Cobbers on the Brain – Page 125 – Student Commentary on the Neurological Sciences

Integrative Cognitive Affective Therapy – The Future of Bulimia Nervosa Treatment

Posted on March 15, 2016 by / 0 Comment

I recently got the opportunity to listen to Dr. Stephen Wonderlich, a Concordia graduate and distinguished clinical psychologist, speak on campus. He began his talk by explaining that his research is focused on the science of eating disorders, specifically bulimia nervosa (BN). BN is a disorder that includes recurrent episodes of binge eating, a subsequent purge episode that those suffering do to rid themselves of the binge they just did, a sense of lack of self-control, and typically a deficit in positive self image. Furthermore, he explained that BN affects predominately females, with about 90% of cases being female.
Dr. Wonderlich offered a couple personal stories of people who suffered from BN, discussing how they often experienced negative childhood events or extreme social pressures to lose weight or obtain a “thin” image. To further explain, he talked about the current excepted treatment theory for BN – Cognitive Behavioral Treatment (CBT). This model begins with focusing on the patient’s low self esteem, which in turn leads to extreme concerns about weight, strict dieting, and eventually binge eating. He then discussed the theory he and his colleagues have been developing – Integrative Cognitive Affective Theory (ICAT) – and its mechanisms of action. He explained how ICAT focuses on the emotions of the subjects by analyzing the subjective experience, physiological reaction, expressive component, and behavioral reaction of the subject. Furthermore, he mentioned that many published articles explain that negative emotions precipitate eating disorders. These aspects provide the groundwork of ICAT.
Dr. Wonderlich then explained the role of the brain in emotion generation and regulation, with the dorsal system of the brain being responsible for emotional generation, and the ventral system being responsible for regulating and managing emotion. The two emotional circuits work in accordance – and in people suffering from BN, these two systems may not work as effectively as they could. From extensive testing and research, it has been found that with increased negative emotion comes increased activation of the brain’s reward center in BN patient. Additionally, when bulimic people plan a future binge, their amygdala calms down. Therefore, the thought of food for bulimic people leads to a reward response. This phenomenon is what drives Dr. Wonderlich’s work in the connection between negative emotional states and the induction of a bulimic episode.
Lastly, Dr. Wonderlich talked about the treatments for BN and how he and his team have developed a manual using ICAT that is being disseminated around the world. He explained that the treatment first works to increase positive emotions and then to find a way for patients to tolerate the negative emotional states. The results of the study showed that integrating ICAT and CBT had profoundly positive outcomes, and that the the large majority of the subjects involved continued with the treatment. This, to me, is amazing – a novel treatment for a very serious disorder can now be implemented in order to improve the lives of those that suffer from BN.
Getting the chance to hear the leader of this potentially groundbreaking research was undoubtedly enjoyable, and I am very intrigued to learn of what the future holds for ICAT and Dr. Wonderlich’s team. I also really appreciated Dr. Wonderlich’s ability to integrate the effects a Concordia College education had on him and his future. For me, I feel even more thankful to be given the opportunity to go into the community and influence the affairs of the world. Luckily, I had the chance to talk with Dr. Wonderlich about his work and the road he took to get to where he is today. I found myself further interested in neuroscience and medicine, and I hope I can continue to integrate the two areas in my future career.

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Bulimia a Drug?

Posted on March 15, 2016 by / 0 Comment

Bulimia Nervosa is of concern among adolescents and can be extremely hard to identify. Along with the difficulty in identification many side effects accompany bulimia. Some include the erosion of the enamel from teeth, popped blood vessels, digestive complications, and reproductive impairments. When talking about bulimia more models are suggesting similarities between bulimia and drug addiction.
The new theory describes impulsive versus compulsive behaviors and how they lead into each other especially when looking at bulimia. Impulsive actions lead into compulsions by repetitively taking part in an activity where a reward is being earned but then turns into a compulsion when that individual needs to take part in the activity to avoid a more negative effect from occurring.
Bulimia is usually initiated in adolescents and there are certain individuals that are at higher risk than others, the two main risks for impulsive behaviors are state-based and trait-based. When talking about state-based a lack of self control is being had by the individual. Trait-based is when negative urgency takes place and negative urgency is defined as the tendency to act rashly when distressed, is characterized by high neuroticism, low conscientiousness, and low agreeableness.
Bulimic actions are then reinforced by distraction and negative reinforcement which is very similar to what occurs with drug addiction and can be the reason why it is difficult to stop.
Now knowing the similarities between the addictiveness of drugs and bulimia we as a society will be more informed and aware of the signs of bulimia to help individuals who are struggling with the disease.

Disease/Health

Could Meghan Trainor Actually Save the United States from Bulimia Nervosa?

Posted on March 15, 2016 by / 0 Comment

Meghan Trainor—along with many other celebrities and companies in the United States—has boldly proclaimed her support of the body image acceptance movement.
She’s “All About That Base,” and is encouraging others to accept the bodies they have.
Her aim is to decrease the negative body image that so many young adolescents and adults have developed growing up in a culture that idealizes and idolizes ultra-thinness. By encouraging the acceptance of our bodies, the advocates like Meghan Trainor likely hope to see a decrease in eating disorders—such as bulimia nervosa (BN).
However, there is curious research into the psychology and chemistry of BN that happens to suggest a lot more than just a negative body image factor at play.
The True Predispositions
First off, some people are more predisposed to developing BN than others—we all have to eat, we all like to eat junk food, and we all want to lose weight, but not all of us develop BN.
This predisposition seems to be the beginning of a complex development process.
Predisposition can be genetic, and can be determined based on how much self-control one has—which is somewhat determined chemically through serotonin and dopamine regulatory measurements.
The predisposition also is linked to a person’s attitude. If a person has a negative affect—meaning they are very likely to be in a negative mood—they are more likely to develop BN as well.
With these predispositions, when a person is placed in the right environment, BN develops.
The True Development
In this development process, the person first acts on impulse. Likely the person is in a “bad mood” maybe due to negative body image, or maybe due to stresses in life. They are also likely on a diet. When they have reached the point of exhausting their self-control and/or ability to deal with negative stressors, they binge eat.
This binge eating, in the impulsive stage, acts as a positive reinforcement reward. The brain is given what it wants and the person feels satisfied.
After the binge, the person will feel they have undone what they have desired to accomplish and purge their binge. This begins the cycle again. The cycle eventually leads to more compulsive actions.
The compulsive stage is similar to drug addiction. The patient seeks out the binge in the same way a heroin addict seeks out heroin.
The binge now provides more of a negative reinforcement. The binge takes away negative stressors in life via distraction, and/or satisfies the body of foods it has been deprived of during a diet.
The True Perpetuation

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The interesting thing about BN is not the negative self-image and strive for a perfect body, but the way in which the disease perpetuates.
Because the disease adopts reward functions that mimic drug addiction, the ideal body image becomes a secondary reason for the disease.
If the negative self-image was taken away—like Meghan Trainor and others are trying to do—it is likely that people who suffer from BN would still suffer from addictive and harmful behaviors. This is due to their predisposition to these types of behaviors with low self-control complexes in combination with high negative affect.
Yes, the negative affect that results from negative body image would be removed—but the negative affect caused by other stressors in life would not be, and could result in the same reward seeking cycles with other diagnosis—such as drug addiction, alcoholism, or gambling.
The impulsivity of these patients and their lack of ability to deal with negative emotions will likely persist and lead them to other harmful behaviors if negative body image is eradicated in this culture.
The True Promising Solutions
So, in getting to the root of Meghan Trainor’s likely goal—no, she is not going to rid the world of bulimic-like tendencies. She may succeed in lowering the rates of eating-disorders, but in the case of patients suffering from BN, it will likely take shape in a different harmful behavior.
While her songs are catchy and her intentions are good, Meghan’s ideas are not going to solve the problem. What is? Further research into cognitive functions of bulimic patients and their emotion regulation patterns, as well as further research into the regulatory roles of both dopamine and serotonin in decreasing impulsivity.

Disease/Health

The Addictive Nature of Bulimia Nervosa

Posted on March 13, 2016 by / 0 Comment

In the United States, we have some real problems with our bodies. It become a bit obvious when you look at the constant deluge of advertisements thrown at us saying that we are too fat, too thin, too scrawny, too puffy, too wrinkled, too young, too old, too medicated, or not medicated enough. It’s no wonder that our national self image is in the tank.
But beyond making it easier for corporations to pick our collective pocket, there is a real danger to our national health that comes with hating how we look. The number of eating disorders in the United States has risen to affect almost 20 million women and 10 million men at some point during their lives. This means that almost 10% of the current population will have struggled or is currently struggling with some form of eating disorder.
Once an eating disorder has developed it becomes incredibly difficult to be cured. As seen in bulimia nervosa, the brain chemistry of the afflicted person is warped to accommodate the disorder. In bulimia, the initial susceptibility to the disorder is triggered by a number of possible factors including personal stressors, general anxiety, and negative body image.

In order to feel some relief, the person makes an impulsive decision to binge eat which activates dopamine receptors in their brain and provides a euphoric feeling. However, after binging, the person regrets overeating and feels compelled to eliminate the excess calories consumed leading to a purging episode. By exercising control over this one aspect of their lives, people in the throes of the binge/purge cycle are comforted and actually rewarded for this behavior by a positive neurochemical response to their actions including dopamine activation and serotonin inhibition.

The impulsive act quickly become compulsive because brain chemistry adapts to the increased dopamine signaling by decreasing active dopamine receptors. This means that these people now have a higher threshold for normal dopamine signaling are because of this are more at risk for developing depression. Thus the cycle of binging and purging becomes a requisite aspect of everyday life as people with eating disorders experience symptoms very similar to drug addiction.
To escape the cycle, certain types of cognitive or emotional regulatory treatment have been utilized but with limited success. One of the best ways to help a person struggling with an eating disorder is to establish a supportive network that they can rely on. So until our society wises up to the dangers that are quietly infiltrating our lives, make sure to be aware of the signs and symptoms of eating disorders and take care of your loved ones.

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Bulimia Nervosa: a model of deficient serotonin signaling

Posted on March 13, 2016 by / 0 Comment

Bulimia nervosa is a serious, potentially life-threatening eating disorder characterized by a cycle of binging and compensatory such as self-induced vomiting in the purpose of compensating for binge eating. This condition is known to be heavily psychological, with BN commonly associated with negative urgency, the tendency to act in brash actions in response to negative stimuli.
Overall, with this psychological condition come mechanisms in the brain leading to this behavior. One neurological occurrence occurring with BN patients revealed in recent studies is serotonergic signaling. In the brain, there are commonly bottom-up and top-down interactions between significant components of the brain, the amygdala and OFC. These structures work together to regulate many neurotransmitters and neuromodulators, ultimately providing a system to control your emotion. These connections have a role in controlling serotonin (5HT) and dopamine (DA) signaling.
Many experimental designs have demonstrated that low levels of serotonin signaling are associated with greater rates of sensation seeking and reckless behavior, together with greater levels of both negative and positive affect. Considering the system of interest, less serotonin means less top-down and bottom-up signaling between the Amygdala and OFC system in the presence of strong emotion. This results in a stronger and more lasting emotional response, and a reduced ability to consider the long-term consequences of ones actions.
In many brain areas, serotonin modulates dopamine activity. In these instances, with less serotonergic signaling, dopamine levels rise, altering behavior in with increased reward-seeking and risk-taking behaviors. Additionally, high levels of DA activity in the amygdala-OFC circuit are associated with high rates of rash or reckless acts. Overall, subjects with psychological disorders and specifically Bulimia Nervosa have shown to have significantly less serotonin signaling in the brain. This supports the described behavior, with BN patients being unable to control their severe behavior in situations of strong negative emotion.
Serotonin signaling is associated with many psychological disorders, and behaviors associated with emotion. One study showed an inverse correlation between romantic relationship satisfaction (RRS) and level of serotonin signaling. RRS is measured in subjects in relationships, and is imperative for mental and physical health. Often serotonin signaling is measured by a transporter called serotonin transporter promoter polymorphism (5-HTTLPR), a protein essential for function of serotonin, and is often linked to genetic factors. Overall, it was found that those with higher levels of serotonin transporters found higher RRS, but lower social interaction anxiety. These findings demonstrate a correlation between 5-HT signaling and satisfaction within a relationship, showing an interesting perspective regarding the mechanism in which serotonin affects emotion. With a lesser ability to control strong emotion, contentment within a long-time relationship is compromised.
Estrogen and the menstrual cycle have been shown to alter serotonin signaling furthermore. Studies have revealed estrogen has an inhibitory affect on serotonin, leading to a deregulation of dopamine signaling. This finding correlates to the statistic that 11-12 year old girls have the highest rates of Bulimia Nervosa. With a spike in estrogen levels, less serotonin signaling is present to regulate the emotions associated with dopamine. Moreover, rash behaviors such as purging, exercise, or dietary restriction lead to deregulation of the menstrual cycle and decrease the level of available estrogens. This ultimately causes serotonergic disturbances, and cannot be corrected until the individual re-regulates eating patterns.
All in all, serotonin signaling has been linked to depression, anxiety, and many eating disorders. Without serotonin signaling, a loss of control of emotion occurs, leading to abnormal behavior. The role of these neurotransmitters and the role they play in behavior can ultimately be an important focus for future research.

Disease

Novel Brain Scan Technique Could Definitively Diagnose Alzheimer's Disease

Posted on March 2, 2016 by / 0 Comment

What is Alzheimer’s Disease?
Alzheimer’s Disease (AD) is a progressive neurodegenerative disorder that destroys ones memory and many other important mental functions. At a basic level these symptoms are caused by a dysfunction of neurons and the communication of neurons, the synapses. For many years two defining characteristics of AD found in postmortem brains of AD patients were neurofibrillary tangles and amyloid plaques. These two very “sciency” words essentially mean large accumulations of certain types of proteins that cannot get broken down. Along with the tangles and plaques, recent studies have shown a correlation between AD and type 2 diabetes. It seems that in people with AD the insulin signaling pathway in the brain, yes insulin does play a role in the brain, is damaged. The insulin pathway in the brain has been shown to play a key role in our learning and memory. In people with type 2 diabetes their insulin receptors are resistant to insulin. In other words people with type 2 diabetes do not have a problem producing insulin, like people with type 1 diabetes, but their body simply does not respond the way it should to insulin. Researchers believe that insulin resistance is one of the causes of the symptoms seen in AD.
How do we Diagnose Alzheimer’s now?
According to the Mayo Clinic the current action for diagnosing AD is to perform memory and impairment tests, look for behavior changes, look at medical history and rule out other ailments that could be causing these symptoms. Once all of this is done then a doctor may diagnose a person with AD. With that said the only sure fire way to correctly diagnose a person with AD is by looking at the brain postmortem.
Can we diagnose AD with more certainty and earlier?
Recent research at two Canadian universities may have found a way to achieve an earlier and more definitive diagnosis. By studying postmortem brains of patients with AD the researchers discovered an enzyme that gathers around the plaques and tangles characteristically found in AD brains. Not only does this enzyme gather around AD specific plaques and tangles but it seems to stay away from other similar plaques. Using this knowledge researchers were able to develop a small radio-labeled molecule that can bind specifically to these plaques and tangles. The important part about this radio-labeled molecule is that is can show up on PET scans of the brain. Currently there are still some obstacles before this type of diagnosis can be used on for AD patients. For one the radio-labeled molecule has yet to used on humans and the diagnosis would be very expensive.

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Alzheimer's Disease: A Disease Worth the Research

Posted on March 2, 2016 by / 0 Comment

There is no getting around it – Alzheimer’s Disease is devastating. It affects the lives of not only those afflicted, but also their families and friends. And it’s not even one of those things that just weighs on the minds of those involved; it often becomes the center point in familial dynamics. Many times having a family member diagnosed with AD comes with months and years of assistance, planning for the future, and constant stress and worry. And this is for good reason – the disease affects the memory, thinking, and behavior of the patient, with the symptoms worsening over time. But recently, I have heard points being made that an AD diagnosis could possibly be something everyone experiences, whether they live long enough to develop it or not. Before discussing that, however, it’s important to understand what exactly goes wrong in the brains of AD patients.

Although the exact cause of AD has been extensively researched, it is still largely un known. What has been examined is the connection to a faulty breakdown of amyloid precursor protein, or APP. APP is a single-pass transmembrane protein expressed at high levels in the brain that’s broken down into the AB oligomer (ABO) AB-40 by various enzymes. In a normal brain, APP is broken down into AB-42, a slightly larger ABO, about 5% of the time. . At low levels like this, AB-42 is cleared easily by the natural systems in the brain. However, in the brains of AD patients, APP is broken down into AB-42 about 40% of the time, which results in much higher levels of the larger oligomer. At these high concentrations, it begins to aggregate, which leads to the activation of the microglia in the brain. These microglia then destroy and remove cells in an attempt to clear the large AB-42 aggregations. This leads to neurodegeneration – a major factor in AD. Now, there are various other abnormal processes occurring in the brains of AD patients, but it is thought that the aggregation of large ABO’s in the brain could be the most significant.

So, does this eventually happen in everyone’s brain? Does everyone eventually begin to have AB-42 build up, microglia activation, subsequent neurodegeneration, and eventual memory loss and cognitive decline? Current research wo uld suggest that the answer is no; however, I think it’s interesting to explore the possibility that the answer is actually yes. What if this process started with some people at an earlier age than others, or for some it doesn’t start until they would hypothetically turn 110 years old?

It’s a scary thought, that’s for sure. But it also raises a controversial question: should we continue funding AD research if everyone eventually gets it? Is there even a point? One side may say that the amount of money put into AD research is too high, and that even if we did find a “cure” for the disease, a different one would eventually take its place. Another side focuses on the severity of AD itself, how many people it affects, and how AD needs to be further studied. I, personally, take the second side. I think of the multitude of individuals and families that are affected by the specific effects of AD – memory loss and cognitive decline. Although I personally haven’t been affected by the disease, I cannot begin to imagine the toll it must take on those who have. To those backing the side that suggests researching AD is a waste, I can’t help but ask if there could possibly be a worse disease to take the place of AD. But, like many subjects in neuroscience, no clear-cut answer can be determined today. Therefore, the many scientists devoting their lives to trying to understand this disease should continue with their efforts, it is worth the research.

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Could Diabetes lead to Alzheimer's Disease?

Posted on March 1, 2016 by / 0 Comment

In the world of medicine, Alzheimer’s Disease (AD) a hot topic in the recent decades. With it affecting over 90,000 Americans annually, the prevalence of this disease is on the rise. While a majority of research has focused on possible cures or reversing the degenerative affects of this disease, recent studies have taking a different approach to tackling this topic. Rather than concentrating efforts to fix or cure the degenerative effects of Alzheimer’s, researchers have begun to look into preventative care methods and causal mechanisms for this disease. One such correlational condition to Alzheimer’s is type II diabetes.
Characterized by insulin resistance, type II diabetes, also known as adult-onset diabetes, is a disease in which the body is unreceptive to insulin leading to higher concentrations of glucose in the blood. It has also been shown to disrupt many of the neurological pathways leading to development of Alzheimer’s. Insulin has been shown to regulate brain metabolism and energy balance in the hypothalamus along with stimulating memory formation, association, and retrieval in the hippocampus and forebrain. The binding of insulin also plays a major role in cognitive functioning and has been linked to many neuroprotective properties.
Most commonly, patients with Alzheimer’s display two distinct neurological characteristics: senile plaques and neurological tangles. Large clumps of amyloid fibrils (amyloid-beta peptides) are what make up senile plaques. While the aggregation of these peptides chains has shown to be toxic, recent studies have proven that this is not the leading cause of Alzheimer’s symptoms. Rather, it has been cited that the loss of plasticity or neuronal signaling that has been most strongly associated with Alzheimer’s like symptoms and is correlated with the formation of oligomers of Alpha-beta peptides called, Alpha-beta oligomers. These toxins have now been considered responsible for the synaptic loss that encompasses Alzheimer’s disease.

Without the ability for the body to be receptive to insulin, the brain is not able to function properly and can lead to the neurological tangles and plaque build ups as previously described. Because of this, it is essential when discussing preventative care methods to include a healthy diet. This may be the number one preventative care treatment as a healthy diet, along with exercise, significantly decreases the chances of developing type II diabetes. It is important to note that individuals with type I diabetes are not as high of a risk of developing AD since their symptoms can be treated with an insulin agonist. This is because patients with type I diabetes are not resistant to insulin, instead their bodies are not able to naturally produce insulin. Therefore, when given an artificial insulin supplement, the body will function properly.

As a society, if we do not seek to improve our diets, not only will our immediate lives be altered, but the long-term conditions of our lives could be severely compromised. While it may appear that this may just be a biological issue in the science community, if we wish to truly improve the lives of people around the world and in our nation, we must view this as an economic issue as well. Healthy food needs to be more accessible for everyone or else there will be a substantially larger population of people living in high needs nursing homes, contributing to the national economic deficit.

Disease

Connecting Alzheimer's Disease with Insulin Signaling in the CNS

Posted on March 1, 2016 by / 0 Comment

Alzheimer’s Disease (AD) is a disastrous neurological degenerative disease that effects more and more people each year. Cures and treatments for AD have been minimal at best and until recently didn’t show much promise. It was originally thought that the build up of amyloid beta plaques start overwhelming portions of the brain and eventually kill neurons, however, a recent study found that the removal of these plaques from the brain didn’t show in improvement of cognitive functioning in the patients. What instead was found was accumulated amyloid beta oligomers (AβO) causing a synaptotoxin effect.
A new direction of research was observed. The role of insulin in the brain. Until recent years the brain was considered an “insulin-insensitive organ”, but recent research has shown the central nervous system to rely on many insulin actions for potential neuronal survival and other important functions.
Insulin, from the pancreas, travels through the blood stream to the blood brain barrier (BBB) where it crosses and enters the CNS. Here it is known insulin helps regulate brain metabolism by acting on the hypothalamus. Insulin acts on insulin receptors (IR) which are found in various forebrain areas important for memory formation, consolidation, and retrieval. Clearly, insulin signaling is important in memory functioning, and AD has memory disfunction as a primary symptom.
Another recent study found that a build up of AβOs in various areas in the brain could potentially result in a disfunction of IR in neuronal membranes by pushing the IRs intracellular deeming them useless. This would result in a direct cognitive disfunction in whichever area in the brain the IR is associated with, for instance in the hippocampal forebrain would cause memory impairments.
This connection between AD and insulin signaling in the brain opens up a new door for research. It is possible new treatments for AD could arise from the new research of the insulin pathways in the forebrain. Unraveling these mysteries could could reveal powerful therapeutic opportunities for this devastating disease.
Citation:

Easing the anguish of Alzheimer’s disease

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Alzheimer's and Diabetes: The Link We've Been Missing

Posted on March 1, 2016 by / 0 Comment

Until recently the brain was thought to be a insulin-insensitive organ. It has been discovered that there are various actions of insulin in the brain. Insulin acts on the hypothalamus to control brain metabolism and body energy balance. Insulin signaling also plays an important role in all aspects of memory. It is required for synaptic plasticity and learning.
Amyloid plaques are a key trait of Alzheimer’s and for a long time was thought to be the reason for memory loss. After examining brains post mortem there is no correlation between the amyloid plaques and memory loss. The cognitive decline was found to be connected to synapse damage.
Alzheimer’s and diabetes have very similar pathophysiological and clinical traits. Brains with Alzheimer’s disease have defective insulin signaling which leads to synaptic dysfunction and memory issues.
There is currently research being done to discover if the mechanisms that underly impaired peripheral insulin signaling in type 2 diabetes and alzheimer’s are related.
So what does this mean? This means that there may be a direct link between the underlying mechanisms of type 2 diabetes and Alzheimer’s. The current mechanism of Alzheimer’s is pretty unclear. It cannot be diagnosed until after death and because of that it is even more difficult to study.
Now we see that having a healthy lifestyle may not only save you from type 2 diabetes but also Alzheimer’s disease.

That might not be enough for some people, fortunately diabetes are a well researched and treated field. It is difficult to treat Alzheimer’s, because we don’t understand the mechanism. Finding this connection could lead to some treatment choices after the damage has begun. Using anti diabetic treatments for patients with memory loss could be on the horizon.