Everyone knows that to live a healthy life, we must eat good food and exercise. Despite this knowledge, two-thirds of Americans are considered overweight or obese. The United States has the highest rate of obesity in the world. Obesity is associated with diabetes, depression, sleep apnea, cardiovascular, and many other health issues. The scariest part of this story is the increasing rate of obesity in children. If this obesity epidemic isn’t stopped soon, there will be many costs including rising health care costs.
Society has created the view that those who are obese are just lazy people. While obesity can be a result of personal choice, brain dysfunction and genetics can play a role too. Overnutrition, which includes the high fat and carbohydrate diet, leads to an increase in weight and insulin resistance. This leads to inflammation and oxidative stress. This causes the structure of the brain to change. In obese patients, the hippocampus’ size is diminished. This part of the brain plays a role in memory processing. There is a correlation between obesity and memory dysfunction. This pathway also causes dysfunction in appetite behavior. There is research looking at how insulin resistance and hypothalamic inflammation causes people to lose their ability to control hunger. Simply, people are not able to stop themselves from eating even when they are full. This would begin the cycle of overnutrition again. This suggest the idea that obesity can be a result of addiction to food.
There are genetic components to obesity that are being researched. The major one I want to highlight is leptin. Leptin is a hormone that triggers a response that tells you to stop eating. It is created by fat cells and inhibits the neuropeptide Y (NPY) neuron. When NPY isn’t inhibit, it signals to the brain that a person needs to eat more because they’re hungry. Leptin stops this neuron from signaling. When the gene that encodes for leptin is knocked out, leptin can’t be produced. This results in a person feeling hungry and having strong cravings. This eventually leads to overeating and obesity.
This topic caused an interesting debate in our class. We had to decide if obesity was a true brain disorder or if it was the result of personal choice. There wasn’t a definite consensus. I don’t think you can put it down to one or the other. I can see both sides to the argument, and that’s why I believe obesity to be a combination of the two. There is some personal choice at the start of the obesity path. We choose what we eat and if we exercise or not. Once we choose to eat high fat and carb foods, this is where the brain disorder can begin. This is definitely true of those who are genetically predisposed to obesity (leptin patients). This addiction is hard to break, but we still have the choice to stop it. While there will always be debate over obesity and how to fix it, it is important to continue this research on obesity since it effects so many.
Resources:
Obesity in the USA
https://moodle.cord.edu/pluginfile.php/390940/mod_resource/content/0/obesity%20a%20brain%20disease.pdf
http://neurochemistry2014.pbworks.com/w/page/88796942/Is%20Obesity%20a%20Brain%20Disease
Obese (Un?)Intelligence
Last week in neurochemistry we talked about obesity and discussed all throughout the week if obesity was a brain disease or not. The article that was paired with the discussion last week was certainly interesting and discussed many of the chemical pathways and chemical consequences of being or becoming obese. We discussed the chemical effects of over nutrition and how repeated over nutrition can reinforce pathways that contribute to becoming obese.
I personally didn’t “buy” the claim that obesity was a brain disease and remained an outspoken proponent that obesity is a product of repeated negative choices or habits. If obesity is indeed a brain disease, it reduces the choices that we make down to near-robotic physical responses to neurochemical signals. This proposition cheapens the power of our choices and allows individuals to point blame at someone else, or something else.
Beyond the controversy and discussion caused by this article I found a claim of the paper to be incredibly surprising. The paper we read found a relationship between obesity and lowered IQ and significant structural changes in the brain. Another paper I found proposed that the structural changes were due to higher concentration of lipids in the blood getting into the brain and causing oxidative stress. We have seen time and time again throughout this semester that oxidative stresses are how many neurological diseases progress.
Not to trivialize this important topic and disregard the detrimental health effects obesity can cause, but I would like to leave you with this thought. What you see here is a picture of an MRI taken of a popular figure in today’s culture. Mr. Simpson here could be regarded as borderline obese and just take a look at how small his brain is.
Who's to Blame for Obesity?
Let’s face it, when you see someone who is heavy set the first thought that you probably have is that their excessive weight is due to a lack of will power or laziness, but what if I told you that the root of their weight gain is actually caused by a diseased state of the brain? There has been recent research that says that obesity may be more than just a lifestyle problem, but a problem in the chemical pathways in the brain dealing with the consumption of food.
One of the major chemical pathways that is usually dysfunctional in an individual who is overweight is the reward pathway that is activated after the consumption of food. This pathway normally is activated when there are any calories in your intestines, which then eventually activates the release of dopamine in your brain, which is the major neurotransmitter responsible for the feeling of pleasure we often associate with the consumption of our favorite foods. The major chemical that allows this pathway to flow smoothly is found in the intestines and is called OEA (oleoylethanolamide). OEA is normally created in the presence of lipids, or fats, in the diet and following their synthesis they activate one of the major nerves in the body that travels to the brain known as the vagus nerve, where it then triggers the release of dopamine, and gives us that satisfied feeling. OEA regulates feeding in and body weight in vertebrates by way of this dopamine reward system because the dopamine release in the brain is a signal for us to know we have eaten enough. This reward pathway can become dysfunctional if for some reason an individual’s level of OEA upon food consumption is below normal. If OEA levels are lower than normal in the intestines it would require an increase in the amount of food consumed in order to increase the levels of OEA enough to trigger a sufficient release of dopamine to cause that satisfied feeling that results in a cessation of food consumption. This increase in the amount of food needed to trigger this reward pathway obviously would lead to over-eating resulting in unwanted weight gain, but because of how this pathway works the person would feel that they needed to consume this extra food because without it they do not get that satisfied feeling after eating. There are a couple of ways that one’s OEA levels can become decreased: a genetic mutation encoding for the production of OEA in the body, or a diet consistently high in fat. Since a majority of people with low OEA are due to a high fat diet I will focus on how this kind of diet affect your reward pathway. Essentially what a high fat diet does is that it decreases your body’s sensitivity to the presence of lipids in your digestive tract which causes your body to produce less OEA. This leads to higher levels of fats needing to be consumed in order to achieve normal levels of OEA to trigger you food reward pathway in your brain. This tolerance to fat in the digestive tract is very similar to what is seen in many addictive behaviors such as drinking and drug use, in that in order to achieve the same “high” more of the substance is required, and in our case the substance being abused is fat. In the United States fat consumption is at an all-time high, so it is no surprise that we see this type of problem in a large portion of our population considering how much fast food and other high fat foods are major staples in our everyday diets.
Now the next time you see or know someone who is overweight make sure that you consider that their weight gain is likely due to more than their lack of motivation to go hop on a treadmill or will power to eat better they may have a chemical imbalance in their nervous system that may not be so easy to overcome.
Obesity: Not (Completely) Our Fault
Obesity is a growing problem that transcends boarders across the world. There’s the ongoing argument about the battle of free will and people’s genetic disposition towards being obese. Many people argue that being obese is a personal choice and that it’s the person’s inability to “put down the fork” and exercise properly that leads to them being obese. However, what if I told you that new evidence is pointing towards obesity being a brain disorder? What if I told you it wasn’t completely up to free will? Would you think I’m crazy? Let me explain.
It is believed that people are predisposed to having brain defects inhibiting their ability to control their choices regarding eating and overeating. This inability is caused by neurodegeneration in specific areas of their brain which control their executive reasoning, reward system, and overall cognition. Early stages of life have a great effect on our brain development as we progress through life. Our diets have the ability to lead towards proper development or improper development.
High fat diets lead to the disruption of our blood brain barrier which controls the exchanges between our blood stream and our brain tissue. The blood brain barrier is highly specific because the cells which make up the lining of our capillaries are highly compacted (aka have tight gap junctions). These “epithelial cells” have tight gap junctions which are surrounded by the end foot of astrocyte cells (clean-up/ helper cells of the brain). The astrocytes wrap around the gap junctions of epithelial cells in order to add another level of specificity to the exchanging of molecules and ions with the brain tissue. High fat diets disrupt this highly specific barrier by down-regulating mRNA which encodes very important proteins. These proteins hold epithelial cells tightly together producing the tight gap junctions which are vital to a properly functioning blood brain barrier. When these gap junctions are loosened there is the ability for dangerous molecules to be exchanged into the brain causing damage. The damage in the brain is usually due to oxidative stress leading to neurodegeneration, very similar to what we’ve seen in other neurodegenerative diseases before.
High fat diets are high in triglycerides which also disrupt the blood brain barrier. Triglycerides inhibit leptin and insulin receptors on the blood brain barrier that allow for proper transport of these molecules into the brain. These molecules (leptin and insulin) lead to the brain’s response telling us to stop eating because we’re full. When triglycerides inhibit the transporters for these molecules, we’re unable to properly transport them into the necessary regions of the brain thus we continue to eat. This is how leptin and insulin resistance is created in the body, commonly found in obese individuals.
Obese individuals brains exhibit volume deficits in their hippocampus and hypothalamus (regions associated with memory and executive functions [decision making]). These deficits are due to improper exchange with the blood brain barrier due to high fat content in their diets currently, when they were children, or even when they were in the womb. These findings put a lot of responsibility on the parents to provide adequate nutrition for their children early in life in order to lead to proper brain development.
I used to believe completely that obesity was a choice. After reading more into research regarding brain defects causing inability to feel “full”, to properly use our executive functions, and have our memory center altered, I truly believe obesity is an actual brain disorder. Depending on how your mother’s diet was during pregnancy and how your diet growing up was, some people are predisposed to be obese. Will power has a lot stacked up against it for some people whose brains are telling them to keep eating even though they shouldn’t. It’s a vicious cycle that is better to be avoided than broken.
Until Next Time,
Sebastian
More Than Meets the Eye: Obesity in the United States
While obesity and weight issues continue to be a huge problem in our society today, the most recent research suggests that obesity may in fact be a brain disease. Some scientists have argued that after excessive overnutrition, the body tends to accumulate more and more fat. As overnutrition occurs, inflammation in the hypothalamus and insulin resistance may occur, in addition to general weight gain. This inflammation and resistance may lead to a variety of problems, including fat tissue expansion via lipolysis, impaired energy and food intake control via hypothalamic gliosis, and cognitive deficits via impaired insulin secretion. Many of these issues will in some form cycle back, causing more weight gain and obesity, or more structural brain changes and cognitive deficits. However, much more research needs to be done in this area.
Personally, I am skeptical of such a hypothesis. While I agree that obesity may result from some brain dysfunction, there are still huge social and economical factors that play a large role in this epidemic that is overcoming our country. For example, while obesity has become a huge problem, relatively little has been done to combat this by our government. Apart from healthier school lunches, much of government funding goes to supplying underprivileged with food, regardless of its nutritional value. I’m not saying we shouldn’t be attempting to stop hunger, but I feel more action should be taken that is directly focused on reducing obesity. For example, I think Berkeley, CA is on the right track, marking a one cent tax per fluid ounce on sugary beverages.
In terms of social factors, nutrition awareness needs to start earlier, with parents supporting healthy food choices for their kids beginning at birth. I firmly believe that although there are some genetic influences, obesity can be prevented by making the choice to eat healthy from the beginning. If kids are fed healthy foods by their parents, it is more likely that they will develop healthier eating habits, resulting less weight gain as they age and metabolism slows. Nonetheless, this is of course coupled with economic factors, as more nutritious foods are generally more expensive, compared to their unhealthy alternatives. And again, government regulation plays a role, as one may argue for government subsidies on fresh fruits and vegetables.
Now I don’t claim to be a politician or expert on government, but I do know that obesity, brain disease or not, is a huge problem that is growing in the US, quite literally. Something needs to be done, and it needs to be done soon. Until then, keep eating your fruits and veggies, and help encourage your kids’ to do the same.
Bipolar Disorder – What is it?
This past week, we were discussing bipolar disorder. From this broader topic, our group spent quite a bit of time discussing whether or not it should be considered a real disease, is it over diagnosed, and is it a “cop out” diagnosis. It is very difficult to determine any of these without first looking at the background effects it has on neurological function inside the brains of those affected and treatment.
Bipolar disorder is diagnosed as individuals that experience extreme swings in mood, with the manic stage lasting at least a week and the depressive stage lasting at least two. That means you extremely moody significant other who switches from hot to cold over the course of the same day are most likely not bipolar. Individuals with bipolar disorder go from periods of depression to periods of “manic” activity, and the effects are very difficult for them to carry on in day-to-day functions. This is where the diagnosis gets tricky. According to the “go-to” diagnostic book (cinder brick is more like it!), the DSM-IV, there are so many aspects of the manic stage and depressive stage that most people would be hard pressed to not find themselves having two or three conditions of each.
At this point, you are probably wondering what happens in the brain? What goes wrong? The research is there, and while our class probably only scratched at the surface, it was enough to make my head spin! One of the main causes we found in our readings was oxidative stress. Oxidative stress is when our bodies produce too many free radicals and are unable to balance the system with antioxidants. This is not something as simple to fix as drinking more pomegranate juice and eating more spinach. Oxidative stress is more like a domino effect. When one domino falls, the rest don’t just stand there and deflect the falling domino, but rather fall in a chain reaction. The cascades that follow include affecting the secretions of our immune system called cytokines. Wait, immune system? Yup, you read that right. These inflammatory cytokines can have a prolific effect in increasing our manic moods and our depressive moods. In unaffected people, you can kind of see this in the effect of the “runners high.” So how do we cure the progression of this disorder?
There are many current treatments for bipolar disorder, one of the most common being lithium. Why lithium? Turns out that sufferers tend to have a sodium concentration inside their 2-5 times higher than everyone else. Lithium was originally intended to help replace some of that sodium with another element that does not have such a significant factor in regulating out bodies. The only problem was that in order to actually be effective, we needed to consume 10 times the concentration of sodium, and our cells would burst under that high of a concentration. Think of it this way, in your coin purse you have quarters, nickels, dimes, and pennies. We are going to call the quarters the sodium and the nickels the lithium. Since we are trying to flush out the quarters (sodium), we are going to replace each quarter with five nickels (lithium). It doesn’t take a much time to realize that pretty quickly you run out of space and your coins begin to spill over everywhere. So why do we still prescribe lithium? Lithium, actually in smaller doses does a remarkable job! It has significant therapeutic properties, and it is believed that it has the ability to target the affected (higher concentration) cells first and leave our “normal” cells be.
That’s a lot of science, and not a whole lot of discussing. Rather than give you the answer to our debate, how about some thought provoking questions – the ones that started our discussion. Does the increasing trend in diagnosis correlate with the change in how we treat our children? Is the “everyone is awesome for participating” attitude at fault? Think back to when you were a teen; is the prevalence of diagnosis higher? If so, why? When do people get diagnosed, is it because they’re trying to justify something or their actions? And if you really want to poke the bear, is bipolar disorder real?
The Hidden Neurological Disorder
Many degenerative disorders such as Parkinson’s disease or ALS show very distinct physical and mental symptoms that others can directly see. Bipolar disorder however, is slightly different. It is obvious to many that diseases such as Parkinson’s are debilitating, however this is not as evident in those who have bipolar disorder. The effects can be seen by those that are close to those affected, however in general, bipolar patients are forced to hide their disease in order to function normally in society. There are several different neurological causes that have been hypothesized however there is still more that has to be examined. Likewise, there are current treatments, however they are not particularly effective, fixing only one side of the issue and making bipolar patients feel somewhat empty.
What Characterizes Bipolar disorder?
Bipolar disorder is a manic-depressive illness that is characterized by long periods of depression, followed by long periods of mania. That is, patients go through prolonged periods of highs and lows, which tend to get more polarized over time.
Pathways Causing Bipolar Disorder
Several different pathways have been identified as potential causes of bipolar disorder. The dopaminergic system has been seen to be overactive in the manic stage and almost non-existent in the depressive stage. The glutamatergic system is also unregulated in bipolar disorders. Excess levels of glutamate have been shown to lead to excitotoxicity. Another culprit in the disorder is excessive inflammation. This inflammation is characterized by cytokine cascades which lead to cellular immune responses. This is also a primary cause of depression, thus a characteristic of the depressive state. And finally, like most other neurological disorders, high levels of oxidative stress and mitochondrial disfunction have been observed in bipolar disorder. Brain energy generation is increased in mania and decreased in depression.
Treatment Options
Current treatments of bipolar disorder target the intensive manic stage that patients experience, by administering mood stabilizers which inhibit dopamine. Many of these drugs are similar to the drugs that are used to treat psychosis, again, showing how much is unknown about the disease as a whole. However, several different neuroprotective strategies may prove to be effective treatments for bipolar disorder. N-acetyl cysteine is a precursor to a free radical scavenger. This may sound menacing, however it is essentially just a specific antioxidant (ones that we hear about in green tea or veggies). It has shown to modulate glutamate levels, thus crossing off one of the causes of the disease. Anti-inflammatory medications have also been shown to lessen the depressive stage of bipolar disorder. Drugs such as celecoxib or even aspirin have been shown to induce these anti-inflammatory benefits. Omega-3 fatty acids have also shown decrease the prevalence of nerve disorders. This occurs due to anti-inflammatory benefits as well as an increase of BDNF that occurs with an increase of Omega-3 fatty acid consumption. Finally, statins have shown anti-inflammatory and anti-oxidative properties which, as previously mentioned, are beneficial for bipolar disorder treatment.
There is still much that must be done now to better understand and treat bipolar disorders, however until that point, there must be greater public acceptance and understanding for those that are currently going through and suffering the highs and lows of the disorder.
Breaking Down the Vicious Cycles of Bipolar Disorder
Bipolar disorder, also known as manic depressive illness, is a mental disorder characterized by extreme unusual shifts in energy, mood, and activity levels, impacting the ability to carry out day-to-day tasks. Although it is not a neurodegenerative disease like other previous topics discussed, bipolar disorder is neuroprogressive. Tissue damage and structural changes occur in areas involved in mood regulation increase the risk of recurrence of episodes and reduce the effectiveness of treatment. Several factors have been identified to contribute to the neuroprogression in BPD. First, let’s break down the symptoms and diagnosis of this disorder.
Symptoms
Bipolar disorder is characterized by extreme manic and depressive mood episodes. Cycles between manic and depressive episodes vary in frequency and severity from one individual to another.
Manic episode symptoms: mood changes consisting of a long period of feeling overly happy or outgoing mood or extreme irritability (hypomania), talking very fast, jumping from one idea to another, racing thoughts, easily distracted, increase in activities such as taking on a variety of new projects all at once, overly restless, sleeping little, unrealistic belief in one’s ability, impulsive behavior, engaging in pleasurable, high-risk behaviors
Depression episode symptoms: extended period of feeling sad or hopeless, loss of interest in previously enjoyed activities, including sex, problems in concentration, memory, and decision-making, restless/irritable, changes in eating, sleeping, or other habits, thoughts of death or suicide, including suicide attempts
Diagnosis
The onset of bipolar disorder occurs due to genetic influences, stress, and other factors such as substance abuse. Someone with a bipolar family member is at an increased risk for developing the disorder, but onset is not guaranteed. Bipolar disorder usually develops in early adulthood, with half of all cases starting before age 25. Bipolar disorder worsens if left undiagnosed and untreated. Unfortunately, bipolar disorder is often misdiagnosed as ADHD or major depression due to similar symptoms, and by the time it is properly diagnosed, manic and depressive cycles are much more severe and difficult to treat. Here is a brief overview of the different bipolar diagnoses according to the DSM (Diagnostic and Statistical Manual of Mental Disorders):
Bipolar I: manic or mixed episodes persisting for at least 7 days or severe manic symptoms that require hospitalization, depressive episodes also occur, persisting for at least 2 weeks
Bipolar II: pattern of hypomania episodes and depressive episodes, but no full-blown manic episodes as observed in Bipolar I
Bipolar Disorder Not Otherwise Specified (BP-NOS): symptoms of illness exist and are out of the person’s normal behavior but do not fit criteria for Bipolar I or II
Cyclothymia: mild form of BPD, episodes of hypomania and mild depression present for at least 2 years, symptoms do not meet requirements for any type of BPD
Rapid-cycling: 4 or more episodes of mania, hypomania, mixed states, or depression within one year, more common for those with first bipolar episode onset at a younger age
Neuroprogression of Bipolar Disorder
The underlying mechanisms behind the progression of the disease remain largely a mystery. However, recent findings have identified structural changes and factors involved in the neuropathology. Grey matter loss in the anterior cingulate cortex of the brain has been observed in those with Bipolar disorder, particularly the anterior limbic regions. These areas of the brain are associated with cognitive functions including executive control, emotional processing, reward anticipation, and decision-making.
Recent research has identified inflammation and oxidative stress as factors involved in the neuropathology of BPD. These factors are also present in neurodegenerative diseases such as Alzheimer’s disease. Excess levels of dopamine, a neurotransmitter involved in reward behavior, and glutamate, an excitatory transmitter, are present in BPD brains. Excess levels of dopamine and glutamate lead to an increase of calcium in the cell, causing oxidative stress, which damages neurons.
Increased levels of cytokines, pro-inflammatory molecules involved in immune responses, have also been observed in those with BPD. When the brain becomes inflamed, it activates cytokines, which increase the number of oxidative species in the brain. Oxidative species damage the cell and eventually lead to cell death. Although increased cytokine levels have been identified, their exact link between the inflammation process and bipolar disorder is still unknown.
Treatment
Bipolar disorder is treated with a variety of medications, usually a combination of mood stabilizers and antidepressants. The most effective mood stabilizer is Lithium, which helps control manic symptoms. Though not much is known as to why Lithium is so effective, it has been suggested to protect against inflammation and oxidative stress. Antidepressants are used to treat the depressive symptoms of BPD, but unfortunately can increase the risk of developing rapid-cycling symptoms. This is why they are often required to be given in conjunction with mood stabilizers like Lithium. Finding the appropriate dosage of both mood stabilizers and antidepressants to treat bipolar disorder is a difficult and painstaking process, often requiring many adjustments to medication and dosages before finding one that best controls the cycles. More research is needed to further investigate the role of inflammation and oxidative stress in the pathology of Bipolar Disorder. With a better understanding of the underlying mechanisms of bipolar disorder, we can create more effective treatment plans and stop the vicious cycles for good.
Bipolar Disorder, more than just Mood Swings
Bipolar disorder, often associated with characters such as Dr. Jekyll and Mr. Hyde, is a very real and serious disorder. Because it is a mood disorder, it can be dismissed by some as “mood swings” or someone being temperamental while in reality, bipolar disorder has biomedical groundings and can be diagnosed quantitatively using biomarkers. Like so many of the diseases or disorders previously mentioned on this blog, bipolar disorder can be caused by inflammation or oxidative stress in the brain. This shared etiology really shows not only how fragile the human brain is, but how diverse its functions are and what can go wrong when those functions are disturbed.
If inflammation and oxidative stress are what bipolar disorder shares with some of the other neurological diseases discussed on this blog then neurodegeneration is where bipolar disorder differs. With other diseases, like Parkinson’s or ALS, show massive neuronal cell death, bipolar disorder doesn’t really follow that path. You might see more glial cell death instead of actual neuron death, which could be what makes bipolar disorder not life-threatening like the Parkinson’s or ALS. Despite this distinction, bipolar disorder is still a serious and debilitating disease and the advances in diagnosis and treatment of this disorder are welcome by the many people it affects.
My Cousin, Bipolar Disorder, and the Stereotypes of Mental Illness
Bipolar disorder is a disease that most people in the general public have heard about but had little experience with. For me, it is a disease that I find extremely interesting, and I attribute that interest to actually knowing someone who suffers with bipolar disorder. One of my cousins is both schizophrenic and bipolar, and seeing how she has been affected by these mental illnesses is very eye-opening. Most of the symptoms that you see when you are with her are the “schizophrenic side” but when you compare interactions with her at different times (like Christmas vs. Fourth of July) it is sometimes evident of her “bipolar side,” as well. My cousin is someone who suffers greatly from these diseases of the mind; she is unable to have a job and must live in a community that does not allow for complete independence. The medications that she takes also take some of the “life” out of her and have caused additional health problems. It is heartbreaking to think about what her life could have been like, had she not been diagnosed with these disorders. Mental illness is something that has a very negative connotation in today’s society because it is a disease that cannot be “seen”. There are no effects on mobility like Parkinson’s or ALS. It is much harder to ask for help for something like depression or bipolar disorder because it can be embarrassing for the patient. It is for this reason that we should continue research on bipolar disorder (and other mental illnesses) to determine exactly what is happening in the brain and why.
Bipolar disorder (BD) is more than just mood swings. The mania and depression associated with the disorder can drastically alter a person’s life. There are multiple pathways in the brain that are altered/triggered in BD. First, excess dopamine is associated with BD, and when it reacts with an enzyme called monoamine oxidase, the dopamine is broken down. This breakdown causes reactive oxidative species (ROS) to be created. ROS are harmful because they cause the mitochondria of our cells to become stressed, and oxidative stress ultimately results in apoptosis, or cell death. Too much glutamate in the body can also be seen in BD. Excess glutamate causes excitotoxicity, generation of ROS, and cell apoptosis. Finally, inflammation in the brain is a very large part of BD. When there is inflammation, receptors called TNF-alpha and IL-6 receptors are activated. Activation eventually leads to apoptosis and neurodegeneration through ROS and oxidative stress as seen in the other pathways.
Treatment for BD is difficult because there are two opposing extremes to treat. Too much “control” of the depression can elevate manic symptoms, while treating the mania can result in depressive symptoms. It is a delicate balance, and patients with BD are often on a cocktail of drugs to maintain that balance. Lithium is one drug that proves to be very effective at treating BD, but the mechanism behind how it works is unknown. Much of today’s research involves finding out how lithium can control BD in the hopes that understanding that pathway can help us understand what is exactly causing BD.
Bipolar disorder is difficult to live with, but not impossible. Unlike my cousin, many people are able to hold jobs and have families while they are diagnosed with BD. But in addition to having the difficulties and symptoms of BD, they also must deal with the negative stereotypes associated with mental illness. Just because someone requires pharmaceuticals or therapy to stabilize their mood does not make them less of a person. As a society we should not be so quick to judge those with bipolar disorder, or any mental illness for that matter. Eliminate the stigma associated with BD, and others may be less afraid to seek help.