Disease/Health

Let’s Talk About Dietary Fats

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Types of Dietary Fats

Fats are a necessary part of an individual’s diet. Some benefits include organ protection, nutrient absorption, and energy metabolism. There are three main types of dietary fats: unsaturated, saturated, and trans-fat. Saturated fats are solid at room temperature, and are known to increase one’s cholesterol levels, specifically the ‘bad’ cholesterol, LDLs. The most common American foods with a  high saturated fat content include:

  • Pizza and cheese

            Figure 1
  • Whole and reduced fat milk
  • Meat products (beef, sausage, etc.)
  • Grain-based desserts (cookies, brownies, etc.)
  • Variety of fast food

Saturated fat is found mainly in foods from animals, but may also be found in plants such as coconut and palm oil (coconut oil may not be as great as you think)! On the      other hand, we have unsaturated fats. These are liquid at room temperature and are considered to be the ‘good’ fats through improving blood cholesterol levels (lowering LDLs and raising HDLs), easing inflammation, and stabilizing the heart. There are two types of unsaturated fats: monounsaturated and polyunsaturated.

Figure 2
Figure 2
  1. Monounsaturated fats:
    1. Oils (peanut, canola, olive)
    2. Avocado
    3. Nuts (almonds, pecans, peanuts)
    4. Seeds (pumpkin, sesame, etc.)
  2. Polyunsaturated fats:
    1. Oils (sunflower, corn, soybean, flaxseed)
    2. Walnuts
    3. Flaxseeds
    4. Seafood

Within polyunsaturated fats, there are fatty acids known as omega-3. The body is unable to produce omega-3 fats on its known, so it is important to obtain these from one’s diet. These are mainly found in seafood (fish) and walnuts or flaxseeds. Lastly, trans-fats is a fat produced through the process of hydrogenation to elongate shelf-life. This fat is considered to be the most detrimental to one’s health through increased inflammation, insulin resistance, and raise bad LDLs while lowering good HDLs. These are often known as partially hydrogenated oils (PHOs), and are banned in many countries.

Saturated Fatty Acids (SFAs) in the Brain

It has been shown that specific fatty acids, specifically saturated fatty acids (SFAs), are linked to hypothalamic inflammation, disrupt insulin and leptin signaling, as well as trigger inflammatory signaling cascades. The induction of SFAs are able to trigger Toll-like receptor (TLR2/4) signaling. TLR4 activates the response gene, MyD88, activates the kinase complex, IKK. Under conditions of high-fat diets (HFDs), IKK phosphorylates IĸBα, an inhibitor of the pro-inflammatory cytokine producer, NF-ĸB. This allows NF-ĸB to translocate to the nucleus of the cell and transcribe pro-inflammatory cytokines such as TNF-α and IL-1ß, as well as SOCS3. This signaling cascade increases neuronal inflammation in brain tissue as SFAs are able to cross the blood-brain-barrier (BBB) (Jais and Brüning, 2017). SFAs also disrupt insulin signaling through the increased production of ceramides within the brain. Ceramides activate protein kinase C (PKC), which is a primary inhibitor of PI3K. PI3K plays a major role in the insulin signaling pathway, and its inhibition will cause nuclear exclusion of FOXO1 and contribute to insulin resistance (Jais and Brüning, 2017).

Figure 3 (Jais and Brüning, 2017)

How Much Fat Should I Eat?

The dietary intake reference for total fat should be around 20-35% of total calories per day (44-77 grams depending on caloric intake). This intake should primarily consist of mono and polyunsaturated fat, with little saturated fat, and no trans-fat. In a low-fat diet, fat intake should be about 30% of total calories. In high-fat diets, such as Keto, total caloric intake will consist of around 75% of fats due to lack of carbohydrates. The Mediterranean diet, considered to be an ideal diet for humans, provides about 35-40% of calories from fats, focusing on unsaturated fat intake. According to the Dietary Guidelines for Americans 2020-2025, saturated fat intake should be limited to less than 10% of one’s calories per day. In order to do this, saturated fats should be replaced

      Figure 4

with unsaturated fats, primarily polyunsaturated. Also, around 5% of saturated fats in one’s diet are inherent in common foods such as lean meat, eggs, nuts and seeds, and grains. Due to this, there is very little room left for additional saturated fats found in foods with added butter or sugar.

Reference

Jais, A., & Brüning, J. C. (2017). Hypothalamic inflammation in obesity and metabolic disease. Journal of Clinical Investigation, 127(1), 24–32. https://doi.org/10.1172/jci88878

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Ideal Diet

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The ideal diet for humans contains high-quality food that is not processed such as veggies, fruits, whole grains, healthy fats, and protein. (1)

The ideal diet is the Mediterranean diet. This diet has been named the best 4 years in a row. It consists of mostly plant-based foods in addition to whole grains, seeds and nuts, spices and herbs, fruits and veggies, and olive oil. Fish, seafood, dairy, and poultry, are used sometimes while red meat and sweets are used rarely. Above is a hand-drawn diagram of the Mediterranean diet. (2)

Fatty fish and olive oil components of this diet are very healthy and have great benefits. Fatty fish can contain high amounts of omega-3 fatty acids which helps decrease inflammation, triglycerides, blood clotting, and risk of strokes and heart attacks. Olive oil is a monounsaturated fat that can lower cholesterol. The Mediterranea diet overall can decrease an individual’s chances of developing heart disease, stroke, Alzheimer’s, Parkinson’s, and type 2 diabetes. (2, 3, 4)

However, the Mediterranean diet can cause weight gain due to consuming higher amounts of fats from olive oil and nuts than what is recommended. A lower dose of iron from eating a small quantity of meat. Also, a decrease in calcium levels can be seen from consuming smaller portions of dairy products. (2)

The new food guide consists of:

  • 1/2 plate of diverse fruits and veggies
  • 1/4 plate of whole grains (whole wheat, quinoa, brown rice, oats, etc)
  • 1/4 plate of protein (fish, meat, etc.)
  • Water, coffee, or tea (consume less dairy, juice, and sugary drinks)

History of the Ideal Diet

The ideal diet has changed throughout the years. There has been a total of 9 food guides for American citizens approved by the USDA.

The first guide was introduced in 1916 by Caroline Hunt called “Food for Young Children”. It aimed to guide parents and caregivers on proper nutrition for children. This guide included 5 groups consisting of:

  1. Cereals
  2. Fruits & veggies
  3. Meat & milk
  4. Fats & fatty acids
  5. Sugar & sugary foods

In 1917 Hunt and Helen Atwater created a food guide for the whole family called “How to Select Foods”. It included and guided parents and caregivers on ideal meals along with the estimated cost of each meal.

In 1943 the United States Department of Agriculture (USDA) released the “Basic 7” food group guide to the public. This guide was made to help the United States citizens meet proper daily nutrition while rationing on food during World War II. Due to food rationing there the guide did not include serving sizes. The 7 food groups include:

  1. Green and yellow veggies
  2. Oranges, tomatoes, grapefruit, cabbage, and salad greens
  3. Potatoes and other fruits & veggies
  4. Milk and other dairy products
  5. Meat, poultry, fish, eggs, dried beans, peas, nuts, and peanut butter
  6. Bread, flour, cereal, and natural whole grain
  7. Butter and fortified margarine

In 1955 the Harvard School of Public Health (HSPH) introduced a shorted and condensed form of the “Basic 7” to the “Basic 4” which was approved by the USDA. This new guide included the food groups:

  1. Milk – includes the amount each age should consume daily
  2. Meat – 2+ servings per day
  3. Fruits & Veggies – 4+ servings per day
  4. Bread & Cereal – 4+ servings per day

In 1977 Mark Hegstend, a professor at HSPH developed the “1979 Hassle-Free Daily Food Guide”. This guide includes the food groups:

  1. Fruits & veggies – 4 servings
  2. Bread & cereal  4 servings
  3. Milk & cheese – 2 to 4 servings
  4. Meat, poultry, fish, & beans – 2 servings
  5. Fats, sweet, & alcohol – in moderation

In 1984 the “Food Wheel” was developed and introduced by the American Red Cross and the USDA. This updated guide included the daily food groups and appropriate calorie intake. The groups included:

  1. Bread, grain, & cereal – 6 to 11 servings
  2. Fruits – 2 to 4 servings
  3. Veggies – 3 to 5 servings
  4. Eggs, meat, poultry, & fish – 2 to 3 servings
  5. Cheese, yogurt, & milk – 2 servings
  6. Alcohol, sweets, & fats – in moderation

In 1992, the “Food Pyramid” was introduced. The large amount of recommended bread caused negative feedback of this guide. The 6 food groups included:

  1. Bread, cereal, rice, & pasta – 6 to 11 servings
  2. Fruits – 2 to 4 servings
  3. Veggies – 3 to 5 servings
  4. Milk, yogurt, & cheese – 2 to 3 servings
  5. Meat, poultry, fish, beans, eggs, & nuts – 2 to 3 servings
  6. Fats, oils, & sweets – in moderation

In 2005 “MyPyramid” was introduced. The graphic for the updated guide showed the importance of fitness along with adequate nutrition. The food groups include:

  1. Grains
  2. Veggies
  3. Fruits
  4. Milk
  5. Meat & Beans

In 2011 the USDA took a different approach to display food guides. “MyPlate” depicted the food portions on a plate rather than a pyramid, bullet points, or wheels.

This image was updated by HSPH to the “Healthy Eating Plate” and is held as the current food guide to American citizens. It stresses the importance of physical activity and eating healthy grains, proteins, oils, and vegetables that aren’t potatoes.

(5, 6)

Sources

  1. https://www.hsph.harvard.edu/nutritionsource/healthy-weight/best-diet-quality-counts/ 
  2. https://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/mediterranean-diet/art-20047801
  3. https://www.helpguide.org/articles/diets/the-mediterranean-diet.htm
  4. https://www.pennmedicine.org/updates/blogs/health-and-wellness/2019/february/mediterranean-diet
  5. https://www.hsph.harvard.edu/news/magazine/centennial-food-guides-history/#jp-carousel-111354813228
  6. https://guides.lib.unc.edu/nutrition-history/government

 

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Obesity: FAD diets, Keto Diets

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FAD diets and Leptin:

FAD diets promise quick weight loss, but they involve unhealthy and unbalanced eating plans. When proper food is brought back into someone’s diet, they gain weight rapidly. Leptin is a hormone that is important for its role in regulating food intake and energy expenditure. This hormone is produced by fat cells that signal satiety. Leptin is also shown to control the insulin-glucose axis as well as insulin responses. Since it was discovered, leptin has been used as a therapy for obesity and diabetes. Leptin, however, has been shown to be the reason why dieting does not work. With FAD diets, leptin receptors can become resistant the same way people with diabetes experience insulin resistance. The problem with these quick diets and fast weight loss is that the body becomes depleted of leptin, which makes individuals hungry all the time.

Keto diet and Leptin:

The Keto diet is one that causes the body to release ketones into the bloodstream. Most cells prefer to use blood sugar for energy, which comes from carbohydrates, however once on a ketogenic diet, there are very few carbohydrates for the body to utilize. In the absence of carbohydrates and circulating blood sugar from food, the body starts to break down stored fat into molecules called ketone bodies. Once the body has reached the stage of ketosis, most cells in the body will use ketones for energy until carbohydrates are consumed again. During a keto diet, the ability of insulin to regulate blood sugar levels is changed due to the content of macronutrients. During a high-fat diet, individuals can experience insulin resistance and an inability to maintain good glucose levels. While on a keto diet however, it has been seen to help symptoms of diabetes. Some Studies show that the ketogenic diet can increase leptin and decrease insulin, which is unusual because leptin and insulin levels normally change together, with both either increasing or decreasing. During conditions associated with weight loss, like fasting, there was a decrease in both leptin and insulin. During conditions associated with weight gain, like overeating, caused both Leptin and insulin resistance to increase. This shows that the ketogenic diet plays a unique role on the metabolic state and the opposite changes in levels of leptin and insulin also lead to a unique neurohormonal state

Sources:

Alex. (2021, October 31). The problem with fad diets. Ryan and Alex Duo Life. Retrieved November 24, 2021, from https://www.ryanandalex.com/problem-fad-diets/.

Amitani, M., Asakawa, A., Amitani, H., & Inui, A. (1AD, January 1). The role of leptin in the control of insulin-glucose axis. Frontiers. Retrieved November 24, 2021, from https://www.frontiersin.org/articles/10.3389/fnins.2013.00051/full.

Kinzig, K. P., Honors, M. A., & Hargrave, S. L. (2010). Insulin sensitivity and glucose tolerance are altered by maintenance on a ketogenic diet. Endocrinology, 151(7), 3105–3114. https://doi.org/10.1210/en.2010-0175

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The role of leptin in eating disorders and obesity

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Am I hungry or not? 

Leptin is a hormone that decreases your appetite while ghrelin increases it. These hormones aid in determining an individuals weight. However, when there is a malfunction in the signaling pathways an individual can experience weight gain/loss.

Drawing by Hannah Paulson

For people with eating disorders, the decision of what to eat is a complicated snarl of anxiety and guilt. And it’s not much less complicated for people without eating disorders. Our appetites, for what and how much we eat, are regulated by a complex array of hormones, hunger, and desire. When these systems are working properly, everything is great. We eat what we need and want, more or less. Our weight is appropriate for our genes and body type. Our diet is varied and tasty. 

Leptin

As in any complex system, however, things can go wrong. Research has shown us that eating disorder sufferers have problems regulating feelings of hunger and satiety that can perpetuate and perhaps even contribute to the onset of illness. Several key hormones and brain processes have been identified that may be malfunctioning in people with eating disorders. Leptin and ghrelin, discussed below, also interact with a variety of other hunger and satiety signals to help keep our bodies fueled properly. 

Leptin is a hormone produced by fat cells that signals satiety. Researchers at Rockefeller University discovered the leptin gene almost 20 years ago, and researchers soon showed that leptin is one of the many reasons why diets don’t work. As body fat stores go down, so do leptin levels. Lower leptin levels mean that it takes longer to feel full after eating, which serves to bring the body back to its original weight. 

Since leptin is a key component of appetite and body weight regulation, scientists suspected that leptin might be involved in eating disorders. Researchers measured leptin levels in 67 women with eating disorders, compared to 25 healthy women. As expected, leptin levels were significantly elevated in the women with binge eating disorder compared to healthy women, but they were significantly lowered in women with anorexia or bulimia. 

Normally, high levels of leptin are associated with lower levels of endocannabinoids, brain chemicals that, among other things, regulate appetite. Low levels of endocannabinoids should make a person feel less hungry. This isn’t the case in people with binge eating disorder; their elevated leptin levels are actually associated with high levels of endocannabinoids, which could help promote further binge eating.

In bulimia, leptin levels appeared somewhat lower than expected, and lower leptin levels were associated with more frequent binge eating. A later study found that low leptin levels in women with bulimia were also associated with more chronic, severe illness. 

When researchers compared leptin levels in women with anorexia to women who had low weights for other reasons, they found that leptin was significantly higher in the women with anorexia. This blunted leptin response could help explain why people with anorexia are hyperactive and can continue starving themselves for long periods of time. They are hungry, yes, but not as hungry as they should be.

Ghrelin

Ghrelin is secreted by the stomach and acts opposite to leptin. Whereas high levels of leptin help trigger satiety, high levels of ghrelin help trigger hunger. Ghrelin levels typically rise before a meal and decrease afterwards. The hormone is thought to work in part by helping to stimulate the brain’s reward system to encourage eating. 

Scientists found that, in women with binge eating disorder, ghrelin levels were lower than in women with similar BMIs. Other researchers have found similar results indicating that decisions about eating aren’t dictated just by hunger and fullness, but by other emotions as well. 

When researchers measured ghrelin in women with bulimia, they found that levels of this hormone didn’t decrease as much as it did in control women. Since women with bulimia don’t feel as full after a meal, they may be more likely to binge or overeat. In anorexia, ghrelin levels are elevated, as expected with someone who is starving. During the refeeding process, however, ghrelin levels drop dramatically, which could help explain why many people with anorexia struggle to put on weight because their hunger signals aren’t working properly.

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Let’s talk about Obesity: a fast growing global epidemic

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Obesity is now considered as a an epidemic that the public health is currently facing globally than malnutrition/ undernutrition. According to WHO in 2016, 2 billion adults were found overweight, of which 650 million of them are affected with obesity.

In the US, obesity has risen exponentially since the ’60s, which is also reflected with the busy “microwave” lifestyle that most Americans live, if looking at its prevalence in the United States. This thus implies a lack of time and investment in self-care, which in return opens the door for overconsumption of processed foods that are high calories, especially from fats and sugars.

This is very well alive in other parts of the world as well, regardless of the income level of the country. Below is a world map of obesity around the world.

 

Exposure to a high-fat diet and neuroinflammation in the Central nervous system has been shown to increase risks and causes for obesity, besides genetic predisposition. Changes in brain neurochemistry have impacts on the hypothalamus and its regulations for insulin and leptin levels and disrupt food consumption and energy.

This creates imbalance in food intake and energy consumption, caused by the insulin resistance that affect the hunger and satisfaction feelings.

The AgRP signals are released to create a feeling of hunger where as the alpha-MSH from POMC neurons allow for the feeling of satisfaction. The insulin resistance thus causes disruption, where there occurs more food intake than energy consumption. The insulin resistance can be caused by a high-fat diet or genetic mutation that cause neuroinflamation through the release of pro-inflamatory cytokines from the overactivity of mIcroglia and astrocytes.

ABT statement: A high fat diet is a measure trigger for obesity that is worth cutting down when considering underlying health issues, but there are various traditional cuisines around the world that have a fat heavy diet, therefore to what extent can culture be flexible to sustaining better lifestyle?

Artstract:

 

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Insulin signaling and Obesity

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What does insulin do

Insulin is a key regulator of adipose tissue lipolysis, which is the catabolic process leading to the breakdown of triglycerides stored in fat cells and release of fatty acids and glycerol (Langin et al., 2006).  Insulin regulates adipose tissue metabolism through direct effects on adipocytes (a cell specific for storing fat) and through signaling in the central nervous system by dampening sympathetic outflow to the adipose tissue (Shin et al., 2017). So, what about insulin in relation to POMC and AgRP?

 

 

Regulating Hunger

POMC and AgRP neurons

The insulin receptor is expressed in both AgRP and POMC neurons. Insulin can both inhibit AgRP and POMC through hyperpolarization or can activate these neurons as a result of heterogeneity (Shin et al., 2017). Insulin and leptin act directly on neuronal subsets in the ARC of the hypothalamus to control energy homeostasis. POMC neurons are activated, while AgRP neurons are inhibited. Then the MC4R-expressing neurons in the PVN. If one is fasting, the AgRP levels are increased and the POMC levels are reduced which leads to decreased MC4R signaling. When one has eaten, AgRP levels are diminished and POMC levels increase, which triggers MC4R signaling, stimulating energy expenditure (Jais et al., 2017).

 

 

Insulin resistance in Obesity and Type 2 Diabetes

 

Insulin resistance in Obesity and Type 2 Diabetes is classified by decreased insulin-stimulated glucose transport and metabolism in adipocytes and skeletal muscle and by impaired suppression of hepatic glucose output. In this situation, insulin binding, receptor phosphorylation, and phosphorylation of IRSs are reduced. In general, this means that PI3K activity associated with both IRSs is impaired (Langin et al 2000).

 

 

 

Why is this Important?

Figure 1: https://www.cdc.gov/obesity/data/prevalence-maps.html#overall

According to the CDC, the US obesity prevalence was 42.4% in 2017-2018. Obesity can lead to other disorders including, heart disease, stroke, type 2 diabetes and certain types of cancer. These are among the leading causes of preventable, premature death (CDC et al., 2021).

 

 

What can I do to prevent this?

Healthy Plate

There isn’t necessarily a diet you can do to help prevent insulin resistance in your body, you must be willing to change your lifestyle all together. Obviously, everybody knows you should eat healthy, this isn’t new information, but it is important that when eating unhealthily it is in moderation. Although you should not skip meals because this causes your insulin and blood sugar levels to go up and down leading to more body fat (Moore et al., 2019). Try your best to adopt healthy habits slowly and they will become permanent.

 

 

 

 

 

 

Works Cited

 

Centers for Disease Control and Prevention. (2021, September 30). Adult obesity facts. Centers for Disease Control and Prevention. Retrieved November 22, 2021, from https://www.cdc.gov/obesity/data/adult.html.

 

 

Jais, A., & Brüning, J. C. (2017). Hypothalamic inflammation in obesity and metabolic disease. Journal of Clinical Investigation, 127(1), 24–32. https://doi.org/10.1172/jci88878

Kahn, B. B., & Flier, J. S. (2000). Obesity and insulin resistance. Journal of Clinical Investigation, 106(4), 473–481. https://doi.org/10.1172/jci10842

 

 

Langin, D. (2006). Adipose tissue lipolysis as a metabolic pathway to define pharmacological strategies against obesity and the metabolic syndrome. Pharmacological Research, 53(6), 482–491. https://doi.org/10.1016/j.phrs.2006.03.009

 

 

Moore, W. (n.d.). Insulin resistance diet: How to use Diet to prevent diabetes. WebMD. Retrieved September 23, 2019, from https://www.webmd.com/diabetes/diabetes-insulin-resistance-diet.

 

 

Shin, A. C., Filatova, N., Lindtner, C., Chi, T., Degann, S., Oberlin, D., & Buettner, C. (2017). Insulin receptor signaling in POMC, but not agrp, neurons controls adipose tissue insulin action. Diabetes, 66(6), 1560–1571. https://doi.org/10.2337/db16-1238

 

 

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Obesity and the Endocannabinoid System

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Obesity Basics 

Figure 1: https://www.cdc.gov/obesity/data/prevalence-maps.html#overall

Obesity has been identified a top 10 global health problem by the World Health Organization. According to the CDC, nearly 42.4% of the adult population in the US were obese in the year of 2017. In figure 1, the color of each state represents the percentage of obese individuals in that state within 2020.

An important contributor is increased caloric intake without increased physical activity. An increase in calorie consumption is conducive to an increase in appetite from increasing craving and liking of food. The main brain system involved in craving and liking is the endocannabinoid system (ECS).

The Endocannabinoid System

The ECS functions to adjust behavior and metabolism according to food availability. Its action range from regulating sensory responses to developing preference for the consumption of high caloric food. In today’s world it appears that the ECS favors obesity and metabolic disease as food is readily available, especially “junk” food.

The ECS receptor in the brain is the cannabinoid-1 receptor (CB1). Researchers have examined the effects of activating and deactivating this receptor has on the body.

CB1

Cannabinoids and endocannabinoids bind this receptor. Figure 2 represents a simple schematic of the retrograde signaling of the ECS system.

Figure 2: A basic representation of ECS signalling in neurons. https://gaiaguru.co.uk/cannabinoid-receptor-1-basics/

Cannabis has been documented as promoting eating through strong cravings and an intensification of the sensory and hedonic properties of food. It has been demonstrated that the hyperphagic actions of THC (one of the psychoactive constituents of cannabis) were mediated in large part by cannabinoid CB1 receptors. Additionally, researchers saw that, systemic anandamide (an endocannabinoid) administration caused an increase in food intake. Later experiments confirmed that other endocannabinoids (2-AG and noladin ether) also increased food intake. Therefore CB1 agonists promote eating behaviors that lead to obesity.

In addition to CB1 agonists, researchers determined that CB1 antagonist suppressed food intake. They found that mice without CB1 receptors had a reduced sensitivity to the motivating properties of food, exhibiting reduced rates of responding for food and lower breakpoints when given a task to obtain food. In effect, the stimulatory actions of cannabinoids on eating resembles the changes that occur in food deprivation: levels of

Figure 3: CB1 receptor activation induces inhibitory effects on insulin signaling. doi:10.3390/ijms20092109 

anandamide and 2-AG increase after fasting. Therefore, this shows that endocannabinoids have an effect on the food intake of the brain without any drug influence.

In figure 3, you can see how some researchers believe CB1 signaling can affect insulin signaling that could in turn mediate weight gain. This activation of the CB1 signaling can be done by endocannabinoids (anandamide) or cannabinoids (THC).

Figure 4: doi:10.3390/ijms20092109

In figure 4, it describes the different locations of CB1 receptors and their pathological implications. As you can see the ECS is implicated in many agents of obesity development.

Overall, CB1 agonists show to increase wanting and liking of food AND CB1 antagonists show to decrease these. The endocannabinoid system plays an important role in the development and control of obesity. However, the exact mechanisms of these neurotransmitters on a cellular level are still not completely understood. Therefore, research must continue to clarify how endocannabinoids and cannabinoids can mediate obesity and how they might be able to be a part of treatment.

References:

https://www.cell.com/trends/endocrinology-metabolism/fulltext/S1043-2760(15)00140-X

https://www.mdpi.com/1422-0067/20/9/2109

https://gaiaguru.co.uk/cannabinoid-receptor-1-basics/

https://www.cdc.gov/obesity/data/prevalence-maps.html#overall 

https://doi.org/10.3389/fnins.2017.00293 

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How You and I Can Help Keep People Safe in Contact Sports

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Concussions are no joke, and it’s nice to see that people are finally beginning to take them seriously both on and off the field. The most dangerous part of a concussions is the chance of re injury, which means the most important piece to helping people with concussions is to stop them from a secondary impact. This is usually done by stopping players from playing for a while, but in order to do that the first step is recognizing the problem, which can be a challenge for many reasons. Such reasons include wanting to keep playing, dismissing it as a headache, or even ignoring the concussion to keep a player on the field. As concussions have become more recognized and dangerous, players and coaches need to change that mentality to one of a fast recovery. One of the best ways to get that first recognition and fast recovery in is by using the SCAT test.

The SCAT test is designed to be both user friendly and efficient, combining two of the key problematic factors regarding concussion diagnosis. Every coach, family member, and player should be able to use this tool effectively due to the functional layout and simplified instructions. By having these tools accessible to the public, concussions can be traded much more efficiently provided they are given the attention they deserve.

Below is an image of the first page of a SCAT-3 test as it would be administered in the field. One of the main strengths of the test besides its ease of use is the ability it has to cover all its bases. The test begins with important baseline information, such as level of consciousness and basic cognition, which are the most important indicators of a severe concussion. From there the test moves to a self-report, which can be both helpful and harmful depending on how it’s used. If this test were stand-alone it could lead to a series of issues, but the SCAT test instead uses it as a part of the baseline establishment, which allows for much more important information to be gathered by the observer. The test then goes into an in depth analysis of how the test taker performs on a variety of physical and cognitive tasks, with a score value assigned to each test. It may seem like a lot to the casual observer, but the level of detail combined with the ease of administration makes these tasks both manageable and effective at diagnosing a concussion. After the tests are done a concussion diagnosis can either be made or ruled out, and if a concussion is determined to exist the test outlines the next steps to take for seeking help.

Source For SCAT Test

There is still much work to be done regarding concussions and public opinion, but focusing on catching them before they can cause permanent damage is an important first step in recognizing the severity of concussions and moving towards a safer recovery period for people that live in high contact potential scenarios like contact sports or manual labor. In conclusion, ask your local coaches if they would be willing to have a copy of the newest SCAT test on hand, they never know how important it could be for their team!

Source for Featured Image

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Concussion & Behavioral Changes

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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
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Protection of the most important organ from concussions, the Brain

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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 

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