During the COVID-19 pandemic, researchers looked for medications that could reduce inflammation, prevent blood clots, and protect organs from damage. One compound proposed as a potential therapy is BPC 157, a small synthetic peptide.
COVID-19 is understood as more than just a respiratory infection; it is also a vascular disease. The virus damages endothelial cells that line blood vessels, leading to inflammation, clot formation, and impaired blood flow. These processes contribute to complications such as lung injury, heart problems, liver damage, and neurological symptoms. Because BPC 157 shows strong endothelial protective effects in animal studies, researchers hypothesized that it might reduce some of the harmful vascular effects seen in COVID-19.
BPC 157 interacts with the nitric oxide (NO) system, through activation of endothelial nitric oxide synthase (eNOS). NO is important for maintaining healthy blood vessels by promoting vasodilation, limiting clot formation, and controlling inflammation. Some studies also suggest NO has antiviral effects. BPC 157 may help regulate NO production, potentially improving blood flow and vascular stability in COVID-19 patients.
In animal models, BPC 157 has been shown to reduce injury in organ systems, including lungs, heart, liver, and brain. It has also demonstrated anti thrombotic effects and a reduction inflammation in experimental settings. These findings overlap with many of the complications observed in COVID-19 cases.
However, despite these promising mechanisms, there is currently no clinical evidence showing that BPC 157 works in humans with COVID-19. Most data come from animal research, and human trials with this peptide are limited to other conditions. No large, controlled studies have tested its safety or effectiveness specifically for viral infections or COVID-19.
Over the past decade, Ozempic has risen to prominence as one of the leading drug treatments for those with type II diabetes. The active ingredient in Ozempic, semaglutide, works by mimicking our body’s natural GLP-1 hormone, lowering blood sugar by increasing insulin production and decreasing glucagon release. In the same vein, Wegovy functions identical to Ozempic but the only difference is that Wegovy is prescribed specifically for weight management while Ozempic is for type II diabetes.
As these drug’s popularity surges, however, a multitude of ethical concerns have emerged, particularly concerning Ozempic’s intended purpose which is increasingly overshadowed by its appeal as an easy path to weight loss. One of the main ethical concerns against prescribing semaglutide drugs for weight loss is that it will leave those who ‘need it most’ for therapeutic purposes worse off (Ryan et al. 2025). This is because there are more people affected by their weight than type II diabetes - here is where the controversy kicks in.
Arguments against prescribing these drugs for weight loss are firmly grounded in the idea that the overwhelming majority of people (at least in the U.S) who request this drug for their weight, are victims of their own lifestyle. Rather than working on one's lifestyle, people see these drugs as an easy way out of the problem they have caused, and continue to cause. Similarly, it can be argued that the U.S government takes the same stance because prescribing semaglutide’s is easier than dealing with population obesity caused by issues with the healthcare industry. Additionally, there is growing fear that the widespread use of semaglutide could reinforce fat-phobic rhetoric due to the notion that getting one’s body ‘back into shape’ is considered a moral activity.
On the other hand, there are many viable reasons to prescribe semaglutide drugs for weight loss, starting with combating obesity. While most perceive obesity as someone who is just lazy, it is needless to say that it is much more complicated than that. In addition to treating obesity, prescribing semaglutide offers a less risky therapy compared to bariatric surgery due to the differing side effects of each. Common side effects for bariatric patients include nutritional deficiency, anaemia, osteoporosis, neuropathy, calcium oxalate urolithiasis and infertility, while common side effects of semaglutide include nausea, vomiting, diarrhea, bloating, and constipation.
The point of this blog is not to be comprehensive, rather it is meant to spark interest and encourage further self research into the subject. While I briefly spoke on some arguments for and against prescribing semaglutide for weight loss, there is far more to uncover. Such as: How does long term use of Ozempic or Wegovy affect female reproduction? Should those who struggle with their weight be bailed out by this drug, or should they be encouraged to change their lifestyle first? Should the U.S government reallocate its subsidies for Wegovy to Ozempic? Who takes priority when requesting Ozempic, diabetics or obese patients?
Work Cited:
Ryan, N., & Savulescu, J. (2025). The Ethics of Ozempic and Wegovy. Journal of medical
Isaiah Charles Austin was one of the most highly touted recruits in the country. He had attended Grace Preparatory Academy in Arlington, Texas. The senior standout averaged a double double and was able to be represented in the 2012 McDonald’s All-American game, 2012 Adidas Nations Camp, and 2012 Jordan Brand Classic. His ranking soared after this season as he was the number 3 overall recruit according to ESPN. And this allowed him to have offers from almost every power 5 school in the nation. He ultimately decided to go to Baylor. The Texas native continued to have success at the college level, where he was able to be part of the Big 12 All-Rookie team, Big-12 All Defensive team, and Third Team All- Big 12. He was even able to be a key contributor to the NIT championship team in 2013. Everything was falling into place for Isaiah, as the NBA was very much in his sights after two years at Baylor; until it wasn’t.
Just days before the 2014 NBA draft, where Isaiah was supposed to accomplish his dreams of making it to the NBA, he learned that he had been diagnosed with a mild case of Marfan Syndrome. A routine EKG during his pre draft workout had revealed this condition. Marfan Syndrome is a rare genetic disorder that can affect the connective tissues surrounding the body. It will interfere with the functionality of the eyes, heart, blood vessels, and parts of the skeleton. The fibers that anchor organs and other bodily structures are all affected. For Isaiah, he unfortunately follows under the common build for those with Marfan Syndrome as he has disproportions in the lengths of the limbs in his body. Standing at seven foot tall, he is subject to some of the ramifications that come with the disease. Defective fibrillin genes may cause some of the bones in the body to make an individual taller than normal. This affects the size of the arms, legs, fingers, and toes as well. A mutation in the transforming growth factor beta (TGF-beta) gene will cause a cascade of connective tissue problems throughout the body.
For this topic, I wanted to focus on the heart as we have been delving into the physiology of the heart. And more specifically, I wanted to understand why Marfan Syndrome affected the heart physiologically to the point where someone like Isaiah Austin was not allowed to compete professionally in the NBA. Marfan Syndrome can potentially be life threatening. And for Isaiah to find out he had Marfan Syndrome so much later in life, is a pose of concern. The features were not so obvious until they did an x-ray scan that revealed the enlargement of his heart due to the condition. Doctors were concerned about a potentially fatal aortic dissection because of his aorta that was enlarged. The physical activity from basketball requires demands on the heart that would deem too risky for Isaiah to participate in. They would render him medically ineligible to play.
Marfan Syndrome, from a physiological perspective, can affect the heart in a multitude of ways. It can begin by weakening the connective tissue that surrounds the aorta, as well as its valves. Because of this, aortic aneurysm can occur. Other conditions such as aortic dissection and mitral valve prolapse can happen, too. An enlarged aorta is subject to tearing and a life threatening case of aortic dissection may occur. Blood can potentially seep into the inner layers of the aorta wall through regurgitation. The heart will have to work too hard as the left ventricle can become too large, and it will lead to heart failure. As far as aortic aneurysm is concerned, the aorta can weaken and widen. That leads to a bulge forming from the widening and causes problems at the aortic root where the aorta leaves the heart. Rupturing of the aorta is extremely problematic, as life-threatening hemorrhage is subject to occurring. Blood pressure will drop significantly and one can be dead in just minutes. With heart valves, the flaps on the mitral valve can potentially become “floppy” and prevent closing. Because of this, the blood may leak backwards into the heart leading to aortic regurgitation. As far as some other cardiac effects are concerned, the irregular heartbeats that happen by way of Marfan Syndrome will lead to the shortness of breath and heart palpitations. Because of the effect on such regulatory pathways in the heart, individuals are subject to lightheadedness and chest pain. In less common scenarios, the pulmonary artery can become dilated due to Marfan Syndrome. And this will cause issues as the increased pressure on the lungs, will cause a strain on the right side of the heart and potentially lead to heart failure.
For Isaiah Austin, his story did not end there. The NBA honored him on draft night by making him a ceremonial first-round pick. And two years later, he was able to grace the court again to play professionally. Because his condition was mild, further testing in 2016 cleared him to play with close watch on his heart from doctors. He was not cleared by the NBA, who carried stricter guidelines as far as cardiology was concerned. But his own doctors allowed him to continue playing as he pursued opportunities overseas. He was able to play multiple seasons in Europe and Asia. And he has also been able to play locally here in the United States through Ice Cube’s BIG3 Basketball League.
If you are wondering how he was able to be cleared, I was too. And I took a dive into how exactly he was able to play with Marfan Syndrome all these years since. Because his condition was mild, his aorta was still structurally stable. The root diameter remains the same size. His cardiac output was monitored and it still was efficient. So, measures such as his stroke volume, left ventricular structure, SA node, and oxygen carrying capacity were all rendered to be normal. The sympathetic nervous system is functioning properly. And his mitral valve would be able to handle the workload of a professional basketball setting. There should be less indication of regurgitation. And the fibers surrounding his connective tissue were not extremely weakened by his condition. All of the systems in the heart have been carefully monitored by clinicians. Many CT and MRI scans are done. He constantly wears a heart monitor when playing or doing physical activity. He also goes under blood pressure testing regularly.
Beyond the scope of just basketball, Isaiah had been instrumental in increasing the public awareness of the rare genetic condition. In addition to that, Isaiah has helped foster many people who had similar physical features of his own to get tested for Marfan syndrome. This encouragement of early detection saved lives and helped people get diagnosed that would not have any other way. Isaiah continued to advocate for those dealing with Marfan Syndrome as a motivational speaker and symbolic figure of what you can still do. He has highlighted the importance of genetic testing for the disease. He is living proof that one can find alternative ways to live out their dreams through proper medical care and fulfill meaningful roles in society.
American College of Cardiology/American Heart Association. (2022). 2022 Aortic disease guideline: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Journal of the American College of Cardiology, 80(24), e223–e393. https://doi.org/10.1016/j.jacc.2022.08.004
Brooke, B. S., Habashi, J. P., Judge, D. P., Patel, N., Loeys, B., & Dietz, H. C. (2008). Angiotensin II blockade and aortic-root dilation in Marfan’s syndrome. The New England Journal of Medicine, 358(26), 2787–2795. https://doi.org/10.1056/NEJMoa0706585
De Backer, J., Renard, M., Campens, L., & Muino-Mosquera, L. (2021). Cardiovascular management in Marfan syndrome and related conditions. European Heart Journal, 42(39), 3939–3947. https://doi.org/10.1093/eurheartj/ehab302
Groth, K. A., Hove, H., Kyhl, K., Folkestad, L., Gaustadnes, M., Vejlstrup, N., & Østergaard, J. R. (2015). Clinical review: Marfan syndrome—A clinical update. European Journal of Human Genetics, 23(1), 124–133. https://doi.org/10.1038/ejhg.2014.62
Maron, B. J., Udelson, J. E., Bonow, R. O., Nishimura, R. A., Ackerman, M. J., Estes, N. A.,
& Thompson, P. D. (2015). Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: Task Force 3: Hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and other cardiomyopathies, and genetic cardiovascular diseases. Journal of the American College of Cardiology, 66(21), 2362–2371. https://doi.org/10.1016/j.jacc.2015.09.035
Loeys, B. L., Dietz, H. C., Braverman, A. C., Callewaert, B. L., De Backer, J., Devereux, R. B.,
& MacCarrick, G. (2010). The revised Ghent nosology for the Marfan syndrome. Journal of Medical Genetics, 47(7), 476–485. https://doi.org/10.1136/jmg.2009.072785
I think most of us have heard people say, “Oh, I ate dirt as a kid, so I won't get sick”. But what is the extent of this “protection” from illnesses? Well, I was one of those kids; I used to play all the time outside, digging in the dirt and ruling the playground (if I didn't like you, you didn't come on the playground when I was on it 🙂). From time to time, I'll accidentally lick my fingers full of dirt and not think much about it. But as I grew up, I heard people say, “If you ate dirt as a kid, you should be fine”. Per the Environmental Protection Agency, children in the U.S. consume about 200–800 mg of dirt per day (Hauptman &Woolf, 2017). This seems like a lot, and it also gives my mom reason to ground me anytime I end up with dirt on my clothes (because I always wore white for some reason).
However, when looking at the literature, studies on animals raised in sterile environments, such as rabbits, mice, guinea pigs, and rats, have shown failure of proper immune system development (Gerald, 2003). It is said that their lymph nodes and Gut-associated lymphoid tissue (GALT) did not achieve the right shape or composition and could not initiate a normal immune response (Gerald, 2003). Furthermore, exposure to certain microbiomes causes lymph nodes and GALT to enlarge and reorganize, and develop T/B lymphocytes. Germ-free mice had increased inflammation of the lungs and colon, which was the result of hyperactivity of T cells linked to these disorders in both mice and humans (Brigham and Women's Hospital, 2012). The overall literature points out that exposing the germ-free mice to microbes during their first weeks of life, but not when exposed later in adult life, led to a normal immune system (Brigham and Women's Hospital, 2012).
Now, as a graduate student, I understand why people say they will not get sick because they “ate dirt”. Of course, kids should just shove a handful of dirt in their mouth (I might have), but it overall points to the bigger idea of the development of children and how nature and environment can shape not only our experiences, but also our biological and metabolic functions. Now I open the discussion…with the recent global pandemic and years of restrictions, reduced social interaction, and increased hygiene measures, how might the immune systems of today’s children develop differently? Of course, not EVERY plays in the mud or “eats dirt”, but what could the implications be for their health?
References
Brigham and Women’s Hospital. (2012). Getting the dirt on immunity: Scientists show evidence for hygiene hypothesis | ScienceDaily. https://www.sciencedaily.com/releases/2012/03/120322142157.htm?utm_source=chatgpt.com
Callahan, G. N. (2003). Eating Dirt. Emerging Infectious Diseases, 9(8), 1016. https://doi.org/10.3201/EID0908.030033
Hauptman, M., & Woolf, A. D. (2017). Childhood Ingestions of Environmental Toxins: What Are the Risks? Pediatric Annals, 46(12), e466. https://doi.org/10.3928/19382359-20171116-01
Olszak, T., An, D., Zeissig, S., Vera, M. P., Richter, J., Franke, A., Glickman, J. N., Siebert, R., Baron, R. M., Kasper, D. L., & Blumberg, R. S. (2012). Microbial exposure during early life has persistent effects on natural killer T cell function. Science, 336(6080), 489–493. https://doi.org/10.1126/SCIENCE.1219328
So I always complained about being cold and anemic (yes, I should take my iron pills, but I forget and alarms don't work for me), but I never realized how much it was affecting my performance in Taekwondo. I’ve been practicing Taekwondo for over a decade now, and it’s my favorite sport. If you’ve ever watched MMA, and you see those flashy, high kicks? Yes, many of them come straight from Taekwondo.
Taekwondo (TKD) is a type of Martial A,rts sport that mixes endurance and power, with fast, explosive kicks that require both strength and accuracy. To master basic kicks, you must constantly train your muscles for speed, accuracy, and flexibility. Ever since the lecture on skeletal muscles, I’ve wondered how Taekwondo athletes develop fast vs. slow-twitch muscle fibers. As we know from Dr. Campisi, skeletal muscle is composed of a mix of fiber types that range from slow to fast. We have type I (slow-twitch),and type IIa/IIb (fast-twitch), which all vary in their fatigue-resistant ability and use of energy. Because Taekwondo relies heavily on explosive, anaerobic movements, elite athletes tend to have a higher proportion of fast-twitch fibers, particularly Type IIa and IIb, similar to other power athletes (Sladic, 2025).
Now, my anemia can complicate this. A study in rats showed that iron deficiency can cause Type IIa fibers to shift toward Type IIb fibers, which are fast but fatigue very quickly. Interestingly, slow-twitch fibers remained mostly unchanged (Swearingen,1986), which may explain why I could perform better in shorter rounds but struggled over longer sessions (AKA, I always tell coach 30-second rounds). Some of you have even noticed how those staircases in the library kill me every day (let's be honest, who does it not kill).
Another interesting fact about TKD (which I hope gets more research), is the difference between old-school and modern Taekwondo. When I started, old-school Taekwondo was all about power and speed, whereas modern, it's more point-based, focusing on techniques and head-level kicks. We all know about plasticity and how muscles can adapt/ change muscle fibers over time. I wonder whether athletes from the old-school era (me) had a higher abundance of fast-twitch fibers compared to today’s competitors. Regardless, I still need to take my Iron and I’ll be sure to keep you posted on how it affects my Taekwondo performance!
References
Sladic, N., Cular, D., Babic, M., Kezic, A., Tomas, T., & Zubac, D. (2025). Neuromuscular Profile of Top-Level Youth Taekwondo Competitors Assessed Through Tensiomyography-Croatian National Youth Taekwondo Team Example. https://doi.org/10.51371/issn.1840-2976.2025.19.2.1
Van Swearingen, J. (1986). lron Deficiency in Athletes: Consequence or Adaption in Strenuous Activity. www.jospt.org
Research on African elephants (Loxodonta africana) offers insight about the metabolic consequences of abnormal prolactin secretion. This is important as it can help assess elephant health in relation to the conservation and care of these animals. But not only that, it identifies parallels in elephant and human health that were previously unknown.
Natalia Prado and colleagues examined the metabolic health biomarkers in acyclic female elephants with either abnormally high or low prolactin levels. They found that both extremes of prolactin secretion are harmful, but in distinct ways.
They saw that high-prolactin elephants showed significantly lower levels of thyroid hormones (TSH, T3, and T4), lower glucose and LDL cholesterol, yet higher total cholesterol. These markers point towards hypothyroidism and suggest that a disrupted thyroid system may be caused or aggravated by elevated prolactin.
In elephants with low prolactin levels, they saw increased body condition scores (BCS), insulin, HDL cholesterol, cortisol, and testosterone. The combination of higher insulin and body fat signals possible insulin resistance, which is a precursor to metabolic syndrome.
These results show that elephant metabolic health is just as complicated and intertwined as human health. That abnormal prolactin not only disrupts reproductive cycling but also profoundly affects energy balance, lipid metabolism, and the stress in elephants.
Both elephants and humans are vulnerable to the metabolic consequences of abnormal prolactin, including thyroid dysfunction and insulin resistance.
This study greatly sheds light on metabolic and endocrine systems in elephants that we did not previously understand. And while there were similarities between humans and elephants, we have to keep in mind that there are slight physiological changes that can make a big impact (such as… body mass… and musth in male elephants). So while we gained great insight into the elephant’s metabolic pathway and endocrine system, further studies need to be made into these complex systems.
Prado, N.; et al. (2023). Abnormal prolactin secretion is associated with changes in metabolic health biomarkers in acyclic female African elephants (Loxodonta africana). Science Direct. https://www-sciencedirect-com.dml.regis.edu/science/article/pii/S2773093X23000466?via%3Dihub
PCOS—Polycystic Ovary Syndrome has long been viewed as a hormonal disorder affecting women of reproductive age but it is still being researched. And recent findings from physicians such as Jia Zhu and her colleagues indicate that PCOS is part of a broader metabolic and reproductive disorder. Findings suggest that genetic risk factors can be detected as early as childhood which would be beneficial in the management and treatment of this disease (Covino-Deaso, 2025).
There is research shown that children of women with PCOS have had a negative metabolic impact of the syndrome. This includes but is not limited to higher risk of obesity and insulin resistance. Zhu used a polygenic risk score (PRS) to identify the association between PCOS and genetics and found that a higher PRS was associated with obesity, type 2 diabetes, coronary artery disease and androgens alopecia. The higher PRS and symptoms can be viewed in children as early as 6 years old and more importantly before puberty. This suggests that PCOS may not be hormonal or at the very least independent of the typical ovarian association.
PCOS symptoms include fatigue, low sex drive, fluctuation in weight, excessive body hair, and ovarian cysts. There is an error in communication between the hypothalamus, pituitary gland and ovaries, as we know to be a negative feedback loop. Due to a dysfunction of this HPO axis the luteinizing hormone (LH) is in excess (La Marca & Indefrey, 2020). LH is involved in the ovulation cycle and its hormonal balance is what leads to the natural progression of ovulation, followed by the luteal phase and then back to the follicular phase.
We should use genetics to our benefit and research these markers. This could possibly increase the number of PCOS cases as those with PCOS are often misdiagnosed or undiagnosed because there is not a definitive diagnostic test. Black and Hispanic women are impacted most by PCOS as they are at a higher morbidity due to cardiovascular disease and diabetes as high risk factors in the population. There is something to be said about the access to proper care and diagnoses of PCOS within these communities due to explicit bias in health care (Engmann et al., 2017). In a perfect world justice and beneficence would be used to make such a test available to everyone regardless of race and socioeconomic background. A delaying of proper diagnoses leaves individuals in the lurch—not possibly receiving a diagnoses until their symptoms become severe and obvious.
Engmann, L., Jin, S., Sun, F., Legro, R. S., Polotsky, A. J., Hansen, K. R., Coutifaris, C., Diamond, M. P., Eisenberg, E., Zhang, H., Santoro, N., & Reproductive Medicine Network (2017). Racial and ethnic differences in the polycystic ovary syndrome metabolic phenotype. American journal of obstetrics and gynecology, 216(5), 493.e1–493.e13. https://doi.org/10.1016/j.ajog.2017.01.003
We all know how vital sleep is to our overall health, but it might play a bigger role in our brain health than we previously thought.
We know that a good night’s sleep is important, as it allows our brain to strengthen important neuronal connections, clear toxins via the glymphatic system, restore the brain’s ability to focus and think clearly, and so much more. It is vital that you get at least 7 hours of sleep a night so your brain can reach NREM and REM sleep. It is also important you have a good night’s sleep, as poor sleep has been linked to an increased risk in Alzheimer’s.
In Alzheimer’s disease, there is a buildup of proteins amyloid-beta and tau. The buildup of these proteins in and around the neurons will lead to neuronal death. This neuronal death leads to cognitive and memory diseases such as dementia and Alzheimer's. (There are currently more than 6 million people in the united states living with Alzheimer's).
With such a prevalent disease, researchers are constantly looking for preventative or altering medicines. And within this search, an unlikely candidate might prove helpful.
Suvorexant, a DORAs drug (dual orexin receptor antagonists), has been developed to help combat the effects of insomnia. By blocking orexin, patients are able to fall asleep - but it might help with their brain health too!
In a recent clinical trial of 38 volunteers (between the ages of 45 and 65 who were relatively cognitively healthy), they were split into a placebo and treatment group. The treatment group received suvorexant and the amyloid-beta levels and phosphorylated tau in the cerebrospinal fluid was measured across each group.
They saw a 10 - 15% drop in phosphorylated tau and a 10-20% decrease in amyloid-beta. With the reduction of both of these proteins, it can lead one to believe it will help in neuronal death and eventually Alzheimer's. And while the long-term effects of suvorexant have not yet been studied, it proves promising.
So perhaps sleep is more important in diseases such as Alzheimer's than we previously believed.
Lucey BP, Liu H, Toedebusch CD, Freund D, Redrick T, Chahin SL, Mawuenyega KG, Bollinger JG, Ovod V, Barthélemy NR, Bateman RJ. Suvorexant Acutely Decreases Tau Phosphorylation and Aβ in the Human CNS. Ann Neurol. 2023 Jul;94(1):27-40. doi: 10.1002/ana.26641. Epub 2023 Apr 20. PMID: 36897120; PMCID: PMC10330114.
U.S. Department of Health and Human Services. (2025, September 18). Insomnia drug may lower levels of alzheimer’s proteins. National Institutes of Health. https://www.nih.gov/news-events/nih-research-matters/insomnia-drug-may-lower-levels-alzheimers-proteins
Have you ever wondered why we have hangovers? We know that alcohol causes them, but how? After doing some research I found that your liver actually creates acetaldehyde when it breaks down the ethanol from the alcohol you overconsumed. Acetaldehyde causes many of the common effects of hangovers, such as headaches, nausea, and fatigue. The levels of acetaldehyde also build up overnight. As you sleep, your brain does not enter REM sleep since it is suppressed by alcohol. Many people fall asleep quicker, but wake up feeling much more tired since we are unable to complete our REM cycle.
Hangovers often hit teens harder due to many factors, the main one being binge drinking and inexperience with alcohol. A point of conflict in the United States is the argument that the drinking age be lowered to 18, like many other countries in the world. They bring up the argument of the “forbidden fruit.” The idea behind this is we as humans have a natural instinct to want what we can’t have. Therefore if we grow up not able to possess alcohol, we will hold it in higher value than if we grew up with access to it. Another argument for lowering the drinking age is that in our current culture, teens resort to drinking in dangerous, isolated, or unsafe areas, while unsupervised. This leads to bad decisions without adult/law enforcement intervention, and often without health professionals around.
On the other hand, many argue that the brain isn’t fully developed until the age of 25. However, we are allowed to vote and be tried as an adult by age 18. They also state that drinking at a young age has statistically been shown to increase the likelihood of an addiction in the future. Another common fear is that this would bring alcohol into high schools, where 18 year olds spend the day hanging out with 17, 16 and 15 year olds. Personally I am conflicted on this issue. I do think that waiting until 21 was way too long, however I do not want the rate of drunk driving to go up, nor do I want the rate of alcohol addictions to go up in the United States.
Knuces, Laura. “The Science behind a Hangover.” Supplements and Health Tests, 13 Sept. 2001, www.thorne.com/take-5-daily/article/the-science-behind-a-hangover?gad_source=1&gad_campaignid=23211254821&gbraid=0AAAAADLUbJUrebw306nZHd62hELi3G_Dm&gclid=Cj0KCQiA0KrJBhCOARIsAGIy9wD9KKety_WeLAKKSeTq-d8A-epp6NsgWm7jtRctkADt3PBDt5-704IaApWiEALw_wcB.
Tapert, Susan F., et al. “Alcohol and the Adolescent Brain: Human Studies.” Alcohol Research & Health, National Institute on Alcohol Abuse and Alcoholism, 2004, pmc.ncbi.nlm.nih.gov/articles/PMC6601673/.
Imagine your immune system as a sharp security squad, always on the lookout for threats like viruses or bacteria. But what stops it from mistakenly attacking your own body? That's the root of autoimmune problems, like arthritis (where it hits your joints) or type 1 diabetes (where it targets insulin cells). The 2025 Nobel Prize in Physiology or Medicine honors Shimon Sakaguchi, Mary E. Brunkow, and Fred Ramsdell for discovering "peripheral immune tolerance"... the body's smart safety net that keeps things calm after early training in the thymus, where cells learn to tell "us" from "them" (Brunkow, 2025).
Let's break it down step by step. In 1995, Sakaguchi experimented with mice missing specific T cells (key immune fighters) and saw their bodies turn against themselves in total mayhem. He identified "regulatory T cells" (Tregs) as the level-headed guides that step in and say "hold up," calming excessive responses to protect your own cells (Sakaguchi, 2004). Then, in 2001, Brunkow and Ramsdell studied mice with wild, uncontrolled immunity (nicknamed "scurfy" for their rough skin). They pinpointed the FOXP3 gene as the main switch for creating Tregs. If it's damaged, no Tregs get made, leading to nonstop self-attacks – much like IPEX syndrome in human babies, who suffer severe autoimmunity from birth (Brunkow et al., 2001).
By 2003, Sakaguchi linked it all: FOXP3 transforms normal T cells into these peacekeeping pros, spreading tolerance throughout the body, not just in the thymus (Sakaguchi, 2004). Why wait until 2025 for the prize? Nobels hold off until the ideas prove their power in the real world. After 2003, research took off tying FOXP3 issues to common diseases like multiple sclerosis and lupus, creating enhanced Tregs in the lab, and starting patient tests in the 2010s. In the 2020s, new treatments boost Tregs or target FOXP3 to prevent organ transplant failures, enhance cancer therapies without harming healthy tissue, and ease long-term inflammation. It's basic science evolving into everyday breakthroughs (Young, 2025)
At its core, nature thrives on balance, not just raw power. Push tolerance too far, and infections win; dial it back too much, and self-damage ramps up. This shifts how we see physiology… from constant germ wars to smart self-control. What's coming next, like custom-tuned immune systems? The body hides more surprises than we know.
References:
Brunkow, M. E., Jeffery, E. W., Hjerrild, K. A., Paeper, B., Clark, L. B., Yasayko, S.-A., Wilkinson, J. E., Galas, D., Ziegler, S. F., & Ramsdell, F. (2001). Disruption of a new forkhead/winged-helix protein, scurfin, results in the fatal lymphoproliferative disorder of the scurfy mouse. Nature Genetics, 27(1), 68–73. https://doi.org/10.1038/83784
Brunkow, M., Ramsdell, F., Sakaguchi, S., Francisco, S., & Osaka, U. (2025). PRESS RELEASE The Nobel Prize in Physiology or Medicine 2025 “for their discoveries concerning peripheral immune tolerance.” https://www.nobelprize.org/uploads/2025/10/press-medicineprize2025.pdf
Sakaguchi, S. (2004). Naturally Arising CD4 + Regulatory T Cells for Immunologic Self-Tolerance and Negative Control of Immune Responses. Annual Review of Immunology, 22(1), 531–562. https://doi.org/10.1146/annurev.immunol.21.120601.141122
Young, L. J. (2025, October 6). 2025 Nobel Prize in Physiology or Medicine Awarded for Discoveries Key to Treating Autoimmune Disease. Scientific American. https://www.scientificamerican.com/article/2025-nobel-prize-in-physiology-or-medicine-awarded-for-discoveries-key-to/
Where is the G-Spot, and does it even exist? The G-spot is a structure that sparks so much enthusiasm and remains as one of the most debated mysteries. It is a complex region, thought to be located on the anterior vaginal wall behind the pubic bone and along the urethra. It is named after a 1950 seminal paper published by gynecologist Ernst Gräfenberg (Gräfenberg-spot), which explored the Role of the Urethra in Female Orgasms, more specifically, an erotic area that would swell with sexual stimulation (Vieira-Baptista et al., 2021). Depending on who is asked, the G-spot is thought to encompass many different anatomical structures. The G-spot is described as being composed of epithelial, glandular, and erectile tissue, but also as a fibroconnective sac and/or an increased density of microvessels and small nerves. (Vieira-Baptista et al., 2021).
While researching this subject, I have found that a few groups are publishing original investigations. Some have conducted cadaver dissections and histological examinations, whereas others have assumed its location/composition. There are a lot of anecdotal stories of female patients as to where they derive their sexual pleasure. Women have reported sometimes ejaculating non-urine fluid during orgasms, another possible evidence for the existence of the G-spot. Although there is inadequate information to show that the ejaculated fluid is anything other than urine, more analysis should be conducted. Some have found that the fluid contained high levels of prostatic acid phosphatase in the ejaculate compared to what can be found in urine (Hines, 2001). Prostatic acid phosphatase is also found in high amounts in the male ejaculate and originates in the prostate, which produces components of the male ejaculate. Some research has hypothesized that any non-urine female ejaculate would likely come from the female paraurethral glands, also known as Skene’s glands or ducts, as it may be analogous to the male prostate. This could be evidence of there being a female prostate and, therefore, the G-spot.
Some studies have concluded that women with higher education levels and better sexual function were more likely to report having a G-spot (Vieira-Baptista et al., 2021). I do wonder what scale they used to measure better sexual function, as it was not explained. However, I do believe that women with lower sexual health literacy may be unable to put a name to this concept, which underscores the importance of providing accurate and accessible information regarding the promotion of sexual health literacy. This should be a reason for us to support research equity! Let’s be honest, female sexual behavior is not universal, and for centuries, sexual anatomy related to pleasure has been understudied and underdiscussed. Hopefully, talking about this helps normalize curiosity and aids in destigmatizing female sexual anatomy. Research on female anatomy should not be considered optional, and increasing clinical, anatomical, and psychological studies would help to close the gender gaps in sexual health research.
Hines, T. M. (2001). The G-spot: A modern gynecologic myth. American Journal of Obstetrics & Gynecology, 185(2), 359–362. https://doi.org/10.1067/mob.2001.115995
Vieira-Baptista, P., Lima-Silva, J., Preti, M., Xavier, J., Vendeira, P., & Stockdale, C. K. (2021). G-spot: Fact or Fiction?: A Systematic Review. Sexual Medicine, 9(5), 100435. https://doi.org/10.1016/j.esxm.2021.100435
