I realized I needed to pace myself when it comes to how much I put into my studies. People had told me Honours was going to be difficult, but this is much more difficult than what I expected.
The course I chose is Clinical Anatomy and we had our first techniques exams in March. Most of our learning was crammed into 2 months of intense studying and understanding of human anatomy. This would be the first time I had written a test in 5 years, so I had decided to give it my all, because I had wanted great marks. Yet, after the techniques exam was done, I felt I had failed. It felt as if all the hard work I had put into studying was for nought. I had to accept that I wasn’t cut out for academia or lower my expectations of myself.
With all the intense learning and studying for techniques, I had stopped taking care of my mental health. Therefore, I had a breakdown. I was burnt out and the year wasn’t finished. I didn’t realise how much I had put into getting great marks. Yes, I enjoyed myself, and yes, I received great marks, but the cost wasn’t worth it. I had to find a way to balance my studies and the other parts of my life, otherwise I wouldn’t survive 2022.
It’s been a few months since then and I’m getting better at finding the balance. Now, I’m working to achieve good marks. The lesson I learnt was to be realistic about my expectations regarding Honours and myself. Yes, Honours is difficult, intense and sometimes crazy, but that doesn’t mean I won’t enjoy Honours.
Mary Poppins (1964) said, “In every job that must be done, there is an element of fun. You find the fun and ‘snap’, the job’s a game.”
Finding the fun in writing this, was finding a way to incorporate the quote.
Goodluck to all the future Honours students. Remember to take care of your mental health and yourself.
Hey, I am Gomolemo. A young individual from Gauteng who is aspiring to be a scientist. I cannot share a whole lot more about myself right now, but I will share something in particular. The final semester of my undergraduate studies was the most nerve-wracking time of my life. I would try to make the most of my days but my thoughts were always about doing well on my final exams, ultimately getting my degree and then furthering my studies. On top of that, I would check my email regularly to see if any of the universities I had applied to do my honours at had accepted me.
Once the exam season had finally ended and the long-awaited festive season was approaching. I received an email confirming my admission to UCT. To say that I was happy would be an understatement. I was over the moon! I could not wait to share these amazing news with my family and friends. As excited as I was though, I realised that going to UCT would mean that I would have to move to a different province and stay in a place that was completely new to me. Extremely far from friends, family and home – my comfort zone. However, I will admit that in high school my friends and I would constantly say, “I can’t wait to leave high school. I will finally feel grown and independent.” Needless to say, that is every teenager’s dream. However, it started to feel like everything was suddenly happening way too fast and I felt like I was no longer ready to be grown and independent. On the other hand, I kept thinking that it really could not be all that bad. I would be just fine, right?
Soon after New Year’s Day, I finally made it to Cape Town. I was overwhelmed with a feeling of excitement and a dash of fear. But surely I would be just fine, right? A few days into my stay I eventually got to meet my stream convenor and classmates for the first time. Surprisingly, many of my classmates were just like me, in that they had now moved to a place which was totally unfamiliar to them. It was during our orientation that we realised that the journey we were now embarking on would not be as terrifying as we had imagined. Although we had all just met, we discovered that together we would form the best support system for one another. Our similarities would be what allow us to form a strong bond which would make those days away from family and friends slightly bearable. Our connectedness would be the source of strength and courage needed to help us through the eventful year ahead of us.
It certainly did not take me months to finally believe that I would be just fine. All my uncertainties and fears were slowly overcome with each passing day. That was all thanks to my stream convenor, lecturers and most importantly my classmates. A small group of compassionate and friendly people who somehow showed me that change is not always scary. They revealed that stepping out of your comfort zone allows you to live a fulfilling life in which you discover your abilities and potential. You learn to stand on your own and experience moments that will allow you to grow as an individual. So with all that I have shared, trust me when I say that throwing yourself into the unknown seems daunting. But take that leap of faith because in the end, you will be just fine.
Imagine the things your body is capable of. Imagine even the little things like stretching, scratching that itch, talking, and eating. Now, imagine not being able to do any of that, each ability you’ve had for as long as you can remember slowly eroding away. Every little thing we may take for granted like being able to swallow, being able to speak, or just being able to move our bodies is a gift that a person with amyotrophic lateral sclerosis (ALS) soon loses.
ALS is a neurodegenerative disease characterised by the progressive death of motor neurons in the spine and the brain that control voluntary muscle movements. The death of these neurons leads to the subsequent death of muscle cells. The loss of motor neurons spreads to other parts of the body leading to the inability to move, eat and swallow, and speak. Eventually, this fatally leads to the muscle and nerve cells of the diaphragm – the most important muscle involved in breathing – also dying. Now, symptoms and disease progression may vary, but ultimately one’s life and loved ones are affected severely.
There is unfortunately no current cure for ALS. All that can be done right now is supportive care that can potentially increase life expectancy but at the cost of quality of life. The difficulty in finding effective long-term treatments is due to our lack of understanding of how this disease occurs. There are a multitude of genetic and environmental factors that play a role in ALS, so the picture is quite complex. One fundamental question underpinning ALS pathogenesis is: “Why do those neurons die?”
Firstly, cell death is divided broadly into two categories. We have accidental cell death that is uncontrolled and typically caused by direct chemical or physical injury. Then, we have regulated cell death (RCD) that is controlled and regulated by our own cells. One major kind of RCD is “apoptosis” which is typically triggered by death ligands (molecules that signal cells to undergo RCD) and a caspase cascade (a chain reaction of caspase molecules that result in apoptosis). It was originally thought that motor neuron death was caused by apoptosis, but inhibiting it did not protect neurons in ALS. Then, “necroptosis” was suggested as a mechanism. It’s another form of RCD that’s typically caspase-independent and driven by inflammation. However, if we get rid of MLKL – a critical component of necroptotic signalling – we find no changes in neuronal death.
A group of researchers in Australia aimed to find a mechanism underlying neuron death in ALS. That led them to “ferroptosis”. Ferroptosis is a relatively newer discovery and also a form of RCD that is iron-dependent and caspase-independent. Ferroptosis is typically caused by iron dysregulation and glutathione peroxidase 4 (GPX4) depletion that result in lipid peroxidation and cellular membrane damage (lipids are a major component of cell membranes). GPX4 is a major regulator of ferroptosis as it is acts as a defense against lipid peroxides, preventing widespread cellular damage. It does require glutathione (GSH), an antioxidant, in order to do so. See, as it turns out, accumulated iron, lipid peroxidation, and glutathione depletion were found in spinal cord and brain tissue of affected ALS individuals. See the link here?
To test if ferroptosis was indeed the cause of cell death in ALS, the researchers tested the effect of GPX4 on neurons from ALS mice. The result? ALS mice had lower levels of GPX4, and iron levels were dysregulated as expected. Overexpressing GPX4 in these mice showed a positive effect. There was a decrease in lipid peroxidation, therefore cell death was decreased, and disease onset was delayed thereby extending the mice’s lifespan. Additionally motor function was somewhat preserved although disease progressed as usual upon onset.
Does it really amount to much though?
These might not seem like groundbreaking discoveries. After all, the ALS mice still displayed neurodegeneration, indicating that we’re yet to uncover the full picture, let alone find a suitable long-term treatment. But we’ve made progress. Highlighting ferroptosis’s role in ALS opens up new avenues for treatments and discovery. Just from the researcher’s suggestions alone, perhaps selenium (a component of GPX4) or GSH treatments may be useful; iron chelation to remove excess iron might also hamper degeneration. Just knowing that ferroptosis exists and is involved in ALS gives us the power to target it in the future. Perhaps this is just the beginning. Ferroptosis is slowly being linked to other neurodegenerative diseases. Understanding it and how to influence it has the possibility of building the foundation upon which we can treat other diseases as well. Every step we take towards learning more and more about the diseases that plague us is a step towards building a world where people don’t have to suffer from them.
Reference
Wang, T., Tomas, D., Perera, N.D., Cuic, B., Luikinga, S., Viden, A., Barton, S.K., McLean, C.A., Samson, A.L., Southon, A. and Bush, A.I., 2022. Ferroptosis mediates selective motor neuron death in amyotrophic lateral sclerosis. Cell Death & Differentiation, 29(6), pp.1187-1198
Are the pharmacokinetics of cerebrospinal fluid (CSF) able to predict brain target concentrations of various drugs? What role does the blood brain barrier (BBB) play in the distribution of drugs within the central nervous system (CNS)? What is the relationship, in terms of drug distribution, between the different compartments of the brain? These are some of the questions explored in a review paper by de Lange and Danhof (2002).
Knowledge about distribution within the central nervous system is important for drugs that have brain target sites, such as antidepressants, anticonvulsants, anaesthetics, antibacterials and anticancer agents. In the clinical setting, direct measurement of the concentration of these types of drugs poses many challenges. Historically, most often drug concentrations within lumbar CSF were used as a proxy for the concentrations achieved in the brain – however the role of the blood-brain barrier and blood-CSF barrier in the complex relationship of drug distribution within the different compartments of the CNS requires further research. The compartments of note include the brain extracellular fluid (ECF), intra-cellular brain compartments, as well as ventricular and lumbar CSF.
There are multiple factors that may affect drug distribution within the CNS. Firstly, the blood-brain barrier (BBB) and blood-CSF barrier (BCSFB) affect the entry and distribution of drugs into the different CNS compartments. The BBB is found at the cerebral endothelial capillaries, which have tight junction proteins that restrict the movement of mainly hydrophilic drugs. The BCSFB is slightly more permeable than the BBB. The characteristics of these barrier systems have significant implications for the distribution of drugs in the CNS. Secondly, there may be distinct differences in the pharmacokinetics of drugs within lumbar CSF compared to ventricular CSF, due to diffusion as well as CSF dynamics. Thirdly, in terms of the physicochemical properties of drugs, the size, charge and lipophilicity of the drug affect its ability to passively diffuse. In this case, lipophilic, small and non-charged drug molecules are favoured when it comes to transcellular diffusion. On the other hand, hydrophilic, large and charged drug molecules rely more on paracellular diffusion, although this type of transport is mediated by the tight-junctions of the BBB and BCSFB, that preclude molecular transport based on size. Cerebral blood flow could also affect drugs crossing the BBB, with an increase in blood flow resulting in a greater influx of highly permeable drugs across the BBB. In addition, the extent of plasma-protein binding of a drug will affect its transport across the BBB and BCSFB. The turnover rate of CSF will also have an effect. Enzymes found at the BBB and BCSFB affect drug metabolism, which acts as a barrier for drug entry into the brain. In addition, pathological brain conditions can affect the permeability of the BBB. This creates repercussions for the transport of drugs across the barrier into the brain. Drugs can also cross the BBB and BCSFB by active transport, which involves the use of ion channels and pumps, including influx and efflux transporters. Some endogenous influx transporter proteins may assist drug entry into the brain, and efflux transporters may actively pump drugs out of the brain.
Considering the multitude of factors that affect drug distribution within the different CNS compartments, it seems logical to try to find a method of measuring drug concentrations as close to their presumed site of action as possible. This is important for antibacterial drugs, where a minimum inhibitory concentration (MIC) needs to be reached in order to kill off the bacteria – for example when treating bacterial meningitis. If we are still only using lumbar CSF concentrations as a proxy for brain drug concentrations, we are in the dark about the actual drug concentrations being achieved in the affected brain tissue. This has significant implications for determining whether sufficient dosages are being prescribed in the clinical setting in order to achieve the best patient outcomes.
Most drugs that target the CNS have their target sites within extracellular regions, thus extracellular brain concentrations of these drugs provide the most relevant information. Cerebral microdialysis is a method, although invasive, that may be able to measure drug concentrations achieved at specific regions in the brain. Imaging techniques, despite having significant limitations, may be non-invasive methods for obtaining better drug concentration information as well. These techniques include positron emission tomography and magnetic resonance spectroscopy.
The review concludes that the value of CSF concentrations of drugs in predicting the effect of the drugs in the brain is highly limited, and thus methods to measure drug concentrations closer to their site of action in the brain need to be further developed.
Reference
de Lange, E. and Danhof, M., 2002. Considerations in the use of cerebrospinal fluid pharmacokinetics to predict brain target concentrations in the clinical setting. Clinical pharmacokinetics, 41(10), pp.691-703.
Do you consider yourself a night owl? Do you struggle to fall asleep and wake up early in the morning, hitting the snooze button a few too many times? This may be the cause of a genetic mutation, meaning we now have a medical excuse for missing that 8 am lecture.
Researchers from The Rockefeller University discovered a genetic mutation, altering the timing of the biological clock. The result of this is a common sleep syndrome called delayed sleep phase disorder (DSPD) or “Night Owl Syndrome”. It is estimated that a whopping 15% of people in the United States struggle with this disorder.
Normally the intrinsic circadian clock promotes 24-hour rhythms, that are essential for daily human activity and body functioning. The 24-hour cycle consists of a negative feedback loop where transcription factors, Clock and Bmal1, produce inhibitors (of the Per and Cry family). These inhibitors gradually repress the transcription factors which are eventually silenced and therefore no longer produce inhibitors. Once all the inhibitors have degraded, the transcription factors regain their maximum potency, thus starting the cycle all over again.
The researchers sequenced the genes that form the mammalian circadian clock from the DNA of a patient thought to have DSPD. A mutation in the CRY1 gene was found, a gene already implicated in the circadian cycle. This gene mutation results in an altered protein expressed leading to the inhibitor being hyperactive. A hyperactive inhibitor causes the activators to be repressed for too long, extending the circadian cycle by at least half an hour.
To test whether the circadian abnormalities in this individual were related to the observed modification of CRY1, information on sleep patterns was obtained from the proband’s family members. The individuals were genotyped for the presence or absence of the candidate allele. Delayed sleep behaviour was found to be common among family members of both sexes and across several generations. This led the researchers to conclude an autosomal-dominant inheritance pattern.
So besides being an easy excuse as to why you overslept, this discovery may lead to the development of drugs in the future based on this mechanism that has been uncovered. Perhaps a drug that would reduce the activity of the hyperactive CRY1 protein in individuals with this disorder. Additionally, I believe that more research should be done around this since the human circadian cycle is known to not only regulate sleep but also hunger and levels of metabolites and hormones. How does the CRY1 mutation in people with DSPD affect this? Hopefully, the answer to this becomes clear soon, but until then I’ll carry on hitting my snooze button a few too many times.
Reference
Patke, A., Murphy, P. J., Onat, O. E., Krieger, A. C., Özçelik, T., Campbell, S. S., & Young, M. W. (2017). Mutation of the Human Circadian Clock Gene CRY1 in Familial Delayed Sleep Phase Disorder. Cell, 169(2), 203-215.e13. https://doi.org/10.1016/J.CELL.2017.03.027
With this piece, I am going to take you back to the very beginning and set the scene, it’s 2021, I am in my room preparing for the final exams of my undergraduate studies and I received an email that had me smiling for the rest of the day, it read: “Congratulations! You have been firmly admitted to the BMedScHons program at UCT in 2022.”
The day I arrived in Cape Town, from Joburg, was filled with so much anticipation, I had never experienced such a cocktail of emotions before, a mixture of excitement and joy laced with fear and anxiety. I got to my room at res and before doing anything else sat down and wrote down all the things that I was grateful for at that moment, little did I know that this would be an important grounding exercise for me throughout the year. This was followed up by me writing down my hopes and goals for the year on a blank A5 sheet. I put down a variety of things both academic, like improving time management and asking as many questions as possible; and some personal things, like strengthening my relationships and working on my overall health through reading, journaling, and eating. I had placed this beautifully decorated sheet strategically on my wall so that it was the first thing that I saw when I woke every morning. I was fully prepared for the year ahead, or so I thought. The reality of what the honour’s year was to bring first hit me when I was faced with an excel spreadsheet titled “Student Year Planner 2022”, and I quickly realized that what I had ahead of me was a beast, truly going into the lion’s den and looked my little sheet and was filled with doubts, could I get through this? This question still looms over me as I write this.
As the real work began, I found it harder to stick to those goals I had written down. I could feel my mental health deteriorating exponentially, and with the people I love being so far away, I felt more alone than ever. For the first time it had got to me in such a way that I was unable to compartmentalize; separating my personal struggles and worries from my academic commitments/requirements became an incredibly difficult feat, and with this year being one that I planned to find myself and determine whether this whole ‘being a scientist’ thing is really for me, you can imagine how heartbroken this made me feel because it made me think that maybe I wasn’t cut out for this. Nonetheless, I continued pushing forward and taking on each day and its lessons.
When the second half of the year started, I decided to revisit that list of goals I made and made the necessary adjustments that would allow me to be more flexible with the changes that come with this honour’s year. The old list is now stored away and now I wake up to see my new redesigned list of goals, it’s not as beautifully decorated but it is a better fit for the person I have grown to become. Despite the rocky beginning, this year has shown me just how resilient I am, I will not give up even when my world is literally shattering around me, which it has several times, and despite the pain and discomfort, I do believe that the struggles that I faced this year were necessary for me to truly appreciate this trait in myself. I have also learned the importance of having a great support system, I had always thought this meant only my immediate family, but this year showed me that that support is through a variety of different people: from friends to lecturers to my incredible supervisors and lab colleagues who I truly appreciate for all their guidance and mentorship, and for handling me with such care and compassion.
I am going through the remaining months of this year, feeling immensely grateful for the lessons I have learned in and out of the classroom and lab. I’ve had the opportunity to learn many valuable lessons about myself and have met such amazing people who have shown me that what makes this life beautiful are those little moments in between the chaos, when you share a laugh with a friend, or when you have random dance parties as a mid-week pick-me-up to energize and relieve stress. So, with this last stretch, I want to allow myself to fall and get back up again, I want to open myself up to more opportunities and forgive myself for the mistakes that I made while trying to figure things out because I am capable of achieving a lot more than I think or even believe sometimes.
And finally, thank you 2022 Honours year, you are truly a gift, I really see and appreciate that now.
Patience. That is what the past couple of months have been teaching me. Patience. Waiting over 6 weeks for equipment to arrive in order to start your experiments for your thesis tends to do that, I think.
In the meantime, I have thrown myself into learning as much as I can with the research group my project falls under. They are the best bunch of people, all interesting and unique and kind and helpful. I got a teeny taste of what it is like working as a team sorting through old patient files and documenting certain details on a group spreadsheet, and enjoyed celebrating with everyone once the task was finished. We had a debrief session after this period of working through some pretty heavy and hectic patient files (mostly dealing with motor vehicle accident traumatic brain injuries) and it was a safe space to process the emotions of reading through the files over the past couple of weeks. I learnt about everyone’s different hobbies outside of the research space; they range from yoga, to dungeons and dragons, to sewing and baking. We talked about work-life balance, and coping mechanisms, and celebrated the birth of the baby boy of one of the researchers in the team. I think what I love most about science at the moment is the people, and how they can shape your experience of working in a lab. Interacting and getting to know different researchers and their stories has been the best thing, and I know that in whatever direction I take my studies, people will be a part of that story. I think this is really special and something to be treasured, along with scientific progress and academic accomplishments and all that. Isn’t there a saying that rather than what you did or said, people remember how you made them feel? Well so far I have felt very welcomed and encouraged working with this wonderful group of people, who also happen to be spectacular scientists I can look up to and be inspired by.
Okay, back to waiting for the equipment to arrive and stressing about my project…
In school, it goes without saying that acquiring excellent marks throughout the year is a goal most students aim to achieve. However, there is a lot more to the honours year than just bagging distinctions and simply calling it a day – or rather one of the longest years. Some lecturers emphasize that this is a year where you get to expand your knowledge by delving into the scientific work which you find most fascinating; while learning some of the most important techniques researchers use to build this body of knowledge. My supervisor on the other hand refers to it as the year of “trial-and-error”. He says it is the year wherein you’ll gain some lab experience that will either make you joyful and proud or that will just make you cry and super stressed. I couldn’t agree with him more, especially while I was standing in the lab repeating an experiment for the fourth time!
I genuinely felt like giving up at that point. But following a series of numerous attempts at the same experiment, I eventually realized that simply adding a slightly higher volume of enzyme to my reaction tubes could have produced the best results. All I needed to do was to tweak the protocol. And much like me, researchers constantly find themselves having to tweak some of their techniques and protocols to produce effective treatments that aim to alleviate numerous diseases. For instance, acute myeloid leukaemia (AML). This blood and bone marrow cancer has limited treatments with high success rates due to their lack of specificity and their association with life-threatening side effects. Additionally, some of the available treatments cannot be administered to AML patients because they lead to graft-vs-host disease. Consequently, specific and more effective treatments still need to be produced to treat this cancer.
Recently, a much greater effort aimed at developing such specific treatments is being made. The latest research has revealed the use of chimeric antigen receptor (CAR) – T cells as an alternative and novel form of cancer therapy, which boosts the immune system to fight cancer. CAR- T cell therapy has shown exceptional success rates compared to conventional treatments as it targets specific antigens which are expressed by cells known to lead to the development of a particular disease. In some cases, researchers genetically modify natural killer (NK) cells as opposed to T-cells due to their cost effectiveness, reduced side effects and longer lifespan. For instance, work done by Albinger (2022) is proof of concept of a treatment which specifically targets AML cells. Essentially, they set out to generate CD33-targeted CAR-modified natural killer (NK) cells. They focused on CD33 because it is a potential antigenic target frequently expressed on leukemic blasts and cells that prompt leukaemia.
In order for Albinger (2022) to achieve their objectives, they first collected AML cells from patients and then isolated primary NK cells from healthy volunteer donors. They then tweaked or rather genetically modified (by lentiviral transduction) primary NK cells to express a second-generation CD33-CAR. In vivo functional studies of CD33-CAR-NK cells in humanized OCI-AML2 xenograft mouse models which reflect physiological conditions of a human host were performed. Qualitative and quantitative analysis using flow cytometry and confocal microscopy were also done.
In the end, their work showed considerable results proving that the use of CD33-CAR-NK cells could be a potential treatment for AML. In vitro experiments, in the OCI-AML2 cell line, showed that the CD33-CAR-NK cells had stronger cytotoxic activity against AML relative to untransduced NK cells. The in vivo experiments where a single dose injection of CD33-CAR-NK was administered showed effectual clearance of leukemic cells and a greater reduction in leukemic burden relative to untreated mice or mice receiving untransduced NK cells. In vivo experiments where multiple doses of CD33-CARNK cells were administered also showed minimized leukemic burden. The confocal microscopy images obtained from some of the experiments showed low GFP-positive leukemic cells and the presence of intact CAR-NK in the bone marrow of CD33-CAR-NK treated mice. Another one of the major observations made from Albinger’s (2022) work was that the use of the single and repetitive doses of CD33-CAR-NK cells in the mice did not cause any noticeable changes in weight, appearance or behaviour. Additionally, no signs of cytokine release syndrome or graft-vs-host disease were observed.
In conclusion, the results prove that CD33-CAR-NK could be a suitable treatment for AML. Moreover, targeted therapies may assist in improving the prognosis of many patients with AML. This form of therapy could also be applied in the treatment of other types of cancer. However, further research about the identification of unique antigens needs to be done to produce more effective targeted therapies while minimizing undesirable side effects in patients.
Reference: Albinger N., Pfeifer R., Nitsche M., et al. (2022) Primary CD33-targeting CAR-NK cells for the treatment of acute myeloid leukemia. Blood Cancer J. 12, 61.
Despite medical advances, uneven access to healthcare still contributes to gender inequality. The female combined oral contraceptive pill has been on the market for sixty years and has empowered women, giving us autonomy over our bodies. As reviewed by Dr. Stephanie Page and colleagues in Frontiers in Endocrinology, the variety in female contraception contrasts with male contraception which consists of condoms, withdrawal, and a vasectomy. Only 16% of global contraceptive use is male-driven, with the ‘latest’ commercially available male contraceptive being the condom, which was established two hundred years ago. Inadequate male contraception emphasises how society places the responsibility of safe sex on women.
Though the proof of concept of androgen use to suppress spermatogenesis was established by the WHO almost fifty years ago, male hormonal contraception is unavailable and pharmaceutical companies have abandoned male contraceptive development. Predictive models suggest novel reversible male contraception could decrease unplanned pregnancies by 30 to 40%, improving the mental, physical, and economic well-being of women and their families, and decreasing population growth. The perceived lack of market for male contraception highlights the commercially driven pharmaceutical industry.
Surveys show that 50-85% of men are willing to use male hormonal contraception. To date, however, only eight male hormonal contraception efficacy studies have been conducted, some of which were terminated prematurely due to mood-altering side effects. An unequal standard of healthcare between genders is seen by the side effects of the female ‘pill’ which include headaches, nausea, weight gain, mood changes, and more. Dimethandrolone undecanoate (DMAU) is an oral and injectable male hormonal contraceptive that acts on both progesterone and androgen receptors. Studies show it is safe, well-tolerated, and markedly suppresses gonadotropins and sex hormones, with few or no symptoms of hypogonadism. Yet male hormonal contraception commercial availability remains unseen.
While men bear no risks of childbirth or abortion, women are forced to use contraception as the benefits outweigh the risks. The benefits may only outweigh the risks for men if there were additional health benefits, for example, reducing long-term disease risk. Prolonging development, for an expectation yet to be explored for women, augments the burden of responsibility of pregnancy that society has already placed on women, diminishing the reality of the “shared risk”.
Through education, increased awareness, and engagement of pharmaceutical companies, male hormonal contraception can be materialised. This will improve the health and wellbeing of women, and decrease global burdens.
References • Page, S. T., Blithe, D. & Wang, C. 2022. Hormonal Male Contraception: Getting to Market. Front Endorcrinol (Lausanne). DOI: 10.3389/fendo.2022.891589 • Roberts, M. 2019. Male pill – why are we still waiting?. BBC News (online). Available: https://www.bbc.com/news/health-47691567.
Health Science Reviews 