzheimer’s patients and believed to contribute to the disease itself. Although there are no treatments found for Alzheimer’s so far, the researchers are looking into inhibiting the MAPK pathways mentioned above in order to slow the progression of the disease.
Like Alzheimer’s, Parkinson’s disease is another prevalent neurodegenerative disease related to oxidative stress. It is characterized by the accumulation of the Lewy bodies in the brain causing an increasing loss of dopaminergic neurons, and promoting inflammations by activating p38, ERK and JNK pathways. Mutations in multiple genes have been associated with Parkinson’s disease. Although various studies suggest that MAPK pathways contribute to the neuroinflammatory responses and cell apoptosis in Parkinson’s disease, due to its complexity of the pathway, it is very difficult to be diagnosed and cured. An alternative treatment that has been performed on the Parkinson’s patients is called the deep brain stimulation, although it does not cure the disease, it could effectively help the patients manage some of its symptoms.
Amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease is caused by the mutation of the gene which encodes for SOD 1 (Cu/Zn superoxide dismutase) which ultimately results in the death of motor neurons. Although it is unclear how mutations of the SOD 1 gene results in ALS, the researchers believe that the activation of p38 MAPK pathway in motor neurons is important for ALS progression.
Many researches have been done on the neurodegenerative diseases introduced above in order to not only understand but also treat them. Although tons of money and efforts have been put into the studies of the MAPK pathways, due to their complexity, we still have a lot to learn about them. I am certain that life must be very difficult for patients with any of the diseases mentioned in this article, and no one will be able to understand exactly how difficult it is until one gets the disease. Therefore, I believe no matter how difficult to single out one pathway and how complex each pathway is, we should put in more and more resources into researches of these diseases. And eventually, we will be able to cure these patients.

Disease/Health/Hot topics

Research that Gives You the Shakes! Or Cures Them!

Posted on October 23, 2012 by / 0 Comment

If you could prevent Alzheimer’s, Parkinson’s, or Lou Gehrig’s disease, would you? More than likely; with the current research carried out in control of the MAPK (mitogen-activated protein kinases) neurochemical pathway in your brain, these and other diseases can be examined and eventually treated directly. These diseases are all linked through different pathways that the same MAPK works in your brain. It is important to note that when it comes to the brain, the inner workings are very complicated, interconnected, and overlap with one another even with the same chemicals like MAPK.
The belief in Alzheimer’s disease in relation to MAPK is that brain cells are being told to die off faster than in a healthy adult. Oxidative stress tells the brain to have its cells self-destruct. From stress in the brain, a cascade of activities occurs involving MAPK, ultimately leading down to cells telling them to self-destruct. Loss of brain cells from this pathway has contributed to Alzheimer’s disease significantly with the obvious loss of areas of the brain in memory. Current research has been looking into blockage of the MAPK pathway that is telling these cells to die off, and lead to Alzheimer’s.
Parkinson’s disease is another detrimental one that is due to loss of control in motor function in the brain. MAPK pathways lead to inflammation of the brain and its cells that lead to death of the brain cells. In Parkinson’s patients, areas of the brain that regulate motor control are experiencing cell death from inflammation. The precise pathway for control is not yet known, but has been researched extensively, especially through the Michael J. Fox Foundation for Parkinson’s disease Research. Understanding of this pathway will help in understanding of how to regulate it and stop the progression of Parkinson’s and even help in early detection of its early symptoms.
Lastly, Lou Gehrig’s disease (amyotrophic lateral sclerosis) is due to mutated genes that lend ultimately to cell death. The areas affected are mainly motor control areas as well. The start is due to mutated genes that start signaling the MAPK pathways that will give rise to motor neuron death. The outcome becomes muscle loss, paralysis, and eventually death. Prevention of Lou Gehrig’s disease could be best understood through drugs that could stop different particular steps in the MAPK pathways.
These diseases are very detrimental to those that they affect, and that they may all be linked through very closely related paths is of extreme significance. Research on any of these diseases may affect each other; advances in one area can be important or influence treatment methods in another area. With further research, we can start to see what drugs will halt cell self-destruction and inflammation that lead to these diseases, and which ones will have the fewest complicating side effects in the brain. As with most treatments, one area that is fixed can lead to complications in other areas. The more we can understand MAPK and how it works in the complicated thing we call the brain, the more we can prevent and treat these diseases.
Photo courtesy of: http://feww.wordpress.com/tag/pesticides/

Community/Disease/Health/Hot topics/Uncategorized

Vicodin, Morphine, Heroine, Oh My!

Posted on October 18, 2012 by / 0 Comment

In society today, doctors give out pain medication in the class of opioids like they are candy. For things from a tooth ache to surgery, the range of ailments which one can be prescribed opioids for is rather large. Opioids include codeine, hydrocodone (vicodin), oxycodone, and morphine. You may be thinking: why is this a problem? Isn’t it a good thing that doctors are helping people manage pain? That answer is rather complicated…
First, opioids can be highly addictive. The addictive factors of opioids means that it is supposed to be regulated and there are steps doctors are supposed to take when prescribing as well as follow-up steps after prescribing. But speaking from experience, it is not very hard to be prescribed these drugs. Doctors giving out addictive drugs to people who are likely not in the need of them can cause many societal problems such as prescription pills being sold on the street.
Second, while the drugs I listed above are the opioids regulated medicinally, heroine is also classified as an opioid. Part of the problem with these drugs is people do not understand what they actually do. Opioids work so well in managing pain because they block pain receptors in the spinal cord. This means that pain signaling cannot reach the brain to alert it of the pain. The difference in the drugs from codeine to heroine is the amount of the signal being blocked.
Most people would not try heroine because of its addictive and harmful effects on the body. But then the question becomes if you wouldn’t take one form of opioid, why would you take any?
Messing with signal pathways to the brain can have many adverse side effects. Are doctors doing their due dillagence in perscribing such serious drugs for something that a simple over the counter pain medication might help with? So next time you have the option of taking even the smallest dose of an opioid, even if it is prescribed by a doctor, ask yourself, are you really in enough pain to jeopardize the risks associated with opioids?

Health/Hot topics

Opioids, a Pain Killer? Or Cause of Pain?

Posted on October 15, 2012 by / 2 Comments

Pain — A spasm in your back, a toothache, recovering from a fracture or dislocation, a degree of discomfort following surgery; it comes in many forms, but usually gets treated with some form of pain pill from Tylenol to hydrocodone (Vicodin).

The reason many of the drugs that help relieve pain are effective is because of their ability to target the process of pain signaling in the body. However, a specific group of these painkillers, known as opioids, have a serious risk of dependence and addiction and are frequently abused.

Why is this?

Opioids, many people may be familiar with their common names; they include but are not limited to: Morphine, codeine, hydrocodone, and oxycodone. These opioids are commonly prescribed by physicians for treatment of either chronic pain, or a post surgery treatment to take the edge off. While they may have varying side effects for different people who use them, opioids are very effective in targeting and almost completely numbing the human body’s ability pain signaling pathway. That would help explain why after their wisdom teeth get pulled most people are clamoring for some Vicodin.

Opioids do their job of stopping pain in several different ways, but one that really sticks out is the ability to slow, and even stop the process known as nociception. This process is responsible for taking in signals from nerves in the body and transferring them to the brain to be “felt” as pain. When these signals are on their way to the brain, nociception is responsible for the release of many neurotransmitters, and Substance P. When someone thinks about Substance P, they should just think of P for pain, because its role in the body is to make the body’s sensitivity to the pain signal being transferred very strong. So, after its release the neurons really start to fire and the signal gets shot up into the brain with some fervor. It is important for opioids to inhibit the release of Substance P. However, is it a good thing to stop the body from feeling pain?

Why not?

It was brought up in a class discussion, but why can’t we simply take opioids and not have to feel pain? There is one huge drawback to opioids, they are have a high rate of addiction and physical dependence. Something that is able to affect the brain in such a drastic manner can cause many harmful problems if abused. Maybe people who have been affected by a heroin addiction will attest to that. Heroin is also known as morphine diacetate, is a synthetically produced opioid that is highly addictive and known for incredible negative withdrawal symptoms, including insomnia, vomiting, and involuntary spasms of the body. Also to note, these symptoms can begin to show a presence as early as six hours after taking the drug.

Heroin is just another opioid, which before it became widely abused was just another attempt at altering morphine to make it more effective. The stories of addiction to heroin are very similar to most who abuse any opioid; almost impossible to overcome without treatment, because of the severe emotional and physical distress caused to the body.
So it is important to answer the question do opioids cause more pain than they relieve?