Skin Color Has a Biological Basis. Race Does Not

Foreword by Susan Eckert (teacher)

This post is written as a collaboration between student and teacher. The topics in this post are challenging and complex. As a teacher, I have been dwelling on the genetics of race for years now and always felt that I did not do the topic justice in the classroom. I see this post as an opportunity to work with a student and make some progress on how to more effectively teach my students about the biological basis of race (beyond just saying there is none). All science in this post and the entire blog is supported by evidence. However, this post, like many on the blog, gives both student and teacher the space to discuss the intersection of science and morality. Science is a distinctly human effort to understand the natural world and it does not exist in a vacuum--history and context matters.

The Biology of Melanin by Shannon Huhn (student)

Did you know that your skin is the largest organ of your body, your first line of defense against pathogens and your primary defense against the sun's damaging rays thanks to melanin? Melanin is an invaluable pigment that is found in all humans (and in many other organisms)--its key functions that protect us from Earth’s harsh conditions are necessary for our survival. For example, did you know that the melanin you produce protects you every time you step outside? One of melanin’s prime functions is to protect the epidermis (the top layer of your skin) from the ultraviolet (UV) radiation from the sun. Melanocytes, cells where melanin is produced, can absorb UVA and UVB rays that can be harmful to your skin and increase the risk of skin cancer by damaging DNA. This is why your skin gets darker during the summer--your body produces more melanin in response to increased sun exposure.

The classic "farmer's tan" which results from the skin responding to increased UV exposure by producing more melanin. Source

Melanin also has some lesser known advantageous features, such as the ability to absorb scattered light rather than light beams within the eyeball, which can sharpen visual perception. Melanin is the biggest contributor to eye color--dark colored irises have a higher concentration of melanin and lightly colored irises have a lower concentration of melanin. There is no blue or green pigment that produces eye color in humans--it's all melanin and the way the light scatters as it hits the iris.

Different properties of melanin have been influenced by human evolution. For example, two different types of melanin have been the result of evolution. Eumelanin and pheomelanin can influence how dark or light your skin tone is--those with lighter skin have higher amounts of pheomelanin, and those with darker skin have higher amounts of eumelanin. Interestingly, we all have roughly the same amount of melanocytes and what differs is the amount and type of melanin the melanocytes produce. Since each person has different levels of these two types of melanin based on genetics/ancestry and the environment, there is a large variety of skin tones across the globe and in the US. Here is a TED talk on the beautiful variation of skin color among humans.

Variation in skin color in a family. Source

However, the amazing biological purpose of melanin has been stained through the detachment of its biological importance with the creation of the concept of race and the idea of racial superiority. The result of white colonizers adding value to skin color and associating darker skin with inferiority in 16th and 17th century North America set the foundations for a country that thrived in the hands of slavery and discrimination by creating complex systems that blatantly favored those with lighter skin. Although many Americans believe that we have made great strides to create a more equal nation, this simply isn’t true. Slavery and racial inferiority haven’t disappeared. The system has evolved from slavery to Jim Crow to the “war on drugs” to mass incarceration and police brutality. Most recently, this phenomenon has manifested with the murders of Black Americans at the hands of police officers, sparking greater media coverage across the country. Americans of all ages, races, and ethnicities have taken to the streets to demand change in institutions that only benefit those with lighter skin.

Black Lives Matters protestors in NYC on June 9th, 2020. Source

As the fight for racial justice continues in the coming political era, it is imperative that we keep biological concepts straight. That is, we must remember that the properties of melanin and melanin production that create skin color were caused by human evolution. It is our duty to keep in mind that race is a social construct; society’s perception of race has been convoluted by bigotry and hatred. However, the claims of racial superiority have persisted for so long that it would do more harm than good to try to detach the biology of melanin and the social constructs that have followed. We must educate ourselves on the biological and social aspects of skin color, and how we benefit from centuries-old systems. Without this, we will never be able to amplify Black voices and create a future that is just and equitable for all, regardless of one’s complexion.

Genetics and Race by Susan Eckert (teacher)

I'm going to get straight to the point: there is no biological basis of race. It is a social construct and my primary goal is to provide enough knowledge about the variation of the human genome to allow the reader to easily refute those that try to use science to promote an agenda of racist ideology. The idea of a biological basis for race has a long and dark history based on biological determinism, which led to eugenics, the justification of genocide, colonialism, and slavery. When I started college in 1990, I knew that I wanted to pursue a career in genetics. My freshman seminar was about eugenics and we read Stephen Jay Gould's Mismeasure of Man. Stephen Jay Gould was a paleontologist, evolutionary biologist, historian of science and a well-known science communicator. The book forcefully criticizes against biological determinism that used skull measurements, known as craniometry, and psychological testing, and then assigning worth to an individual based on these measurements. There has been some criticism about the book's data analysis but the premise of the book I stand behind.

Craniometry. Source

If there is no biological basis for race, the logical question is where did the idea of biologically distinct races come from. We can trace the use of science to promote distinct races back to the publication of a book in 1775 by a German physician and scientist named Johann Friedrich Blumenbach, who used craniometry to create a model of five distinct races. With advances in genetics, we can easily analyze whether there is a genetic basis for race and the answer is a definitive no. If we work with the popular notion that there are five distinct races (African, European, Asian, Oceania, and Native American), there is more genetic variability within the races than between them. Homo sapiens are 99.6-99.8% identical. There are no trademark alleles (specific versions of a gene) that distinguishes one supposed race from another. Skin color is often used to distinguish race and as Shannon explained above, the type and amount of melanin produced determines an individual's skin color. Genes that control melanin production, however, are a tiny part of the human genome and they assort independently of traits that racists use to promote their agenda, namely intelligence and behavior. White supremacists have moved on from craniometry to misrepresenting genetic data to support their view. Some white supremacists do have a solid understanding of genetics but they cherry pick the data to align with their racist world view. Apart from being morally repugnant, the approach of finding data to align with a preconceived notion is anathema to how science works.

. . . 

One year, I had a class that gently teased me for declaring one too many times that I used to be a genetic counselor. I can see their eyes rolling if they read the next sentence. Teaching is a second career for me--prior to teaching I was a genetic counselor. Why am I stating this yet again? Well, because for 9 years, I was focused solely on human genetics and a patient's ancestry played a role in both medical research and clinical care. In a medical setting, those in healthcare do routinely ask about a patient's ancestry. The operative word is ancestry, sometimes ethnicity, but not race. Gathering data about ancestry played a role in the clinical and research genetic setting because although there is no biological basis that supports distinct races, humans do cluster into broad geographical regions and knowing the ancestral history of an individual is helpful for disease screening. Mutations that arise in an egg or sperm are random but how the environments acts upon these mutations is anything but. If a mutation provides an advantage for survival and reproduction, then we say that the environment selects for that trait and it becomes more common in the population. This is called natural selection and it's the reason why people whose ancestors lived in equatorial regions tend to have more melanin: like Shannon explained, the molecule protects cells from damaging UV rays. An excellent film from the Howard Hughes Medical Institute's BioInteractive division beautifully explains the evolution of skin color as it relates to biogeography. Sometimes, though, evolution results in a disease gene being more common in people who live or whose ancestors lived in a specific region. Two classic examples are sickle cell anemia and cystic fibrosis. Sickle cell anemia is more prevalent among those living in an area where there is a high risk of malaria. Being a carrier for the disease gene (one disease gene and one gene without the sickle cell mutation) provides protection against the deadly disease. It's also more prevalent among those whose ancestors lived in areas where malaria was a risk even though the selective pressure is no longer present. Cystic fibrosis, on the other hand, is more common among White individuals, although why is still a mystery.

. . . 

So what does this all mean for the classroom? How do I teach about race when we get to the genetics unit in AP Bio? Should I even talk about it at all? It's not a topic that most biology textbooks tackle and it's not specifically in my curriculum. Genetic variation, however, is and that is why I have gone there, although not at the level I would like, and why I will continue to explore the topic with my students. The general population holds a lot of misconceptions about the biology of human variation and that of course includes students and teachers as well. Some teachers are tackling it head on. And resources to help teachers navigate the topic in the classroom do exist. 

It's crucial to stress that even though there is no evidence for a biological basis for race, we can't simply say we don't see color and act as if the social construct of race and racial identity do not matter. Instead, we should understand the role evolution and biogeography play in human genetic variation, fight racism with scientific knowledge, commit to ending racial injustice, and learn about and celebrate human genetic and cultural diversity.

Addendum: There are many hyperlinks in this blog post. The articles I (Susan) have linked to below are the ones I recommend the most.
An excellent blog post that tackles the genetics of human variation in more detail
An article in the journal Nature Genetics that dives much deeper into the science
An article in The Atlantic that focuses on the difficulty of teaching race in HS biology classes

If you have questions or concerns about the content of this post, please email Susan Eckert at seckert@montclair.k12.nj.us or suseckert@gmail.com

How Advances in Optometry work for the Colorblind.

    Did you know that about 8.5% of the world’s population is color blind with 8% being male and 0.5% being female? That may sound like a small number, but even that calculates to 680 million people worldwide. Color blindness is a recessive disorder that affects how your eyes receive wavelengths of light, which in most cases disrupts the function of red-green receptors in the retina. This can be the difference between a person differentiating two different colors, not being able to see the difference, or not seeing those colors at all. The reason why people are affected is that color blindness is a sex-linked genetic disorder, inherited by parents. Fortunately, modern science has allowed for fascinating treatments for this disorder.

Model of the Human Eye

    There are a few things to understand in order to truly grasp the incredibility of the advances in optical sciences. Embedded within each and every organism's cells lie DNA, the genetic material that codes for every physical characteristic about the organism. Specifically, a section of DNA, the gene, would code for an assigned trait of an organism. Through a process called transcription, a DNA sequence is transcribed on mRNA as it is produced. A few edits are completed on the mRNA to splice out the unnecessary sequences transcribed. The protein is translated from this mRNA in a ribosome. In this case, the cones of the retina are made up of multiple disc-shaped transmembrane proteins. The human eye receives light in the retina. It differentiates the wavelengths of light, or color, with a variety of color receptors, also referred to as cones. The gene that codes for the red-green receptors that are sensitive to red and green light is located on the X-chromosome.

X(right) and Y(left) chromosomes

    A chromosome is made up of 2 strands of double-stranded DNA wrapped around histone proteins for structure. The X-chromosome is one of the 2 sex chromosomes that contain genes that code for traits specific to what biological sex the organism is. Most of the genes on the X chromosome encode proteins that have nothing to do w/ the physical structures associated w/ sex. Females have two X-chromosomes without the Y-chromosome while males have one X-chromosome along with a Y-chromosome. With only one X-chromosome, it is impossible for a male to be a carrier of this disorder, the male either has the disease or does not have it. For females, the possibility of not showing for the trait is more likely, either as carriers of the trait or homozygous dominant which is not having the recessive gene for color blindness at all. The possibility of being color blind depends on your parents' genotype but in all cases, there is a higher chance of being color blind as a male than as a female. This explains the statistic from the first paragraph.

    Now that you know how people inherit this disorder, how exactly does one treat it? For some time, color blind people had the option to wear contact lenses saturated in the color they could not see. This significantly improved the sight of color in some. Although these improved the color perception, they still did not correctly simulate what functional color perception looks like. For some time there was no way to truly do that. That was until a glass researcher, Don McPherson, Ph.D., along with other members of EnChroma invented a pair of glasses that properly display each wavelength of visible light for color blind people. Normally, the cones in the retina have overlapping regions as a way to increase efficiency however when each cone overlaps too much, poor color discrimination occurs. The EnChroma glasses use a filter to cut out these overlapping wavelengths. One can only imagine how long this took to develop, especially since optometry is a fickle and ever-evolving study.

EnChroma's colorblind glasses

    Unfortunately, there are some extreme cases where people are born without color receptors called achromatopsia. This is also a genetic disorder that is linked to the X-chromosome. It is less common and a recessive trait. Sadly, there is no cure or treatment for this even with these special glasses. These glasses utilize the defectivity of the receptors so without cones or completely dysfunctional one's glasses would have nothing to work on.

    Your eyesight is precious. It is almost everything you know and remember. You would not be able to read this article without it. Since this is the case, it is important you treasure everything you see, from shape to color to depth. And if you are color blind, rest assured that there are options and treatments for you that are quite eye-deal.

Venom the movie...REAL??? not clickbait almost died

The products of evolution are fascinating and complex. Life intersects in countless interlocking processes, and we find many of these to be beautiful. There are some ways of life, however, that are less photogenic, and those are the kind I want to talk in this post. Specifically, one of the reproductive strategies we find most disturbing: behavior-altering parasitism, in which the behavior of the host is altered to maximize the success of its parasite.

(like this guy)

So what does that mean? In this case, we’re not talking behavior like the usefulness of a cough for spreading germs. We’re talking a perceptive shift that changes the way that that host interacts with the world. For most of us, the most familiar example is rabies. The basic physical symptoms of the rabies virus are fever, headache, and vomiting, with partial paralysis at later stages, but behavior is also affected, causing anxiety, confused agitation, and hyperactivity. Weirdly, the infected develop a fear of water. Nocturnal animals become active during the day. Behavior becomes increasingly reckless. 

Saliva collecting in the mouth is probably the most well known symptom of rabies.

This all happens for a reason. Digging a little deeper, the direct correlation between these symptoms and transmission of the parasite is obvious. The deranged nervous behavior makes it much more likely that the infected animal will pass on the rabies to another host, while the aversion to water and drink in general keeps saliva (through which rabies is passed) collected, pooling, in the mouth. All the better to infect you with! 

The Baculoviridae family of viruses cause even grosser effects. Acting on caterpillars, they cause their hosts to gorge themselves providing nutrients for the parasite. When the virions (virus bits) are ready to leave the host, the caterpillar’s cells begin producing enzymes that “dissolve the animal into goo.” This scatters clumps of infected material that can be ingested by future hosts! (Yay recycling!) 

Another great example of parasitically altered behavior is toxoplasmosis. Rodents that consume fecal matter from infected animals become more reckless and less fearful of predators-- even, dramatically, attracted to the scent of cat urine. 

(Interestingly, mice that have been cured of toxoplasmosis remain unafraid of cats, suggesting a lasting structural change in the brain.) 

This all, of course, makes those infected mice much more likely to be eaten by a cat: the definitive host. Definitive hosts are what you might call final or “preferred” hosts, a stable environment in which the parasite can kick back, reach maturity and reproduce. 

Not only mice and cats are affected by toxoplasmosis. Considered a neglected parasitic infection in the US, it causes "mild flu-like symptoms" at worst in those humans whose immune systems are able to battle the parasite. Most immune systems are; according to the CDC, over 40 million people in the States carry the parasite, with only a tiny fraction showing symptoms. But it can cause death if your immune system is compromised by something like AIDS, and if you become infected while pregnant (or just before you get pregnant), the results for your kid could be equally serious. The effect could be as obvious as losing the baby, or symptoms (seizures, blindness, or mental disability) might only surface in that child years after birth. Some scientists think that the effect of toxoplasmosis on the general (human) population is even more staggering. One fairly prolific proponent of this is Jaroslav Flegr, a parasitologist and evolutionary biologist who has written about toxoplasmosis' influence on everything from traffic accidents to sex ratios, mental illness and human personality. Much of this writing, to summarize very simply, discusses the increased recklessness also seen in infected mice. 

This effect on the mice is called parasite-increased trophic transmission, in which the host behavior is altered to make that host more likely to be eaten by an animal at a higher trophic level (in layman’s terms, a predator), thus passing on the parasite through ingestion (in layman’s terms, eatin it). 

Behavior-altering parasitism is a wide-ranging strategy, not only exhibited by viruses like rabies and protozoa like Toxoplasma gondii, but crustaceans, insects, and parasitic worms (like leeches and tapeworms). 

(above) A horsehair worm with cricket host.
(below) A flatworm (green dude) with a snail host 

(both images from wikipedia)

It can also lead to more complex behaviors than increased recklessness. For example, the larvae of the wasp Hymenoepimecis argyraphaga are grown in Leucauge argyra spiders. Before they finish killing the host, those larvae inject the spider with a chemical that alters weaving behavior. The spider, before dying, weaves a different sort of web for the larvae to pupate in, one specifically to keep their cocoons supported and dry. These more complicated changes in behavior are what are most spectacularly cool to me. 

Another very dramatic change in behavior is caused by the Cordyceps genus of fungi. Acting on insects, it is also known as the zombie ant fungus, due to its effects on its host. Spores attach to the ant and "dig" down into its exoskeleton, where they spread out along the muscles. David Hughes (an entomologist who's studied zombie ants) describes how the fungus replaces the ant from the inside out: "We found that a high percentage of the cells in a host were fungal cells. In essence, these manipulated animals were a fungus in ants’ clothing." The results of Hughes' team's research suggest that the fungus directly manipulates the legs and mandibles of the ant, like a puppeteer, and that a "large proportion" of the fungal cells seem connected to each other in a 3D network, working collectively to control the different behaviors required from the different parts of the host's body. Infected ants are moved to ideal places for the fungus to reproduce, over time (perhaps even years) creating mass graves of strange, overgrown little corpses. Cordyceps out of control can destroy an entire colony of ants, robbing itself of its own legs, so to speak, and so there is a balance struck by the ecosystem that continues to be researched, where just enough ants are infected to help the fungus grow without stranding itself. (This is really cool- other fungi that don't harm the ants help protect their colonies from cordyceps.)

We don’t understand the mechanisms behind every kind of behavioral change yet, but one that isn't too difficult to wrap our brains around is altered neurochemical communication. So what does that mean? The brain is a physical thing. Thought and action both start as energy between neurons. If you alter the brain’s ability to communicate to the body or itself by messing with the chemicals that allow that communication, you alter the behavior. For example, the emerald cockroach wasp injects venom directly into the brain of its host, messing with the chemical balance and therefore with the brain’s responses to threatening stimuli (the escape! responses triggered by something frightening, like a wasp trying to inject stuff into your head). 

(image from wikipedia)

The host becomes usefully paralyzed without any interference on the part of the wasp to the parts of the brain responsible for movement control. Put simply: the physical ability of the host to move has not been touched. What has been changed is that the host is no longer stimulated to move-- it has no motivation, there is no incentive to react. In its way, this solution is as satisfyingly elegant as anything else evolution has produced. Energy is more efficiently spent changing the host’s innate reaction to stimuli--cutting off behavior at the source-- than simply handling the behavior once it happens. 

We often like to consider our rational thinking as something divorced from our physical selves. These parasites remind us that even the mind is just a collection of physical components-- hormones, proteins, impulses, chemicals-- that can be attacked by an outside force, just the same as our muscles and organs. Isn’t it cool?

Chia seeds: the "runner's food"

The Tarahumara are a group of indigenous peoples who live in northwestern Mexico and are renowned for their long distance running ability.  These people have a tradition of running close to 200 miles over the course of a few days to reach different settlements they had.  How were they able to accomplish this?  The answer is their diet!  Specifically the chia seed, which is a staple in every Tarahumara meal.   Chia seeds come from the Salvia hispanica and Salvia columbariae plants. The Salvia columbariae is the plant that is native to the region of the Tarahumara people.

Salvia columbariae plant (source)

Now, I bet you’re wondering: What could possibly make these tiny seeds so special?  Well, these seeds are chock full of NUTRIENTS!  That's right, chia seeds are an excellent source of omega-3 fatty acids, antioxidants, fiber, and protein.

Examples of omega-3 fatty acids (source)

Omega-3 fatty acids are extremely beneficial for the average runner as they help to relieve stress off your joints during and after a run. By relieving pressure off your joints, chia seeds reduce your likeliness of getting an injury. Omega-3 fatty acids also boost HDL cholesterol levels which protect against heart disease and stroke. Chia seeds are full of antioxidants that help keep the fats in the seed from going bad. However, antioxidants are also beneficial to the human body by reducing the production of free radicals which can damage cells. Chia seeds also contain soluble fiber. Fiber is a type of carbohydrate that we eat, but that the body cannot completely break down. Soluble fiber is important to the body as it helps to stabilize blood sugar levels. It does this by slowing down the digestion rate of other nutrients to prevent spikes in blood sugar levels and reduce the likeliness of heart diseases. Soluble fiber helps feed the "good" bacteria in your stomach that breaks down food. The high levels of soluble fiber also allows chia seeds to absorb 10 to 12 times its weight in water. This is why chia seeds can be used as an egg substitute in vegan baking. Protein composes approximately 14% of chia seeds by weight. This is pretty high in comparison to other plants. Protein is important as it reduces appetite and is helpful for weight loss. The high protein levels of chia seeds is what gave the Tarahumara people sustenance on their lengthy journeys.

Chia seeds also have an interesting reaction when placed in water.  When mixed in a glass of water, chia seeds will develop a gel-like substance surrounding the 1mm in diameter seed that is approximately 12x the original size of the seed.  This happens because chia seeds have a high amount of mucilage (a soluble fiber), a hydrophilic shell, and the ability to absorb over 10x their weight in water.  This gel-like substance is formed for a variety of reasons.  First of all, it is used to cover wounds that the seed has endured to block the entrance of pathogens and other bacteria into the seed.  Mucilage also works to spread seeds through the roots of the Salvia columbariae plant.  Finally, mucilage works to incubate the seed while it germinate.  When the seed comes into contact with water, mucilage absorbs some of the water to surround the seed with moisture while it germinates.  Mucilage also has some pharmaceutical applications.  Chia seeds can be used as an organic ACE inhibitor because of it's mucilage content.  An ACE inhibitory enzyme is activated when chia seeds are soaked in water.  ACE inhibitors are produced synthetically to treat high blood pressure and other heart diseases.  What ACE inhibitors do is that they inhibit the production of angiotensin II which is a substance that narrows your blood vessels.

Chia fresca drink

This gel-like substance that surrounds chia seeds is also the basis of a popular drink of the Tarahumara people called chia fresca.  I recreated this drink by mixing 1 Tbsp. of chia seeds into 10 oz. of water and letting it sit for 5-10 minutes (the longer it sits, the more gel-like it will become).  Honey or citrus can be added for flavoring as well.

Although it is refreshing, I found the texture of the gel to not be very appetizing and instead opted for sprinkling some chia into a morning smoothie.

Chia seeds are an extremely versatile, nutrient-rich seed with origins in ancient warrior fuel that can improve not only your running capabilities, but your overall health as well.

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Sleep Hallucinations: Why Do They Happen?

Have you ever experienced a dream so vivid, it might as well have been real? Do you recall a time where you’ve seen spiders crawling up your walls, a monster at the end of your bed, or even heard faint singing when dozing off? If you said yes to either of these questions, you’re not alone. These are parasomnia hallucinations— hallucinations that occur as a result of abnormal activity of the nervous system.

There are two main types of these hallucinations: hypnagogic and hypnopompic. What’s the difference between the two? Hypnagogic hallucinations occur between the transition from wakefulness to sleep, while hypnopompic hallucinations occur from sleep to wakefulness. These hallucinations are more common than you think, it was found in a recent study that 37% of a sample of 4972 people reported experiencing hypnagogic hallucinations and 12.5% reported hypnopompic hallucinations.You may remember being in a hypnagogic state when you doze off on the couch and the sound of the TV slowly turns into a distorted jumble of words and sounds, or when you listen to a song so much that you may catch it in your dreams. Sometimes, if you have repeatedly performed an action like playing a video game, this may make a surprise appearance in your hypnagogic hallucinations; this is known as the “Tetris effect,” where one repetitive act is manifested in parasomnias or dreams.

Occurring in bursts between five to ten minutes, hypnagogic states are the most common form of sleep hallucination. Hynagogia occurs as a natural part of sleep for some individuals with heightened brain activity, especially those frequently in high-stress environments, those who experience repetitive situations, or even after viewing very stimulating media. Though hypnagogic states are not entirely understood, it is widely believed that the transition between types of brain waves from wakefulness to sleep are the culprit. When falling asleep, the transition begins with alpha waves, which are released during times of relaxed consciousness, to theta waves, which occur during early sleep, to delta waves, which are characteristic of deep sleep. This transition normally occurs in the process of falling asleep, however, when hypnagogic states occur, the distribution of these brain waves is uneven, and the brain begins to “turn off” specific areas of the brain faster than others. This leads to certain regions of the brain such as the occipital lobe or the cerebellum to stay “on,” forming visual hallucinations and certain falling sensations. 

Hypnagogia’s ugly sibling, hypnopompic states, are often described as much more unsettling, scary and vivid, and can be difficult to distinguish from reality. Hypnopompia is the transitory period between sleep to wakefulness, and is far less common than hypnagogia. Unlike the faint and often abstract images that individuals experience in hypnagogia, those who experience hypnopompic states report solid and seemingly tangible figures that they are able to touch, smell, or speak to.

Henry Fuseli’s “The Nightmare” is believed to be one of the earliest 

depictions of a hypnopompic state.

Unlike the natural and lulling quality of hypnagogic hallucinations, hypnopompic states are considered more like little brain “glitches” that occur as a result of abnormal electrical pulses in non-REM sleep stages, or deep sleep, where dreaming does not occur. Why is this important? In REM sleep, the brain experiences intense electrical activity from the brain stem, which leads to dreams, however, once your REM cycle ends, you enter NREM (non-REM sleep) which is characterized by virtually no electrical activity in the brain stem; this is where you brain is “quietest” and is also known as deep sleep. Since there are no dreams occurring normally in NREM, it is often the most common stage to wake up in, however, in some circumstances, the brain stem sends out slight pulses of electrical activity during NREM, making two things happen A) dream synthesis mechanisms are activated (just as in REM) and B) your brain sends signals that something is abnormal and makes you begin the process of waking up. All of this combined and you begin the process of waking up, but your dream mechanism is still activated, making you hallucinate in a groggy, in-between mode. Not only this, but a link was recently found between these states of hypnopompic and deficits in serotonin and dopamine, giving many of these hallucinations an unpleasant and negative theme.

Stages of Sleep, the Blue is non-REM sleep

All in all, hallucinations such as these can be, well, unpleasant. So what can you do to reduce hypnopompic and hypnagogic hallucinations? Scientists believe that reducing intense stimuli a few hours before bed can be effective in reducing the frequency of such states, which means put down your phone, stop watching horror movies, and start meditating a little bit before bed. If these hallucinations persist, it could be a sign of more serious disorders, so talk to a sleep specialist if need be.

Dopamine, Schizophrenia, and...Creativity?

Of all the psychotic disorders, schizophrenia happens to be one of the most common. Within the American population, roughly 1.2% (or 3.2 million people) have it. It is also a relatively slow acting disorder. This type of psychotic break is classified by a mental separation from reality. The majority of people who have schizophrenia see symptoms arise during their late teenage years and early twenties. However, there are outliers that start to see symptoms during their forties and fifties. The main symptoms that are evident with this condition are hallucinations, abnormal behavior, and isolation. Based on these traits of the disorder it could be concluded that it has ties with neurotransmitters and the inner workings of the brain. There are two main groups that classify the symptoms of schizophrenia: positive and negative. The positive symptoms are normally repetitive actions that are challenging to control while the negative symptoms take away a function/feeling. Some examples of positive are: hallucinations, delusions, and racing thoughts. For negative the symptoms are: apathy, lack of emotion, and non-existing social functions. In addition to dopamine, glutamine plays a role in the development of Schizophrenia. Glutamine is an "excitatory neurotransmitter" in the brain, so it helps to active neurons and other brain cells. This means that the multiple brain areas that are involved in schizophrenia are connected by a circuit of brain cells that rely on glutamate to communicate. Surprisingly, the exact causes of schizophrenia are unknown but it's accepted that the disease results from an interplay of environmental factors and genetics. It has been commonly known to develop over time due to numerous things such as: drug use, trauma (emotional), brain changes, genetics, and pregnancy complications. The common assumption among researchers is that it is a combination of those causes.

The Symptoms observed of Schizophrenia
(Source)

As mentioned before, schizophrenia is connected with neurotransmitters. Dopamine happens to be one of those neurotransmitters that contribute to the symptoms seen in schizophrenia. Therefore, an overactive dopamine system could result in this disorder. This was proven through the medications that block dopamine receptors, specifically D2 receptors. When they block the receptors, the symptoms of schizophrenia subside. Essentially, the D2 receptors which reside in the thalamus and the striatum, have a change in binding potential as a result of the disorder. If schizophrenia is left untreated in patients, there is an increase in the amount of receptors in the striatum. To further delve into this topic, some authors came up with an experiment to test the D2 receptor density in people who are creative. Ultimately, the result was that more creative people had a lower D2 receptor density in their thalamus just like patients with schizophrenia. 

Dopamine Receptors in the synapse (Source)

Due to the less density of these receptors in this area of the brain, it was concluded that both creative and schizophrenic people have brains that don't filter out as much information as the average person does. This allows them to come up with a different train of thought compared to other people. For creative people, this means new and unique ideas while for people with schizophrenia it explains their abnormal thought process. (Articles on dopamine in relation to creativity: #1, #2, #3)

To put some of this into perspective, dopamine has been observed to have a hyperactive transmission in the prefrontal cortex of the brain of schizophrenia patients. This is generally the area where decisions are made, so if an overload of dopamine is within that area, it causes not only impaired judgement but also the execution of odd behaviors. Additionally, dopamine dysregulation has also been observed in the amygdala which is as essential for emotional processing as the prefrontal cortex. 

  

The affected brain areas by dopamine (Source) 

With the function of dopamine being well known among scientists, the overlap between it and neurological disorders are inevitable. Dopamine is known as the pleasure reward or the "feel good neurotransmitter." Therefore, it affects mood, motor function, and decision making. However, dopamine is reliant on the cycle of motivation, reward, and reinforcement, which makes it harmful in excess. If that normal cycle changes, dopamine will be released in overdrive and make you feel good... for a short amount of time. It is much like a "high" and the long term version of this would be schizophrenia, except the amount of dopamine is so much that the negative effects (such as hallucinating) are experienced but the reward feeling isn't.  

Migraines Are Not Just Headaches

Last year, I was diagnosed with chronic migraines. This was in the middle of my junior year, which led to an extended absence from school for many months. Something as simple as standing or looking at my phone felt impossible. I can still recall my first migraine attack as clear as day, and I cannot describe the head pain I went through. It was so severe that I went to the hospital and was admitted and stayed for a week, getting MRIs and CT scans. I slept for the entire week, until one medication finally worked and I was discharged. I thought it was a freak thing, and I wouldn't get another migraine, but oh boy was I wrong. Little did I know my migraine journey had just begun, and I would suffer from chronic migraines for months to come, and face debilitating complications.

You may be wondering, "What is a migraine? Isn't it like a bad headache?"

Before I had suffered from migraines, I too thought it was just a bad headache. I didn't realize the severity of it, and I didn't know how it could impact someone's day to day life, until I experienced them. Migraines are a neurological condition that are frequently characterized by intense, debilitating headaches. In my case, it was accompanied by nausea, vomiting and extreme sensitivity to light and sound.

This is a visual representation of what it is like to experience double vision, which I frequently experience with migraines. 

The causes of migraines aren't fully understood, but genetics appear to factor in. Migraines typically affect women, and it does run in families (it runs in my family). Familial hemiplegic migraine (FHM) has been linked to showing an autosomal dominant pattern of inheritance, and is usually heterogeneous. There are three main causative genes, CACNA1A, ATP1A2, and SCN1A which have been identified through family pedigrees. These three main genes encode for ion channels or ion transport proteins, which lead to the conclusion that HM is a channelopathy. Also, changes in the brainstem and its interactions with one of the nerves (the trigeminal nerve, a major pain pathway) could also be involved. There are lots of unknowns with migraines, and there are so many triggers that could lead to a migraine attack. Factors like hormonal changes, drinking alcohol, stress, sleep changes, weather changes, foods and food additives could lead to an attack. In my case, migraine attacks aren't triggered by anything in particular, as I would suffer from attacks weekly and for days without any medications.

The trigeminal nerve, which is a pain pathway that leads to the face 

There is one aspect of the migraine pain theory that explains that migraine pain happens due to waves of activity by excitable brain cells. The neurotransmitter serotonin plays a role in communication between nerve cells, which can result in the narrowing of blood vessels throughout the body.

Since migraines commonly affect women, changes in estrogen levels can also theoretically lead to migraines. For women, estrogen levels naturally increase during fertile years, and decrease afterwards. Women of childbearing age also experience monthly changes in hormonal levels, which leads to an assumption that migraines can be associated with fluctuating hormonal levels. Some researchers believe that when estrogen levels rise and fall, contractions in blood vessels may be off, which leads to throbbing pain. However, other data suggests that lower levels of estrogen can make the facial and scalp nerves sensitive to pain.

Estrogen can affect serotonin levels, the trigeminal nerve and cause mood changes 

So you might be wondering how migraines are treated. There are a ton of medications you can take to relieve current migraine symptoms.

Typically, there are two medication types that are used to treat migraines. Treatment choices depend on the frequency and severity of headaches. Usually doctors will try to combat migraines at home with over the counter and prescription pain relievers. Excedrin is also a popular medication used, but it usually only works against mild migraines. In hospitals, you will typically receive an IV and be treated with medications such as IV Tylenol or other pain relievers, anti nausea drugs and possibly opioids. Dihydroergotamine (D.H.E.) is a popular medication given in hospitals, but can have side effects of its own such as high blood pressure and vomiting/nausea.

How DHE helps to relieve migraines

If you suffer from frequent migraines like I do, preventative medications can be used. The goal of these medications is aimed at reducing how often you get a migraine and how severe the attacks are. Medications that do this include blood pressure lowering medications (beta blockers), antidepressants (amitriptyline), anti-seizure medications (topamax), and botox injections. Botox works by being injected around pain fibers that are involved with migraines, and Botox is placed in the nerve endings which blocks the realize of chemicals involved in pain transmission. This prevents pain networks from firing, leading to migraine relief.

With a diagnosis of migraines, it might seem like the end of the world. I promise you it is not, you just need to learn how to do things differently and realize that you might be dealing with this condition your entire life. You may need to change your daily routines and realize your journey might be challenging, but it is important to not let it discourage you. You can make modifications, but it is important to not give up on reaching your goals in life.

June is migraine awareness month 

Are Stem Cells The Future of Medicine?

Stem cells have long been prophesied to be the cure to all medical ailments since they were first discovered in mice in 1981. This hot area of research has come a long way since then, yet there are still no FDA proven stem cell treatments. Although many treatments have been shown to have great benefits, many have also come with large health risks to the patients. At this point, 30 years down the road, the question is, are stem cells still the cure of the future, or a thing of the past?

Stem cells are unique because unlike other cells, which are created to carry out one specific function, they can exist as cells without a specific function. These stem cells are essentially "blank" cells, which can be programmed to become a certain type of cell. They undergo symmetric or asymmetric cell division. Symmetric cell division produces two daughter cells with a desired function. Asymmetric cell division produces one cell that is identical to the parent cell and one that performs its programmed function. Asymmetric division is useful because it only requires one initial stem cell to create a virtually endless line of stem cells because after each division there is a new stem cell remaining.

Photo Courtesy of Andre Gorgens

The other cell produced by asymmetric cell division, which is programmed to carry out a certain function, will become one of many types of somatic cells in the human body, such as a nerve cell, a liver cell, or even a blood cell. This is why there was such hope in the medical field that stem cells could be the future cure to many prevalent diseases, such as Alzheimer's, Parkinson's, and many other blood related diseases.

For the most part, stem cells are currently being used for the treatment of less severe medical issues,such as male-pattern baldness, rather than for more severe diseases, as was hoped. Although the treatments for some of these more severe diseases do in fact exist, they are extremely expensive and not accessible to most. The reason for this is the way that stem cells are produced.

The cells most often used in effective stem cell treatments are embryonic stem cells. These cells come from human embryos, This means that embryonic stem cell availability is limited to the amount of embryos that are being created in in vitro fertilization clinics and donated to stem cell research programs. Also, embryonic stem cells have been the subject of controversy Many activist groups, often the same ones that are against abortion, have pushed back against the use of embryonic stem cells in medical treatments. As a result, from the years 1996 to 2007, stem cell researchers in the United States were restricted from receiving any federal funding, leaving them to rely solely on private donations. In many ways, this push back, which has had a serious legislative and cultural impact, has significantly slowed the research of stem cells and could very well be the reason why an efficient method of replicating and programming stem cells has not yet been discovered. While there are stem cells that are found in the adult body, which would seem to be an obvious solution to creating non-controversial stem cell treatments, they are much more difficult to program. Also, many researchers believe that they may cause harmful long-tern and short-term side effects, but more research needs to be done to prove this.

Photo Courtesy of San Francisco Chronicle

Luckily, stem cell research has continued and positive legislative change has come. In 2009, President Barack Obama issued an executive order allowing many stem cell researchers to begin receiving federal funding. Only 5 years later, the results of a groundbreaking trial showed that it was possible to restore vision in legally-blind patients using stem cell treatments. After seeing the renewed promise of stem cell use in medicine, research sped along at record pace. Fueled by legislation such as the 21st Century Cures Act, the field of stem cell research expanded greatly. Currently, the ISSCR (International Society for Stem Cell Research) has over 4,000 active stem cell researchers across the globe, looking for a way to make stem cell treatments more effective and more accessible. Although the study of stem cells has had its setbacks, with continued political and cultural attention, it can once again become the medical promise of the future.

Photo Courtesy of the Associated Press

President Obama signing the 21st Century Cures Act into law.