Community/Disease/Health/Hot topics

Obesity: Is it our fault?

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This week we discussed an article that claims obesity is a brain disease and that over-nutritious diets change our brain chemistry.  In contrast the to “eat less, exercise more” theory, these authors implicate countless mechanisms in the brain as the source of obesity.  Mainly, the over-nutrition during development, such as high fat and high carbohydrate diets
Our brain should be able to tell us when we are hungry, “go gather food”, and when we are full, “stop eating”, but in the obese these signaling pathways are modulated and do not work properly.  Leptin and insulin are the main signaling molecules in these pathways.  However, there is commonly insulin resistance and down regulation of leptin receptors in obese patients brains.  The picture below is an image of two mice, the one on the left does not have leptin receptors and is unable to tell when it is full so it just keeps eating, while the one on the right is a healthy mouse.

Obesity is really a downward spiral, once the balance is disrupted, it is hard and nearly immposible to make right.
During development, if exposed to over-nutritious or high caloric diets energy and food intake control will be impaired.  This will lead to overnutrition and weight gain, like seen in the mouse above.  When we eat, our bodies process the food and produce insulin, but because of the over nutrition the body was already exposed to it is possible that the body is now insulin resistant.  This insulin resistance directly impairs our ability to send the signal to stop eating.  In addition, over nutrition leads to weight and adipose (fat tissue) gain.  Adipose tissues produce a molecule called leptin, which is also responsible for sending a signal to stop eating.  But because of the large amount of adipose tissue on obese subjects, leptin resistance occurs.  Without either of these signals, food intake continues, and the spiral begins.

In addition to the signal molecules excess nutrition can structurally change our brains.  For one it is possible to alter the structure of the protective barrier to the brain, or the blood brain barrier.  If this structure is modulated our brains can quite literally become leaky, and let molecule that aren’t supposed to be in our brain, into our brain.  These structural changes can then lead to cognitive deficits.   So not only is one’s physicality altered, but cognition is as well.
Obesity is already a problem in our country, and childhood obesity is on the rise.  It is scary to think that as our population ages, and is exposed to the bad nutrition that is so common in so many households, not only is our population going to be obese, but dumb as well.
Maybe that sounds like a harsh thing to say, but we need to realize that there is a serious epidemic on the rise, and we need to step up and stop it.
Reading this article I kept thinking about the movie WALL-E.   We are going to destroy our planet, and our population, all in one fell swoop.

The solution starts at the beginning.  Proper diet during development is key, and we better start now before its too late, otherwise our entire population will be in that downward spiral.

Disease/Health

Knowledge is Power: power for muscles affected by ALS

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Amyotrophic lateral sclerosis (ALS), a disease made famous by Lou Gehrig, is the most common adult-onset motor neuron disease.  Characterized by upper and lower neuron degeneration, ALS patients commonly present with spasticity and atrophy of the limbs since the neurons responsible for voluntary movement and muscle power are compromised.
The most common form of ALS is the sporadic form, making up 90 percent of patients, while the familial form only makes up 10 percent and is associated with several genes.  The cause of ALS is still greatly undefined, but recent research has shown that calcium disturbances, endoplasmic reticulum stress, and mitochondrial stress may be implicated in the disease pathology.
Under normal conditions calcium levels are low inside our cells, and is stored in our endoplasmic reticulum (ER) and mitochondria.  However, calcium is responsible for proper cell signaling, and signal transduction.  Making it very important in nerve cells.
The ER is responsible for proper protein synthesis and folding.  If proteins are misfolded they become dysfunctional and accumulate in the ER, causing ER stress.  Protein synthesis starts at the ribosome; after the protein chain is put together by the ribosome it enters the lumen of the ER where proteins called chaperon proteins are able to guide the folding of the new protein.  Chaperon proteins can also try and refold already misfolded proteins.  Unfortunately, many chaperon proteins are negatively affected by calcium.
This is where researchers suggest ALS comes into the picture. Many wonder why only motor neurons are targeted in ALS, and this theory may answer the question.  Motor neurons are more susceptible to calcium influx because they have more calcium permeable channels.  Based on this new research the greater levels of calcium in these motor neurons negatively impact the proteins responsible for proper protein folding.  Since proteins aren’t being folded properly, there is increased stress in the ER.
There are a number of proteins that are supposed to alleviate this stress, these proteins decrease regular protein synthesis and increase the level of proteins that can relieve this stress.  But in ALS patients there is so much stress that extensive activation of this process eventually triggers apoptosis, or cell death.

So what can we actually do with this information?
This new research will serve as a way to develop pharmacological treatments.  One way, suggested by the researchers, was to promote the proteins that are supposed to alleviate ER stress, but without inducing cell apoptosis.  There are, however, many gaps in our knowledge about ALS and this mechanism, so even though we have potential, a lot has yet to be seen.
Unfortunatley, ALS is a fairly rapidly progressing disease, and the disease will typically take the patients life within 2 to 5 years after diagnosis.  The fact that the disease only attacks motor neurons, not cognitive neurons like Alzheimer’s, makes the disease that much harder to watch.
We need to expand on this information about ALS, because at the moment, ALS seems to attack anyone, and we here time and time again that knowledge is power.

Health

Discussion on Concussion

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Many people associate concussions with football and boxing, but the reality is, concussions affect between 1.6 to 3.8 million athletes yearly in a variety of contact sports, including hockey, soccer, basketball and the list goes on.
Concussion, or mild traumatic brain injury (mTBI), is biomechanically induced, meaning it’s causing by a mechanical injury (i.e. a blow to the head).  The acceleration and deceleration forces initiate a number of events, beginning with the disruption of neuronal cell membranes.  This disruption to the membrane quite literally makes the cells leaky.
I don’t know about you but a leaky brain doesn’t seem like a very good thing.
These leaky membranes allow for the flux of ions into and out of the cell.  This disrupts cell signal transduction, increasing oxidative stress, axonal swelling, and potentially the severing of axons.

Now, none of those symptoms are good things obviously.  They negatively affect memory and cognition in the short term, and if the injury isn’t given enough time to heal its effects can become permanent.  This is why there is so much discussion about concussion.
Parents are concerned about the physicality of contact sports.  No one wants to be injured, and no one wants their injury to affect their ability to think and process information.  That’s why concussions can be so scary, to parents and the athletes alike.
Unfortunately, no two concussions are alike.  There is a series of guidelines for diagnosing concussions, but when athletes are allowed to return to play is incredibly variable.  This is where athletes face the majority of stress and pressure from coaches.  Its seems like the question, “when can you play again?” is always being asked.  But returning to play too early can be just as traumatic as the concussion itself.  If an athlete returns to play before their injury is fully healed it can increase their chance of getting a second injury and increase the chance of getting a worse injury.
I feel like we have tried so hard to change the games in order to lessen the number of concussions athletes’ experience.  But all of the protective headwear and new rules, have they really made a difference? Or have they just allowed for greater contact?
Concussion has short term and long term consequences on the brain, and repeat injury can cause a number of other deficits, and I think to truly decrease the number of concussions we see, athletes coaches and parents alike need to understand and communicate the dangers of playing with a concussion and the increased risk of a second injury.
To view a video about concussions, and how they occur click here.

Disease/Health/Hot topics

Marijuana: the real story behind endocannabinoids

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Everyone in the United States seems to have this stereotypically view of marijuana.  When we hear about it, we think of all the pop culture references from music by rap singers, TV shows like Weeds, and movies like Pineapple Express, but what we don’t think about is why it was used in the first place.
The use of marijuana for medicinal purposes predates recorded history, and the earliest record of its use for medicine was in 1500 BC by the Chinese.  Even in today’s society marijuana can be prescribed for treatment of chronic pain, seizures, muscle spasms causes by MS, nausea caused by chemotherapy, poor appetite, glaucoma, cluster headaches, the list goes on.
And the reason it works? THC (tetrahydrocannabinol)

Our response to marijuana is based on the fact that our body produces molecules called endocannabinoids, which are structurally similar to THC.  The two main endocannabinoids we produce are called Anandamide (AEA) and 2-arachidonoylgylcerol (2-AG).  After these molecues are synthesized, they enter the extracellular space and bind to CB1 and CB2 (cannabinoid) receptors initiating the response.  THC acts on these receptors in the same way.  After the activation of these receptors a number of pathways are turned on or altered, many of which affect signal transduction in the brain, and of course the common side affect of marijuana, appetite.
Unfortunately, THC does have some downfalls, like it’s psychotropic effects, which contribute to marijuana’s addictive qualities.  However, researchers are looking for ways to synthesize an alternative to THC, because of its numerous benefits.
A potential alternative, could alleviate some of the social consequences of using and prescribing medicinal marijuana, but it is important to think about the pharmacological characteristics of taking THC in the form of marijuana.
Marijuana can be taken as a liquid extract, eaten, vaporized, or the most common, smoked.  Now, smoking marijuana has its benefits over the others, because in this form THC enters the body the most rapidly.  Pharmacologically this is important because the therapeutic qualities become apparent much more quickly.  For example, if one feels a cluster headache coming on, and they use their medicinal marijuana, they can essentially stop the headache before it starts.  Whereas, if they were using a THC alternative in the form of a pill, the results may not be quick enough to provide the best therapy.
So, before you pick a side of the legalization of medicinal marijuana, really look at the benefits that were listed here, and weigh the very few consequences, because they are greatly outweighed by the therapeutic properties that THC provides.

Disease/Health

Iron-Chelator? I thought the super hero was Ironman…

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A few weeks ago we discussed the new idea that iron levels in the brain potentially have implications in the development of Parkinson’s disease.  As a progressive neurodegenerative disease, affecting about 2% of the elderly population, Parkinson’s disease (PD) is typically associated with tremors, rigidity, and instability, and also cognitive deficits.
Biologically, these symptoms are caused by the progressive loss of dopaminergic neurons (neurons that release dopamine) and the formation of Lewy bodies (abnormal protein clumps).  However PD has also been shown to be associated with oxidative stress and metal accumulation, this is where iron comes into the picture.
In general iron accumulates in the brain with age and is regulated by a number of proteins, many of which also regulate the amount of iron allowed in the blood stream.  Iron is essential for many processes such as DNA synthesis, neurotransmission, oxygen transport, and metabolism.  In regards to Parkinson’s, an imbalance of iron in the brain can lead to greater levels of free radicals leading to oxidative damage of DNA and lipids, as well as proteins like alpha-synuclein.  If there is oxidative damage to alpha-synuclein it will misfold and can lead to protein aggregates called lewy bodies.
There is no cure for Parkinson’s disease, we can only treat the symptoms.  Common treatments include, Levodopa for motor dysfunction, Dopamine agonists to promote dopaminergic signaling, and physical therapy to improve mobility and gain balance, and potentially we will be able to treat the symptoms associated with iron now.
Due to this new evidence, a new form of treatment for Parkinson’s has been identified.  Iron chelators have the ability to lower iron availability; this is done by binding to free iron.  The decrease in free iron will decrease instances of misfolding of protein as well as lower concentrations of free radicals, and overall keep iron levels in the brain in check.
Some research has shown that ingesting foods with antioxidant capabilities could also be a therapeutic treatment for PD.  Green tea for instance contains catechins, specifically one called Epigallocatechin gallate, or EGCG for short, which have the ability to chelate iron but also have important neuroprotective action and potentially anticancer agents.   Now, I am not a tea drinker, but there are plenty of other foods that contain catechins such as apples, blackberries, grapes, chocolate, and red wine.  (For more interesting facts about catechins as well as the foods that contain them follow this link, Catechin Facts)
So what does this mean for the average person? Well, it is important to have balance.  That’s what it comes down to most of the time when talking about the brain.  We don’t want too much and we don’t want too little.  It obviously wouldn’t be a good idea to go on a low iron diet, iron is an essential nutrient, but at the same time too much iron isn’t the greatest either.
Although there is no cure for Parkinson’s at this time, research on iron mechanisms in the brain has identified promising new treatments for the disease, and hopefully a cure is around the corner.
 
 

Disease/Health

Food or Thought: not food for thought

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It’s not a new idea that the majority of the food people eat here in the US is unhealthy; we are a nation of convenience.  Fast food, ready to prepare meals, and boxed items are staples in many households, mine included.  Because of the quality of food many of us eat, doctors are concerned with the rise of obesity, high blood pressure, high cholesterol, but it is new idea that your diet may also affect your chances of developing Alzheimer’s disease (AD).
If you are not familiar with Alzheimer’s, it is a neurological disorder characterized by memory loss and dementia, due to neurofibrillary tangles and amyloid plaques.  While environmental and genetic factors are known to cause AD, recent studies have shown having type 2 diabetes is also a significant risk factor for Alzheimer’s.  While not everyone with type 2 diabetes is overweight, lack of physical activity and weight seem to be contributing factors. The link between type 2 diabetes and AD is thought to come from the insulin resistance built up in the brain, characteristic of type 2 diabetes.  This insulin resistance greatly affects the transportation and effects of insulin in the brain.  Many of the problems characteristic of AD can be attributed to a lack of insulin, since insulin has a role in neurotransmitter release as well as learning and memory.
So if we know our diet can affect our chances of developing type 2 diabetes, and type 2 diabetes can affect our chances of developing Alzheimer’s, will you change your diet?
You may say yes now, but how many of us will actually go and start eating differently?
At what point do we say enough is enough, and actually make a change?
Its come to a point where we now have to choose between out favorite foods, and our cognitive abilities.  Food or Thought, not food for thought.
I feel like there has to come a point where we finally say, “hey, this food is bad for me I probably shouldn’t eat it” but then actually listen to ourselves.  So much of the time we eat what is poor for our health anyway.
This could potentially become a huge problem in our nation.  Obesity is rising, type 2 diabetes is rising, so theoretically Alzheimer’s will begin to rise. In addition to the actually prevalence rising, the age of onset is decreasing.  Potentially people in their thirty’s could start to develop Alzheimers! What does that mean for our health care system, our work force, and the overall health of our population?  Well, I can tell you it wouldn’t mean good things.
We need to wake up and realize that our diet is having major effects on our living conditions.  Essentially, our lifestyle is negatively affecting our lives.
If there is one thing that I have learned in our Neurochemistry class, it’s that there is a very fine line between too much and too little neurotransmitters, like dopamine and norepinephrine.  And when our neurochemistry is out of balance some very bad things begin to happen.  We should be doing everything we can to take care of our bodies, and keep these neurotransmitters in balance; this would help better ensure our neurological health and well-being.
Is this new information about a link to Alzheimer’s going to change your diet? I’ll be honest, it probably won’t change mine, and that is not something I am proud of.
Click here to view our public service announcement about this topic.

Disease/Health

Mystery and Motivation

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Lithium has been used to treat bipolar disorder for nearly half a century now, even though lithium’s therapeutic mechanism has remained an enigma.  No one is absolutely sure how lithium is working with bipolar, let alone how bipolar disorder is developed.  However, new evidence has come to light about lithium’s mechanisms, specifically on the enzyme Glycogen synthase kinase 3 (GSK-3), that may open the door to understanding this disease and why lithium works so well.
GSK-3 has also been shown to play roles in a number of diseases other than bipolar, such as Alzheimer’s, Type II diabetes, and a few forms of cancer.   So this research involving GSK-3 could provide many therapeutic treatments.
Lithium, a monovalent ion with a positive charge, has now been shown to have neuroprotective and neurotrophic, or cell survival, effects.  This is believed to stem from the direct inhibition of GSK-3, along with a few other mechanisms.
When GSK-3 is active it is central to a number of signaling pathways, including cellular proliferation, inflammation, and apoptosis or cell death.  GSK-3 activity is regulated by a wide variety of kinases, one in particular is Akt.  Lithium essentially activates Akt by allowing it to complex with other proteins and be phosphorylated.  Active Akt will then go on to inhibit GSK-3 by dephosphorylating it.  Inhibition of GSK-3 down regulates the activity of the proliferation, inflammation and apoptotic pathways.  Also, by inactivating GSK-3, a number of genes that promote neuroprotection are able to be transcribed, since they are inhibited by active GSK-3.
This would be considered a good thing in regards to neurodegenerative disorders like Alzheimer’s because this would prevent the continuation of neuronal cell death, hence the neuroprotective and neurotrophic effects of lithium.
Based on this research Lithium can have potential therapeutic effects for a number of diseases, such as bipolar, stroke, Huntington’s disease, Alzheimer’s disease, Parkinson’s disease, Retinal degeneration, Fragile X syndrome, Amyotrophic lateral sclerosis (ALS), Multiple sclerosis (MS), spinal cord injuries, HIV infections, Prion disease, alcohol-induced neurodegeneration, Down syndrome, Tardive dyskinesia, and Schizophrenia, and I’m sure the list will grow as more research is done.  Lithium has been shown in a variety of animal models to treat, or at least slow the progression of many of these diseases.  This extensive list should be a great motivator to continue research on lithium’s mechanism and its therapeutic properties.
But is lithium too good to be true?
It is too early to tell.  There needs to be many more animal models for some of these diseases being treated with lithium before we can really see what kind of effect lithium will have in humans.  Even though lithium has been used for the last 60 years to treat Bipolar disorder, its true effects on healthy humans aren’t entirely known, and there is a lot of research left to be done.
However, it is exciting to think that a therapy has been sitting under our noses for half a century, and now it may make its entrance as an invaluable part of many treatment plans.   There is still a lot of the mystery yet to uncover, but hopefully it will work as a motivation.
 
More information on Lithium (how it is prescribed now and it’s side effects):
http://www.webmd.com/vitamins-supplements/ingredientmono-1065-LITHIUM.aspx?activeIngredientId=1065&activeIngredientName=LITHIUM

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Capstone: not what I thought, but what I wanted…

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Before taking my capstone course at Concordia, I definitely had a bias towards any course that carried the “capstone” tag. The sound of the word itself had always led me to believe that any course with this title was one that was designed to be extremely rigorous and in a way the “final mountain” to climb in order to graduate. But as I conclude my semester long neurochemistry capstone course, I have realized that it is the exact opposite of what I led myself to believe. Not in the sense that the class was easy by any means but more so in the sense that this was a class that was set up in a way that was completely foreign to me.
 
Instead of learning in the classical classroom setting where the professor lectures and the students take notes only to be followed by quizzes and tests in the future, we were really challenged as students to learn in a new way. All of a sudden tests and assignments didn’t matter as much in this class. We still had them, but not in the general sense that we become so accustomed to in our first 3 years of college. We found ourselves being graded on critically thinking and real-world problem solving. We sought ways to create targets for new drugs and diagnose diseases in a different manner, things that seemed like they had real world application in the world right now. We learned how to take a problem, think critically, and then communicate results and engage in dialogue about the issue. I think back to our Wednesday’s where each of us had a specific topic that all pertained to one large problem or topic that we were discussing about as a class. Explaining our topics to fellow classmates caused us to engage in discussion about our topics, the problem as a whole, and how to solve the problem.
 
One of the things that I am most happy that we did was the Friday discussion time as well as the blogging. This forced us to take concepts that we learned in class that were extremely scientific and deep and take them and communicate them to a general audience while still explaining the science and getting a point across. The discussions led us to apply a topic to not just the scientific or medical community, but a wide range of other communities as well. This class in short was the first class that I think I have ever taken that is a science class but at the same time explains science in terms of society and politics and everything else at the same time. This is why it was such a different way to learn, because it put science in a completely different light than we were used to.
 
So as I have said before, I am extremely pleased with my capstone experience. It was nothing like I had thought it was going to be and everything that I thought it should be. It had me take all of the knowledge and skills that I have gained while at Concordia and put them into the area of study that I am most interested in while at the same time challenging me to apply these skills to the real world. It is safe to say that my view of what a capstone course is has completely changed. More than doing some big project or paper, this class has showed me what it is like to apply what I know to society in order to make a difference. After all, shouldn’t that be what a capstone course is all about? I think this type of class is what seniors need as we all prepare to graduate and go out into this world on our own.

Disease/Health

The odd truths about autism and its diagnosis

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It’s hard to find a disorder in this world that is more tricky than autism. Unlike the having to flu for example, it has become much more trivial as to determining if someone has autism or not. Many people are aware of what autism is, but unaware of how it is diagnosed and how we can maybe treat it.
 
There are many odd sociological trends as to the diagnosis of autism that don’t really make sense in the realm of how diseases are generally diagnosed these days. Long story short, much of what is used in the diagnosis of autism is based on largely subjective criteria in my opinion instead of the hard scientific facts that we have become accustomed to. For example children with parents who are upper-middle class and higher are more generally diagnosed with autism. Now how can this be? Well it’s no secret that these families are able to afford top quality medical care as well as multiple opinions. Social status aside, I think that the real problem lies within the criteria that have been set out in diagnosing this disorder.
 
These criteria are fairly numerous as you can see below.

This figure just gives an example of some of the criteria that are used in determining if someone has autism. Granted this from the DSM-IV and not the DSM-V, it still gives you an idea of the things that medical professionals look for. Like I said before, these criteria are so subjective. Once doctor could pronounce a child to not have autism, but the next one could pronounce the same child to have autism. That is my problem with this system. Also, medical professionals are trying to diagnose children at a younger and younger age all the time. I think that it is unfair to judge a 2 year old child on “failure to develop peer relationships” among other criteria. I mean what are you supposed to do, watch the kid at daycare and see if he plays with building blocks effectively with the other kids? And how do you assess children who just have a naturally quiet personality? I can’t help but think that some perfectly healthy yet quiet kids would be unfairly diagnosed as well. I think that this is at least in part the reason why we are seeing such an increase in autism diagnosis in the past decade.
 
Now that I have vented a few of my opinions about the system I can explain some of the science that is behind autism. Limited science has shown that autism is linked to CNV’s in a person’s genome. These are copy number variants, which are basically just alterations to a few different genes in the genome. These alterations of genes make cell adhesion very difficult and in turn make it difficult to form synapses and achieve synaptic plasticity. Unfortunately there aren’t really any drugs that can change a persons’ genome back to a healthy one. With that being said treatment options with autism revolve largely around therapy, as no real medications have been tested with great efficacy. I think that this paper has made me more aware of autism above anything else. It has helped me to form the opinion that we definitely need to conduct more research to learn more about this disorder, as it seems that we don’t have too much to go on at this point when compared to other disorders.

Disease/Health

Is fat our fault??

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America is fat. Fat is America. You can say it whichever way you choose but the message is still the same, we are the most obese country in the world. But is it our fault? We recently read a paper that explored the possibility of obesity being a brain disorder rather that a disorder that is caused by our diets and overeating. Shockingly there is a significant amount of evidence that would lead us to believe that obesity is indeed a brain disorder. However, before you go out and buy yourself a Big Mac because “it’s not my fault that I’m fat” you should listen a little closer.

This article made the case that obesity as a disease starts for somebody while they are in the womb of their mother. They argued that the chances of a child having the brain disease of obesity is predicated on the diet of the mother. When a mother eats a very unhealthy diet, then those nutrients are shared with the child in her womb. The child becomes accustomed to the high level of fat in his or her diet and when they are born, their brain is already programmed into the diet that their mother had. The researchers also conducted a study in mice that supported their argument that offspring exhibit the dietary trends of their mother. This is some supporting evidence that obesity could in fact be a brain disease.
 
To further the argument, the paper as well as our class took a look at two different types of neurons that are in the brain that have both been linked to obesity and/or appetite in general. The first was NPY/AGRP neurons, which are neurons that seem to stimulate appetite when people are hungry. This obviously is something that is overactive in obese people. Personally I looked at the other category of neurons, the POMC neurons. These neurons decrease appetite and tell your brain when you are full. These neurons are activated by leptin and insulin. Insulin of course is released after you eat, ordering your tissue to absorb glucose from the blood to make energy for your body. Leptin is the hormone that is released when you are full. Obese people have deficient POMC neurons. So when they eat, the body releases insulin and leptin but the POMC neurons do not become activated and so the brain is still under the impression that you are hungry, when really you may not be.
 
Sure all of these examples were nice to learn about, it was an aspect of obesity that I had never heard about. But take this with a grain of salt, because there is clearly other research out there that suggests that obesity is also caused by diet alone. I believe obesity to be a combination of both a disease, but at the same time a disease that was initially caused by the choices one makes about their lifestyle. So while research such as this gives us insight into potential treatments and drug targets to combat obesity, it should not reinforce the idea that overeating or unhealthy eating is acceptable. Like I said this problem is still largely in our hands. We need to eat right to get right, your body will thank you.

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