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Unlocking the Secrets of Endocannabinoids: The Surprising Role They Play in Our Health and Well-being

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What Are Endocannabinoids?

Endocannabinoids are naturally occurring molecules that are similar in structure to the active compounds in cannabis. These molecules are produced by the body and interact with the same receptors as THC, the main psychoactive compound in cannabis.

Structure

There are two main endocannabinoids: anandamide (AEA) and 2-arachidonoylglycerol (2-AG). Anandamide has a chemical structure consisting of an ethanolamine head group, an arachidonic acid chain, and an amide bond linking them together. 2-AG, on the other hand, consists of a glycerol backbone with two arachidonic acid chains attached to it via ester bonds. Both endocannabinoids are synthesized on demand from membrane phospholipids and are rapidly metabolized to terminate their signaling effects.

Structures of the main endocannabinoids, anandamide and 2-AG, which... | Download Scientific Diagram
Figure 2. Structures of the main endocannabinoids, anandamide and 2-AG.

Receptors

The two main receptors that are relevant to endocannabinoids are CB1 receptors and CB2 receptors. CB1 receptors are primarily found in the brain and central nervous system, while CB2 receptors are primarily found in immune cells and peripheral tissues.

Endocannabinoids, such as anandamide and 2-arachidonoylglycerol (2-AG), bind to these receptors to regulate various physiological processes, including pain, appetite, mood, and inflammation. CB1 receptor activation is associated with the psychoactive effects of cannabis, while CB2 receptor activation is associated with anti-inflammatory effects.

Research has also shown that there are other receptors that can interact with endocannabinoids, such as TRPV1 receptors and GPR55 receptors. These receptors may have additional roles in mediating the effects of endocannabinoids in the body.

Signaling Pathways

CB1 and CB2, are G protein-coupled receptors (GPCRs) that are located throughout the body. When endocannabinoids bind to these receptors, they initiate a signaling cascade that leads to various physiological effects.

When an endocannabinoid binds to a CB1 receptor, it activates a G protein that can lead to the inhibition of adenylyl cyclase, which in turn reduces the production of cyclic adenosine monophosphate (cAMP). This leads to a decrease in the activity of intracellular enzymes such as protein kinase A (PKA) and mitogen-activated protein kinases (MAPKs), which ultimately results in the inhibition of neurotransmitter release from presynaptic neurons.

In addition, CB1 receptor activation can also lead to the activation of ion channels such as inwardly rectifying potassium (K+) channels and voltage-gated calcium (Ca2+) channels. This can result in the hyperpolarization of the postsynaptic membrane and a decrease in the excitability of neurons.

On the other hand, when an endocannabinoid binds to a CB2 receptor, it can activate several signaling pathways, including the inhibition of adenylyl cyclase and the activation of PI3K/Akt and MAPK signaling cascades. CB2 receptor activation can also lead to the inhibition of intracellular calcium release and the activation of potassium channels, which can contribute to the anti-inflammatory and immunomodulatory effects of endocannabinoids.

Endocannabinoids in Neurodegenerative Disease

The paper discussed in class highlights the potential roles of cannabinoid receptors in various diseases of the central nervous system (CNS). The authors describe the potential therapeutic benefits of targeting these receptors for the treatment of neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease.

The authors describe the endocannabinoid system as a key regulator of neurotransmitter release, synaptic plasticity, and immune function in the CNS. They discuss the role of CB1 receptors in regulating the release of neurotransmitters such as glutamate, GABA, and dopamine, and the potential therapeutic benefits of CB1 agonists in modulating these pathways.

The authors also describe the potential therapeutic benefits of CB2 receptor activation in the treatment of neuroinflammatory and neurodegenerative diseases, as well as pain and psychiatric disorders. They discuss the anti-inflammatory and immunomodulatory effects of CB2 receptor activation, as well as its potential role in regulating microglial activation and neurogenesis.

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Metabolic Syndrome’s Relationship with the Hypothalamus

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Artstract By Hailey

 

Metabolic syndrome is a combination of conditions that increase one’s risk for type 2 diabetes, heart disease, and stroke. It is characterized by excess fat in the abdominal areas, high blood pressure, and high blood sugar.1 

High Fat Diet

One of the things that can cause metabolic syndrome is inflammation via a poor diet. Specifically, a high fat diet filled with saturated fatty acids that are in food like cake, butter, chocolate, and red meat. This inflammation starts in the hypothalamus. The hypothalamus functions to control homeostasis. Some fats and oils are also linked to insulin and leptin resistance. Leptin resistance causes someone to eat more and more because it becomes harder for them to feel full. Insulin resistance leads to high blood sugar and many other physiological comorbidities. With a diet high in saturated fatty acids, the hypothalamus cannot control normal homeostatic processes like blood sugar or appetite.

This inflammation in the hypothalamus occurs through many cell signaling pathways. One pathway in particular is affected by saturated fatty acids. In figure 1, we see saturated fatty acid (SFA) triggers activation of IKK and NF-κB to produce the expression of pro-inflammatory genes in the hypothalamus like SOCS3 and cytokines. In fact, inhibiting this signaling pathway inhibits insulin and leptin resistance.2

Figure 1. Pathway of Inflammation in Hypothalamus

Hypothalamic Dysfunction

As stated earlier the hypothalamus controls the body’s homeostasis. With a high fat diet causing inflammation in the hypothalamus, there are other things that may come of it. Hypothalamic dysfunction can lead to brain tumors, infertility, and osteoporosis. Metabolic syndrome can cause hypothalamic dysfunction, so it is important for body and brain health to prevent and treat it.3

America’s Relationship with Food

The answer to this problem seems simple: eat less saturated fats. But, it is not simple. The United States has had a problem with obesity and metabolic syndrome for decades. The U.S. Department of Agriculture found that Americans eat 20% more calories in 2000 than in 1983 and consumption of added fats rose by two thirds. Additionally, fast food (which is often full of saturated fats) makes up about 11% of an average American’s diet. This may be due to the convenience of these meals. We often find ourselves spending more time at work than at home with no time to make a home cooked meal, so we rely on drive-throughs to get our meals.4

How Can We Address This?

  1. Quality over quantity
    • The focus needs to be on good nutrition. Food assistance programs in the United States has helped to address hunger overall, but not healthy nutrition. Programs need to improve access to more quality foods.
  2. Integrate healthy nutrition into health care
    • Although nutrition exists within health care, food and nutrition needs to be raised to the same level as medication. This can be done through prescriptions. Prescriptions for meals and food would help support a patient in their journey to good health.5

Making healthy food more assessable is a crucial step to address the problem of obesity and metabolic syndrome. Accessibility will help Americans prevent and treat hypothalamic dysfunction as well as obesity and metabolic syndrome overall.

  1. National Heart, Lung, and Blood Institute. (2022). What Is Metabolic Syndrome? https://www.nhlbi.nih.gov/health/metabolic-syndrome
  2. Jais, A., & Brüning, J. C. (2017). Hypothalamic inflammation in obesity and metabolic disease. The Journal of Clinical Investigation, 127(1), 24–32. https://doi.org/10.1172/JCI88878
  3. Mount Siani. (2023). Hypothalamic Dysfunction. https://www.mountsinai.org/health-library/diseases-conditions/hypothalamic-dysfunction#:~:text=Symptoms%20may%20include%20feeling%20cold,lack%20of%20interest%20in%20activities.
  4. Public Health. (2023). Why Are Americans Obese? https://www.publichealth.org/public-awareness/obesity/#:~:text=As%20for%20what%20is%20driving,food%20and%20too%20little%20exercise.
  5. Aubrey, A. (2022). The U.S. diet is deadly. Here are 7 ideas to get Americans eating healthie NPR News. https://www.npr.org/sections/health-shots/2022/08/31/1120004717/the-u-s-diet-is-deadly-here-are-7-ideas-to-get-americans-eating-healthier
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Obesity Effects on the Brain

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Artstract by Jessica Howard

Obesity can have multiple harmful effects on a person’s life. Most of us know mostly about the physical effects such as increased risk for heart disease. But there are also harmful effects to the brain, specifically the hypothalamus. The hypothalamus is the part of the brain in charge of homeostasis of the body using hormones. This includes, temperature regulation, energy expenditure, and eating habits. One important hormone that the hypothalamus uses to balance energy expenditure with calorie intake is insulin (Sateil & Olefsky, 2017).

How Energy is normally regulated

Normally, in the hypothalamus there are chemicals in the brain that control food intake and energy expenditure. The agouti-related peptide (AgRP) is inhibited by insulin while proopiomelanocortin (POMC) is activated by insulin. This causes the body to decrease its food intake while increasing its energy expenditure. AgRP expressing neurons normally activate melanocortin receptor expressing neurons (MC4R) which leads to increased food intake and decreased energy expenditure. POMC expressing neurons act as inhibitors of MC4R neurons which decreases food intake and increases energy expenditure. Insulin is an important part of keeping these two systems balanced for energy homeostasis (Sateil & Olefsky, 2017).

Salteil, A. R., & Olefsky, J. M. (2017). Hypothalamic inflammation in obesity and metabolic disease. The Journal of Clinical Investigation 127(1), 24-32. Doi:10.1172/JCI88878.

What Goes Wrong?

Obesity caused by a high fat diet activates stress signals in the hypothalamic neurons which release things called cytokines and other inflammatory responses. These responses lead to a decrease in sensitivity of the AgRP and POMC expressing neurons, this is also known as insulin resistance. This means that the neurons no longer respond as strongly to the presence of insulin. So AgRP neurons aren’t getting inhibited and POMC neurons aren’t getting activated, this means that there will be an increase in energy intake and a decrease in energy expenditure (Sateil & Olefsky, 2017).

One way which insulin is inhibited is by the activation of the MAPK pathway. This triggers the activation of JNK signaling which is a mediator of insulin receptor substrate proteins, which help transmit signals from insulin to create a cellular response (Shaw, 2011). In other words the JNK signaling inhibits insulin receptor substrate proteins by phosphorylating them, which deactivates them. This leads to insulin resistance in that cell. When this happens in AgRP neurons they are no longer inhibited and food intake increase, which then leads to more weight gain that serves to continue the insulin problem (Sateil & Olefsky, 2017).

Salteil, A. R., & Olefsky, J. M. (2017). Hypothalamic inflammation in obesity and metabolic disease. The Journal of Clinical Investigation 127(1), 24-32. Doi:10.1172/JCI88878.

What Can Be Done?

Obesity is a very serious condition that can cause great harm to all organs in the body, not just the brain. That is why it is important to seek treatment sooner rather than later. It is best to start with your doctor and get recommendations for a dietitian. A dietitian can help you create a meal plan that is balanced and healthy. It is also important to get regular exercise that with increase your heart rate, like swimming or fast walking. It can also be helpful to join a local weight loss group. This will offer you both a method of accountability and support from others facing similar challenges. It is also important to seek support from your family and friends. Tell them what you are trying to accomplish so that they can also help keep you accountable and keep you from any tempting situations. By sticking with your plan it is possible to lose weight and get better to live a longer healthier life (NHS inform, 2023).

References

NHS inform. (2023). Obesity causes and treatments. causes & treatments – Illnesses & conditions . Retrieved April 15, 2023, from https://www.nhsinform.scot/illnesses-and-conditions/nutritional/obesity#:~:text=The%20best%20way%20to%20treat,a%20local%20weight%20loss%20group

Salteil, A. R., & Olefsky, J. M. (2017). Hypothalamic inflammation in obesity and metabolic disease. The Journal of Clinical Investigation 127(1), 24-32. Doi:10.1172/JCI88878.

Shaw, L. M. (2011, June 1). The insulin receptor substrate (IRS) proteins: At the intersection of metabolism and cancer. Cell cycle (Georgetown, Tex.). Retrieved April 15, 2023, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3142458/#:~:text=The%20IRS%20proteins%20are%20a,in%20response%20to%20insulin%20stimulation.

 

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The Truth About Fad Diets and Diet Culture

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artstract by Olivia Pederson

What is a Fad Diet? 

We have all heard and seen that the south beach diet, the keto diet, the 3-day diet, the juice diet, and many more of these types of diets are recommended for fast weight loss, but this is 100% wrong. These diets are all called ‘fad diets’ which mean that they are popular for a short time, have no standard dietary recommendation, and made pseudoscientific claims for fast weight loss. These diets are not supported by clinical research and often make unsubstantiated statements about health and disease.

45 million Americans go on diets each year, and roughly 50% of them use fad diets. These diets usually only last a couple weeks to a couple months, but once the diet is over it is easy to fall back into the way people were eating before. This turns into a diet cycle that doesn’t end. This cycle can lead to poor health outcomes such as eating disorders, malnutrition, anemia, metabolic abnormalities, and impaired quality of life.

New Years Resolutions and Social Media

The beginning of the new year brings up this idea of new years resolutions. January is a very common month to see these new diet trends make an appearance as well as weight loss products. In the United States alone, 80% of people fail their new years resolutions by February. This is done by not following healthy lifestyle changes over an extended period of time.

Social media plays a large role in diet culture and fad diets. These social media platforms influence many peoples lifestyle behavior or social norms. These fad diets are usually promoted by celebrities or by people who are a part of a company to sell a product. Many of these diets and products promoted for weight loss are not evidence-based. Social media also portrays unrealistic body standards to people, especially young people. There are always people posing or flexing their body instead of relaxing and showing what they actually look like, which can really effect how people see their own bodies. It is important to take each social media post with a grain of salt because it is more than likely not accurate.

The Science Behind Obesity

The hypothalamus in the brain controls a number of neuroendocrine functions that integrate metabolic feedback and control energy balance. Insulin plays an important role here because it is used to help turn food into energy. Leptin is another important character here because it is a hormone released from fat cells and regulates long-term energy balance. These two signals are essential in hypothalamic control of energy balance.

The image above shows this mechanism. The hypothalamus senses and integrates feedback from certain hormones that circulate in the body. Insulin and leptin act on neuronal subsets of the hypothalamus to control energy balance. Through certain excitation and inhibition of specific neurons, energy usage and food intake is balanced out. If the body is resistance to leptin and insulin, the pathway does not get excited and inhibited in the correct way which leads to more food intake (weight gain) and less energy usage.

This image shows the many pathways involved in metabolic inflammation of the hypothalamus. This image just shows how complex inflammation is and how many moving parts there are. Inflammation of the hypothalamus affects many different cells types such as microglia, astrocytes, oligodendrocytes, and macrophages. Understanding the way that all the pieces fit together can help understand that obesity can be connected to the brain and help ways to properly treat obesity.

Proper Lifestyle Changes

Proper weight loss is complex and there are many factors that play into it. Each persons body is different and needs different levels of nutrients so it is essential to not follow other peoples diets exactly. Looking at the food pyramid and creating balanced meals is the first step to changing a lifestyle. The focus should be on eating foods that make you feel good and not just cutting out foods.

Physical activity is also important. Exercise of any kind can release certain chemicals in the brain to make you feel good. The focus should always be on what makes you feel the best. Knowing the lifestyles changes and knowing the science behind obesity can help people understand themselves more and seek out help from a trusted healthcare provider if they don’t see any changes. There are treatments options such as medication and surgeries that can help people if traditional eating and exercise changes do not work.

 

 

References:

Healthy Eating Plate

en.wikipedia.org/wiki/Fad_diet

reidhealth.org/…/fad-diets-the-new-years-resolutions-worst-enemy

reidhealth.org/…/fad-diets-the-new-years-resolutions-worst-enemy

doi.org/10.1172/JCI88878

Community/Disease/Health

Metabolic Syndrome: The disease you may not know is there

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Abstract by Anna Dekkenga

Is Metabolic Syndrome the same as Obesity?

  Metabolic syndrome is defined as a cluster of conditions that occur together, increasing your risk of heart disease, stroke, and type 2 diabetes. Some of these conditions could include high blood pressure, high blood sugar, excess body fat, and abnormal triglyceride or cholesterol levels. All these conditions, together, lead to metabolic syndrome. But just because someone suffers from high blood pressure or abnormal cholesterol levels doesn’t mean they also have metabolic syndrome. However, any of these conditions increase a person’s risk of having metabolic syndrome.

  So, obesity is considered a symptom of metabolic syndrome. They are not one in the same. And just because a person is obese, just like I mentioned above, doesn’t mean that they suffer from metabolic syndrome. Even vice versa, if a person is at a healthy weight, they may suffer from metabolic syndrome. This can be seen below, pictured in Figure 1.[1]

Figure 1. Metabolic syndrome: you can’t always see it.

 

 

 

 

 

 

 

 

 

 

 

What’s the cause of these symptoms?

  According to Alexander Jais and Jens C Bruning, “obesity has been known to induce a state of systemic low-grade inflammation that contributes to the development of numerous comorbidities.”[2] Not only can inflammation lead to many of these health-related issues, but it can also cause major changes in the brain, specifically in areas that keep homeostasis and systematic metabolism in check.

  But what starts inflammation? A high fat diet leads to inflammation in the brain, as well as insulin and leptin resistance which will be discussed more later. A diet high in fat consists of pastries, biscuits, creams, cheese, cheese crackers, and many types of popcorn. Although eating these foods may be a contributing factor, it all depends on moderation.

  More specifically, hypothalamic inflammation is the main link to the development of metabolic syndrome. The hypothalamus is a structure that is located deep within the structure of the brain, it can be seen in Figure 2. The hypothalamus plays a major role in the body; it acts as the body’s “smart control coordinating center.”[3] The hypothalamus controls many neuroendocrine functions, or the relationship that occurs between the nervous system and endocrine system. These functions help to regulate energy homeostasis.

Figure 2. Location of the Hypothalamus.

 

 

 

 

 

 

 

 

 

 

 

 

 

Insulin and Leptin

  As previously mentioned, leptin and insulin levels are both affected by a high fat diet. Leptin is a hormone that helps to regulate energy levels by directing the central nervous system to adjust food intake accordingly. In other words, leptin tells the body when to stop eating and if leptin become dysregulated, a person may not know when to stop. The hormone insulin has a similar role. Insulin’s main role is to regulate the amount of sugar in the blood. When insulin is dysregulated, this most likely leads to high blood sugar which, as previously stated, leads to metabolic syndrome in many people. [4] [5]

 

Figure 3. The role of leptin in the body.
Figure 4. Insulin resistance in the body.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Healthy lifestyle changes

  1. Choose heart healthy foods (fruits, vegetables, whole grains. Limit alcohol, sugars, and saturated fats)
  2. Exercise regularly
  3. Manage stress
  4. Don’t smoke
  5. Get enough sleep
  6. Medications for weight loss, cholesterol, blood sugar, blood pressure, etc. [6]

So, what?

  Why should you care about any of this information? Well, in the United States alone, 1 in 3 adults suffer from metabolic syndrome. Although, most people don’t even know that they have this condition. So, it’s important to understand the risk factors and to take care of yourself. Statistically, you know someone with this disease. A person who leaves metabolic syndrome untreated will have a shorter lifespan than a person without the disease, the body must work much harder. Keep your body happy and healthy, it’ll love you for it. [7]

References

[1] Metabolic Syndrome

[2] Hypothalamic inflammation in obesity and metabolic disease

[3] The Hypothalamus

[4] Leptin and Leptin Resistance

[5] The Role of Insulin

[6] Metabolic Syndrome Treatment 

[7] What is Metabolic Syndrome

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Sleep for the brain

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Sleep as we know consumes 6-8 hours of the average persons 24 hour day. Therefore, taking either 1/4 or 1/3 of your day. To say that sleep is important would be an understatement as it is very much needed for the brain to function.

Sleep is when our body takes a break to regenerate and goes through different stages throughout sleep. Those stages include wake, N1, N2, N3, and REM; stages N1 to N3 are considered non-rapid eye movement (NREM) sleep. The wake stage depends on if someone has their eyes open or closed in preparation of sleep, if the eyes are open beta waves are at play or if they are closed alpha waves are evident. Once the body begins to fall asleep stage 1 becomes apparent, the light sleep, which lasts a total of 5% for sleep time and has active theta waves. Stage 2 (N2) is when sleep spindles and K complexes are active and accounts for 45% of sleep. Sleep spindles have an important role in memory consolidation and K complexes function to maintain sleep and memory consolidation. Stage 3 is when the body repairs and regrows tissues, builds up bone, muscle, and strengthens the immune system. Stage 3 can also be referred to as deep sleep with the delta waves being most active and accounting for 25% of sleep. Lastly, REM sleep which has beta waves and is when dreaming or nightmares are most likely to occur.1

In time, older adults experience more insomnia and an earlier wake time possibly due to changing circadian rhythm that goes along with age. Therefore, imbalance of the circadian rhyme causes problematic secretion of melatonin and cortisol. Cortisol and melatonin are inversely related as an individual wakes up cortisol rises throughout the day and upon going to sleep melatonin rises and cortisol goes down. Other factors such as blue light have been shown to have an effect on sleep. Take for example how melatonin functions to be the hormonal signal for preparing the body to sleep and having melatonin disrupted by abnormal evening light exposure. This light exposure from the backlit of the computer or bright room setting causes reductions in melatonin secretion.  Thus effecting sleep in ways such as prolonging sleep onset latency, decreasing rapid eye movements, and changing slow wave sleep.

Why does the blue light have more of an effect compared to white light? Well knowing that the circadian system has peak sensitivity to around 450-480nm light within the blue portion of the spectrum, blue light therefore can increase an individual’s alertness and suppress melatonin excretion. LEDs are in computers, TV, smartphones, tablets, as well as some light bulbs and have a blue range of around 460nm.2

Chemically in the brain there are a few pathways at play when sleep is activated. Those pathways include cAMP, MAPK, and CREB. It has been found that activity in these pathways is gone in memory deficient mice and that exposure to constant light may disrupt hioppocampal oscillations of MAPK activity causing deficits in contextual memory persistence. Therefore, if MAPK is inhibited at its peak activity it lowers the persistence of memory. Overall, cAMP, MAPK, and CREB pathways are found to be most active during REM sleep and having sleep disturbances especially during REM sleep may have impairments in hippocampus-dependent memory.3

Sleep is important and it is important to try and get the best sleep each night considering it may have a direct impact on your mental health status especially with age looking at memory function.

 

Work cited:

1. Patel AK, Reddy V, Shumway KR, et al. Physiology, Sleep Stages. [Updated 2022 Sep 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK526132/

2. Shechter, Ari, Elijah Wookhyun Kim, Marie-Pierre St-Onge, and Andrew J. Westwood. 2018. “Blocking Nocturnal Blue Light for Insomnia: A Randomized Controlled Trial.” Journal of Psychiatric Research 96 (January): 196–202. https://doi.org/10.1016/j.jpsychires.2017.10.015.

3. Worley, Susan L. n.d. “The Extraordinary Importance of Sleep.”

4. Xia, Zhengui, and Dan Storm. 2017. “Role of Circadian Rhythm and REM Sleep for Memory Consolidation.” Neuroscience Research 118 (May): 13–20. https://doi.org/10.1016/j.neures.2017.04.011.

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Antisocial Personality Disorder: A Difficult Case to Solve

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The Neurological Impact on Psychopathy

Psychopathy, or now more commonly known as antisocial personality disorder, in the simplest definition is the neuropsychiatric disorder that is commonly associated with deficient emotional responses, lack of empathy, aggression, manipulativeness, and lacking behavioral controls. This definition makes it clear that there must be some difference in the brains and/or genes of those with this disorder. Gene expression specifically has recently been linked to those with ASPD compared to those without. Genes that have been found in people with ASPD- RPL109, ZNF132, CDH5, and OPRD1 genes-have also been linked to genes found in those with autism. Similarly, there was findings that psychopathy is normally passed down from the father to son, possibly because of the XY genes of males compared to the XX gene in females. PEG10 is one paternally imprinted gene that was connected to the passing down of ASPD. Furthermore, another neurological change in those with psychopathic behaviors is related to dopamine release. Dopamine released from the cerebellum also has regulatory functions in social behavior. There is a connection between the cerebellum and antisocial behavior along with immune response-related pathways enrichment in those that express psychopathic behavior (1).

This illustrates the parts of the brain that are different in those who have ASPD. (5)

Diagnosis of ASPD

The overall consensus on how many people in the United States have ASPD is 1-4%. However, how does one determine this serious diagnosis? First, there are other antisocial disorders that have similar symptoms to ASPD. Borderline personality disorder includes unstable moods or manipulating behaviors, both overlapping with ASPD. Narcissistic personality disorder is diagnosed by looking for inflated sense of self-importance, which is also similar to those with ASPD. The only way to correctly differentiate between ASPD and other personality disorders is through behavior analysis by a psychiatrist or psychologist. People can begin developing ASPD traits in their early teen years or late childhood. This age makes diagnosis difficult because it can also be mistaken for ADHD, depression, or oppositional defiant disorder. Specific behavioral symptoms that a professional may look for during diagnosis is physical aggressiveness, reckless behaviors, blaming others, breaking the law, etc (2).

The different clusters of personality disorders, with ASPD falling into cluster B. Differentiation between these can be difficult. (4)

Is there a cure?

There is no cure. There is medication and therapy that may help the person control the effects of the disorder; however, there is no way to completely cure a person from ASPD. Therapy can include cognitive behavioral therapy that focuses on changing one’s thinking and behavior. Therapy can also include group therapy or family therapy. Family therapy could be important for the people that live with someone who has ASPD. ASPD does not just affect the person with the disorder, but also people around them, which is why it is so important to understand what the disorder entails. The stigma around having the disorder might negatively influence if people want to recognize it within themselves or want to get help (3).

Conclusion

Antisocial personality disorder has not been studied enough to where we have many long-term treatment options. However, new research is finding the links between this disorder and genes or neurotransmitter releases. Understanding brain chemistry is important in understanding what exactly causes such a behavior and possibly find more ways to diagnose the disorder.

Citations:

  1. Tiihonen, J., Koskuvi, M., Lähteenvuo, M., Virtanen, P. L. J., Ojansuu, I., Vaurio, O., Gao, Y., Hyötyläinen, I., Puttonen, K. A., Repo-Tiihonen, E., Paunio, T., Rautiainen, M.-R., Tyni, S., Koistinaho, J., & Lehtonen, Š. (2019). Neurobiological roots of psychopathy. Molecular Psychiatry, 25(12), 3432–3441. https://doi.org/10.1038/s41380-019-0488-z
  2. Antisocial personality disorder: Causes, symptoms & treatment. (n.d.). Cleveland Clinic. Retrieved April 5, 2023, from https://my.clevelandclinic.org/health/diseases/9657-antisocial-personality-disorder
  3. Antisocial personality disorder – Diagnosis and treatment. (2023, February 24). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/antisocial-personality-disorder/diagnosis-treatment/drc-20353934
  4. Types of personality disorders. (2018, November 12). Priory. https://www.priorygroup.com/mental-health/personality-disorder-treatment/types-symptoms-of-personality-disorders 
  5. News, N. (2021, April 14). The neural basis of psychopathy. Neuroscience News. https://neurosciencenews.com/psychopahty-neural-basis-18234/
Disease/Health/Hot topics

A World Without Empathy: An Insight into Antisocial Personality Disorder

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pexels.com stock photo by Darya Sannikova

 

Antisocial personality disorder (ASPD) is a mental health condition characterized by disregard for the rights of others, impulsivity, and a lack of empathy. Environmental factors such as childhood experiences, parenting style, and social influences can contribute to the development of ASPD. Childhood abuse, neglect, and inconsistent discipline can increase the risk of developing ASPD. Parental antisocial behavior, substance abuse, and criminal behavior can also contribute to the development of the disorder. Additionally, exposure to peer pressure, deviant behavior, and criminal activities can increase the likelihood of developing ASPD. Environmental factors can interact with genetic predispositions to shape the development of the disorder, highlighting the importance of early intervention and prevention efforts [4].

 

Genetics

Antisocial personality disorder (ASPD) has been found to have a strong genetic component, with heritability estimates ranging from 40% to 70%. The LINC00951 gene has recently been identified as a potential genetic risk factor for antisocial personality disorder (ASPD). Research has found that individuals with ASPD have decreased expression of LINC00951 in the prefrontal cortex compared to those without the disorder. This gene is involved in the regulation of neuronal gene expression and plays a role in the development of the prefrontal cortex, a brain region implicated in the pathology of ASPD. Decreased expression of LINC00951 may contribute to impaired prefrontal cortical function, which is associated with the impulsivity and disregard for others’ rights characteristic of ASPD. Further research is needed to fully understand the role of LINC00951 in the development of ASPD [3].

 

ASPD and the Brain

Recent advances in neuroscience have shed light on the neural correlates of antisocial personality disorder (ASPD). Studies have found differences in brain structure and function between individuals with and without ASPD. For example, reduced gray matter volume in the prefrontal cortex, amygdala, and hippocampus have been observed in individuals with ASPD. Functional imaging studies have also revealed abnormalities in brain regions involved in emotion processing, decision making, and empathy. These findings suggest that ASPD may be associated with dysfunction in neural circuits involved in social and emotional processing. Further research in this area may help to inform the development of more effective treatments for ASPD.

 

History and Current Terminology 

Antisocial personality disorder (ASPD) has a long history of various names and classifications. Early descriptions of the disorder can be traced back to the 1800s, when it was referred to as moral insanity. The term sociopathy was later introduced in the early 1900s, followed by psychopathy in the mid-20th century (Figure 1). In the 1980s, the Diagnostic and Statistical Manual of Mental Disorders (DSM) introduced the term antisocial personality disorder, which is still in use today. The current DSM-5 criteria for ASPD include a persistent pattern of disregard for the rights of others, impulsivity, and a lack of remorse or guilt. Despite changes in terminology and classifications, the core features of the disorder remain consistent [2].

Figure 1. Antisocial behavior disorder and other mental health disorders

 

ASPD Subtypes

Antisocial personality disorder (ASPD) can be classified into two subtypes: primary and secondary. Primary ASPD is characterized by fearless dominance, manipulativeness, and a lack of anxiety. These individuals may display charisma and leadership skills, but their behavior is often harmful to others. Secondary ASPD is characterized by impulsivity, aggressiveness, and a lack of remorse or guilt. These individuals may engage in criminal behavior, substance abuse, and risky behaviors. The distinction between these subtypes can be useful in understanding the different underlying mechanisms and treatment approaches for ASPD. However, the diagnosis of ASPD is often based on the presence of a set of specific criteria, rather than subtype classifications.

 

Treatments

Antisocial personality disorder (ASPD) is a challenging condition to treat, as individuals with the disorder often lack motivation to change their behavior and may not perceive their behavior as problematic. However, there are several treatments that have been shown to be effective in reducing symptoms of ASPD. Cognitive-behavioral therapy (CBT) can help individuals with ASPD learn new coping skills, identify and change negative thought patterns, and improve interpersonal functioning (Figure 2). Medications such as mood stabilizers and antidepressants may also be useful in managing conditions such as depression or anxiety [1].

Figure 2. Drug treatment and talk therapy may be helpful for antisocial personality disorder, however this condition is very challenging to treat.

 

Resources

[1] Haelle, T. (2022, October). How to treat antisocial personality disorder. EverydayHealth.com. Retrieved April 5, 2023, from https://www.everydayhealth.com/antisocial-personality-disorder/treatment/

[2] Kiehl, K. A., & Hoffman, M. B. (2011). The criminal psychopath: History, neuroscience, treatment, and economics. Jurimetrics. Retrieved April 5, 2023, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4059069/

[3] Tiihonen, J., Koskuvi, M., Lähteenvuo, M., Virtanen, P. L., Ojansuu, I., Vaurio, O., Gao, Y., Hyötyläinen, I., Puttonen, K. A., Repo-Tiihonen, E., Paunio, T., Rautiainen, M.-R., Tyni, S., Koistinaho, J., & Lehtonen, Š. (2019). Neurobiological roots of psychopathy. Molecular Psychiatry, 25(12), 3432–3441. https://doi.org/10.1038/s41380-019-0488-z

[4] Tuvblad, C., & Beaver, K. M. (2013, September). Genetic and environmental influences on antisocial behavior. Journal of criminal justice. Retrieved April 5, 2023, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3920596/

Disease/Health/Uncategorized

Behind Antisocial Personality Disorder

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Antisocial Personality Disorder is characterized by aggression, impulsivity, and lack of empathy that can lead to criminal behavior.1 Terms such as psychopathic and sociopathic are not used in formal diagnosing and is not in the DSM-IV-TR. Psychopathy was originally used to describe psychopathic inferiority. These terms are now referred to as antisocial personality disorder in the DSM-IV-TR. Although, psychopathy is commonly known as an extreme version of antisocial personality disorder. Antisocial personality disorder and psychopathy are sometimes used interchangeably. In order to diagnose someone with antisocial personality disorder, they need to be over the age of 18. If someone is showing characteristics of antisocial personality disorder like impulsivity and disregard for others under the age of 18, a diagnosis of conduct disorder would be needed.2

Like every other mental illness, antisocial personality disorder has treatment options. Currently, the treatment options include medication and therapy.

Treatment for antisocial personality disorder (and psychopathy)

  • Cognitive behavioral therapy: CBT seeks to break down existing thought connections in which a trigger causes a harmful action by the creation of new connections with more positive outcomes.
  • Antipsychotics: Since individuals with psychopathy can be violent and aggressive in their thoughts and actions, antipsychotic drugs may help to reduce the urge to harm others.
  • Mood stabilizers: Mood stabilizers can reduce the agitation that can lead those with psychopathic tendencies to act violently.

Although antisocial personality disorder is nothing that can be changed, harm reduction and symptom management can improve quality of life.3

Culprits Behind Antisocial Personality Disorder

Antisocial personality disorder, like many other mental illnesses, has been thought to stem from genetic and environmental factors. Two genes in particular are overexpressed, RPL10P9 and ZNF132. RPL10P9 and ZNF132 are found to be expressed in the cerebellum.4 The cerebellum can play a role in the regulating social dominance and aggression.5

Environmental factors largely rely on being in an adverse environment. A study involving adopted children showed that an adverse adoptive home environment in addition to genetic factors can result in psychopathology. In a twin study on peer group norms, it was found that when aggression was favorable the genetic disposition was more likely to be expressed.6

Stigma

Those with antisocial personality disorder are thought of as monsters. They are often cast out from society. We see people with antisocial personality disorder in prison or death row. While these people are cast out, they are not given a chance to change. And once they are labeled as “psychopath,” they do not get a chance to live outside of that label. All of this is detrimental for the person’s quality of life. The life expectancy for someone with antisocial disorder is roughly 13 years earlier than those without antisocial personality disorder.7 Giving those a chance to receive treatment could possibly change this outcome.

Treatment around antisocial personality disorder is limited and the stigma around it may contribute to this problem. Current treatment has high rates of dropout. People with antisocial personality disorder tend to not take treatment seriously and lack understanding of their own condition.3 New treatments need to be explored to remedy this. Additionally, the threat antisocial personality disorder imposes on the general public due to the high rates of criminal activity in this disorder prove that treatment is important and it’s important to catch this early.

People with antisocial personality disorder must not be cast aside and be forgotten about. People with this disorder are still human and therefore must be treated with dignity and respect. They need a fighting chance to better themselves.

  1. Tiihonen, J., Koskuvi, M., Lähteenvuo Markku, Virtanen, P. L. J., Ojansuu, I., Vaurio, O., Gao, Y., Hyötyläinen Ida, Puttonen, K. A., Repo-Tiihonen, E., Paunio, T., Rautiainen, M.-R., Tyni, S., Koistinaho, J., & Lehtonen Šárka. (2019). Neurobiological roots of psychopathy. Molecular Psychiatry, 25(12), 3432–3441. https://doi.org/10.1038/s41380-019-0488-z
  2. Meyer, G. R., & Weaver, C. M. (2013). Case studies in abnormal behavior. Pearson Education, Inc.
  3. Leeson, Cathy. (2022, October 13). What is a psychopath? Signs, causes, and treatment. Therapist.com. https://therapist.com/disorders/psychopathy/
  4. Gene Cards: The Human Gene Database. (2023, March 21). RPL10P9 Gene – Ribosomal protein L10 pseudogene 9. https://www.genecards.org/cgi-bin/carddisp.pl?gene=RPL10P9#expression
  5. Chen, C. H., Schott, A. L., & Schnaude, D. (2019). Cerebellar modulation of the reward circuitry and social behavior. Science, 363(6424). https://doi.org/10.1126/science.aav0581
  6. Tuvblad, C., & Beaver, K. M. (2013). Genetic and environmental influences on antisocial behavior. Journal of criminal justice, 41(5), 273–276. https://doi.org/10.1016/j.jcrimjus.2013.07.007
  7. Krasnova, A., Eaton, W. W., & Samuels, J. F. (2019). Antisocial personality and risks of cause-specific mortality: results from the Epidemiologic Catchment Area study with 27 years of follow-up. Social psychiatry and psychiatric epidemiology, 54(5), 617–625. https://doi.org/10.1007/s00127-018-1628-5
Community/Disease/Health

The Making of a Psychopath

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What is a psychopath?

Most likely when you think of a psychopath, you probably think of a person like Jeffrey Dahmer, Ted Bundy, and John Wayne Gacy. Although they may be categorized as psychopaths, what actually defines them as such? Yes, they were serial killers, but that’s not a required “symptom” of a psychopath. So, what is a psychopath then?

Psychopathy is a very extreme form of antisocial personality disorder (ASPD). A person cannot be given the diagnosis of psychopath, those are merely traits given to a person who suffers from ASPD. ASPD is just one of the ten types of personality disorders. The Diagnostic and Statistical Manual of Mental Disorders defines ASPD as an individual who shows a continued pattern of disregard and violation of other peoples rights, emerging around the age of 15 with three or more of the following symptoms:

  1. Repeatedly breaking the law
  2. Repeatedly lying for personal gain or pleasure
  3. Impulsivity
  4. Irritability and aggression towards others
  5. Reckless disregard for the safety of others
  6. Consistently irresponsible
  7. Lack of remorse
Figure 1. A few characteristics of a psychopath.

 

Nature vs. Nurture

When we talk about any personality trait or quality a person has, scientists like to refer to the “nature” of the person as well as the “nurture.” Nature refers to the biological makeup, or the genetics a person has. Nurture, on the other hand, is how a person grew up, how they were treated as a child, and their life experiences. Figure 2, below, shows these contributing factors. It’s believed that both nature and nurture contribute to the life of a psychopath. Although there is a strong biological component, which will be explained later on, there are also environmental factors that contribute to this disease. Some of these factors may be neglect, abuse, and poor parenting.

Figure 2. The nature vs nurture of a human.

Neurobiological Roots of Psychopathy

When determining what could be going wrong in the brain, researchers found that those who were diagnosed as antisocial with psychopathic traits showed abnormal glucose metabolism and opiodergic neurotransmission in their brain. Abnormal glucose metabolism that leads to hypoglycemia has come to be one of the strongest predictors for violent crimes. One study followed individuals for eight years, hypothesizing that decreased glucose uptake in the prefrontal cortex of the brain led to violent crimes being committed by antisocial males. Over this eight year period, researchers were able to determine that 27% of the violent crimes could be explained by the decreased glucose uptake. From this study, researchers determined that substances that increase glycogen formation and decrease the risk of hypoglycemia could act as potential treatments for impulsive violent behavior.

Conclusion

Labeling someone as “psycho” or “crazy” is something many people do. But, neither of those terms are diagnoses. If a person truly is “crazy,” they most likely suffer from  an antisocial personality disorder with psychotic features. Nature and nurture both play a major role in understanding what creates a psychopath. But, most importantly, there are multiple neurobiological roots that contribute to this disease. Glucose metabolism, and opiodergic neurotransmission are two that researchers know about currently. Knowing whether or not there is more that contributes to the root of psychopathy isn’t quite known but researchers hope to understand more in the future.

 

References:

Antisocial Personality Disorder: Often Overlooked and Untreated

How Glucose Metabolism Works

Low Blood Sugar (Hypoglycemia)

Low non-oxidative glucose metabolism and violent offending: An 8-year perspective follow-up story

Nature vs. Nurture

Neurobiological roots of psychopathy

Psychopathic Personality Traits and Environmental Contexts: Differential Correlates, Gender Differences, and Genetic Mediation

The role of the opioid system in decision making and cognitive control: A review

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