About 1.6 to 3.8 million sports and recreational concussions occur in the USA each year. 1 in 5 of these individuals will develop mental health concerns and disorders. Signs and symptoms that are severe can last as long as 6 months. Females, the elderly population, athletes, and individuals in the military are the most susceptible to concussions. Females are more susceptible because of weaker and thinner neck muscle fibers. Below is an image showing these differences: (3, 5)

Mental Health symptoms after experiencing a concussion include but are not limited to:

• social anxiety
• irritability
• anger
• depression
• feelings of overwhelm
• general anxiety
• mood swings
• emotional lability
• impatience
• difficulty concentrating
• brain fog
• sensitivity to light
• fatigue or burnout
• memory loss
• sleep problems

Researchers have stressed that an individual’s personality doesn’t change after a concussion or traumatic brain injury but their behavior does. Their mood can be altered due to the symptoms of a TBI such as poor quality or lack of sleep, the frustration of not remembering things, feeling burnout easily, developing anxiety, etc. Personality is described to be a part of the person such as their dislikes, favorite food, activities, color, people, etc. How the individual reacts to such variables may change but they are not necessarily gone. This is not to say that personality can’t change because it can be depending on the location of the injury such as Phineas Gage in which his personality and behavior dramatically changed after suffering an injury to his frontal lobe. The diagram below shows the impact of the incident on the damaged regions.  (7, 1)

One study found that experiencing a TBI can increase your chances of developing a mental health disorder by 439%. Many people suffer from social anxiety, irritability, anger, depression, feelings of being overwhelmed, general anxiety, mood swings, or emotional lability (uncontrollable or inappropriate crying) after their injury. (3)

Concussions disrupt the communication between neurons and the blood vessels along with damage white matter within the brain. The damaged pathways will take a couple of weeks to heal but full recovery is expected for nonrepeated or infrequent concussions. In 30% of individuals who experienced concussions noticed a long-lasting slow and disruptive cognitive processing and responses. (1)

Females, the elderly population, and individuals who have had prior experiences of concussions, seizures, migraines, learning, mood, and anxiety disorders are the most susceptible to experiencing PCS (post-concussion syndrome). PCS is when the individual has prolonged symptoms and has continued experiencing such signs and symptoms past the expected recovery time given by doctors. The NINDS found that 20% of individuals who were in the military had experienced injuries during Iraq and Afghanistan. Of this 20%, 83% obtained a concussion or mild traumatic brain injury. Depression after sustaining a concussion is a common symptom. These individuals are twice as likely compared to individuals without TBI’s, to be at higher risk for self-harm and attempting suicide. Depression may contribute to the struggles that come with social interactions after a concussion as the person becomes easily fatigued and irritable due to intense lighting, loud noises, or too much movement and stimuli. (5)

Overall, concussions can lead to behavioral changes due to the symptoms and signs followed by the incident. Seeking professional help on how to manage these symptoms and signs is encouraged.

Resources:

1. https://www.cognitivefxusa.com/blog/personality-changes-after-a-brain-injury-or-concussion
2. https://www.nih.gov/news-events/news-releases/mental-health-disorders-common-following-mild-head-injury
3. https://sciencenordic.com/biology-denmark-depression/head-injury-can-cause-mental-illness/1395035
4. https://www.cognitivefxusa.com/blog/multiple-concussions-effects-and-treatment
5. https://www.medicalnewstoday.com/articles/326227#complications
6. https://www.spokesman.com/stories/2019/apr/03/researcher-mental-health-issues-often-progress-aft/
7. https://www.npr.org/sections/health-shots/2017/05/21/528966102/why-brain-scientists-are-still-obsessed-with-the-curious-case-of-phineas-gage

We all want to keep our friends and family safe. That includes protecting them from outside harm and making sure that they won’t get hurt. The problem is that it cannot always be prevented. One example of an adolescent child getting hurt is through a concussion and it is even more common to occur if that child is in sporting events. A concussion is described to be a traumatic brain injury (TBI) resulting from a blow to the head causing the brain to move back and forth at a fast pace [1]. This rapid and sudden movement causes the brain to form chemical changes and sometimes damage important brain cells [1]. A picture of what the brain is exposed to during a concussion is shown in the figure below. Concussions are potentially very dangerous as any damage to your brain can cause detrimental long term effects. 

A study on the neurometabolic cascade of concussion went into detail on what goes on in a person’s head when their brain experiences a concussion. Biomechanical injuries caused by a concussion lead to ionic flux and glutamate release triggering voltage gated ion channels [2]. This leads to the brain increasing ATP pumping to restore homeostasis, but in turn causes depletion of cellular energy reserves leading to multiple dysfunctions such as altered neurotransmission [2]. This shows a possible energy crisis involved after a concussion, possibly impairing other important mechanisms throughout the body. Because of this, important mechanisms may not be able to perform as adequately after the concussion symptoms have subsided. 

With these multiple changes happening in your brain, this can result in possible axonal injury causing potential damage to important sections. According to the same study on concussions, axonal injury causes disruption in transports resulting in impaired cognition, slowed processing, and slowed reaction times [2]. This implies that concussions can lead to impairment and possible destruction of neuronal receptors leading to become difficult in processing information and possible difficulty in motor behavior. This is scary to think about because this makes it possible that concussions could even cause paralysis. 

After a person experiences a concussion, there is a chance that post-concussive symptoms will stay. It should be known that while they are rare for a person who experiences one concussion, these symptoms can become more likely to occur in somebody that has had multiple concussions in a short period of time. Such as if they had repeated blows to the head in a football game. Some of these long term symptoms include but are not limited to headache, dizziness, memory problems, irritability, insomnia, depression, sensitivity to noise and light, and sometimes it can even cause a personality change [3]. With these effects in mind, it is no wonder why people say it is important to wear your bike helmet.

From these studies on concussions, people should be able to understand the dangers of concussions when doing a very physical activity that can involve the safety of your well being. The brain is the most important organ in your body and it is every person’s job to make sure it is protected from any outside harm it may come across. 

1. https://www.cdc.gov/headsup/basics/concussion_whatis.html
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4479139/ 
3. https://www.healthline.com/health/post-concussion-syndrome#symptoms 

The Basics

A concussion is a condition of neurological signs and symptoms that are caused by a biomechanical force to the brain. Symptoms of a concussion include headache, nausea or vomiting, dizziness, poor balance, light/noise sensitivity, fatigue, memory problems, confusion, etc. The cause of a concussion is a bump, blow, or jolt to the head or body that causes the head to move rapidly back and forth, as seen in Figure 1. The sudden movement of the head causes the brain to “bounce” around or twist in the skull causing injuries to the brain. The injuries to neural tissue caused by a concussion are predominantly functional or microstructural. Functional injuries include ionic shifts, metabolic changes, and impaired neurotransmission. Microstructural injuries include axonal stretch, axonal disconnection, inflammation, cell death, and cytoskeletal damage.

Concussions & Sports

Between 1.7 to 3 million sport-related concussions happen each year with around 300,000 of those from American football. About 5 in 10 concussions gounreported or undetected. According to a study published in 2005, there are about 0.41 concussions per NFL game with 67.7% of concussions involving impact by another player’s helmet. 92% of players who sustain a concussion return to practice in less than 7 days. This data is shocking; however, it is from 16 years ago. The technology to prevent concussions in football and the concussion protocol have changed. Nevertheless, the deadly costs of repetitive hits to the brain are being revealed.

Chronic Traumatic Encephalopathy (CTE)

CTE develops gradually from an accumulation of blows to the head or repeated concussions. Symptoms vary between individuals but tend to resemble other degenerative brain conditions like Alzheimer’s disease: memory loss, depression, mood swings, personality change, fatigue, anxiety, frustration, etc. There is no diagnostic test for CTE, thus, a diagnosis cannot be confirmed until the post-mortem brain can be examined. Football players have a high risk of developing CTE as they are subjected to repetitive head injuries.

From a study of 202 brains from deceased players of American football, CTE was diagnosed in 177 players (87%), including 110 of 111 former NFL players (99%). The most common cause of death for participants with mild or severe CTE pathology was suicide, 27% vs. 47%. 86% of former NFL players hadsevere CTE, compared to 56% of former college players and 56% of semiprofessional players. The level of neurofibrillary tangles correlated positively with the severity of CTE. Neurofibrillary tangles (NFTs) are abnormal accumulations of the hyperphosphorylated (too activated) protein

tau. Normally, tau supports the structure of the neuron by stabilizing microtubules which help guide nutrients and molecules down the cell. Within tangles, hyperphosphorylated tau detaches from the microtubules and stick to each other, forming tangles that block the neuron’s transport system from inside the cell. In figure 2 you can see the mass amounts of NFTs in a region of Aaron Hernandez’s brain. Additionally, there were deposits of amyloid- in all stages of CTE. This protein forms plagues that disrupt communication between neurons.

NFTs and amyloid-  plaques are key markers of Alzheimer’s disease and associated with symptoms of impulsivity, depression, apathy, anxiety, explosivity, aggression, memory loss, and confusion. Among those that showed CTE pathology, 42.3% presented with cognitive symptoms in life, 43.2% showed behavior/mood symptoms, and 14.4% presented with both cognitive symptoms and behavior/mood symptoms.

Aaron Hernandez

A particular case study of CTE in a football player showed severe CTE pathology and the symptomology described with severe CTE. This case is of Aaron Hernandez.

Aaron Hernandez was a tight end for the New England Patriots until his career ended with his arrest for the murder of Odin Lloyd. Two years after his conviction for first degree murder, Hernandez committed suicide within his prison cell. Pre-mortem, professionals thought he had CTE, but this was confirmed after his death when

researchers were allowed to examine his brain. For a little bit of background Hernandez had been playing football since high school. He had many of the symptomology of CTE: changes in mood, aggression, depression, mood swings, personality changes, and memory loss. His brain: through Figure 3 you can see there is an atrophy of his brain specifically in the fornix and hippocampalregions. They also saw perforations of the septum pellucid and deposits of tau that you can see on this picture. Also, you can see that he had a lot of ventricular enlargements.

The researchers who examined Hernandez’s brain claim that it is the worst case of CTE they have ever seen in someone of his age of 27 years old.

After the death of Hernandez, his family filed a lawsuit against the New England Patriots and the NFL for being fully aware of the damage that could be inflicted from inflicted from repetitive impact injuries and not disclosing, treating, or protecting Hernandez from those dangers. They have since dropped this charge.

CTE makes a murderer?

I’m not sure that a neurodegenerative disease can make a murderer. In my opinion, neuronal dysfunction can be an aggravating trigger for homicidal tendencies. But this does not mean having CTE excuses such heinous acts. Instead, I believe CTE is a serious disease that is experienced by the many who experience repetitive traumatic brain injuries and shows itself as a change in key brain functions. CTE is something that should put fear in athletes, coaches, parents, and society. The development of CTE changes the brain and changes the person. And the truth is staring us in the face, if individuals continue to hit their head whether it be in combat, self-injury, accidents, or football they may see a change in themselves only explainable by CTE.

Sources:

https://www.nhs.uk/conditions/chronic-traumatic-encephalopathy/

https://heavy.com/sports/2020/01/aaron-hernandez-cte-photos-brain/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6916416/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3624697/

https://jamanetwork.com/journals/jama/fullarticle/2645104 

When addressing the role of the high fat diet and obesity, it is important to evaluate the types of fats in a given diet. While a high fat diet can lead to increase in obesity, a low fat diets as intervention for obesity is not supported. Rather, increasing the intake of unsaturated fatty acids over saturated fatty acids, carbohydrates, and proteins, can be beneficial for the obese population. Therefore, one must evaluate the types of fat intake that one is receiving, and aim to increase and supplement polyunsaturated fatty acids and some monounsaturated fatty acids when reversing obesity and insulin resistance.

So, what are the types of fat? Which types are “good?”

Trans fat is a byproduct of hydrogenation that is used to turn healthy oils into solids to prevent from becoming rancid. It has no known health benefits and is banned in the United States. It is known to increase the amount of LDL cholesterol in the bloodstream, while reducing the good, HDL, cholesterol. It also causes massive inflammation, and contribute to insulin resistance.

Saturated fats are solid at room temperature. They are found in red meats, whole milk, cheese, coconut oil, and baked goods, etc. A diet that is rich in saturated fats can increase total cholesterol.

Monounsaturated and polyunsaturated fats are good fats that come from vegetables, fish, nuts and seeds. In particular, monounsaturated fats have a single carbon to carbon double bond. Foods such as olive oil, avocados, nuts, and foods familiar to the “Mediterranean diet” are high in monounsaturated fats. Polyunsaturated fats are essential fats. They are required for normal body functions and humans need to obtain them from food sources. They have two or more double bonds. They are used for many different processes in the body, mainly for building cell membranes, cover our nerves, and are used in blood clotting, muscle movement, and controlling inflammation. Eating polyunsaturated fats instead of saturated fats or highly refined carbohydrates reduces LDL cholesterol and lowers triglycerides. The two main types of polyunsaturated fats are omega-3 and omega-6 fatty acids.

Omega-3 fatty acids can be found in salmon, flaxseeds, walnuts, and mackerel, shrimp, hemp and chia seeds, among others. Omega-3 fatty acids are known to prevent and treat heart disease and stroke, they reduce blood pressure, raise HDL, lower triglycerides, and restore leptin and insulin sensitivity, especially in the obese population. The figure below shows how omega-3 PUFAs protect cell membranes through exerting anti-inflammatory effects through modulating NF-kB signaling, NLRP3 inflammasome, PPARa/y, GPR120, and TGF-B signaling. Omega-6 food sources include vegetable and corn oils, sunflower seeds, peanut butter, eggs, and almonds, and they have been linked to protect against heart disease.

The ratio of omega-3 to omega-6 fats is important, especially in regards to inflammation and it is recommended that rather than decreasing the amount of omega-6s in your diet, which can be anti-inflammatory, it is better to increase your omega-3 intake.

Overall, while some fats are harmful to our health and bodily functions, and contribute to diseases like obesity and insulin resistance, high quality fats like polyunsaturated fatty acids can actually protect and reverse obesity and insulin resistance. 

Understanding The Epigenetics of Addiction

Addiction has been a pervasive problem that has plagued human history since we began recording it. Addiction is an issue we are still grappling with, even in developed nations. In the United States, nearly 21 million people have one or more addictions but only 10% of them receive treatment. [1] This costs the US economy north of $600 billion annually and has resulted in 700,000 deaths from overdose between 1999 and 2017.¹ These are abysmal numbers. I will try to shed some light on what some of the causes of addiction are, as well as a brief overview of the neurochemistry of addiction.

Neurochemistry of Addiction

Before we try tackling the chemistry, lets introduce the key brain structure in addiction. Arguably, the most important part of the brain in addiction is the nucleus accumbens (NAc). This is the area of the brain that all drugs of abuse act on in some way.[2] All addictive drugs cause an burst of dopamine (DA) release in the NAc. ⁴ While this is the structure that will be referenced in this article, it should be known that many more areas of the brain play a role in addiction. A comprehensive review can be found here.[3]

Now to introduce one of the chemical messengers in addiction: FosB. FosB has been found to be expressed after exposure to nearly all drugs of abuse. ⁴ After repeated drug exposure, the levels of FosB only increase in the brain. As the levels continue to climb, a person’s sensitivity to natural rewards and drugs increases (as does the likely hood of voluntarily consuming more drugs). ⁴ FosB causes epigenetic changes in the brain, which increase the likelihood that someone will do drugs. This is one of the causes for the vicious cycle of drug abuse.

Causes of Addiction—Epigenetics

I will not try and explain every cause of addiction in this post for two reasons:

1. 1. It will be a very long list
   2. We don’t know what all of the causes are

However, I will provide a brief overview so we can better understand the causes of addiction, both social and molecular. A recent literature review finds 50% of variance in addiction is dues to genetic variation, while the other 50% is due to environmental variance[4]  First, lets explore the genetic variation, but to do this we have to understand some basic epigenetics.

One of the most fundamental aspects of epigenetics, is the ability of a histone protein to become acetylated (i.e. stick a acetyl group onto a histone). Normally, the histone protein tightly binds DNA and prevents it’s transcription into mRNA. However, when the histone protein is acetylated, it loosens up and allows the DNA to be transcribed (see the following image for a visual).[5]

In addiction, histone acetylation occurs after acute exposure to stimulants like cocaine or amphetamine (meth). [6] Interestingly, these acetylations occur near promoters of c-fos and fosB in the nucleus accumbens (NAc). Earlier in this article, we mentioned how fosB  is one of the molecular causes of promoting addiction. Now we know where it is coming from and why.

Conclusion

Drug addiction is still a problem in modern society. We have seen that epigenetic changes occur in the brain after exposure to drugs of abuse. This causes mental and physical changes to the person that increases their likelihood of continuing to consume drugs. Hopefully through studying the science behind what causes addiction, we can develop new treatments and improve on prevention strategies.

Sources

[1] https://www.addictioncenter.com/addiction/addiction-statistics/

[2] Scofield, M. D., Heinsbroek, J. A., Gipson, C. D., Kupchik, Y. M., Spencer, S., Smith, A. C., Roberts-Wolfe, D., & Kalivas, P. W. (2016). The Nucleus Accumbens: Mechanisms of Addiction across Drug Classes Reflect the Importance of Glutamate Homeostasis. Pharmacological reviews, 68(3), 816–871. https://doi.org/10.1124/pr.116.012484

[3] https://www.brainfacts.org/-/media/Brainfacts2/In-the-Lab/Animals-in-Research/Brain-Illustration-Reward.jpg?h=367&iar=0&w=650&hash=F19DD0579346B918C0126E49A1FB7B4D32967584

[4] Reul, J. M. (2014). Making memories of stressful events: A journey along epigenetic, gene transcription, and signaling pathways. Frontiers in Psychiatry, 5. https://doi.org/10.3389/fpsyt.2014.00005

[5] https://www.google.com/url?sa=i&url=https%3A%2F%2Ftheory.labster.com%2Fhistone-acetylation%2F&psig=AOvVaw3ybLsvI2s_wjYfMn32Uz1y&ust=1634161272580000&source=images&cd=vfe&ved=0CAsQjRxqFwoTCPjCv6TrxfMCFQAAAAAdAAAAABAT

[6] Renthal, W., & Nestler, E. J. (2009). Histone acetylation in drug addiction. Seminars in cell & developmental biology, 20(4), 387–394. https://doi.org/10.1016/j.semcdb.2009.01.005