Imagine sitting down to dinner with family and friends to enjoy a nice, healthy meal. Now snap back to reality and think of how busy your life is and how often you decide to go out to eat. In today’s society eating seems to be more like a distraction, interrupting people from their fast-paced lives. As a result, people are looking for the quickest options for breakfast, lunch, and dinner. However, by eating out too often people are developing unhealthy eating habits. At times these eating habits might exceed what is optimal leading to obesity.
You may be thinking “ok yeah I gained a few pounds but what’s the problem with that?”. One of the main problems is the rise in the number of cases of type 2 diabetes caused by obesity. In fact the number of cases of diabetes is rising at an alarming rate worldwide. According to WebMD Health news the number of people diagnosed this diabetes has double to a reported 350 million cases since 1980. Type 2 diabetes occurs when the body produces insulin, but either not enough insulin is produced or the body does not properly use the insulin which is produced. This is called insulin resistance. Since the purpose of insulin is to transport glucose (sugar) into the body’s cells to use as energy, a result of insulin resistance is too high of glucose levels in the blood and not enough sugar in the cells. Therefore, your body is basically starving. Although type 2 diabetes has been around awhile, new research has hinted at a link between type 2 diabetes and Alzheimer’s disease dementia.
The key link between type 2 diabetes and Alzheimer’s disease appears to be the affects of insulin resistance in the brain. According to the article discusses in class, insulin acts through a series of important processes to regulate neuron survival, aging, as well as memory and learning. However, when people have type 2 diabetes insulin found in the brain may not properly regulate these important biological processes. This can lead to improper regulation of the biological processes resulting in overproduction of beta-amyloid and tau proteins. When beta-amyloid protein builds up forming plaques, the brain is more susceptible to oxidative stress which can result in the death of brain cells. Likewise, if too many tau proteins are constructed they begin to bunch up causing a deficiency of nutrient transport in the brain and therefore the death of brain cells. So what can be done to help fix this situation?
The best way to help with this situation is to try and avoid developing type 2 
diabetes by eating healthy and working out regularly. Eating healthy and working out will help fight off obesity and therefore type 2 diabetes. However, as stated in the introduction everyone is very busy and working out regularly may not be possible. This raises other, broader questions about American society and its eating behavior like, “Should it be the government’s responsibility to step in and regulate the food industry to force the general public to eat healthier?” and “If the link between Alzheimer’s disease and type 2 diabetes is true, what actions should be taken to help children and young adults who are developing type 2 diabetes at younger ages than normal?”.
Although, it is extremely unlike that everyone who eats out will develop unhealthy will develop type 2 diabetes and therefore Alzheimer’s disease, it is important to be aware of the possible implications your everyday decision may be having on you, your body, and possibly American society as a whole.
Sources:
http://onlinelibrary.wiley.com/doi/10.1111/j.1582-4934.2011.01318.x/full
http://diabetes.webmd.com/news/20110627/diabetes-rates-double-since-1980
http://vegetarian.procon.org/files/1-vegetarian-images/usda_food_pyramid_large.jpg
Insulin and Alzheimer's
5.4 million people of all ages have Alzheimer’s Disease (AD) in the US, 5.2 million of that 5.4 million are ages 65 and older, according to Alz.org. This statistic means that 1 in every 8 older American has Alzheimer’s. Alzheimer’s is the 6th leading cause of death in the US and payment for care of those with AD is estimated to be $200 billion. The following link goes to a site with lots of information on Alzheimer’s Disease symptoms, diagnosis, statistics, treatment…etc.
http://www.alz.org/downloads/facts_figures_2012.pdf
Recent findings have led experts to consider AD to be Type 3 Diabetes. The findings have been based on insulin’s effect (or lack thereof) on aging and brain cell death. Experts have found a correlation between people who have type 2 diabetes and those who develop AD. In fact, the correlation goes all the way back to weight gain: weight gain (chronic) leads to obesity, which sometimes leads to Type 2 diabetes which now is found to lead to AD.
Experts think that a decrease of insulin in the brain or a decrease in the “potency” of insulin in the brain is what leads to cell death and then to all the effects of AD including memory loss, inability to do simple task or tasks once able to do, time or place confusion and changes in mood and personality. What they are finding as the cause of AD is a lowering of insulin effect in the brain which causes an enzyme to activate far more often than it should, which leads to hyperphosphorylation of a protein labeled as the τ (tau) protein. Hyperphosphorylation of tau leads to the proteins aggregating, which blocks functions of brain cells and causes them to be broken down, leading to lower brain functions. Sorry for the neurochemical jargon. Basically what all that mumbo-jumbo means is that insulin stops the “bunching up” of tau proteins and keeping the brain cells from breaking down.
One thing we talked about in our group discussions is whether research should be focused on how to prevent AD or to creating a “quick fix” drug with minimal side effects. And the overall consensus was that prevention was the best route because preventing AD also can help prevent type-2 diabetes. Also messing with insulin in the body is risky because insulin has other jobs besides blood glucose control and brain cell survival.
Another topic was the ethics of trying to end the aging process and whether or not it is worth all the time and effort and money that would go into it. Again we had a general consensus that it wasn’t worth all the time and effort because the older you get the more chance you have of developing numerous age-related illnesses and disabilities. Another aspect is if we slow the aging process, will we age differently in terms of brain vs. body. What I mean by this is if slowing the aging process works, will it slow body aging, brain aging or both? Will our brains be “younger” than our bodies, vice versa, and what effect on the individual will this have?
As you can see, there still remains a lot of work in order to understand exactly what AD is and how we can go about preventing or treating it.
Next week is glutamate and its role on opioid addiction.
Aging, Diabetes, Alzheimer's and Insulin
In class this week, we talked about the connection between Insulin, Diabetes, and Alzheimer’s Disease. In type 1 diabetes, the cells of the pancreas that create insulin stop producing it. One of the most common ways of combating this disease is to give regular insulin shots. Type 2 diabetes is characterized by insulin resistance: although the body may have regular levels of insulin, the effect of insulin is decreased, usually from fewer receptors. Alzheimer’s disease is characterized by dementia: as state where the patient suffers impairments to cognition, reasoning and communication skills as well as confusion about the time and place and delirium for a prolonged period of time. Connections seen between Alzheimer’s disease and diabetes or insulin resistance has caused some to call it type 3 diabetes.
Insulin controls the uptake of glucose into cells so that they can be active and use energy. In the case of insulin resistance, insulin is unable to fully perform its job of having cells take in glucose. This has been theorized to be part of why Alzheimer’s patients have cognitive defects: in the dearth of glucose, they are less responsive which leads to mental impairment. To deal with low levels of energy, sometimes the cell will also consume important molecules for the cell’s integrity or be unable to produce important molecules leading to cell death; which, in the case of the brain leads to even more irreversible mental impairment.
Another key function of insulin is the role that it plays in aging. In all animals, insulin controls the expression of age related characteristics (think about things like grey hair, facial hair, and so on); insulin levels are responsible in part for the age of our bodies. One of the defining characteristics of the aging brain is that it develops insulin resistance and consequently becomes mentally impaired. This supports the belief that all brains will eventually develop dementia like symptoms and that Alzheimer’s disease only brings it about sooner. One implication of that is that this will lead to sooner onset of dementia in people who have diabetes. This could prove to be a problem for our nation as generations with higher levels of diabetes get older.
A Frightening Proposition
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.