Obesity is obviously a growing epidemic throughout many countries including America. There is rarely a day that goes by where I do not hear some mention to obesity on the television or radio. One of the complications which accompany this obesity is type 2 diabetes. Type 2 diabetes occurs when our bodies stop responding properly to insulin. Insulin allows our cells to take glucose in and glucose is important because it is the primary fuel for our body.
Obesity and Type 2
A key step involved in the development of type 2 diabetes is insulin resistance. Insulin resistance often precedes the clinical onset of type 2 diabetes by ten to twenty years. It is caused by abnormally high circulating fatty acid levels, these fatty acids signal to our muscle and liver cells stopping the normal response mechanisms to insulin. This is what causes the rise in blood sugar levels. An interesting fact about type 2 diabetes is that it can be reversed. Proper diet and exercise can lower blood sugar levels and in fact reverse the problems associated with insulin resistance. Not surprisingly, anti-diabetic drugs have been developed. These drugs redistribute fat from the muscle and liver cells to adipocytes, or fat cells.
Insulin Restistance
Although considered to be largely a preventable disease, diabetes 2 has shown to have a genetic linkage. It is interesting to consider the effect that our food industry has had on the development of type 2 diabetes. There is no doubt that it is a disease which is on the rise. So is cancer but what is interesting when comparing a disease like cancer and diabetes is the age component. The incidence of cancer is rising throughout the U.S., but then again so is our lifespan. We expect to see more cancer with advances in medicine which extend our lifespan and treat other disease more effectively. This “excuse” is not present for type 2 diabetes. It does not have the strong age dependent correlation that cancer, heart disease and neurological diseases have. So our food industry is producing food which raises our risk towards developing type 2 diabetes. There are healthy, organic options available throughout grocery stores. I completely agree that there are disorders which disposition certain people towards developing obesity, and certainly some more than others. In many of these cases however I believe that simply exercising, and eating healthy could prevent or solve many problems.
Bipolar Disorder
This weeks’ topic is Bipolar Disorder. Bipolar disorder (BD) has two types; one and two. BD 1 is characterized by manic and depressive episodes while BD 2 by hypomania and depression. Mania is an excited mental state characterized by physical hyperactivity. Hypomania is just a less severe form of mania. The fact that the exact mechanism underlying the pathology of BD is unknown is not unusual among mental illnesses. There are several hypotheses to why BP occurs. The particular pathway involving a signaling molecule, arachidonic acid, currently prevails as the most plausible. Arachidonic acid (AA) is a chemical signaling molecule. In the brain, AA acts as a signaling molecule that leads to various biological effects. Many of the metabolites, or breakdown products of AA, lead to inflammation.
Bipolar
There are three principal drugs involved in treating BD; Lithium, sodium valproate and carbamazepine. It is unknown how exactly these drugs act. It is known that they all lead to reduction of the Arachidonic acid pathway. This is why the AA cascade is believed to be involved in BD.
There are many questions surrounding bipolar disorder. The arachidonic acid pathway is just one mechanism that may explain the disorder. How much of the disease is caused by genetics, environmental factors or nutritional imbalances in undetermined. Due to the fact that so much is unknown, science and medicine should be hesitant to both rule out and accept hypothesis. It is entirely possible that hypothesis other than the AA pathway are involved in BD. The brain is a complicated, mysterious place but that is what makes it so interesting.
High Fructose Corn Syrup is Delicious
It really is. The ingredient that gives pop that sweet, mesmerizing taste. I could guzzle liters of it without blinking. If I could live off soda (and the occasional steak), I would in an instant. My pop consumption is off the charts due to its addicting, refreshing tastes. And I’m not the only one. According to a self-performed study, Americans drink the equivalent of roughly 24 cans of pop a week, translating to 288 ounces (over 8.5 liters!).(1)
What should we know about high fructose corn syrup and its effect on the body? HFCS is a popular industrially due to being cheaper and artificially sweeter than its natural sugar alternatives. I’m sure you are well acquainted with controversy surrounding this common ingredient in not only pops, but many other beverages and processed foods. You’ve probably seen the corn propoganda commercials where they claim “your body can’t tell the difference” and I’m sure you have a local dietitian (2) around the neighborhood that busts out a torch and pitchfork every time you pop a tab on your favorite soft drink. While both sides have some valid points (my heart/diet hopes desperately the former is unequivocally correct), research has shown a relationship between high fructose corn syrup intake and leptin and insulin levels in your body. Leptin and insulin play direct roles in obesity.
To understand the role of HFCS in this context, we must first understand the role of insulin and leptin in regulating our food intake. Our article this week essentially stated that low levels of leptin and insulin stimulate higher food intake, while normal or higher levels lead to decreased food intake. One crucial area in the brain responsible for this effect is the hypothalamic arcuate nucleus. In this case, we are interested in three types of neurons: POMC, NPY, and AgRP. POMC neurons decrease food intake and increase energy expenditure when activated, while NPY and AgRP increase food intake when activated. POMC neurons are stimulated by insulin and leptin, while NPY and AGRP neurons are more activated when leptin and insulin levels are low. In a normal functional body, these two systems work together to provide homeostasis in the body. If someone is losing too much weight, NPY and AgRP neurons will not stimulated by the lack of leptin/insulin and will “urge” the body to regain weight. If someone has an elevated level of insulin/leptin from increased food intake, POMC neurons will decrease food intake while NPY/AgRP’s effects will be essentially inhibited from their normal function. Insulin and leptin also can affect genetic expression of these neurons, inhibiting NPY while increasing the expression of POMC neurons. Consequently, insulin and leptin resistance can lead to increased food intake and obesity. Leptin and insulin are adiposity signals, meaning they rely on signals from fat stores for their function.
Ideally, we want to avoid low leptin/insulin levels or resistance. What role does HFCS play in the function/levels of leptin and insulin? A study in 2009 provided some not so exciting results for avid pop guzzlers.(3) Consumers of excess fructose (instead of typical glucose or sucrose) showed increased conversion of excess sugars into fats (in a process known as de novo lipogenesis (DNL)). HFCS also decreased insulin sensitivity. If the body can’t respond normally to insulin, it will act as if there is a deficiency which, as seen above, can lead to increased food intake and obesity. In another study, fructose consumption was linked to low ciruclation levels of insulin and leptin.(4) Fructose, unlike glucose, doesn’t stimulate insulin secretion. Insulin-regulated glucose metabolism is hypothesized to play a role in leptin secretion. Thus, both leptin and insulin are decreased, leading to increased caloric intake and further obesity. Besides influencing leptin and insulin levels, HFCS also alters metabolic hormones so we don’t feel full. These manufacturers know what they’re doing.
While it truly pains me to say this, high fructose corn syrup opponents may indeed have a point. It would be wise to reduce HFCS in order to prevent obesity and the diseases, such as type II diabetes, that often result. Sticking to natural sugars like sucrose and glucose in substitution for synthesized fructose can help reduce caloric intake (while it is probably unwise to overindulge in those sugars either). Even if we aware of these problems, can the possible consequences of high fructose diets deter us from indulging in soda and the plethora of other processed food containg HFCS? It’s up to the consumer.
(1) – Americans named Nathan Rodeberg.
(2) – Or dentist. The effect of pop on teeth will unfortunately not be addressed in this blog post.
(3) – Stanhope et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Journal of Clinical Investigation 2009 119(5):1322-34.
(4) Teff et al. Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women. Journal of Endocrinology and Metabolism 2004 89 (6): 2963-2972.
(5) Google Images.
A Knitting Prescription
Bipolar Disorder
Bipolar disorder affects almost six million American adults and is characterized by episodes of depression and mania. The onset of bipolar disorder is often in late adolescents, but it can develop at any stage in life. Mood stabilizers such as lithium, divalproex, carbamazepine, and lamotrigine seek to suppress the swings between mania and depression to treat Bipolar Disorder. Of the mood stabilizers only lithium and lamotrigine, to a lesser degree, are effective at treating both mania and depression. The other stabilizers try to reduce mania, which is thought to indirectly improve depression by “breaking the cycle” and keeping patients out of bipolar episodes altogether. There is also a horde of other drug types, such as antipsychotics and anti-anxiety drugs, which can be indicated for treatment of bipolar disorder under certain circumstances. Every drug has a list of possible side effects that range from mild to (in my opinion) worse than the issue they are treating. This brings me to the topic I wish to talk about this week.
Overmedicated and Unsatisfactory
One of the points made clear by this weeks review was that the underlying cause of bipolar disorder and the reason treatments like mood stabilizers work is still quite unclear. The mood stabilizers are labeled as such not because of a known mechanism of action, but simply from an observed effect. When this is compounded by the possible side effects and the lack of a clear empirical way of diagnosis, I see a lot of room for error. I do not want to sound too critical because I know that psychological disorders seldom have a clearly understood etiology, but trial and error doesn’t seem like a good way perform medicine. That said, I don’t have a better way to go about treating bipolar disorder so take complaints with a grain of salt. However, I do have an idea about what might be done.
Brain Health
I think there might be ways to improve mental health without completely relying on pills. This is a controversial idea, especially in America, because Americans love pills. Our busy lives demand that we continually find the most time-effective way to go about our day. Unfortunately, this applies to our health. Many Americans would much rather take a blood pressure medication than exercise or eat healthier, both of which take time and effort to do. The healthiest approach would be to take the medication along with exercise and diet changes. Brain health should be treated similarly. I think therapy, support groups, and hobbies should supplement medications. Stimulating the brain through contact with other people and enjoyable diversions has the potential to improve mental health significantly. The best part about my suggestion is that it is risk free; taking up knitting may not prevent a bipolar episode, but it sure won’t cause one, which is more than taking up a new medication can say.
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001924/
http://www.dbsalliance.org/site/PageServer?pagename=about_bipolar_overview
Defensive Bipolar
While I was wondering around the internet searching for information on bipolar disorder, I stumbled across an interesting blog by a person (Bp) who was diagnosed with bipolar. This person’s story was interesting to me because Bp displayed the normal symptoms of bipolar, but that was not all. Later on he developed other symptoms. Bp was diagnosed with bipolar at age 14, and was promptly placed on medication (Risperdal). Bp complained that the medication induced a vegetative state, and went off the medicine wanting to try therapy. Then Bp started to hear a voice in his head, named Maverick. Maverick would take over Bp’s body. When Bp asked his therapist about this new development, he was told that it was just a defense mechanism for dealing with people. He was then put on Lithium, and it only got worse. So then Bp went off medication.
This got me thinking about what bipolar really is, and I thought, what if bipolar is just a defense mechanism as well? Maybe mania is a faulty coping mechanism for major depression? Almost like a rebound. Then once your body is exhausted from the manic state, it slumps back down into depression? This is similar to Multiple Dissociative Disorder (multiple personalities). Multiple personalities are just coping mechanisms for dealing with stressors. For example, a woman who was raped by her father every night, created different personalities, one to deal with the rape, and one to live normal school life. Eventually, she created other alters as well.
Bp’s story also got me wondering, how effective treatment by pharmaceuticals is. As of right now, the DSM-IV just tries to objectively diagnose the disorder, and then pump the patient full of drugs. It needs to reform to give us objective suggestions for treatment based on the individual, not just generalized. I think in Bp’s case, actual cognitive therapy would have been way more helpful than a prescription. I think psychologists need to seriously consider the patient when proscribing treatment because every disorder is really unique. Everything is very subjective, and it’s hard to diagnose a subjective disorder. What are your thoughts?
Beethoven Without Bipolar: The Cost of Creativity
This week’s discussion topic was on bipolar disorder. So far we have only focused on the negative effects of bipolar disorder and finding ways to treat it. I am going to take a different perspective on the disease and hopefully shed an alternative light on mental illness.
Can you imagine a world without Beethoven’s Ode to Joy (from his ninth symphony) ringing through churches? And we can’t forget his Moonlight Sonata and the seasonal Fur Elise. Or the daunting Funeral March of his seventh symphony. This music of the late 18th century has captured the hearts every listener for centuries and possibly centuries to come. People have mixed, rearranged and borrowed from Beethoven’s work into present day. Beethoven has been featured in countless modern films such as Fantasia, Mr. Holland’s Opus, Misery, Along Came Polly, The King’s Speech and even Die Hard and Austin Powers in Goldmember. Many others are also included on this list. Even advertisement agencies also use snippets of Beethoven’s work in present day televised commercials. This demonstrates the impact of Beethoven’s musical talent as well as his legacy as his music continues to entertain us for over more than 2 centuries.
Image from: http://omahype.com/event/beethovens-ninth-2/
But, what if it never happened? What if the music inside of Beethoven was never released from his mind? What if something in Beethoven’s genetic make-up allowed him to excel in music and create the enticing melodies that have captivated the world? What if the deeply emotional and soul-filling music could not have been made because some of his inspiration was taken away? What if much of his inspiration came from something that modern people would call a “disease”? Would we have tried to cure him of the disease and have missed out on his timeless piece of music that we have used and reused since the late 18th century? Perhaps we will never know the answers to these questions. But I guess the question I’m trying to pose is: Does mental illness, and more specifically bipolar disorder, carry all negative baggage or can some good come from it? Now for those of you who do not know supposedly Beethoven had a form of bipolar disorder though it was not officially diagnosed. Beethoven went through bouts of depression and then into manic phases, in which he would compose his deepest most emotionally saturated works.
I know that many people may argue against me, but what if Beethoven’s bipolar disorder, with the creativity provided by these drastic mood swings, allowed him to compose the timeless pieces we have today? If that is the case maybe we should take note of the good that may come from some types of mental illness like bipolar disorder. There are many musicians, actors, and artists that have been “diagnosed” with bipolar such as Amy Winehouse, Sinead O’Conner, Vincent van Gogh, and Virginia Wolfe. Perhaps some their success can be attributed to bipolar. Now I’m not trying to say that bipolar makes you successful. I am just trying to play the devil’s advocate. Maybe we should shy away from the negative reputation that bipolar has and look at some of the good aspects. Bipolar disorder is not something that you should wish upon anyone, however it’srtant to keep in mind that not all parts of mental illness are completely negative.
Read more about the connection between bipolar and creativity/inspiration at:
http://serendip.brynmawr.edu/exchange/node/1726
http://www.springerlink.com/content/w68x7qp16374380x/
http://www.manic-depression.net/symptoms/creativity_symptom_of_bipolar_disorder.htm
Get more information about bipolar disorder and its timeline and discovery at:
http://www.thebalancedmind.org/learn/library/about-pediatric-bipolar-disorder-timeline-english
Learn about other famous individuals with bipolar at:
http://www.famousbipolarpeople.com/
And read more about Beethoven in modern culture at:
http://classicalmusic.about.com/od/classicalmusic101/a/aa021906_2.htm
http://classicalmusic.about.com/od/onestopbeethoven/qt/beethoven_movie.htm
Bipolar Disorder in Children- Efficient and careful diagnostic tools needed.
Bipolar disorder is generally defined as recurrent periods of mania and depression (Bipolar I) or hypomania and depression (Bipolar II). According to the website of National Institute of Mental Health (NIH), the lifetime prevalence of bipolar spectrum disorders is 0 to 3 % among adolescents, depending on assessment measured and the range of the spectrum considered. The prevalence of child onset bipolar is not well-established because there is no clear boundary of diagnosis and most of the symptoms overlap with other disorders such as Attention Deficit Hyperactivity Disorder (ADHD) and Schizophrenic disorders.
According to the article we read for class, ‘Bipolar disorder and mechanisms of action and mood stabilizers’ by Rapopart.et.al, 2009, the mechanisms of bipolar disorder are believed to be due to imbalance neurotransmission, disease progression with worsening, cognitive decline, and progressive brain atrophy which can result in impairment of executive functioning, episodic memory, and sustained concentration. In neuroanatomical aspects, there is also thinning of the cortical mantle, widening of cortical sulci, and dilation of the lateral ventricles in bipolar patients. Neuroinflammation and excitotoxicity(incidence of neural cell death due to over activation) are found to be underlying causes in Bipolar disorder. Neuroinflammation is due to increase Arachidonic Acid, a polyunsaturated omega-6 fatty acid derived from diet, and excitotoxicity is due to elevated brain glutamate/glutamine(excitatory neurotransmitter) ratio, and increase dopamine ,a neurotransmitter that is usually found to be increased psychotic symptoms, levels.
In this blog, early onset bipolar symptoms and diagnosis in children will be discussed. Some general notable facts about bipolar disorder from the article, ‘The effect of the first manic episode in affective disorder: a case register study of hospitalized episodes’, by Kessing, Lars.1998. include –
– “ Younger age at onset was associated with increased risk of developing a manic/circular episode for patients who presented with a depressive first episode “(Kessing, 1998)
– “Courses of episodes were the same for patients for whom the first manic episode occurred later during the illness. Duration of intervals between episodes declined steadily with the number of episodes. “(Kessing, 1998)
– The study found out that bipolar patients had the same rate of recurrence throughout the illness irrespective of at which episode or at what time their first manic episode occurred.
– Patients who presented with depression but later developed mania were younger at onset than patients who remained unipolar. (Kessing, 1998)
According to the article, ‘A Summary of Clinical issues and Treatment Options’, by Canadian Network for Mood and Anxiety Treatments (CANMAT), ‘early onset is often defined as occurring before the age of 25. The younger the age of onset of bipolar disorder, the more likely it is to find a significant family history of the condition. Early onset bipolar disorder most commonly begins with depression.’ (CANMAT, 1997) ‘Depression with psychotic features may be a predictor of future full-blown bipolar disorder in the early onset group. Rapid cycling, mixed states, and psychotic features are more common in early onset conditions.’ (CANMAT, 1997) Hallucinations and delusions are also common precursor symptoms associated with bipolar disorder.
Principal components analysis of early intervention symptoms in children with and without bipolar diagnosis in Children, according to Fergusa.et.al, 2003, include-
- Depression, II. Irritability/Dyscontrol, III. Mania, and IV, Psychosis/Suicidality.
Around age 7 and 8 – “ The depression component (I) explained 14.2% of the variance and included nine symptoms (severe fatigue, periods of sadness, increased sleep, low self-esteem, more withdrawn, suicidal thinking, change in appetite, cries easily, and excessive guilt).
From age – 1 onward and greater incidence seen by age 3 – The irritability/dyscontrol component (II) explained 14.1% of the variance and included seven symptoms (temper tantrums, poor frustration tolerance, impulsivity, increased aggression, decreased attention span, hyperactivity, and irritability).
Around age 7 and 8 – Mania component (III) explained 11% of the variance and included six symptoms of mania (racing thoughts, extended mood elevation, pressured speech, grandiosity or delusions, bizarre behavior, and brief mood elevations).
Around age-9 onward – Psychosis/Suicidality component (IV) explained 10.2% of the variance and included five symptoms (hearing voices, paranoid thoughts, suicidal gestures, suicidal attempts, and obsessive thoughts).
According to the article, component II, ‘Irritability or dyscontrol‘ is the earliest symptom to discriminate the bipolar children from the other groups. This factor, according to the article, includes ‘temper tantrums, poor frustration tolerance, impulsivity, increased aggression, decreased attention span, hyperactivity, and irritability’. This factor is also supposed to be associated with later clusters of more classic manic and depressive symptoms that can lead to a diagnosis of bipolar illness. The symptoms in this category also overlaps with those of ADHD and they are believed to be the earliest precursors to classic bipolar see in adults and some adolescents, according to Fergus.et.al, 2003.
Diagnosing bipolar disorder, especially in children, is not a clear cut process and should not rely only on the established guidelines of symptoms. The diagnosis should take into consideration both the unique bipolar symptoms that are apparent in adolescents and adults and if necessary, also compare the symptoms with anatomical brain abnormalities from imaging brain scans.
Homelessness and Mental Illness: A Lethal Combination
This week, Fargo-Moorhead recognizes National Hunger and Homelessness Week, a time to raise awareness about the on-going problem of homelessness—not just in the big cities of New York, LA, and Chicago—but here in the frozen land of MN and ND, in our very own backyards. Whether or not it is acknowledged, homelessness is a problem in virtually every community. The National Coalition for the Homeless estimates that across the US on a given night, between 500,000 to 1 million Americans experience homelessness.
What people in our community may not know, however, is that an estimated 1,000 to 1,500 individuals in the Fargo-Moorhead area are homeless. The 2009 Wilder Research report, which gathered information from homelessness people in the Fargo-Moorhead area on one night in October by combing shelters, transitional housing, soup kitchens, and unsheltered areas like parking lots and alleys, found a total of 443 homeless people. Considering the total number of homeless individuals in our region, this figure is undoubtedly higher. Every year, local shelters like the YWCA and Churches United for the Homeless report maximum capacity and utilization.
While homelessness itself is a devastating experience, there’s evidence that mental illness is more prevalent among homeless individuals, compounding the problems they already face. The same Wilder report of the F-M area found that over 40% of the individuals surveyed had been recently diagnosed with schizophrenia, bipolar disorder, major depression, anti-social personality disorder, or PTSD. This finding reflects a host of social research that has found a nation-wide association between homelessness and mental illness, particularly bipolar disorder and schizophrenia. Based on this research, it is likely that mental illness is a factor that contributes toward homelessness. Being able to effectively diagnose mental illness and make treatment available to at-risk populations could potentially reduce the problem of homelessness.
What is bipolar disorder?
This week, the Concordia neurochemistry class discussed the issues with diagnosing and treating bipolar disorder, a condition that seems to be over-represented in homeless individuals. Bipolar disorder is characterized by uncontrollable and debilitating extremes of mood, which cycle between two states: mania (extremely high mood and energy levels) and depression. People with bipolar disorder are on a “roller coaster” of emotion, cycling between moods every few days, weeks, or months (depending on severity). Understandably, this can be very difficult to deal with personally, and can impair relationships and social functioning.
Diagnosing bipolar disorder is difficult. Like all mental illnesses, it cannot be detected with a quick-and-easy blood test or x-ray. Instead, a psychiatrist or psychologist needs to spend enough time with the individual in order to determine if the rapid cycling of moods is occurring and interfering with normal functioning. This can be tricky because the depression, mania, and sometimes psychotic behavior can look very much like other mental illnesses—like schizophrenia or certain types of personality disorders.
Treating bipolar disorder
The use of medication in treating bipolar disorder has been met with some success. Treating the disorder often involves a combination of medications in order to target both depression and elevated mood (mania). This is usually done through using anti-depressants and anti-psychotics. Another option that has shown relatively high success rates is the use of lithium carbonate, a natural element. Lithium is widely used now as an mood stabilizer in bipolar disorder, balancing the extremes of low and high mood. Exactly how lithium is effective in bipolar disorder, however, is still relatively unknown. What happens in the brain when a person takes lithium?
Researchers have a couple of ideas. One suggestion is that lithium prevents too much of a substance in the brain called myo-inositol from being produced. Too much myo-inositol may contribute to the rapid cycling in bipolar disorder. Another hypothesis is that lithium decreases signaling in a biochemical pathway called GSK-3. This pathway is also believed to possibly contribute to the symptoms of bipolar disorder. Finally, lithium may also decrease the levels of arachidonic acid in the brain, an omega-6 polyunsaturated fatty acid found in cell membranes. This substance is important for a variety of biological functions, including chemical signaling and cell growth in the brain. Arachidonic acid causes inflammation and may damage cells of the nervous system if too much is released. Lithium may protect nerve cells by decreasing arachidonic acid.
So should doctors be prescribing lithium if they don’t even know how it works in the brain? Lithium has been in use for years and shown to be an effective mood stabilizer in many cases of bipolar disorder. While too much lithium can be toxic, doctors are aware of what they are dealing with and do their best to balance the potential benefits of the drug with the associated risk of harm. Most of all, it is important that people who take lithium are aware of both the benefits and possible risks, and make a choice they feel comfortable about.
Making treatment available
Medications like lithium or other treatment options like therapy have been shown to be helpful in treating bipolar disorder. Unfortunately, sometimes the people who need these resources the most do not have access to it. Many people, not just homeless people, can’t afford medical insurance to get the treatment they need. Additionally, not all insurance companies recognize mental illnesses equally as a legitimate condition. While drugs may be covered by insurance companies, other options like therapy and counseling may not be, limiting the options people have. This inaccessibility of treatment has made it very difficult for people with mental illness to get the help they need. Increasing awareness of mental disorders like bipolar disorder and their social implications may help increase the availability of treatment and services to people who need them the most.
Events this week in Fargo-Moorhead
This month, the Fargo-Moorhead community is doing the Fill the Dome project for a fourth year in a row. Students around the area are collecting enough donations to fill the 80,000-square-foot Fargodome with food for local pantries and shelters. Each year, the project collects hundreds of tons of food. The project is wrapping up next week!
Students in Concordia College’s Echo Band are teaming up with the F-M Coalition for the Homeless to create awareness of homelessness as well as raise funds for local organizations. Their concert will be held Tuesday evening in the Centrum, Knutson Campus Center.
The Lake Agassiz Regional Library in Moorhead is holding Holiday Season Amnesty for patrons with overdue materials and fines! $2 will be forgiven per donated non-perishable food item. Donations will go to local food pantries serving the homeless and needy.
For the full 2009 Wilder Research report of the Fargo-Moorhead area, visit:
http://www.wilder.org/download.0.html?report=2354
Bipolar Disorder: We Need A Pokeflute
Bipolar disorder is one of the most well known neurological disorders, characterized by alternating states of prolonged depression or manic states (the term is often misused, such as to characterize a moody friend). Because two different states exist, it is difficult to administer one single drug that can alleviate both symptoms. Thus, mood stabilizers are often used to treat mania, while antidepressents seem to be the obvious choice for treating the depression stage.
Common mood stabilizers used today include lithium (administered as various salts), carbamazepine, valproic acid/valproate, and lamotrigine. These drugs have shown varied effectiveness in depressing the elevated mental state seen in mania or hypomania. However, these drugs were not designed with a certain mechanism of action in mind. Instead, hypothesises have to be made to predict how these drugs actually work neurologically. The paper our class reviewed this week put forth the “arachidonic acid cascade” hypothesis. Arachidonic acid is a polyunsaturated fatty acid that plays a role in many biological processse, including neurotransmission, gene transcription, sleep, memory, inflammation, and behavior. Too much arachidonic acid are linked with inflammation, ischeme, and convulsions. According to this AA cascade hypothesis, the aforementioned mood stabilizers may regulate mania by downregulating the arachidonic acid cascade, thus preventing some of the problems from its overexpression.
The paper only focused on treating mania. Treating the depressive state of BD is a whole new beast. Bipolar depression is three times more common than mania. The mood stabilizers mentioend above (except lamotrigine, to a small extent) are not able to treat depression effectively. It would be natural to assume that antidepressants would be a good treatment. However, most antidepressants increase the likelihood of switching back to mania, which is obviously not a desirable alternative, even when used in tandem with mood stabilizers.
An (not completely accurate) analogy would be considering a Snorlax, Pokemon #143. Consider the manic phase of Snorlax to be an aggravated, aggressive state (usually resulting in an intense pokebattle). Like in BD, this phase is much less common than the depressive state, the state we usually associate with Snorlax. In this “depressive state”, Snorlax is just sleeping and generally lethargic about the world around it. View an antidepressant as chucking a ton of apples at the Snorlax so it will wake up (come out of depression). If you do succeed in waking the Snorlax, it is likely it will instantly convert into a “manic state”, understandably angry from being disturbed so rudely. The antidepressant (apples) may have worked, but it resulted in another undesirable state. What BD needs is a Pokeflute: something that can gently bring the Snorlax out of depression but not bring it to an overactive state. However, since we regrettably don’t live in a fantasy world, this is much easier said than done.
Images obtained from Google Images.
Working Backwards…
Bipolar disorder is a psychological disease characterized by extreme mood change. The highest point, termed mania, is a period of extremely good mood and impulsivity, while the lowest point, depression, is characterized by deep sadness or emptiness. Some of these intense emotional symptoms include poor judgment, spending sprees, very high self-esteem, and hyperactivity during mania which transitions into low mood, sadness, feelings of hopelessness, and thoughts of suicide during depression.[i] Interestingly, it is hypothesized that the famous historical figures Edgar Allan Poe, Vincent van Gogh, and Virginia Woolf all had bipolar disorder. In the U.S., the disorder is estimated to affect 5.7 million adults, but surprisingly only about 50% of these people are getting any treatment at all. [ii],[iii] What is stopping these people from getting adequate treatment for this debilitating disorder?
It would probably surprise you to know that bipolar disorder is one of the oldest known illnesses known today. In fact, according to some sources, its symptoms were recognized as far back as the second century.[iv] How does this make sense? How have we not figured out how to treat this disorder effectively?
Quite frankly, scientists simply don’t know what’s going on with bipolar disorder. The medications prescribed to patients for the disorder are essentially a shot in the dark. No one knows how or why they seem to work….sometimes. In fact, most scientific study into bipolar is essentially working backwards from treatment. In other words, maybe if we can figure out what the treatment is doing in the brain, we can figure out what’s wrong with the brain.
One of the front-running hypotheses as to what’s going on in the bipolar brain is called the “arachidonic acid hypothesis.” This hypothesis shows significant promise as to why mood stabilizers like lithium, valproate, and carbamazepine work to stabilize mood swings, especially in the mania stage.
Arachidonic acid, a polyunsaturated fatty acid found in our diet, plays a role in many cellular processes including neurotransmission, membrane excitability, long-term potentiation, gene transcription, membrane fluidity, neurite outgrowth, cerebral blood flow, sleep, and memory.[v] Furthermore, arachidonic acid has been implicated in the excessive neurotransmission of glutamate and dopamine observed in bipolar disorder. In one study, it was shown that NMDA activation increased arachidonic acid incorporation in controls while use of LiCl or NMDA agonist blocked this incorporation.
Lastly, it has been shown that mood stabilizers have some sort of neuroprotective effect over the brain. This makes sense in the context of the arachidonic acid hypothesis because increasing arachidonic acid levels can lead to cell damage and behavioral changes. Therefore, these mood stabilizers could be decreasing arachidonic acid’s cellular affects.[v]
There are still many unanswered questions surrounding bipolar disorder, and many psychological disorders in general. There really comes a point where you have to wonder – what is normal anymore? Will there come a time when we understand these disorders completely? Or will it take learning all the intricacies of the “normal” brain first? I don’t know the answers to these questions, but it seems like (for now at least) the arachidonic acid hypothesis is the best we’ve got.
[i] http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001924/
[ii] http://www.bipolarsymptoms.org/bipolar-statistics/
[iii] http://blogs.psychcentral.com/therapy-soup/2011/03/new-bipolar-study-statistics-suggest-serious-work-ahead/
[iv] http://www.caregiver.com/channels/bipolar/articles/brief_history.htm
[v] Rapoport et al. (2009) Bipolar disorder and mechanisms of action of mood stabilizers. Brain Research Reviews 61; 185-209.