Asian Flush. What is it Exactly?

Do you ever wonder why when you go out with your friends of Asian descent, some of them get very red just one drink in? Many people call it the Asian flush or the Asian glow, and it is a side effect of not having an active form of the enzyme aldehyde dehydrogenase; this enzyme breaks down alcohol and eliminates it from the blood. If alcohol stays in the blood too long it could lead to consequences, the most common side effects are facial flushing, nausea, and rapid heart rate (Edenberg, 2007). The buildup of alcohol metabolism metabolites can have dire consequences to the body, especially in the functions of DNA.

When you consume alcohol, your body processes and gets rid of the alcohol in various steps. First, your body utilizes a chemical known as an enzyme to break down alcohol into smaller components allowing the body for easy absorption. The alcohol consumed is converted into acetaldehyde through the enzyme called acetaldehyde dehydrogenase (ADH). Second, the acetaldehyde is converted into acetate using aldehyde dehydrogenase (ALDH). The end product, acetate, can then be converted into acetyl-CoA, whose primary function is to deliver the acetyl group to the citric acid cycle (Krebs cycle) to be broken down for energy production (González Hernández, et al., 2019).

The problem with me arises when the second step of alcohol metabolism is not achieved and my body is unable to break down acetaldehyde. Why is that? Well, in my genetic lineage I lack the active form of aldehyde dehydrogenase, therefore, I get a buildup of acetaldehyde, a toxic byproduct of alcohol consumption, in my body. Having a buildup of this toxin causes the consequences mentioned in the first paragraph. Additionally, long-term acetaldehyde build-up can cause long-term damage to the body, for instance, acetaldehyde impairs cellular functions and gene expression by forming complexes with proteins and DNA (Setshedi, et al., 2010). Acetaldehyde is a carcinogen that can increase cancer development through multiple processes, including interference with DNA replication, induction of DNA damage, and formation of DNA complexes (Mizumoto, et al., 2017). 

So the next time you go out drinking, pay attention to those around you. You may be surprised at the number of people who have alcohol intolerance. If they refuse a drink, it may be because they know what an increase in acetaldehyde can do to the body. 

References:

Edenberg, H. J. (2007). The genetics of alcohol metabolism: role of alcohol dehydrogenase and 

aldehyde dehydrogenase variants. Alcohol Research & Health, 30(1), 5.

González Hernández, M. A., Canfora, E. E., Jocken, J. W., & Blaak, E. E. (2019). The 

short-chain fatty acid acetate in body weight control and insulin sensitivity. Nutrients, 11(8), 1943.

Mizumoto, A., Ohashi, S., Hirohashi, K., Amanuma, Y., Matsuda, T., & Muto, M. (2017). 

Molecular mechanisms of acetaldehyde-mediated carcinogenesis in squamous epithelium. International journal of molecular sciences, 18(9), 1943.

Setshedi, M., Wands, J. R., & de la Monte, S. M. (2010). Acetaldehyde adducts in                                alcoholic liver disease. Oxidative medicine and cellular longevity, 3(3),                            178-185.

Phantom Limb Pain: the Haunting Effects of Amputation

 Though often unnoticed, there are more than 2 million people living with limb amputation due trauma, disease, cancer, and malformation across the US. Not only is the process of losing a limb challenging for adjusting to daily actions of living and lifestyle, but 60-80% of amputees also experience Phantom Limb Pain (PLP). Phantom Limb Pain is pain sensation to a limb, organ, or tissue following amputation. It can feel as intense as if the area was never amputated. Patients who experience PLP describe stinging, aching, piercing and burning sensations. For many years, patients were hesitant to mention such pain and it was left untreated. While intial understandings of PLP suggested the pain was psychological or that the lost limb itself was causing the pain, modern studies suggest otherwise. Now it is hypothesized that a combination of peripheral, central neural and psychogenic mechanisms are in place. As a result, the pain may be sourced from changes to the neuron at the amputation stump, upregulation of receptors at the spinal cord, or  brain cortical reorganization (where parts of the brain that normally recognize pain are reordered following the amputation). With no cure, a variety of therapies are used to mediate PLP. These include medication to block pain, surgery to remodel the stump or neurons, and other techniques using  stimulation, biofeedback and cognitive behavioral therapy. A new innovative technology called the Next-gen Device is creating a prosthetic with an implanted stimulator that connects to the damaged nerve endings to reinstitute connections and ultimately reduce PLP . Though amputation is avoided as much as possible, it is still used as the best solution for certain conditions. As a result, finding new approaches to help prevent harm in such cases and promote equal oppertunities for high quality of life even with disability is critical.

Subedi, B., & Grossberg, G. T. (2011). Phantom limb pain: mechanisms and treatment approaches. Pain research and treatment, 2011, 864605. https://doi.org/10.1155/2011/864605

Kaur, A., & Guan, Y. (2018). Phantom limb pain: A literature review. Chinese journal of traumatology = Zhonghua chuang shang za zhi, 21(6), 366–368. https://doi.org/10.1016/j.cjtee.2018.04.006

Hormones for the Gold

For the past three years I have been working with a family practice doctor who specializes in the treatment of transgender patients. It is a fascinating branch of medicine that I never would have considered studying until I was actively involved in treating that demographic. In recent months there has been an ethical debate regarding the inclusion of transgender women (biological males transitioning to be female) in the female category of sports. The argument that frequently surfaces is that the previous presence of testosterone in transgender women adds an unfair advantage to their athletic performance.

The three hormones used to treat gender dysphoria in male to female patients are estradiol, progesterone, and spironolactone, but the one I will focus on is spironolactone. Spironolactone is used for a variety of medical reasons--in transgender treatment it is used as a testosterone suppressor. Androgens are hormones that contribute to growth and reproduction, in males it is known as testosterone. Spironolactone is used to suppress testosterone because it is an antiandrogen. Physiologically this means that spironolactone binds to the androgen receptors in the body instead of testosterone binding. This means that testosterone can’t bind to the androgen receptors, which leads to a decrease in testosterone because it is no longer being metabolized in the body. 

After two years of spironolactone treatment it is expected that a patient’s testosterone level stays within normal female range (2-80 ng/dl) as long as they stay on the regimen. This implies, biologically speaking, they no longer have more testosterone in their body than a cisgendered female athlete. With that being said, if someone has been on hormones for at least 3 years and they have testosterone labs stating their levels are within normal female range, why should they not be allowed to compete? Hilton and Lundberg’s article in The Journal of Sports Medicine argues that the muscle mass and strength one gains during puberty significantly impacts future athletic performance. They found that the performance gap between males and females becomes significant at puberty and often amounts to 10–50% depending on the sport. Therefore, those who transition after puberty do not lose these muscular advantages (Hilton and Lundberg, 2021).

Ultimately, the obvious dilemma becomes whether it is just to allow a subset of athletes with a biological advantage to compete with the gender they identify as. Due to the increased number of transgender athletes this debate has become a hot button topic and warrants further discussion. 

Hilton, E. N., & Lundberg, T. R. (2021). Transgender Women in the Female Category of Sport: Perspectives on Testosterone Suppression and Performance Advantage. Sports medicine (Auckland, N.Z.), 51(2), 199–214. https://doi.org/10.1007/s40279-020-01389-3

Eczema and Egg Allergies

 

Gender-Affirming Therapy, Muscle Mass, and Athletics

    As the number of individuals who publicly identify as transgender or gender-fluid increases in the US and worldwide, there has been greater public discussion about addressing the issues of fairness and equity that these individuals face. One of the most common concerns is how transgender athletes, particularly transgender women (people assigned male at birth who identify as female), should be categorized to avoid any unfair advantage. Numerous studies have demonstrated that cisgender men have a significant advantage over cisgender women when it comes to several athletic measures, including strength (Miller et al., 1993), oxygen uptake/VO2 max (Cureton et al., 1986), and lean muscle mass (Perez-Gomez et al., 2007), which is used to justify separate competitive categories for men and women. 

    Transgender athletes are frequently required to have undergone a minimum amount of hormonal, gender-affirming treatment in an attempt to mitigate any biologic advantage or disadvantage due to androgen or estrogen levels. That said, there have been few empirical studies examining the correlation between these hormone levels and athletic performance. The few studies that do exist often have conflicting results. A 2004 study concluded that after 1 year of hormone therapy, transgender female athletes showed a significant decrease in lean muscle mass, but still had significantly higher levels than transgender males - the authors reported that hormone therapy "reduces but does not reverse" the gap in muscle mass between men and women (Gooren & Bunck, 2004). A 2019 study, meanwhile, found a significant decrease in grip strength in transgender women after 1 year of hormone therapy, but only found significant change in lean body mass in transgender men (Scharff et al., 2019). 

    Given the relative uncertainty of the issue, it is clear that more research is needed before any definitive conclusions can be made on the role of gender-affirming hormone therapy in professional sports. There is strong evidence, however, that any potential for competitive advantage trans athletes might have is often outweighed by the challenges posed by the lack of comfortable and inclusive environments surrounding sports (Jones et al., 2016). Regardless of any advantage or disadvantage trans athletes might have based on their anatomy, sports governing bodies have an ethical duty to address the cultural and societal barriers that discourage trans people from participating in athletics. 

References

Cureton, K., Bishop, P., Hutchinson, P., Newland, H., Vickery, S., & Zwiren, L. (1986). Sex difference in maximal oxygen uptake. European Journal of Applied Physiology and Occupational Physiology, 54(6), 656–660. https://doi.org/10.1007/bf00943356

Gooren, L., & Bunck, M. (2004). Transsexuals and competitive sports. European Journal of Endocrinology, 151(4), 425–429. https://doi.org/10.1530/eje.0.1510425

Jones, B. A., Arcelus, J., Bouman, W. P., & Haycraft, E. (2016). Sport and Transgender People: A Systematic Review of the Literature Relating to Sport Participation and Competitive Sport Policies. Sports Medicine, 47(4), 701–716. https://doi.org/10.1007/s40279-016-0621-y

Miller, A. E. J., MacDougall, J. D., Tarnopolsky, M. A., & Sale, D. G. (1993). Gender differences in strength and muscle fiber characteristics. European Journal of Applied Physiology and Occupational Physiology, 66(3), 254–262. https://doi.org/10.1007/bf00235103

Perez-Gomez, J., Rodriguez, G. V., Ara, I., Olmedillas, H., Chavarren, J., González-Henriquez, J. J., Dorado, C., & Calbet, J. A. L. (2007). Role of muscle mass on sprint performance: gender differences? European Journal of Applied Physiology, 102(6), 685–694. https://doi.org/10.1007/s00421-007-0648-8

Scharff, M., Wiepjes, C. M., Klaver, M., Schreiner, T., T’Sjoen, G., & den Heijer, M. (2019). Change in grip strength in trans people and its association with lean body mass and bone density. Endocrine Connections, 8(7), 1020–1028. https://doi.org/10.1530/ec-19-0196

What is a Perfusionist?

 Kaufmann, J., & Kung, E. (2019). Factors Affecting Cardiovascular Physiology in Cardiothoracic Surgery: Implications for Lumped-Parameter Modeling. Frontiers in surgery, 6, 62. https://doi.org/10.3389/fsurg.2019.00062

I wanted to blog about my future career choice as a perfusionist. A perfusionist is someone who operates machines, specifically the cardiopulmonary bypass machine, that keep a patient alive during serious procedures, such as open-heart or open-lung surgery. Another machine that is frequently used by perfusionists is an extracorporeal membrane oxygenation machine (ECMO) that allows for individuals whose hearts and lungs cannot work properly (such as COVID patients or individuals waiting for a heart transplant) in a Cardiothoracic Intensive Care Unit (CTICU). These machines allow an individual’s blood to be circulating and oxygen flowing to vital organs. From a physiological standpoint, perfusionists need to manipulate the body’s normal physiological processes in order to ensure the intended result in surgery. For example, a drug that does this that is administered in almost every open-heart surgery is Heparin, which reduces clot formation in the blood. Like we learned in class, this acts as a “blood thinner” which greatly thins the blood allowing for it to move smoothly throughout the body as well as the bypass machine. Another drug administered is cardioplegia, which reduces the oxygen demand and metabolic rate in the heart muscle, eventually stopping the heart. This allows the surgeon to operate on a motionless heart with no blood in it. For patients on ECMO, a lot of the time a perfusionist has to monitor the oxygenation of the blood. For example, a patient I was showing one time was waiting for a lung transplant and needed to walk around the ICU floor. The nurses have their patients walk on ECMO to reduce other complications related to immobility, as well as preventing pneumonia. When this patient was walking, their SPO2 (Saturation of Hemoglobin with oxygen) went from 80 to 65. Here, the patient had to sit down and rest, and the perfusionist explained to me that as the patient was resting their SPO2 increased and they were reaching normal levels of oxygen-saturated hemoglobin. This relates to the beneficence ethic in physiology because perfusionists help keep individuals alive during invasive open-heart and lung surgeries. I am excited to go into a field of such high demand and I cannot wait to see how the field and technology will expand. 

Addressing Anxiety and Depression in Atopic Eczema Guidelines

Atopic eczema has an association with increased risk of new-onset depression and anxiety, but the nature of this association is still unclear. Atopic eczema (AE) is a common relapsing inflammatory skin disorder in both children and adults. AE causes intense itchiness and discomfort, heavily affecting the quality of life of the individual. These individuals may be more likely to suffer from anxiety and depression due to the appearance of the skin caused by chronic itchiness and discomfort, in addition to social stigmas. Insight into this temporal relationship of AE and anxiety could help guide the clinical approach and recommendations for management. 

Recent AE guidelines from the European Academy of Dermatology and Venereology do comment on the psychological and emotional factors influencing the clinical course of AE, but a study done by Schonmann and colleagues suggests that anxiety and depression should be explicitly addressed in these guidelines. Because AE is so common, if there is risk of increased new-onset anxiety or depression, it would suggest three things: 1) a major population impact, 2) potential for targeted mental health screening in AE individuals and, 3) the possibility of mental health modification through improved AE control (Schonmann et al., 2020). Schonmann and colleagues found that AE was associated with a 14% increase of newly diagnosed depression and a 17% increase in anxiety diagnosis. The risk of depression increased as the severity of AE increased, which provides strong evidence for dose-response association, therefore suggesting a causal mechanism for the association. With these findings, physicians may be able to improve AE control by facilitating more consistent treatments or through anti-inflammatory effects of antidepressants (Schonmann et al., 2020). 

Mental illness is under-diagnosed in people with skin or other chronic diseases (Schonmann et al., 2020), and while this study mainly focuses in the UK, their findings can be applied to the guidelines set by the American Academy of Dermatology (AAD) or any other relevant settings. The AAD guidelines also briefly mention the mental health associations to AE such as depression, but do not comment on the long term mental health implications (Atopic dermatitis clinical guideline).  Overall, the results show an increased risk of new-onset depression and anxiety, which should be considered in the recommendations for management of AE. This could improve current guidelines and limit new-onset mental illness diagnosis. 

Atopic dermatitis clinical guideline. American Academy of Dermatology. (n.d.). https://www.aad.org/member/clinical-quality/guidelines/atopic-dermatitis. 

Schonmann, Y., Mansfield, K. E., Hayes, J. F., Abuabara, K., Roberts, A., Smeeth, L., & Langan, S. M. (2020). Atopic Eczema in Adulthood and Risk of Depression and Anxiety: A Population-Based Cohort Study. The journal of allergy and clinical immunology. In practice, 8(1), 248–257.e16. https://doi.org/10.1016/j.jaip.2019.08.030

Aspirin, Inflammation, and Cancer

        I have always been intrigued with how aspirin, or any pain medication really, works. How is it that the medicine can find the area where you hurt the most and make the pain subside? Like anything else in life, that question does not have as complicated of an answer as I thought. As we learned in Physiology, aspirin works by irreversibly inhibiting COX-1 and weakly inhibiting COX-2. Thromboxane and prostacyclin formation are decreased with an inhibition of COX-1 and prostaglandin formation is decreased with an inhibition of COX-2. Prostaglandins are associated with inflammation, blood coagulation is associated with thromboxanes, and inhibition of clotting is associated with prostacyclins. When you take aspirin, both forms of cyclogeneses are inhibited which decreases blood clots (blood thinner) and decreases pain. 

Something interesting about this interaction is that inflammation has been found to increase the chance of cancer formation in the region of the body where there is inflammation. This is because any type of inflammation makes cells replicate faster. Inflammation is both good and bad. It is an essential process for the body because it heals it but an issue arises when inflammation becomes chronic. If the immune system is constantly active due to a prolonged issue, or constantly activated without an injured area because of an autoimmune disorder, healthy tissues could become damaged. With the constant “battle” going on in an area of inflammation, the more often cells are replicated beyond normal levels, the higher the chances of a genetic mutation occurring which is cancer (Cancer Treatment Centers of America, 2018). Inflammation may also contribute to the formation of cancer since inflammatory responses produce cytokines which have the function of stimulating the growth of new blood vessels. This increase in blood vessel formation can increase the amount of nutrients and oxygen that a tumor receives (CTCA, 2018).  Another possible reason why inflammation may lead to cancer is due to COX-2 derived prostaglandins as they promote tumor growth. They do so by binding their receptors which activates signaling pathways that control cell apoptosis, proliferation, and migration (Wang & DuBois, 2006). It is clearer to see how aspirin would decrease the growth of tumors in this last case as it would inhibit COX-2. 

As of right now, colon cancer is one of the most promising types of cancer to be treated in a preventative way by aspirin. The inflammatory disease colitis increases people’s risk of colon cancer and taking aspirin in low doses over a long period of time has been found to decrease overall development of cancer in some patients (Wang & DuBois, 2006). The downside is that aspirin also thins the blood by targeting thromboxanes which can cause GI bleeding. Aspirin is currently a common drug taken every day for people who are at risk for heart attacks and strokes, and so taking it to reduce cancer risk would not be revolutionary. The issue is trying to combat the negative side effects of it. Researchers are looking into drugs that only target COX-2, but even drugs that only target COX-2 have negative cardiovascular side effects (Wang & DuBois, 2006). 

        I just think it is crazy that something as "simple" and everyday as aspirin could potentially be something used to combat cancer. They say everything causes cancer but it is encouraging to see that there are also a lot of things that prevent cancer that we have yet to find and understand. 

Cancer Treatment Centers of America. (2018). Inflammation linked to cancer, but lifestyle changes may help. CTCA.  https://www.cancercenter.com/community/blog/2018/08/inflammation-linked-to-cancer-but-lifestyle-changes-may-help. 

Wang, D., & DuBois, R.N. (2006). Prostaglandins and cancer. Gut, 55(1), 115-122. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856377/. 

From Baby to Boomer: The Identification of Adult Pluripotent Stem Cells could have New Implications for the Future of Regenerative Medicine

           The debate surrounding the use of stem cells in medicine has been a controversial one to say the least. For years, it was believed that the only viable stem cells capable of regeneration came from human embryos. While many were enthusiastic about the prospects of stem cell therapies for the treatment of terminal diseases, others were abhorred at their nature of isolation, and felt it was unethical to obtain them from embryonic sources. Many media personalities, such as the late Christopher Reeves, were major contributors to stem cell research. Individuals like Christopher Reeves have sought to use their influence to show the world the capabilities of stem cell interventions, but proponents of both sides have remained steadfast throughout the years.

            Previous research has shown that perhaps the isolation of stem cells may not solely have to come from human embryos. An article posted by Seymour et al. in 2015 in the International Journal of Molecular Sciences highlighted exactly this. During most of the history of stem cell research, it was thought that pluripotent stem cells (PSCs) were exclusively embryonic stem cells (ESCs), until the discovery of adult PSCs in the tissues of adult brains and breasts that displayed characteristics like ESCs indicated otherwise. It’s important to note just what a PSC is. A PSC has been determined to be a master cell of sorts, capable of dividing indefinitely, but perhaps more importantly, is also able to differentiate into cells within the three germ layers (ectoderm, mesoderm, and endoderm). These germ layers lay the foundation of embryonic development, and the entirety of an adult human being is derived from the division and expansion of cells of these three layers in utero (Seymour et al., 2015)

 

            Research of these adult PSCs and the genes regulating their creation and function has shown how crucial their role is in the pubescent development of breast tissue, and the continued functionality of the brain. Without them, breast development is often incomplete or dysfunctional, and the plasticity of the brain is often diminished. However, overexpression of the transcription factors for the proliferation of these cells has also been linked to many cancers, which are resistant to contemporary forms of treatment like chemotherapy (Seymour et al., 2015). Therefore, the continued identification of properties and functionalities of adult PSCs and their transcription factors should remain a focus of stem cell research. If a way can be found to effectively manipulate them to maximize their regenerative properties while minimizing their carcinogenic tendencies, it could redefine regenerative medicine, and subsequently, establish a new direction for the future of medicine.

 

Seymour, T., Twigger, A. J., & Kakulas, F. (2015). Pluripotency Genes and Their Functions in the Normal and Aberrant Breast and Brain. International journal of molecular sciences, 16(11), 27288–27301. https://doi.org/10.3390/ijms161126024

The Link Between Evolutionary Biology and Anthropology

Anthropology consistently has linked evolutionary biology with cultural changes. Prior to the early 21st century, many anthropologists incorporated Darwinism into their understanding of cultural evolution. However, recently, more cultural evolution has been shaped by new understandings including the Modern Evolutionary Synthesis. New debates specifically have been revising prior standards to include evolutionary biology and ecology more into cultural anthropology to provide a larger understanding of the link between anthropology and evolutionary biology (Zeder, 2018). Interestingly enough, the article I chose to write on also discussed how there are internal developmental plasticity changes as well, a biological phenomenon that is also extremely important for anthropological changes and understandings. 

Developmental plasticity is described as the way a single genotype can alter and change itself during development in an organism to respond to important environmental cues without altering the DNA of an organism (Zeder, 2018). This is an extremely interesting argument in the world of anthropology and biology because this phenomenon can be argued to be linked to domestication of a species. Climate change specifically has been noted to contribute to these developmental biology changes. For example, the melting of the last ice age has been argued to have led to eliciting a plastic expression of phenotypes to lead to the domestication of some animal species (Zeder, 2018). Due to the environmental changes of the melting ice age, it is argued that in some of these populations, animals adapted and were easier to domesticate due to their evolutionary drive for survival. The constant, stable, and predictable environments that are created by domestication are argued to lead to the permanence of these newly introduced phenotypes and traits (Zeder, 2018). 

This article was particularly interesting to me because it took two of my favorite subjects and morphed them together. The idea of anthropology without biology is difficult to understand and the idea of biology without anthropology and culture is non existence. In this example, cultural changes, like domestication, have influenced evolutionary biology. The idea of anthropology and science working together is incredibly important for those of us interested in medicine and working in healthcare. Understanding culture allows physicians to deeper connect with their patients. Although the example discussed above pertains to evolutionary biology and domestication of animals, it fits into the bigger picture of understanding how culture can influence medicine and the importance of understanding culture to understand biology and how to correctly treat patients through the use of cultural competence.

Zeder, M. A. (2018). Why evolutionary biology needs anthropology: Evaluating core assumptions of the extended evolutionary synthesis. Evolutionary Anthropology: Issues, News, and Reviews, 27(6), 267-284.

The Gut Microbiome and Our Psychiatric Well Being

    You probably know a thing or two about the gut microbiome and how it affects your health. Did you know that the yogurt you had for breakfast or the kombucha you’re sipping on right now contains probiotics that can help balance your gut microbiome? Physiological changes in the gut microbiota may influence obesity, autoimmune disorders, and psychiatric disorders. The most direct ways that the gut microbiome impacts health is by converting nondigestible carbohydrates to short chain fatty acids, action against pathogenic bacteria, and modulation of innate and adaptive immune systems. Now you might be thinking, how is the gut microbiome related to psychiatric disorders if it’s affecting physical body functioning. The answer is that the brain and gut have bidirectional communication that mediate physiological functions. For example, gut peptide secretions are able to enter the bloodstream and stimulate sensory neurons which send afferent projections to the vagus cranial nerve.

    A 2018 review done by Gillard Lach and colleagues illustrate the relationship of the gut microbiome and psychiatric disorders. Factors such as diet, age, genetics, antibiotics, upbringing, and even prenatal stress can all have an affect on the gut microbiome. For instance, they note that researchers have found that maternal stress during pregnancy has induced depressive behaviors in offspring, particularly, in adulthood. They found that this prenatal stress induced changes in offspring gut microbiome composition which increased the HPA axis response to stress. In another example, they indicate how researchers have found that deficient gut microbiomes upregulated the NPY gene in the amygdala and hypothalamus. NPY upregulation was associated with higher anxiety-like symptoms in mouse populations.

    How do we fix a deficitted gut microbiome? Consuming a healthy diet as well as getting enough exercise positively affects the gut microbiome. It has been shown that changing your diet for a 24 hour duration can positively change the gut microbiome. New clinical studies have shown a new class of treatment for those with psychiatric disorders - psychobiotics. Clinical studies have found that those consuming probiotics such as Lactobacillus spp. had lower plasma cortisol and lower scores of self-reported negative moods.

Our gut microbiome is often overlooked when we’re not feeling mentally or physically well. Luckily, it is something that we can remedy ourselves by practicing a healthy and diverse diet. Short term changes to our diet for a period of a day can already yield benefits to our gut microbiome.


Lach, G., Schellekens, H., Dinan, T. G., & Cryan, J. F. (2018). Anxiety, Depression, and the Microbiome: A Role for Gut Peptides. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 15(1), 36–59. https://doi.org/10.1007/s13311-017-0585-0

Tetrodotoxin - a cure for lazy eye?

 

Amblyopia, commonly referred to as lazy eye, is a vision disorder caused by an imbalance in the connections to the visual cortex. Many of us probably know someone with amblyopia or are affected ourselves, as it is nearly impossible to treat after early childhood (Hamilton, 2021). But in some cases where affected adults lose their “good” eye, they regain vision in their amblyopic eye. How can that be?

Well, we have known for years that the brain is remarkably plastic and constantly rewiring itself. In fact, similar results have been observed in monkeys and cats that have had their unaffected eye removed. But losing an eye is a high price to pay just to regain vision in the other. What if instead, you just tricked the brain into thinking that the dominant eye was lost?

It turns out you can do that with tetrodotoxin (TTX), a neurotoxin commonly found in a particular variety of puffer fish. TTX inhibits voltage-gated sodium channels. If sodium can’t enter the neuron, it can’t generate an action potential, which renders it incapable of sending signals. As you might imagine, this can have potentially fatal consequences at high doses (think respiratory failure). But at low doses, the effects are reversible, and a group of researchers at MIT figured out how to exploit that.

By injecting a small amount of TTX into the unaffected eye of cats and mice with amblyopia, Fong et al. demonstrated that you can temporarily inactivate that eye, and effectively convince the brain that it is missing. It only inactivates the eye for about 1 to 2 days, but that’s all the time the brain needs to start rewiring itself. The underlying biological mechanisms are not well understood, but the prevailing hypothesis is that there is potentiation of excitatory synapses feeding the amblyopic eye. This could mean changes in things like NMDA receptors or inhibitory signals, but the bottom line is that potentiation is occurring and having lasting effects (Fong et al., 2021).

Overall, the results of this study are a testament to the plasticity of the adult brain, and even though this method has not yet been tested in humans, the replicability across mice and cats suggests that it could one day be a viable treatment option for amblyopia and perhaps other neurological conditions. 

References

Fong, M.-fai, Duffy, K. R., Leet, M. P., Candler, C. T., & Bear, M. F. (2021). Correction of amblyopia in cats and mice after the critical period. ELife, 10. https://doi.org/10.7554/elife.70023

Hamilton, J. (2021, September 15). Pufferfish toxin holds clues to treating 'lazy eye' in adults. NPR. Retrieved September 21, 2021, from https://www.npr.org/sections/health-shots/2021/09/14/1037096390/pufferfish-toxin-holds-clues-to-treating-lazy-eye-in-adults.