If one were to list the most common fears of people today, they would likely come up with a conglomerate including things like death, heights, spiders, and clowns. My biggest fear, however, is perhaps not so run-of-the-mill: dementia is something that’s all too common and all too detrimental to overlook as a serious life issue. Many young people probably don’t consider it a major concern in their lives – that it would happen years down the road and that it wasn’t really something they could control. Recent research, however, has drawn some surprising connections from dementia and Alzheimer’s to diabetes, particularly type II, which is mostly dependent on lifestyle. When they say that the decisions you make today affect you down the road, this is no exception.
Type II diabetes is characterized by high blood sugar caused by insulin resistance or insulin deficiency. It accounts for 90% of diabetes cases and correlates highly with obesity; both diseases have been growing tremendously in recent years. As serious a disease diabetes is already, there is evidence to show that it is a significant risk factor for developing Alzheimer’s later in life. The link between the two disorders seems to be insulin resistance. Cells resistant to insulin uptake don’t take in as much glucose either, leading to a deficit in energy. This makes the cell vulnerable to oxidation, which is a main cause of neurodegeneration. Another suggested pathway involving insulin resistance involves the dysregulation of lipid metabolism; improper disposal of lipids from brain cells promotes ceramide (a lipid class) accumulation, causing inflammation and toxicity as well as beta-amyloid accumulation, which leads to amyloid plaques and neurofibrillary tangles, resulting in neurodegeneration. Although the causes of type II diabetes include genetic factors, lifestyle is a main contributor, involving obesity, lack of physical activity, and poor diet.
Another risk factor greatly associated with Alzheimer’s development is a dysfunctionality of apolipoprotein E (ApoE). This is largely a genetic risk factor, but recently has been associated with vascular health. ApoE normally works against inflammation and plaque formation in the brain, but certain isoforms of the protein that translate to dysfunctional alleles of the gene. ApoE4 has been found to be the largest known genetic risk factor for developing Alzheimer’s disease; this isoform does not efficiently bind lipids for transport out of the brain, leading to inflammation and beta-amyloid accumulation as mentioned before. There is a mechanism involving vascular health, however, where ApoE4 does not control the inflammatory molecule cyclophilin A in the brain; the resulting increase in cyclophilin A activates the enzyme MMP-9, which causes damage to the blood brain barrier (BBB). Damaging the BBB can lead to many adverse effects, such as allowing neurotoxic chemicals that wouldn’t otherwise be able to cross the BBB into the brain, as well as increasing vulnerability to beta-amyloid deposit and accumulation. Although this is mostly a genetic risk factor via ApoE4, increasing vascular health can possibly counter the damage caused to the BBB, lessening the adverse effects of ApoE4 and lessening the risk for developing Alzheimer’s.
Although there are definitely genetic risk factors that play a significant role in the development of Alzheimer’s, the fact that there is growing evidence for lifestyle contributors should not be ignored. Lifestyle plays a huge role in the development of type II diabetes, which is now linked via insulin resistance to Alzheimer’s. The possible role of vascular health in maintaining the BBB and countering the damaging effects of ApoE4 is a fairly promising one as well, and hopefully there will be more research done to confirm this relationship. Losing the ability to think clearly for myself is one of my greatest fears in life. Taking into consideration these new studies, my lifestyle choices will definitely take a turn for the better. I hope others do the same.
Is Alzheimer's Disease really "Type 3" Diabetes?
A rising health concern throughout the world is diabetes. The number of people diagnosed with diabetes in 1985, around 30 million, increased nearly ten fold to 285 million in 2010. Similarly there has been an increase in the amount of cases of Alzheimer’s disease. Although the increase in these two dispositions may appear coincidental research has shown that there is a correlation between diabetes and Alzheimer’s disease. More specifically research has focused on the role insulin plays in the body and recently the brain.
First, it is important to understand what the role of insulin in the body is. Insulin’s primary job in the body is to allow for cells to intake glucose, or sugar, in order to use as energy. Diabetes is a disease in which for some reason insulin fails to complete its job. There are two main types of diabetes: Type 1 and Type 2, also apart of Type 2 is Gestational diabetes mellitus (GDM) which is the onset of diabetes during pregnancy. According to some researchers there is a “Type 3 diabetes.” Although not universally recognized due to lack of research, Alzheimer’s disease is sometimes referred to as “Type 3 diabetes.” Now you’ll probably ask, how can insulin relate to a neurodegenerative disease like Alzheimer’s? The answer is that insulin’s role in the brain is as important and more complex than throughout the rest of the body.
In the brain insulin is most concentrated and active within the hippocampus and frontal lobes. The hippocampus functions as the memory center of the brain and insulin affects the hippocampus by regulating the neurotransmitter acetylcholine. Acetylcholine basically acts as a bridge between stimulus, insulin, and brain function, memory and learning. The question then arises, what turns a normally functioning insulin receptor inactive? Insulin resistance is the cause of decreased insulin sensitivity and diabetes.
Insulin resistance involves normally healthy neurons becoming unable to respond to insulin stimuli. The picture shows how some insulin receptors are active while others are non-responsive. Because the neurons are not processing the signals from insulin, the cell in not able to take in glucose. This means that the cell does not receive the energy required to facilitate normal cellular functions and excess glucose stays in the blood stream. Without a source of energy brain cells within the hippocampus and frontal lobes enter their termination state and begin to die. Based upon this, researchers focused in Alzheimer’s disease believe insulin resistance is a cause for the neurodegeneration associated with Alzheimer’s disease.
Compared with the rising levels of diabetes throughout the world the number of cases of Alzheimer’s disease is likewise increasing. A likely cause of this correlative increase is due to the poor eating habits that are on the rise in the united states. The onset of diabetes continues to occur at earlier ages and thus the likelihood of earlier onset of Alzheimer’s disease is also expected, although more research is needed on this topic. The genetic consequences of permanent insulin resistance are more likely to cause a predisposition to Alzheimer’s disease in the children of those who possess insulin resistance. Further studies is required to fully understand the consequences of insulin resistance on the brain as well as the development of Alzheimer’s disease based on that resistance.
Sources:
http://www.hbo.com/alzheimers/science-insulin-in-the-brain.html
http://diabetes.niddk.nih.gov/dm/pubs/insulinresistance/
http://www.jci.org/articles/view/59903
http://onlinelibrary.wiley.com/doi/10.1111/j.1582-4934.2011.01318.x/full
Diabetes…An American Epidemic
The number of diagnosed cases of diabetes being classified as type 2 has been rising over the past years in America. The average age of people with type 2 diabetes has been declining as well. But what are the repercussions of more and more people, especially young people, developing this disease?
Type 2 diabetes used to be classified as ‘adult onset’ meaning it presented itself later in life while type 1 diabetes was termed ‘childhood’ as it typically presented itself in childhood or early adulthood. But other than timing of diagnosis, what is the difference between the two types of this disease? In type 1 diabetes, the person’s body is failing to produce insulin. In type 2 diabetes, the person’s body has a lowered number of insulin receptors meaning while there is insulin in the blood, the body is not able to use it properly. When the body does not have enough insulin or cannot use it properly, glucose levels become unbalanced and the body’s metabolism is thrown out of whack.
As more and more children are being diagnosed with an inability to process insulin and therefore glucose, people are wondering what problems this will create later in life. Recent research has found possible links between diabetes and Alzheimer’s form of dementia. How can this be?
While we typically think of insulin as being a hormone which is in the periphery of the body, it is also found in the brain. In type 2 diabetes, the body is trying to use insulin which may lower insulin levels in the brain. Lowered insulin levels in the brain can disrupt other brain chemical levels which ultimately can lead to disorders of the brain such as Alzheimer’s. Alzheimer’s is a degenerative brain disorder caused by depletion of neurons through plaque formation and fiber tangles. It is a disease which puts great pressure on the effected patients family as well as society in general because of the elevated cost for care.
Both these diseases have lifelong implications after diagnoses and can ultimately lead to death. So how can we prevent this inflated rate of diagnoses from continuing?
First, we need to address the issue of increased number of type 2 diabetes cases. Preventative measures for type 2 diabetes include managing weight, cholesterol and other health issues related with obesity. This needs to be done in people of all ages but especially children because overweight children have a higher risk of being diagnosed with diseases like type 2 diabetes at a younger age. People also need to try to be more active. Things as simple as taking a walk around the block or taking the stairs instead of the elevator can help manage weight. By managing these things, the number of cases of type 2 diabetes will hopefully start to go down, especially in children.
Because of a possible link between diabetes and Alzheimer’s, lowering the rate of type 2 diabetes will hopefully help to manage the number of Alzheimer’s patients.
Developing Diabetes Now May Lead to Alzheimer's Disease Later in Life.
This week in class we read an article detailing how the symptoms of type 2 diabetes can lead to Alzheimer’s Disease later on in life. The main issue involved in type 2 diabetes which leads to Alzheimer’s is that your body develops a resistance to your own body’s natural insulin. This leads to many processes in the brain becoming altered with the end result of them acting together to give someone Alzheimer’s.
One of the primary results of type 2 diabetes, the aforementioned insulin resistance, leads to an increased use of insulin in the periphery, that is areas outside of the central nervous system, as well as a decreased flow of insulin into the brain. One result of this lack of insulin is a decrease in the production of acetylcholine, a vital neurotransmitter in the formation of memories. Acetylcholine depends on insulin to induce the breakdown of glucose, a sugar, into pyruvate, which is then oxidized to form Acetyl-CoA which is a necessary to form acetylcholine.
Insulin is also an important signal molecule. It interacts with N-methyl-D-aspartate (NMDA) receptors in order to allow calcium ions into our neurons. This influx of calcium into our nerve cells activates calcium ion dependent enzymes withing the cell. Another important function of insulin as a signal molecule is that researchers have found that the act of insulin signaling in your brain decreases the number of receptors for ADDL’s. ADDL’s degrade your nerve cells by binding to their synapses, which are where the nerve cells pass on either chemical or electrical signals. It has also been found that inhibition of insulin signaling in the brain leads to the hyperphosphorylation of tau proteins within the brain. These tau proteins, which are normally soluble, begin to clump together and interfere with the inner workings of the cell. This happens because the protein GSK-3-beta, which is usually inhibited by insulin, is left unchecked to phosphorylate tau proteins as it pleases.
Another important function of insulin is that it helps with inflammation. Normally, epinephrine, which is anti-inflammatory, is regulated by insulin, but without insulin the ADDL’s in your system continue to inflame the tissue, and in fact create a self-reinforcing process which produces more ADDL’s.
Besides the effects of diabetes on your body, in small groups we talked about what we can do as a society to decrease the prevalence of avoidable diseases like diabetes. One of the major things we talked about in this area is whether the government should get involved in the food choices that people make. Bad food is also cheap food, so a lot of people find it easier to simply go out to eat rather than prepare a healthy meal, should the government help out by subsidizing healthy foods, or by taxing unhealthy foods. One group member even posed the question of whether obese people should be able to qualify for government health insurance. Personally, I think the government should get involved simply because the percentage of the population that can apply for medicare is getting larger and as people still say that it is a service that they want, the government should take steps to ensure that the people entering into the program do not have the risk factors associated with these avoidable illnesses. I know that the idea that the government should give tax breaks to companies that supply their employees with gym memberships has been thrown around. I feel like that is one good way that the government can do something to help people while not stepping on so many toes.
"I seem to have lost myself" – Alzheimer's Disease
In the year of 2006, there are nearly 27 million people who suffer from Alzheimer’s disease (AD) globally. The latest Alzheimer’s statistics estimated that 5.3 million people of all ages have AD in the United States. And these numbers are said to be doubled every twenty years. Most AD patients will eventually lose the ability to perform day-to-day tasks and require caregivers which often are people around the patients (e.g. family members, friends). Without a doubt, AD is one of the most influential diseases in this modern world.
AD is a gradual, fatal disease which the scientists believe is caused by the abnormal activity of two proteins called beta amyloid and tau which form Plaques and Neurofibrillary Tangles respectively. Although there appears to be a strong correlation between AD and the ages of the patients, it is not a normal aging process. In the early stage of AD, these plaques and tangles start to build up in the hippocampus and lose their ability to consolidate short-term memory to long-term memory. As AD progresses onto different stages, the plaques and tangles spread and destroy other regions of the brain, the patients eventually loss the abilities to use languages properly, to solve problems, to have logical thoughts, to control emotions, to access stored long-term memory, and in the last stage, it reaches the part of the brain which regulates the breathing and the heart, and ends a person’s life. There is no direct ways to diagnose AD while the patients are still alive, and there is no cure for it. The medicines available to the public can only slow down the progression of AD.
Many researches have been done on AD related subjects, although the god of science has not yet blessed us with a cure for AD, there are promising evidences which show the correlation between type II diabetes and AD. Studies have found that patients who suffer from type II diabetes are four times more likely to suffer from AD when compared to healthy people. Since both diseases are closely related to insulin resistance and insulin resistance could be controlled by diet and exercises, there might be ways to lower the chances of getting AD. There are many other ways that have been suggested to help prevent AD, such as playing cards, reading, and any kinds of brain exercises.
In America, where more than 35% of the total population is obese and almost 10% of the total population suffer from diabetes. I believe it is very important for everyone in the society to be responsible for themselves, and to make good life choices. My grandmother is in her nineties, and unfortunately, she has been diagnosed with AD. She would sometimes forget if she has had lunch or not, and she also suffers from Auditory hallucinations. All we could do is to hire a personal caregiver to be with her all day and take good care of her. So far it hasn’t been much of a trouble, but everyone in the family are all afraid of one day she might not recognize her family anymore. And it has been really hard on us. After all, AD does not only cause functional loss of the patient, but also brings pain to the patient’s family and the caregivers.
To learn more about AD: http://www.youtube.com/watch?v=9Wv9jrk-gXc, http://www.alz.co.uk/research/world-report-2011
Eating out more often may lead to Alzheimer’s disease
Today in the United States the way of life is becoming increasingly quick-paced. People are more often getting a quick breakfast, lunch or dinner from fast food restaurants. In some, this habit becomes excessive and may lead to weight gain and if not checked, may lead to obesity. This is a problem that exists with many Americans. According to the CDC “more than 35% of U.S. men and women were obese in 2009–2010” Obesity can increase the risk of many diseases such as type II diabetes and it has been found recently that there is a tie to this type of diabetes and the infamous neural degenerative disease known as Alzheimer’s.
Type II diabetes is a metabolic disorder that is characterized by high blood glucose because the body rejects its own insulin to lower these levels. This rejection is also accompanied by low levels of insulin in the body to begin with. We can treat this disease by administering insulin to these patients in order to lower their blood sugar levels and in conjunction with this we can encourage diet and exercise to solve the initial obesity problem. So diabetes is theoretically very easily treatable but obviously has no actual quick cure. When we look at Alzheimer’s there is no great way to treat it and maintain it. It is a continuous degradation of the mind and physical death of neurons and shrinking of the brain. All we can do for these patients is try to slow down the process and hope to make them comfortable.
The connection for these two diseases comes from the role of insulin in the brain. Insulin is important in the central nervous system because it regulates key processes such as neuronal survival and longevity and even plays a role in learning and memory. Type II diabetes’ main effect on its victims is low insulin levels in the body and thus lower levels in the brain. Also accompanying type II diabetes is the reduced insulin transport in the brain. These consequences result in neurons becoming energy deficient and then are susceptible to oxidation decreasing the cells’ functions. A main cause of Alzheimer’s is the accumulation of beta-amyloid masses in the brain that destroy functionality of the neurons around it. Low levels of insulin in the brain cause certain active sites of the cells of the brain to become less active and this indirectly promotes the production of these masses. In short, type II diabetes can possibly result in the acquisition of Alzheimer’s disease.
This connection raises many new thoughts. The way we eat does not solely affect our weight and we’ve known this as those that are obese are often at risk of diseases relating to the heart. Things change when our eating habits begin to affect our minds and their longevity. What can we do to fix this? Should the government begin to regulate the food market? It seems that the general public cannot make the right decisions when it comes to eating. Soon, as obesity rates climb, we will see a dramatic increase in diabetes and then even a climb or earlier onset of Alzheimer’s. If we begin to see an early onset then the average obese person will be able to contribute less creating a burden on society in terms of healthcare taxes. Can we even begin to solve this problem at the basic level of encouraging diet and exercise or do we have to focus on treating Alzheimer’s because we cannot count on people to make good choices about their lives? Education for children may need to be set into place to ingrain the connection of eating, obesity, diabetes, and Alzheimer’s much like we already drill the negative effects of cigarettes and alcohol into our youth.
There are so many things that need to be done about this issue but at so many levels that it is hard to know where to begin or where to focus our energy and attention. There are many negative implications for the future of these diseases as trends seem to be pointing toward a more obese America. At the basis of it all, we need to begin to watch what we eat so we may maintain our minds as we age.
THC and Cannabinoids Involved in Mental Disorder Therapies
Of the most notable mental disorders, anxiety, depression, schi
zophrenia, and eating disorders have been examined with relation to endocannabinoid therapies. The main theme behind endocannabinoids is that there is a direct link between decrease in them and an increase in observed anxieties and depression in tested mice. There was even a proposed method for treating eating disorders with this same assessment. As well, an increase from substances such as medical marijuana that contain and boost endocannabinoid levels in the body would counteract these disorders; the main problem with this method of treatment lays in the correlation, not causation, between marijuana usage and schizophrenia. The pharmaceuticals available to those who seek treatment will be dependent on further mice studies as well as the possible legalization of medical marijuana.
The two types of endocannabinoid receptors, those that bind to the incoming endocannabinoids in the cell membranes of the brain’s neuronal cells, are CB1 and CB2 alpha G proteins. What occurred most frequently in testing mice with the blockage of CB1 receptors was that they were necessary for the management of anxiety symptoms. The parts of the brain that handle stress symptoms were the areas of the brain where endocannabinoids were produced and CB1 receptors were expressed the most there. Additionally, deleting the CB1 receptor gene from mice enhanced depression-like symptoms and the ability to accept rewards. This also targets the feelings of pleasure/reward similar to those that humans experience when achieving a goal or eating a pleasurable food. CB2 receptors, when increased in expression, led mice to show less stress in response to stressful situations or stimuli. Cannabidiol, the non-psychoactive component of medical marijuana, has been shown to stimulate and increase amounts of CB1 receptor binding and counteract depression and anxiety. A future hope in research is that this same cannabidiol will allow for an increase in the pleasurable response from eating such that those with anorexia or bulimia will have proper treatment for once aspect of their disorder.
The overhanging problem with these treatment methods is that the current options are to either create THC or cannabidiol synthetically to produce pharmaceutically, or to use the naturally occurring forms in marijuana plants. The latter, of course, is illegal for medical therapeutic use in the majority of the United States. The draw towards a synthetic cannabidiol is the increase in the ratio of it in comparison to THC, which, in low ratio amounts, has a growing correlation with schizophrenia symptoms in marijuana users. The more THC there is in comparison to cannabidiol in marijuana or other compounds, the higher the likelihood of patients exhibiting schizophrenia-like symptoms. This is partially due to the prolonged activation of these endocannabinoid receptors in marijuana users, demonstrating an increase in likelihood of schizophrenia development in those patients who are already at risk. While this rate of risk is extremely low, it is still a prevalent concern in further developments of therapeutic drugs and legalization of medical marijuana. It seems impractical to produce a drug or legalize one that can result in a side effect as drastic as schizophrenia, but at the expense of treating depression, anxiety, and eating disorders, further research must be carried out to determine the best therapeutic method.
Photos courtesy of Google images.
How Might Medicinal Marijuana Affect Soldiers With PTSD?
Psychiatric disorders are under-reported illnesses that affect the quality of life for the suffering patient. Post-Traumatic Stress Disorder (PTSD) is a subset of anxiety disorders in which one suffers from episodes of panic and anxiety after an extremely stressful situation. These feelings are brought back by a trigger, such as sounds and events that may remind the individual of the initial cause. (See http://www.ptsd.va.gov/ for more information about PTSD. While the stigma associated with reaching out for psychiatric therapy is still very much relevant, receiving this help is becoming both more common and socially acceptable. In response to this, the market for prescription drugs that treat those with mental issues is very profitable. Much is still unknown about all of the chemical pathways of the brain, and new findings may prove important in developing new pharmaceuticals. Activity and signaling in the brain is an area of continued research.
The endocannabinoid system plays a role in areas of the brain that function in memory, mood, cognition, and emotion. CB1R, a type of cannabinoid receptor, is essential for handling stressful situations that may result in anxiety and aggression. When this receptor is removed (referred to as CB1R knock outs), studies show that that mice exhibit increased anxiety and increased aggressiveness, especially in highly stressful situations. In addition, CB1R enables behavioral adaptation following the development of negative memories.
Phytocannabinoids are derivatives of marijuana, or cannabis, which can activate the endocannabinoid system and alter the central nervous system. While parts of the plant can be helpful in artificially stimulating the body’s response to stress, other parts of the plant can lead to negative effects. THC (delta-9-tetrahydrocannabinol) is the chemical compound found in cannabis that is responsible for addictive and psychotropic properties. When abused, the changes to the central nervous system may lead to dependence.
Should marijuana be prescribed for soldiers returning with PTSD? Positive and negative consequences exist and would have to be weighed when making a decision in this case. Stimulation of the endocannabinoid system would lower anxiety levels, decrease aggressiveness, and assist in the elimination of destructive memories. These benefits, however, may not outweigh the harm that could ensue from the use of marijuana by those with PTSD, as it does not usually exist as the solitary problem for these individuals. Alcoholism is common in veterans as is abuse of other controlled substances and illegal drugs. (See http://www.drugabuse.gov/publications/topics-in-brief/substance-abuse-among-military-veterans-their-families for statistics and more information regarding substance abuse among veterans). The addictive properties of marijuana that lead to dependence may be destructive for an individual trying to cope with the stresses and imagery associated with war. Substance abuse of alcohol, marijuana, street drugs, or prescription drugs will only delay the healing that is desired.
Legalization of marijuana is a highly debated and highly controversial issue. While it can treat pain, anxiety, relieve nausea and increase appetite in chemo patients, and relieve eye pressure for those with glaucoma, there are definite risk factors that need to be considered. In the case of use of marijuana to treat the symptoms of PTSD, there is just as much room for debate. More studies will need to be completed before the whole picture can be known.
As with any other treatment, one should consult with a doctor before beginning any sort of action plan. Each individual should evaluate their own needs, genetic and environmental risk factors, and possible benefits before seeking prescriptions for any psychiatric disorder.
Endocannabinoid Manipulation: A New Frontier in Psychotherapy
Last Monday in class we read an article detailing the research of the use of endocannabinoids in the treatment of certain psychiatric disorders. Before we begin it is important that y0u understand what endocannabinoids are and what their normal role is in the human body. Endocannabinoids are a kind of neurotransmitter that is present in the body that influence your perception of appetite, pain sensation, mood and memory. There are two primary endocannabinoids that function in the endocannabinoid system, they are anandamide and 2-AG. These chemicals interact with two different receptors, cannabinoid receptors 1 and 2(CBR1, CBR2). CBR1 is found mostly in the brain, CBR2 was thought to be only present in the peripheral nervous system, but has only recently been discovered in the brain. This being said, the article focuses on how numerous psychiatric disorders affect this system and certain treatments that have been tried in order to remedy them. What most of these disorders boil down to is the matter that the endocannabinoid system, the relationship between the endocannabinoids and their receptors, is out of balance. In anxiety, it has been found that CB1R’s, which act in order to maintain an appropriate anxiety level in stressful situation, as well as to help in the reduction of fear responses in the body and to adapt to such situations in the future are not present in sufficient amounts in order to maintain healthy levels of anxiety, the same goes for CB2R’s. It has also been shown that lack of CBR’s are responsible for depression. Interestingly enough, schizophrenia appears to result from CBR’s being expressed in the wrong places, put another way it is not a matter of the system functioning improperly, but that it did not develop properly. The article also makes it a major issue to point out that cannabinoid use in adolescents and people with certain genetic abnormalities show an increased risk of developing shizophrenia later in life. Another major focus for this article was on the endocannabinoid cannabidiol(CBD) and its effects on these psychiatric disorders. It was interesting to see that CBD would only reduce anxiety once it had passed a certain threshold, whereas up until that threshold, it would actually increase anxiety, the researchers even found that an overdose of CBD would increase anxiety in test subjects. Researchers also found that CBD may have anti-psychotic properties. The article also talks about the interest that researchers have in treating eating disorders through endocannabinoid manipulation. It recounts numerous drugs that reduce nausea for cancer patients, induce appetite in AIDS patients, help with weight loss and help treat spasticity which results from multiple sclerosis.
All in all, it was a very interesting article and it seems to me that the research that these people are doing could lead to some promising treatments for very serious disorders. However, I do have one issue with people saying that because certain people are genetically predisposed to developing schizophrenia with cannabinoid use is not a sufficient reason in and of itself for the continued prohibition of marijuana for personal use. Certain people are genetically predisposed to become alcoholics, but people are not clamoring to ban alcohol for everyone because certain people unknowingly possess this genetic trait. That’s my bit, I’ll leave you until next week with my next rehashing of a scientific article.
Marijuana as a treatment for eating disorders?
There is a great deal of stigmatism about weight in the United States. While there is some media about self-acceptance and building confidence we constantly encounter a barrage of messages (whether intentional or not) through adds, television, magazines, the internet, celebrities that show unrealistic body images. Articles in magazines emphasize quick fix weight loss on the front cover along with celebrities in scant clothing or stories about how someone famous gained 20 pounds (The horror! The horror!). I feel like I see advertisements such as
Every time I’m on the internet. And we do have unrealistic expectations.
| Average U.S. Woman | Barbie Doll | Store Mannequin | |
| Height | 5’4’’ | 6’0’’ | 6’0’’ |
| Weight | 145 lbs. | 101 lbs. | N/A |
| Dress size | 11-14 | 4 | 6 |
| Bust | 36-37’’ | 39’’ | 34’’ |
| Waist | 29-31’’ | 19’’ | 23’’ |
| Hips | 40-42’’ | 33’’ | 334’’ |
Sonenklar, Carol. 2011. Anorexia and Bulimia (USA Today Health Reports: Diseases and Disorders. ) Minneapolis, MN: Twenty-First Century Books.
It’s no wonder that rates of eating disorders continue to increase. A little over a year ago one of the girls I babysat for in high school was diagnosed with anorexia. She is 12 years old. This is when eating disorders got real for me.
First, a few factoids about eating disorders
- An eating disorder is characterized by abnormal eating patterns that attempt to satisfy a psychological rather than physical need. The three most common disorders are anorexia nervosa, bulimia nervosa, and binge eating disorder. Anorexia nervosa is characterized by self-starvation, weight loss, an irrational fear of gaining weight, and a distorted body image. Bulima nervosa is characterized by a cycle of compulsive binging followed by purging through various means, such as vomiting, laxative/diuretic abuse, and extreme exercising. Binge eating disorder is the most common disorder and is characterized by frequent periods of compulsive overeating without accompanying purging behaviors.[i]
- Nearly 10 million females and 1 million males have a form of anorexia or bulimia in the United States. Millions more are struggling with compulsive eating disorder. Additionally, over 70 million people worldwide struggle with an eating disorder.[ii]
- Forty percent of new cases of anorexia are in girls between the ages of 15 and 19.[iii]
Marijuana in the Brain
Marijuana has 2 active chemicals: tetrahydrocannabinol (THC) and cannabidiol, both of which are linked in the endocannabinoid neurotransmitter system. The endocannabinoid system works backwards from many other neurotransmitters because it releases signals from the post-synaptic neuron to the CB1 and CB2 receptors on the pre-synaptic neuron as shown in the diagram below.
THC has been related through studies to the psychoactive, munchies, addictive qualities of marijuana and in high doses can cause or increase anxiety. There have also been studies that show that endocannabinoids interact with the dopamine system, playing a role in drug taking and seeking behaviors. [iv] Cannabidiol has been related to the therapeutic effects which is why marijuana is used in cancer treatments,pain relief, and has also been used as a treatment for schizophrenia.
Marijuana as a treatment for eating disorders
Marijuana has also been used as a way to help AIDS patients maintain a healthy weight as an effect of their disease they lose appetite and stop eating. This is part of the premise of using marijuana as a way to help gain or lose weight because of it’s link to the reward system and studies have shown that endocannabinoids CB1 receptors in the hypothalamus play a large role in food intake. Obviously, this is a very simplified synopsis of how the endocannabinoid system could be linked in a way that would help with the treatment of eating disorders. There is a lot that is still unknown about the endocannabinoid system and all of the parts of the brain of which it is an integral part. One of the objections that one could make about using marijuana as a medical treatment is that it is not specific enough to the effected brain area. Even if scientists were able to create synthetic products to emulate the positive effects of the drug without the addictive or psychoactive effects, there is currently no way to target specifically the hypothalamus, if that is the only part of the brain that is needed to be targeted with eating disorders. Is there enough known about the diseases or the endocannabinoid system to use it as a treatment? Another part to take into consideration is that a large part of the disease is about body image and perception, and while the treatment may help patients gain weight or change some stimuli of eating to positive, is that going to help with body image?
The legalization of marijuana is a complicated subject and there is a lot that we do not know about how the drug effects out brain. It has been shown to have therapeutic effects, whether or not those effects can help with eating disorder treatment is also very complicated and could use more research.
If you or someone you know have an eating disorder or you would like more information about eating disorders visit http://www.nationaleatingdisorders.org/
[i] Sonenklar, Carol. 2011. Anorexia and Bulimia (USA Today Health Reports: Diseases and Disorders. ) Minneapolis, MN: Twenty-First Century Books.
[ii] Sonenklar, Carol. 2011. Anorexia and Bulimia (USA Today Health Reports: Diseases and Disorders. ) Minneapolis, MN: Twenty-First Century Books.
[iii] Eating Disorders Statistics.” National Association of Anorexia Nervosa and Association Disorders. 2012. Accessed: September 29, 2012.