Health and Disease

“Saviour Siblings”: Taking a look at PTT

By Asmita Anand

Published 2:05 EST, Sun October 3rd, 2021

What are Saviour Siblings?

A saviour sibling can be best described as a child created using IVF and genetic diagnostics. They will provide an organ or cell transplant for a sibling who is critically ill and suffering from a fatal disease.

For certain diseases, a human leukocyte antigens identical stem cell transplant can be the only treatment. While stem cell therapy is a very attractive option, finding a donor can be a challenge.

The Technology Behind Saviour Siblings

Preimplantation tissue typing (PTT) is a technology that allows us to test and select embryos in order to treat children in need of stem cell transplants. PTT is also sometimes called HLA tissue typing. Preimplantation HLA typing is a great solution for children requiring stem cell transplants. It is a common treatment used to treat blood diseases such as thalassemia, sickle cell anaemia, and malignant diseases such as leukaemia and lymphoma. [1]

PTT or PGD-HLA was first introduced clinically in 2001 to treat Fanconi Anaemia (FA), a rare but serious genetic disorder that mainly affects the bone marrow. [2] For conditions such as Fanconi anemia, the only treatment option is bone marrow transplantation, which will restore hematopoiesis. Due to the high rate of transplant-related mortality, using HLA identical cord blood transplantation is increasingly attractive. It will help avoid complications and produce a better outcome. PTT provides realistic hope as a radical treatment option for those suffering from congenital and acquired bone marrow failures. FA is the first disorder in which cord blood stem cell transplantation has been performed.

The Procedure

By selecting embryos for the new sibling, we can ensure that the new sibling can provide an exactly matched tissue donation to the child suffering from the life-limiting disease, and hence act as a saviour. Apart from serving as a donor of pluripotent haematopoietic stem cells, the new sibling will also be screened for the same disease through preimplantation genetic diagnosis.

Preimplantation genetic diagnosis (PGD) is used when either one or both parents carry a known genetic mutation and seek to transfer a non-affected embryo. [3] It involves the analysis of artificially fertilised embryos in order to find one with the desired genotype. [4] Preimplantation genetic testing for monogenic disorders (PGT-M) combines both in vitro fertilisation (IVF) in conjunction with PTT.

PGT-M is a standard biopsy procedure performed on cells from a blastocyst embryo. It will also determine whether the embryo has the same inherited genetic mutation that has caused the life-limiting disease in the older child. It is done by testing for the single gene mutation associated with the disease.

The first step would be to create an embryo through IVF treatment. IVF involves the following steps: ovarian stimulation, oocyte retrieval, sperm retrieval, and fertilisation. During IVF, the egg retrieved from the uterus will be fertilised with sperm in a laboratory to produce a zygote. After IVF, the embryo biopsy will be prepared by removing a small number of trophectoderm cells (layer of cells on the outer edge of the blastocyst). While testing occurs for any abnormalities, the embryos will be frozen and preserved for implantation.

Once you find out the results of the biopsied cells, you can then select an embryo free from the same life-limiting genetic disease and simultaneously also a tissue match. This is vital so that the umbilical cord blood of the new sibling can provide stem cells to treat the existing sibling who has the disease.

These unaffected embryos will then be assessed for their HLA compatibility with the sick sibling to find a tissue match. Then, the unaffected and tissue-matched embryo will be ready to be transferred to the woman’s uterus. Once the new sibling has been born as a viable donor, the umbilical cord blood will be taken and used for hematopoietic stem cell transplantation. Umbilical cord blood is a great source of hematopoietic stem cells(HSCs) and has a higher concentration of HSCs than adult blood. These multipotent HSCs will then be used to treat the existing sibling.

Should it be used? Ethical considerations, benefits, and risks

PGT-M is a technically demanding procedure and involves the use of highly specialized molecular biology techniques. [5] Many arguments favouring and condemning PTT are based on the welfare and commodification of the donor sibling. [6]

Many who are against PGD may view it as selective breeding and “reproductive discrimination.” However, it is important to note that PGT-M currently cannot be used to select embryos for ‘designer babies’ as we are still not capable of scientifically determining certain characteristics. It is only used to test for a single genetic mutation.

Another common protest is that the donor baby may not be born for the right reasons and is used as a “medical commodity.” It’s vital to consider the reasons and intention of the parents to have another child. For some, this new baby may not act as a burden as they genuinely wish to have more children. But for others, the same cannot always be said as it’s difficult to gauge the parent’s true motives.

It is also reasonable to question whether individuals should be able to select an embryo simply on the basis that the child born may be the source of life-saving therapies for a sibling.

PGT-M also can be considered ethically problematic, considering affected embryos will be discarded. For some, this is not an issue as they are discarded at a very early stage of development and aren’t as severe as terminating a pregnancy at a later stage. PGD provides the advantage that difficult decisions to terminate a fetus are removed since only tissue-matched embryos will be implanted in the mother’s uterus.

Aside from ethics, we need to also consider the practicalities and other effects of the procedure. Down the line, it can potentially cause psychological effects on the saviour sibling as it may have only come into existence to save their older sibling. Furthermore, there can also be an emotional impact on other family members, along with risks imposed on the mother during the ART (Assisted reproductive technology) cycle. [7]

We also need to consider to what extent the saviour sibling is really “saving” their older sibling. Are cells being removed from the umbilical cord and blood, or is bone marrow or an organ being taken? It’s obvious that removing an organ would cause much more damage to the donor sibling, showing that the spectrum the treatment can cover poses its own issues as to whether it can qualify as ethical. Moreover, it opens up the question of how far we will go with this technology. Because it is reassuring that there are existing strict policies and regulatory frameworks for most genetic biotechnology groups, it is unlikely the technology will be misused, and harm to the donor sibling will be minimised.

Lastly, it is also expensive. The procedure itself is costly and can present another limitation, especially if more than one treatment cycle is necessary before a match and the unaffected embryo is found and pregnancy is achieved.

On the other hand, you could also argue that the care and treatment for a disease long-term are costly, and the procedure may end up being less expensive overall, provided that the treatment works. Not only this, but the child will be free of the disease and won’t suffer anymore.

In summary, PGT-M is highly valued when it succeeds despite its complexities and has been described as “a triumph for common sense.” [4]


PGT-M is an evolving technology, which means there are still more improvements that can be made. This ranges from the current protocols in place to databases containing more thorough information on the outcome of the procedure.

At the moment, we are also facing both technical and biological limitations to the PGD-HLA procedure’s success. These include the limited outcome of finding a suitable embryo and the low rates of live births after using IVF and ART. [7] However, we can improve such limitations by rectifying the issues behind this low IVF success rate (e.g., obtaining better-quality oocytes for biopsy and PGD).

Overall, PTT offers the opportunity to save a life and is something which I believe can be an amazing tool, provided there are no indications for it to cause harm to all members involved and that it is used for the right intentions. Personally, if I grew up knowing I’d saved a life, especially my sibling’s, I would be overjoyed the minute I was born!

Asmita Anand Youth Medical Journal 2021


[1] Preimplantation Tissue Typing. (2019, February 16). IAKENTRO.

[2] Verlinsky, Y. (2001). Preimplantation Diagnosis for Fanconi Anemia Combined With HLA Matching. JAMA, 285(24), 3130.

[3] Preimplantation Genetic Diagnosis, What is PGD – Testing Services. (2016, May 3). Houston Fertility Institute.

[4] Boyle, R. J., & Savulescu, J. (2001). Ethics of using preimplantation genetic diagnosis to select a stem cell donor for an existing person. BMJ, 323(7323), 1240–1243.

[5] O. (2019, August 8). Pre-implantation Genetic Diagnosis (PGD) – ORH Fertility Clinic. Overlake Reproductive Health.

[6] Liu, C. K. (2007). ‘Saviour Siblings’? The Distinction between PGD with HLA Tissue Typing and Preimplantation HLA Tissue Typing. Journal of Bioethical Inquiry, 4(1), 65–70.

[7] Traeger-Synodinos, J., Kakourou, G., Destouni, A., & Kanavakis, E. (2013). Eleven years of preimplantation genetic diagnosis for human leukocyte antigen matching: is there room for improvement? Expert Review of Hematology, 6(3), 215–217.

Pre-implantation tissue typing (PTT) | Human Fertilisation and Embryology Authority. (n.d.). HFEA. Retrieved 7 August 2021, from

I. (2020a, November 25). Embryo Testing: The Difference Between PGT-A and PGT-M. IGENOMIX – With Science on Your Side.

Kuliev, A. (2014). Preimplantation HLA typing: Practical tool for stem cell transplantation treatment of congenital disorders. World Journal of Medical Genetics, 4(4), 105.

In vitro fertilization (IVF) – Mayo Clinic. (2019b, June 22). Mayoclinic.

Kuliev, A., & Rechitsky, S. (2016). Preimplantation HLA typing for stem cell transplantation treatment of congenital and acquired bone marrow failures. Hematology & Medical Oncology, 1(2).

A. (n.d.). Embryo HLA Typing. British Cyprus Fertility Hospital. Retrieved 7 August 2021, from

Health and Disease

Aducanumab (Aduhelm), a cure to the tragedy of Alzheimer’s Disease?

By Asmita Anand

Published 11:20 EST, Sun September 5, 2021


One of the most common types of dementia in the UK, Alzheimer’s disease (AD) is a physical disease that affects the brain.[1] It is estimated that in 2040 there will be over 1.5 million people with dementia in the UK at the current rate of prevalence.[2] Despite the alarmingly high figures, research is being undertaken to tackle this with 126 different agents currently being assessed to treat Alzheimer’s.[3] Recently, the FDA approved a new drug, aducanumab, for clinical use in Alzheimer’s patients after reviewing evidence on its effectiveness in slowing the progression of symptoms in people with early-stage AD.

What we know:

The effect of Alzheimer’s on the brain

In order to understand how aducanumab treats Alzheimer’s, we must understand the effect AD has on the brain. AD is a neurodegenerative disease. During Alzheimer’s, vital communication between neurons is disrupted as many neurons stop functioning, which results in cell death and leads to shrinking of the brain. This process is known as cerebral atrophy. AD disrupts important processes in neural networks such as communication, metabolism, and repair.[4] As these neurons die, a person suffering from AD will begin to lose the ability to think, remember, make decisions and function independently. This is due to pathological changes and damage to multiple brain structures such the cerebrum, cortex and hippocampus.

The exact cause of AD is still unknown. Many scientists believe that two proteins called ‘beta-amyloid’ and ‘tau’ play a huge role in the toxic changes that occur in the brain. Both of these proteins form the buildup of two abnormal pathologies. The first pathologies are plaques (composed of beta-amyloid) which build up slowly in the neurons and are found scattered between nerve cells. The second pathologies are neurofibrillary tangles formed inside cells which result from the accumulation of abnormal tau. But it is important to note that these are not the only factors which contribute to AD. Furthermore, it is due to the lack of universal acceptance of the amyloid hypothesis that aducanumab has been so heavily criticised, which is explored in further detail below. [5] [6]

What are the current treatment options for AD?

At the moment, treatment for AD revolves around helping patients maintain mental function, slow down progression of symptoms, and manage and ease behavioural symptoms. There are several pharmaceuticals available which can help manage symptoms of Alzheimer’s. Acetylcholinesterase inhibitors are the main drugs used to treat AD in the UK. These include donepezil, galantamine, and rivastigmine. These work by preventing the enzyme acetylcholinesterase from breaking down acetylcholine, a critical neurotransmitter. Levels of acetylcholine are very low in patients with AD due to nerve cell death. By preventing breakdown of this vital chemical, acetylcholine levels will increase, leading to reduction in some symptoms of AD. [7]

The last approved drug was memantine in 2004, which is an oral medication. Unlike the cholinesterase inhibitors which are considered ‘symptomatic’ treatment, memantine is considered a ‘neuroprotective’ drug as it may slow the underlying progression of AD. In AD, too much glutamate leaks out of damaged brain cells, and these high concentrations can result in over-excitation of nerve cells, which leads to cell death.[8] [9] Memantine protects the nerve cells by dampening the excitatory effect of the neurotransmitter glutamate. [10]

What is aducanumab (aduhelm)?

It is an antibody infusion targeting amyloid beta protein (Aß), a defining feature of the biology of AD.[11] Current drugs aim at suppressing cognitive symptoms whereas aducanumab is aiming to tackle the underlying cause of AD, which is to both stop and cure it. Aducanumab is aiming to do this by targeting amyloid, clumps researchers believe are responsible for brain cell death.

The antibody will preferentially bind to aggregated amyloid-beta. This will reduce the presence of amyloid plaques in hopes to slow AD progression.[12] These plaques are also responsible for the inability to perform simple tasks and memory loss.

Back in March 2015, an early-stage clinical trial provided evidence that aducanumab drastically reduced beta-amyloid plaques in the brain. However there were some flaws within this trial such as small testing groups but also the assumption that beta-amyloid oligomers decreased. The latest updates have found that the intermediate deposits, ‘beta-amyloid oligomers’ may be the real culprit and not the end state ‘beta-amyloid plaques’.[13] [14] Four years later and Biogen announced that the development of aducanumab will be discontinued. That is until a couple months later the announcement that the FDA would now be considering it for marketing approval.

The Problems:

The Controversy

The FDA granting accelerated approval is under much speculation. As mentioned earlier, the amyloid hypothesis has influenced a large proportion of Alzheimer’s disease research. The amyloid hypothesis is still doubted by many professionals with its more recent ‘failed’ drug trials adding further doubt.[15] The FDA’s ignorance towards data from the trial which showed no slowing in disease progression is alarming considering the “FDA’s own advisory committee last November voted 8 to 1 against approving the drug, citing “lack of strong evidence that the drug works.”[16] In fact, a member of the of the FDA’s expert panel for nervous system therapies has even gone as far to resign over the FDA ruling, STAT reported.[17]

Even if we were to ignore the lack of data proving any clinical benefits of aducanumab on declining disease progression, the question of whether there is a connection between plaque reduction and cognitive improvement still remains uncertain. Some believe beta-amyloid may not be the underlying cause of the disease at all and hence aducanumab may not be the answer.

Furthermore, we need to be realistic. Professor John Hardy of neuroscience at University College London, said: “We have to be clear that, at best, this is a drug with marginal benefit which will help only very carefully selected patients.” It is likely that aducanumab will be better for those with mild AD and cognitive impairment, as opposed to those with advanced AD.

It’s Future and the Challenges that lie ahead

The potential side effects are another reason to approach aducanumab treatment with caution. Patients undergoing aducanumab treatment will need continual monitoring due to its main side effect, amyloid-related imaging abnormalities (ARIA). ARIA-E refers to cerebral edema or brain swelling, whereas ARIA-H refers to cerebral microhemorrhages or micro bleeds in the brain.

While many have heavily criticised the approval, others are praising it with caution under the acknowledgement that it is far from a cure. The accelerated approval of aducanumab (as opposed to standard approval) is paving a new path for other treatments of neurodegenerative diseases. The ‘accelerated approval’ pathway is used for treatments that are “reasonably likely” but not certain to help patients. Furthermore, the revival of aducanumab is also bringing more interest towards research for treatments of neurodegenerative diseases. As Mario Carrillo, chief science officer at the nonprofit Alzheimer’s Association, has said: “History has shown us that approvals of the first drug in a new category invigorates [sic] the field”.

In order for us to ensure aducanumab could truly be the way forward for AD treatment, companies marketing the drug, Biogen and Eisai, should verify its clinical benefits with further study. While the amyloid hypothesis may be doubtful, there is no reason to give up in this direction of treatment yet.


Uncertainty still remains over aducanumab’s future impact; it is yet to be available in the UK and Europe. Nevertheless aducanumab is providing a spark of hope for our endless search for treatments of AD, as it is the first treatment in a very long time. With dementia research having been chronically underfunded in the UK, the need for new life-changing treatments is only increasing.

As it stands currently, aducanumab is not exactly a cure for Alzheimer’s and there are still many more obstacles we will have to overcome. However, it undoubtedly is a remarkable moment and marks a great milestone in dementia research.

Asmita Anand, Youth Medical Journal 2021


[1]Jackie, et al. “What Is the Difference between Dementia and Alzheimer’s Disease?” Alzheimer’s Society, 17 July 2018,

[2]“Alzheimer’s Society’s View on Demography.” Alzheimer’s Society, 2020,

[3]Cummings, Jeffrey, et al. “Alzheimer’s Disease Drug Development Pipeline: 2021.” Alzheimer’s & Dementia: Translational Research & Clinical Interventions, vol. 7, no. 1, 2021. Crossref, doi:10.1002/trc2.12179.

[4]“What Happens to the Brain in Alzheimer’s Disease?” National Institute on Aging, 2017,

[5]“How Alzheimer’s Changes the Brain.” YouTube, uploaded by National Institute On Aging, 23 Aug. 2017,

[6]Leonard, Wendy Mph. “Causes of Alzheimer’s Disease.” Healthline, 2 Sept. 2017,

[7]“How Do Drugs for Alzheimer’s Disease Work?” Alzheimer’s Society, Accessed 2 July 2021.

[8]“Alzheimers Drug Treatments | Royal College of Psychiatrists.” RC PSYCH ROYAL COLLEGE OF PSYCHIATRISTS, 2015,

[9]Liou, Stephanie. “About Glutamate Toxicity – HOPES Huntington’s Disease Information.” HOPES Huntington’s Disease Information, 18 Nov. 2014,

[10]Kernisan, Leslie Mph. “4 Medications FDA-Approved to Treat Alzheimer’s & Other Dementias: How They Work & FAQs.” Better Health While Aging, 19 June 2021,

[11]Jack, Clifford R., et al. “NIA-AA Research Framework: Toward a Biological Definition of Alzheimer’s Disease.” Alzheimer’s & Dementia, vol. 14, no. 4, 2018, pp. 535–62. Crossref, doi:10.1016/j.jalz.2018.02.018.

[12]Staff, Bns. “Aduhelm (Aducanumab).” Alzheimer’s News Today, 1 July 2021,

[13]Yu, Han. “We’ve Got the First Alzheimer’s Drug in Decades. But Is It a Breakthrough?” The Guardian, 2 July 2021,

[14]Sevigny, Jeff, et al. “The Antibody Aducanumab Reduces Aβ Plaques in Alzheimer’s Disease.” Nature, vol. 537, no. 7618, 2016, pp. 50–56. Crossref, doi:10.1038/nature19323.

[15]Sabbagh, Marwan Noel, and Jeffrey Cummings. “Open Peer Commentary to ‘Failure to Demonstrate Efficacy of Aducanumab: An Analysis of the EMERGE and ENGAGE Trials as Reported by Biogen December 2019.’” Alzheimer’s & Dementia, vol. 17, no. 4, 2020, pp. 702–03. Crossref, doi:10.1002/alz.12235.

[16]Doheny, Kathleen. “Controversial New Alzheimer’s Drug: What to Know.” WebMD, 9 June 2021,

[17]STAT. “Member of FDA’s Expert Panel Resigns over Alzheimer’s Therapy Approval.” STAT, 9 June 2021, First Edition&utm_medium=email&_hsmi=132618545&_hsenc=p2ANqtz-83Omcd8InGsFZ56X_VCnvMvUv0khIW5KtkCzv_xmhbJZHfTbrddSvG8vTBOry6QTzlKkA4sVxAEFsNru_nBzJj4xYUhw&utm_content=132618545&utm_source=hs_email.

“Amyloid-Related Imaging Abnormalities.” Wikipedia, 2021,

Servick, Kelly. “Alzheimer’s Drug Approved despite Doubts about Effectiveness.” Science, 2021. Crossref, doi:10.1126/science.abj8372.

Alexander, G. Caleb, et al. “Evaluation of Aducanumab for Alzheimer Disease.” JAMA, vol. 325, no. 17, 2021, p. 1717. Crossref, doi:10.1001/jama.2021.3854.

Schneider, Lon. “A Resurrection of Aducanumab for Alzheimer’s Disease.” The Lancet Neurology, vol. 19, no. 2, 2020, pp. 111–12. Crossref, doi:10.1016/s1474-4422(19)30480-6.


The Placenta: The Often Forgotten, Underrated Organ

By Asmita Anand

Published 4:20 PM EST, Sat June 26, 2021


Many take the role of the placenta for granted. Often discarded as ‘an afterthought of afterbirth’, it’s the only temporary organ with its role of nourishing and protecting the foetus restricted to that of human gestation. Despite its short lifespan, it plays a vital and significant part in the healthy development and growth of the foetus and to the maintenance of mankind.

In recent years, a lot of the attention surrounding placentas have tended to consist of the consumption of freeze dried placenta pills after celebrities have given birth. While some may argue it has nutritional value, a review on human placentophagy [1] discovered no evidence to support the claimed benefits and instead, a higher risk of ingestion of harmful pathogens.

In some cultures, placentas also play an important role in ancient traditions such as burial or placenta prints (art). Although we may have been unaware of the placenta’s vital functions back then, it was always considered more than just medical waste.

The Role Of The Placenta

The placenta plays a critical role during pregnancy, yet many are unaware of the importance of this organ which magically appears. Its role ranges from sustaining the foetus through substance exchange, foetal protection from pathogens and infections to metabolic transfer and hormone secretion.

The main functional units of the placenta are the finger-like chorionic villi, which increase the surface area for substance exchange. Nutrients (such as glucose, fatty acids and amino acids) from the mother are transferred via active transport across the placenta to the foetus through the umbilical cord. Oxygen passively diffuses across the placenta to the foetus, who’s foetal lungs aren’t taking part in gas exchange while in utero. The placenta will also remove waste products including carbon dioxide, water and urea between the maternal and foetal plasma.

The placenta also provides immune protection against infectious diseases to the foetus through the transfer of immunoglobulins from the mother. Lastly, the placenta is hugely responsible for the secretion of various hormones important for foetal growth and development, which prepare the foetus for life outside of the uterus. For example, it acquires the production of both oestrogen and progesterone from the corpus luteum and the first hormone it produces is hCG. [2]

Overall the placenta performs the functions of the lung, liver, gut, kidney and the endocrine system. To sum up, its multifunctionality is awesome and not appreciated enough.

The Formation Of The Placenta

The development of the placenta in pregnancy generally begins once the blastocyst has implanted in the uterine wall. Some cells from the blastocyst, known as the outer trophoblast cells, form the placenta while the others (inner cell mass) form the foetus. Hence the blastocysts consist of both these two distinct differentiated embryonic cell types (the outer trophoblast cells and the inner cell mass) . [3] The placenta is unique as it partly develops from both maternal tissue but also foetal tissue. This also means that the placenta is foreign to the mother’s system as it comprises a mix of both maternal and paternal DNA.

At the end of pregnancy the placenta will undergo several changes to decrease exchange between maternal and foetal circulatory systems. These include the increase of fibrous tissue in the core of the villus and the increase in thickness of foetal capillary basement membranes. [3]

Extraordinarily, the placenta is not rejected by the mother’s body as the trophoblasts do not trigger a maternal immune response. If maternal and foetal blood were to mix, then the mother’s immune system would inevitably kill the foetus. This is because the foetus may not have the same blood type as the mother and an immune system attack in the foetal blood supply can be caused by direct mixing of blood. The syncytiotrophoblast, the outermost layer of the placenta, facilitates the separation of the two bloodstreams.

How And Why Has It Evolved?

All living mammals except marsupials and monotremes are considered to be placental. [4] However mammals didn’t always have one and the placenta was only estimated to have evolved around 150 million to 200 million years ago.

Thus placentas have given mammals a slight advantage over other animal kingdoms by allowing them to supply their offspring with essential nutrients and oxygen vital for the development of the mammalian brain.

If it weren’t for some special viruses, humans may still be laying eggs. Evolutionary scientists have mapped the genomes of cells in the placenta and found that ‘syncytin’, a protein which allowed these cells to fuse into a wall, appeared to come from an ancient retrovirus. Unlike normal viruses, retroviruses are able to enter cells and insert copies of its RNA genome into the DNA of the host. This leads to a change in the genome of that cell. [5] The RNA is converted into DNA during infection allowing it to integrate into the chromosome of the cell. In the case of the placenta, the virus eventually created a viral protein which gave the ability for cells to fuse into a wall that we know now as the placenta. Over many generations this viral DNA must have been passed on until the entire population had evolved, turning it into a fully endogenous retrovirus. This has made retroviral infection a driver of placental mammal evolution. Ed Chuong describes this process ‘as a molecular domestication of an ancient retrovirus element’. Apart from the placenta, remnants of ancient viral infections found in our DNA are also adding more evidence that viral genes are assisting the evolution of new species. [6]

Challenges To Our Understanding Of The Placenta

There are multiple reasons as to why scientists do not know much about the human placenta. A problem that arises when trying to study the placenta is that it is not only logistically but also ethically difficult to study due to its strong link with foetal development. It is difficult to apply research since placentas differ between animals and humans as evidenced from animal studies as well. Since many of us lack this important organ (not being pregnant or a woman), it  accounts for a reason as to why it has been so understudied.

What Is The Future Of Placental Research?

Despite being understudied in the past, scientists are now striving to achieve a better understanding of the behaviour of the placenta and more information on the prevention, detection and treatment of pregnancy problems.

The gatekeeping role of the placenta facilitates its exchange of nutrients and waste between maternal and foetal circulatory systems. However we are yet to uncover the intricacies as to how the placenta is able to do this without triggering an immune response. As Y.W Loke wrote in “Life’s Vital Link”, “This ‘immunological paradox of pregnancy’ has preoccupied immunologists for well over half a century and still the solution remains tantalizingly beyond reach”. “This normally peaceful co-existence between placenta and mother throughout pregnancy is one of the most extraordinary phenomena in reproductive biology.” [7] There is hope that if we are able to understand how the placenta is able to resist rejection, it could lead to a better understanding of preventing organ rejection in transplant patients.

The placenta could also unlock better explanations of how cancer is able to evade the immune system, leading to the possibilities for new cancer treatments. This is due to the similarities between pregnancy and cancer, such as the rapid proliferation, invasion of the host and evasion of the immune system. [8] A study conducted at the Wellcome Sanger Institute [9] found that placental tissue had about five times as many mutations to a single DNA ‘letter’ to body cells which generally have a high rate of mutation. This opens up potential questions as to why the placental tissue is so mutated. Tim Coorens, who was part of the team who conducted the study, suggests its “disposability might provide a clue: as it only “lives” for nine months, it doesn’t need to invest precious resources into repairing itself”.

Furthermore, the placenta is important to our understanding of the health of babies. For example, the size of the placenta in relation to the baby’s birth weight can indicate foetal death risk. [10] There is also hope that by studying the placenta in real time physicians may be able to diagnose complications that arise from pregnancy, such as pre-eclampsia, which is when blood flow to the placenta is decreased.


It is no question that the placenta is critical to human life. Arguably it is one of the most important organs in the human body, impacting both the lifelong health of the mother and child. Fortunately, the Human Placenta Project is currently researching more into the placenta’s development and function through monitoring in real time, to uncover more information about both the least understood and studied organ. [11] As we continue to research more into this wonderfully unique organ, hopefully the “afterbirth” will no longer be an “afterthought.”

Asmita Anand, Youth Medical Journal 2021


[1] Farr, Alex et al. “Human placentophagy: a review.” American journal of obstetrics and gynecology vol. 218,4 (2018): 401.e1-401.e11. doi:10.1016/j.ajog.2017.08.016

[2] “Placental Structure, Function and Drug Transfer.” ScienceDirect, 1 Apr. 2015,

[3] “Placenta and Placental Development – Clinical Relevance.” TeachMePhysiology, 6 Mar. 2021,

[4] Britannica, The Editors of Encyclopaedia. “Placental mammal”. Encyclopedia Britannica, 19 Feb. 2021, Accessed 2 June 2021.

[5] Wikipedia contributors. “Retrovirus.” Wikipedia, 2021,

[6] Mitra, Avir. “How the Placenta Evolved from an Ancient Virus.” WHYY, 31 Jan. 2020,

[7] Loke, Y. Life’s Vital Link: The Astonishing Role of the Placenta. Illustrated, Oxford University Press, 2018.

[8] George, Alison. “The Cancer-Fighting Multi-Organ: 9 Ways the Placenta Is Amazing.” New Scientist, 1 Feb. 2021,

[9] Coorens, Tim. “Somatic Mutations Reveal Widespread Mosaicism and Mutagenesis in Human Placentas.” BioRxiv, 1 Jan. 2021,

[10] Stranden, Anne Lise. “Your placenta may reveal risk of getting preeclampsia.” sciencenorway, 25 Mar. 2020,

[11] “Human Placenta Project.” NICHD, Accessed 3 June 2021.

Fard, Maggie Fazeli. “Book Discusses the Most Underrated Organ, the Placenta.” Washington Post, 5 Aug. 2013,

Nelson, D Michael. “How the placenta affects your life, from womb to tomb.” American journal of obstetrics and gynecology vol. 213,4 Suppl (2015): S12-3. doi:10.1016/j.ajog.2015.08.015

Racaniello, Vincent. “Retroviruses Turned Egg-Layers into Live-Bearers.” Virology Blog, 14 Dec. 2017,

Biomedical Research Neuroscience

‘Patient H.M’ – An unsung hero: The forgotten man who forgot everything

By Asmita Anand

Published 4:40 PM EST, Sun May 23, 2021


In recent decades, scientists have made huge progress discovering how our identities, and memories are made and stored. A patient that transformed our understanding of the way  memory functions are organised in the human brain, is  referred to as ‘the man who couldn’t make memories’; Henry Molaison possessed one of the most famous brains worldwide and bestowed unique insights into the inner-workings of human brains.

Who Was He?

Figure 1: HM in 1953 before his surgery (

Henry Gustav Molaison, also known in medical literature as patient H.M. to protect his identity, was born on February 26, 1926 in Manchester, Connecticut.

As a child, he had a relatively normal childhood. Although it wasn’t long after a minor head injury and a family history of seizures (although the exact aetiology behind his seizures remains uncertain), that Molaison began suffering from severe epilepsy. At the age of 10, he started having absence seizures and 6 years later he developed generalised tonic-clonic seizures. His seizures greatly impacted his daily life and led him to drop out of high school. Later he was also unable to maintain his job and function independently. Molaison’s case was so severe that it couldn’t be treated pharmacologically with high doses of anticonvulsant medication.

After nearly 10 years he turned to Dr William Scoville, a renowned daredevil neurosurgeon of his time, with hope to lead a normal life once again. At the age of 27, his hippocampus was removed in an experimental procedure in an attempt to alleviate the impact his seizure had on the quality of his life. He underwent a ‘bilateral medial temporal lobectomy’, which surgically removed the medial temporal lobe on both sides of his brain. This included the hippocampal complex, parahippocampal gyrus, the uncus, the anterior temporal cortex, and the amygdala, according to Scoville’s own illustrations of his surgical technique. However in around 1992-199, MRI scans revealed that the surgery was less extensive than he thought, but enough to cause the damage it did. [1]

Figure 2: Diagram depicting HM’s brain after surgery compared to a normal human brain (

Although Dr Scoville hoped it would cure the epilepsy, he still wasn’t completely sure whether it would be successful or if there might be any long lasting side effects of this procedure. As a result, both of his thoughts were correct. Molaison’s seizures had stopped but unfortunately he was also left with long term memory loss, leaving him constantly living in the present tense. Later Scoville admitted that the operation was a tragic mistake and has spoken strenuously about the dangerous implications of bilateral mesial temporal lobe surgery.

Different types of Amnesia

There are multiple types of amnesia, such as Retrograde, Anterograde, Transient global and Infantile amnesia. Retrograde amnesia is when someone is unable to recall events that occurred before the development of the amnesia and is commonly used in films and media. [2] Whereas anterograde amnesia refers to a decreased ability to retain new information and is typically caused by brain trauma. [3]

Molaison developed a peculiar form of amnesia and suffered from both partial retrograde amnesia and anterograde amnesia. The latter meant he lost the ability to form new memories, such as the inability to remember what he had eaten for lunch that day, tests that he just done minutes before and names he had just been introduced to. Scoville wrote: “After operation this young man could no longer recognise the hospital staff nor find his way to the bathroom, and he seemed to recall nothing of the day to day events of his hospital life. There was also a partial retrograde amnesia.” [4] This meant that while he could recall memories from his childhood, he was unable to remember almost 11 years of events prior to the operation. 

However, both his personality, intellectual abilities and perception remained unaffected and his IQ increased from 104 to 117. [5] Molaison still had the ability to form non-declarative memories, allowing him to still acquire and develop motor skills, which led to Brenda Milner’s discovery of the distinction between procedural and declarative memories. While his mind became like a sieve, through other testing performed by Milner she discovered that he still possessed short term memory. This led to the notion that this too existed in a separate brain structure to the one he lacked.

Short Term and Long Term Memory

Molaison’s misfortune ended up as a milestone in our understanding of the brain as up until it occurred memory wasn’t thought to be localised in one area of the brain. Dr Scoville and Brenda Milner were the first to make observations and report his case in 1957 in the “Loss of recent memory after bilateral hippocampal lesions”. Since he had difficulty remembering doing the tests in the day, Molaison never grew tired of the numerous experiments he partook in.

It is thanks to Molaison, that today we know that intricate functions are directly connected to distinct regions of the brain. The hippocampus, which is embedded deep into the temporal lobe, plays an important role in forming, retaining, and recalling declarative memories and spatial relationships. It’s also where short-term memories are turned into long-term memories.

Five decades later, referred to as Patient H.M., Molaison’s case grew in popularity due to the publication, which has thoroughly been cited numerous times. Researchers arrived at the conclusion that short term memory was not connected in any way to the medial temporal lobe structures. A particular researcher out of the 100 who studied him, Suzanne Corkin, spent the most time with Molaison interviewing him and working with him for 46 years. In her book “Permanent Present Tense: The man with no memory, and what he taught the world”, Dr Corkin covers how Molaison’s mind was used to understand how our minds and memory work. It also covers his early life and key childhood memories from their personal conversations or careful reporting and research. She wrote about how she went from viewing him as a “subject” to seeing him as a human being. Molaison’s life was not easy as he often struggled at times. After a while he came to understand that while others could retrieve and store memories, he could not. Nevertheless, he remained positive, coping well with his difficult situation and he acts as a true inspiration for his extreme resilience. H.M. once poignantly remarked that “every day is alone in itself. Whatever enjoyment I’ve had, and whatever sorrow I’ve had”. [6] 

His Legacy

Figure 3: Photography by Spencer Lowell (

Sadly Henry Molaison passed away at the age of 82 due to respiratory failure. Despite his death in 2008, his brain still continues to excite and offer further investigation into memory as there is still much to uncover. Mr Molaison was much, much more than a research specimen but a person who despite facing grave misfortune, still managed to show ‘the world you could be saddled with a tremendous handicap and still make an enormous contribution to life.’ [7] Columbia pictures and Scott Rudin have even acquired rights to develop a film based on his life.

As Dr Corkin described as “a beautiful finale to his enduring contributions”, his frozen brain was cut into 2,401 slices postmortem, which have been photographed and digitised into a high-resolution, 3D model for further anatomical analysis, in which we can even view individual neurons!

Molaison once commented: “It’s a funny thing – you just live and learn. I’m living and you’re learning.” Henry Molaison leaves behind a legacy (quite literally through the preservation of his brain!) which shall be remembered by us all and stay within our own memories. His forgetfulness has revolutionized our understanding of the brain, which we can still learn so much from till this date.

To end, as Dr Corkin said “Henry’s disability, a tremendous cost to him and his family, became science’s gain”.

Asmita Anand, Youth Medical Journal 2021 


[1] Annese, J. (2014, January 28). Postmortem examination of patient H.M.’s brain based on histological sectioning and digital 3D reconstruction. Nature Communications.

[2] I. (2020, November 25). Retrograde Amnesia | Symptoms, Causes, Illness & Condition. The Human Memory. amnesia is a form,that occur after the onset

[3] Cherney, K. (2018, September 18). Anterograde Amnesia. Healthline. amnesia refers to a,is a subset of amnesia.

[4] Lichterman, B. (2009, March 17). Henry Molaison. The BMJ.

[5] Scoville, W. B., & Milner, B. (1957, February). Loss of recent memory after bilateral hippocampal lesions. NCBI.

[6] Loring, D. W., & Hermann, B. (2017, June). Remembering H.M.: Review of “PATIENT H.M.: A Story of Memory, Madness, and Family Secrets”. Archives of Clinical Neuropsychology.

[7] Adams, T. (2018, March 22). Henry Molaison: the amnesiac we’ll never forget. The Guardian.

Halber, D. (n.d.). The Curious Case of Patient H.M. Brainfacts.

Gholipour, B. (2014, January 28). Famous Amnesia Patient’s Brain Cut into 2,401 Slices. Livescience.Com.

Shah, B. (2014b, July 1). The study of patient henry Molaison and what it taught us over past 50 years: Contributions to neuroscience Shah B, Pattanayak RD, Sagar R – J Mental Health Hum Behav. Journal of Mental Health and Human Behaviour.;year=2014;volume=19;issue=2;spage=91;epage=93;aulast=Shah

Hodges, J. R. (2013, November 23). Memories are made of this. Oxford Academic.

Shapin, S. (2017, June 19). The Man Who Forgot Everything. The New Yorker.

Billington, A. (n.d.). Scott Rudin Developing Feature Film About Henry Molaison. FirstShowing.Net. a cue from The,in medical circles as H.M.

Biomedical Research

The Race for the Covid-19 Vaccine

By Asmita Anand

Published 7:40 PM EST, Mon April 19, 2021


Ten authorised vaccines. Fifty-eight vaccine candidates still in development. All with the same aim. But just one is needed to stamp out this terrible pandemic.

Around April last year, while most of the world seemed to be shocked with horror by the effects of the pandemic, the race for the Covid-19 vaccine began as scientists hoped to provide immunity to this terrible disease and pulled out their magic card: vaccines.

The Vaccine War

A vaccine has the aim of reducing the severity of disease, making it one of the only magic cards we can currently pull out in an attempt to reduce the increasing mortality rate caused by SARS Covid-19. With the pandemic greatly impacting economies around the world, the vaccine is their ticket out of economic damage, making it the new golden ticket to success.

At the moment there are numerous proprietary vaccine candidates each competing, or have competed, for marketing authorization. The hunt for the vaccine has sparked the interest of both researchers and universities, with some even trialling new technologies that haven’t yet been licensed in a vaccine before. On the surface it seems that this geopolitical competition has pushed scientific discovery to a new level as we find ourselves at the crux of this situation with a huge variety of platforms being used, whether it be vector based, inactivated virus based or mRNA vaccines. Such diversity is welcome in academic research and competition has led to everyone coming up with their own ideas and providing many alternatives giving us a hand of cards from the joker to the king to even an ace, useful for potential variants of the virus.

Therefore, our best shot at tackling the pandemic seems to be the winner of this ‘rat race’. Sigh, this cannot be the best approach.

If we continue in this way, the ‘winner’ will be determined from the amount of financial or industrial help a candidate may have compared to its effectiveness. Furthermore, we’re also likely to use the one which achieves regulatory approval rather than its safety and suitability to public health. Trial protocols are being set up to produce success instead of the aim to prove it protects against the disease and death in hospitalisation.

For example, the FDA is willing to fast-track the roll-out of vaccines while both China and Russia have approved vaccines without waiting for the results of Phase 3 trials. [1] This rushed process could have serious risks and it exemplifies how scientific integrity is being undermined by hyper- competition. Even worse, Russia, Iran and China have even been accused of pandemic brinkmanship and allegedly hacked vaccine research. [2] Everyone wants to make this breakthrough and everyone wants to deal their own magic card.

It seems clear that while the element of competition is providing a fierce environment, it is taking a negative toll on research output. Both commercial and political pressure is pushing for immediate vaccination-roll out. As each country creates their own version, it will be more difficult to make each one available worldwide regardless of their efficacy as they struggle to even vaccinate their own nation.

Most scientists have even anticipated that, like most other vaccines, COVID-19 vaccines will not be 100% effective. [3] This concern only further perpetuates the public’s hesitancy on getting a shot which has been developed over months rather than years with unreliable evidence of success.

So, what should we do instead?

Let us paint an utopian version of this situation. Imagine if we had one global team who had full access to every combination of tools they could need. Imagine if each company feed-backed their findings to help each other out. Imagine if we truly tried using a global effort to solve this global solution. Instead, we’ve constrained ourselves with no freedom to collaborate. For the interest of the public and stopping the disease, vaccines need to be a united effort and not for the reputation or privilege of a particular company or nation.

Generation of collective intelligence will be more efficient and effective to provide robust solutions, especially when trying to find a mechanism to fit in such a strict framework. Even the World Health Organisation has proposed a collaborative efficacy trial, with one of their core functions detailing the coordination of international efforts through global collaboration and cooperation. [4] This builds on the idea of learning from other developers’ mistakes in order to increase productivity and efficiency in manufacturing one of the only current magic tricks we have up our sleeve.


So please, let us end this ‘rat’ race for the benefit of humanity. To conclude, we have already dealt ourselves with the best variety of cards, but we need to now play our hand right in order to successfully stamp out this disease once and for all.

Asmita Anand, Youth Medical Journal 2021


[1] O’Brien, Sarah. “FDA Willing to Fast Track Coronavirus Vaccine before Phase Three Trials End.” CNBC, CNBC, 31 Aug. 2020, track-coronavirus-vaccine-before-phase-three-trials.html.

[2] Light, Felix. Pandemic Brinkmanship: the Geopolitics behind the Race for a Vaccine, 6 Aug. 2020, brinkmanship-geopolitics-behind-race-vaccine.

[3] “Coronavirus Disease (COVID-19): Vaccines.” World Health Organization, World Health Organization, vaccines.

[4] “Accelerating a Safe and Effective COVID-19 Vaccine.” World Health Organization, World Health Organization, 2019/global-research-on-novel-coronavirus-2019-ncov/accelerating-a-safe-and- effective-covid-19-vaccine. 

Health and Disease

Non-Communicable Diseases – A Global Epidemic

By Asmita Anand

Published 5:22 PM EST, Mon March 22, 2021


Unlike communicable diseases, non-communicable diseases haven’t seen a drop in figures in recent years. Known as ‘the product of economic development and globalisation of western lifestyle and diets’, they kill over 40 million people annually (70% of deaths worldwide)[1] and dominate mortality and morbidity in advanced countries. Today they affect people in every continent and from all cultures.

What Are Non-Communicable Diseases (NCDs) and How Are They Caused?  

NCDs can be known as chronic diseases and cannot be spread from person to person.They are usually caused by a combination of genetic vulnerabilities combined with physiological, lifestyle and environmental factors. For example, factors range from living in poverty or polluted surroundings to poor diet, tobacco and alcohol use.  

Figure 1 showing chronic disease risk factors for the four most common types of NCDs

NCDs include a variety of diseases ranging from 5 main groups: cancer, cardiovascular diseases (e.g. heart attacks or stroke), diabetes, chronic respiratory diseases (e.g. asthma) and mental disorders and other mental health conditions. Previously, mental health has been overlooked as a part of NCDs but recently UN member states expanded to a ‘five-by five approach’ to effectively tackle the prevention and control of NCDs [2]. Mental health’s integration along with these 4 common groups of NCDs is important as mental conditions often occur in conjunction with other physical NCDs and their risk factors often overlap. Another large misconception around NCDs is that they mainly affect the developed world, whilst diseases of poverty mainly affect the developing world. This sometimes leads to failure in regarding iit as a global health priority.

What Are The Risks of NCDs? 

Over-nutrition and excessive consumption of sugar, carbohydrates, fats and salts are becoming increasing health risks. These heightened risks are exacerbated by obesity and physical inactivity, which are increasingly apparent in younger age groups. Today these factors are being encouraged due to lifestyle and society changes. 

The prevalence of non-communicable diseases is increasing in richer countries. Unlike the popular belief of NCDs mostly afflicting the wealthy, the incidence of cancer is rising in poorer countries and expected to double by 2030. In 2016 around 70% of cancer deaths were in low to middle income countries [3]. However the incidence of cancer by age is still much greater in advanced countries than in LIDC’s and MIC’s. 

Global Impact

NCDs impact both the rich and poor causing a large burden of disease globally. 

As can be seen above in Figure 2, the majority of countries affected by NCDs, such as Africa and Eastern Europe, are all middle and lower income countries. This is especially true as the estimated percentage increase in cancer incidence by 2030, (compared to 2008) will be higher in  both low (82%) and lower-middle-income countries (70%) compared with the upper-middle (58%) and high-income countries (40%) [4]. Differentiating NCDs by just affluence or poverty isn’t particularly useful to understand the global pattern of disease but instead the result of economic development. Those of lower social and economic positions are more likely to die sooner from NCDs compared to those in higher positions, often resulting in driving these poorer members into more poverty. Reasons for this range from the negative effects of rapid globalisation and development in these poorer countries which often result in undeveloped infrastructure and resources to protect members from NCDs and to prevent engagement in behavioural risk factors for NCDs.

Why Is There An Increase In NCDs? 

An increase in NCDs is likely due to the ongoing shift in global lifestyles. This is especially occurring in developing countries, hence forming the global pattern above. A number of factors support the growth of NCDs, including: 

  • Population ageing 
  • Increase in consumption of sugar, carbohydrate and fat (unhealthy diets), which can lead to both raised cholesterol and blood pressure.
  • Global marketing which encourages unhealthy eating habits (Smoking, alcohol, junk food) targeted at children, adolescents and women in developing countries. These habits then stay with them their entire life and will get passed to the next generation.
  • Growing urbanisation that has an impact on people’s lifestyle (e.g. poor diet and insufficient physical activity leading to obesity, rising levels of air pollutants). 
  • In developing countries, governments tend to make less restrictions (e.g. on smoke-free laws, pollution control, education on diet/alcohol use, urban planning to encourage physical activity).  People in developing countries are more likely to have low life expectancies due to the harsh conditions they live in resulting in higher incidence of disease & illness compared to rich developed economies. 

The Link to Environmental Risks 

NCDs and environmental factors are intrinsically linked, hence climate change and NCDs share the similar goal to reduce emissions that is the cause of air pollution and global warming. Steps to control emissions across energy production, transport systems and food systems will produce benefits for both health and the environment. 

In Figure 2, we can see that in 2016 the second largest risk factor was air pollution after tobacco smoking. Depending on the population and other factors, in places such as Southeast Asia, air pollution would be one of the biggest causes of NCDs. 

Figure 3, Graph depicting selected risk factors by disease group, 2016.

More than 40% of people, mainly in low and middle income countries, are cooking with inefficient technology and fuel combinations leading to the accumulation of harmful smoke in their homes. Evidence is emerging that this has caused an increase in NCDs that includes 24% of cases of stroke, 25% of ischaemic heart disease, 28% of lung cancer, and 43% of chronic obstructive respiratory disease [5].

Neurological and mental disorders can also be associated with chemicals and around 1.3 million deaths from NCDs were caused by risks related to chemicals in 2016. To stop this form occurring, safer use of chemicals and more health measures are being carried out. Apart from health benefits, combating air pollution could also reduce climate change.  

Focused Research on Diabetes 

At the moment, 422 million people have diabetes worldwide and it is becoming a major issue [6].

This figure can be translated to 1 in 11. With the rise of diabetes cases, Technavio analysts have predicted that in 2019 to 2023, the global blood glucose test strips market will grow at a CAGR of over 6%.  Around 39% of this growth will be Americans alone and such a high surge means a lot more money will be spent in this area too. In the UK an estimated £14 billion pounds is spent a year on treating diabetes and its complications [7]. This equates to over £25,000 being spent on diabetes every minute.

One reason for an increase in these figures could be again due to the shifting lifestyles the world is facing.  Obesity rates are one of the main drivers behind the rise of type 2 diabetes. Equally it is also entirely possible that the increasing prevalence of type 2 diabetes is due to earlier and better detection strategies as the symptoms can be hard to spot. 

Many are unaware of the real cause behind a disease such as type 2 diabetes. It is a popular myth that sugar triggers diabetes, as many assume the increased blood sugar levels in diabetic patients must be its root cause. 

It is in fact not caused by a high carbohydrate diet or sugar but a diet that builds up the amount of fat in the blood. An accumulation of microscopic fat particles within muscle and liver cells leads to glucose being unable to reach where it needs to in the cells despite the efforts of insulin. As a result the pancreas produces extra insulin and glucose builds up in the bloodstream, hence increased blood glucose levels. The combination of insulin resistance and pancreatic cell failure leads to type 2 diabetes, making fat the real culprit. In order to decrease insulin resistance, fat intake needs to be decreased. However one should note a diet high in sugar will also lead to many other serious medical conditions if not contributing to the root cause of diabetes. Furthermore a study by HSPH researchers has found a strong association between both processed and unprocessed red meat and an increased risk of diabetes [8]. This reaffirms the idea that a diet avoiding meat, dairy products and overall fatty foods is a much better precaution to developing type 2 diabetes. 

Case Study on Type 2 Diabetes in Sri Lanka

A case study in Sri Lanka has provided the evidence that Type 2 Diabetes is linked mainly to diet, smoking and a poor & inactive lifestyle. Around 25% are suffering from diabetic or pre-diabetic symptoms, and this could double by 2050 [9]. There has also been a rise in BMI in children between the ages of 10-14 and a high number of risk factors are present within the young urban population. In countries like Sri Lanka, there has been a rapid growth of type 2 diabetes. 

This can be attributed to a number of reasons: 

  • Urbanization is increasing up to 59% and influences sedentary lifestyles [9].
  • Diets in Sri Lanka are carbohydrate heavy as rice and curry is a staple meal. This is eaten 3 times a day but is not a problem for agricultural workers as much as it is for office workers, who will have a higher sugar intake. 
  • Many marketing campaigns encourage the use of alcohol and tobacco as currently 29.4% men and 0.1% women smoke [10].
  • Around 68% of people work in industry and services and most use cars and public transport opposed to walking or cycling to travel to work [9].
  • Exercise has not been a priority as many adults work long hours and so have little time for physical activity. Children also follow their parents path as new generations live in a world full of technology coupled with Sri Lanka’s ‘tuition culture’, leaving them with little free time for exercise as well.
  • Another important factor contributing to the onset of diabetes is stress. Sri Lanka experienced a long civil war which led to stress and fear. A Swedish study found that chronic stress for 1-5 years was associated with a 45% increase in risk of both type 1 and 2 diabetes [11]. In response to stress, the body releases hormones which can upset the body’s glucose balance.  

Figure 4 showing the distribution of diabetes in Sri Lanka

What Is Being Done in Sri Lanka to Combat Diabetes?

There is an increased media coverage raising awareness for diabetes as the government is focusing more of their attention on health issues. There has been development of fitness facilities (such as new jogging tracks), more education and public awareness (such as lectures, workshops, screening and treatment centers) and research into diabetes. The Diabetes Association of Sri Lanka has set-up walk-in screening centers in Colombo that people can attend at a modest cost. They have also collaborated with a research team from Kings College London on an intensive screening, education and monitoring program which has identified young people at risk from developing diabetes. As of 2016, they had managed to lower the risk of people developing Type 2 diabetes by 26% in the previous 5 years. A developing economy like Sri Lanka is finding it challenging to afford the cost of treatment that is rising by 25 US$ each year.

They have also found out in a study last year (i.e. 2020) that there is a genetic overlap between type 2 diabetes and depression for female participants [12].

To help lower the risk, prevention is key as attitudes to diet and exercise need to change, which includes the control of sugar, fat and salt. 

What Is the UK Doing to Combat NCDs?

In the UK itself, NCDs account for around 89% of all adult deaths(2016) [13]. The UK is using systems at both local and national levels to try and prevent and intervene early in NCDs. The national government mainly monitors population behaviors and health indicators with a responsibility to enact policies that will optimize the health of their citizens. In 2012, public healthy responsibilities were deferred to local authorities. Local governments are able to work with the community, respond to local needs and also create settings that support healthier lifestyle behaviors. Examples include the NHS health check and National Child Measurement Programme. Both play a key role in preventing NCD, as even local nutrition prompts in a school or leisure centre could make the difference. 

There are many studies and research being done to tackle the epidemic of NCDs as actions such as early immunisations to help lower the risks. Screening programmes and social marketing campaigns such as Change4Life are also making a change. These are run by Public Health England (PHE), who are working with the NHS, to solve this issue nationally and globally. 


Overall, by reducing the four main behavioural risk factors (tobacco use, physical inactivity, harmful use of alcohol and poor diet), a large proportion of NCDs could be prevented. In order to end the huge toll they take in forms of human suffering and the damage they cause to economic human development, serious action is needed on a global, national and even a personal scale to end this horrible epidemic. 

Asmita Anand, Youth Medical Journal 2021


[1]“C3 Collaborating for Health | What Are Non-Communicable Diseases (NCDs)?” C3 Collaborating for Health, 17 May 2018,,for%2070%25%20of%20deaths%20worldwide.

[2]Stein, Dan. “Integrating Mental Health with Other Non-Communicable Diseases.” The BMJ, 28 Jan. 2019,

[3]“The Global Cancer Burden | American Cancer Society.” The Global Cancer Burden,,in%20cancer%20incidence%20by%202030.

[4]Page 13,World Health Organization. “Global Status Report on Noncommunicable Diseases 2010.” World Health Organization, 5 Oct. 2015,

[5]Prüss-Ustün, Annette. “Environmental Risks and Non-Communicable Diseases.” The BMJ, 28 Jan. 2019,

[6]“Diabetes” World Health Organization, 13 May 2019,

[7]Editor. “Cost of Diabetes.” Diabetes, 11 Mar. 2020,

[8]“Red Meat Linked to Increased Risk of Type 2 Diabetes.” News, 13 Jan. 2014,

[9]Curriculum Press. “A Tsunami of Non-Communicable Diseases?” Curriculum Press, 5 Apr. 2019,

[10]Tobacco Tactics. “Sri Lanka- Country Profile.” TobaccoTactics, 5 Jan. 2021,

[11] A. Perceived stress and incidence of type 2 diabetes: a 35-year follow-up study of middle-aged Swedish men.

[12]Kan, Carol. “Genetic Overlap Between Type 2 Diabetes and Depression in a Sri Lankan Population Twin Sample.” PubMed, 2020,

[13]“Noncommunicable Diseases Country Profiles 2018.” World Health Organization, 24 Sept. 2018,

Figure 1 – “Chronic Diseases Fact Sheet.” GACD,

Figure 2 and 4 – Fenton, Kevin. “Tackling the Epidemic of Non-Communicable Diseases.” Public Health Matters, 27 Feb. 2014,

Figure 3 – “Environmental Risks and Non-Communicable Diseases.” The BMJ, 28 Jan. 2019,


NCD – Non-Communicable Disease

LIDC – Low Income Developing Countries

MIC – Middle Income Developing Countries


What Makes a Good Doctor? The Balancing Act Between IQ and EQ


Many would argue that medicine is a prestigious career. A doctor is expected to treat, improve and save patient lives. But does this cookie-cutter definition really describe a “good” doctor? 

There is no doubt that the medical profession is not for the faint-hearted. So, what sets apart this profession, and what differentiates the ‘good’ doctor from the “bad”? In this essay, I am hoping to explore this rather complex, intriguing question and analyze whether this perceived notion of a doctor, in reality, is ‘good’.

Medicine is an intellectually demanding career. After years of hard work at medical school, doctors are expected to apply their skills to patients with conditions of varying complexities. A doctor at times may not have a clear and immediate solution as exemplified by Covid-19. 

The key here is the problem-solving aptitude, ability to cope with difficult & demanding situations by being resilient and empathetic to patient wellbeing. The Intelligence Quotient (IQ) that measures academic or cognitive intelligence may be too narrow to cover all the skills required, individuals with a high Emotional Quotient (EQ) may achieve higher success. EQ refers to the person’s ability to perceive, control, evaluate, and express emotions.1 Evidence is emerging that EQ is as important for patient outcomes as it is for business and relationship success.2 

Therefore, the perfect concoction of qualities of a good doctor is formulated by IQ and EQ – the Intelligence and Emotional Quotients. 

So how does EQ contribute? 

Emotional intelligence can best be described as the ability to monitor one’s own and other people’s emotions, to discriminate between different emotions and label them appropriately, and to use emotional information to guide thinking and behaviour.3 

In fact, in the UK much of this is evaluated as early as the application to medical school. Physicians work in both emotionally demanding and highly complex environments. A Loyola Medicine study4 demonstrates that an educational curriculum for physicians in training improves their emotional intelligence, which may help protect against burnout.

Key competencies of a good doctor: 

Communication and Social Skills 

Doctors need to first communicate to understand their patient’s issues and then effectively explain the diagnosis, using clear, simple language emptied of medical jargon. Physicians with high EQ have the ability to recognize, relate and influence a patient’s emotions to make them feel empowered and hopeful. 

Relationships and Caring 

It’s important to not view patients as a list of medical problems but as opportunities to build confidence and trust between patient and doctor. When patients are cared for and listened to, they are more likely to comply with medical recommendations and return for follow-up visits, leading to strong relationships and positive interactions with clinicians and health care administrators. 

Self-Awareness and Self-Regulation 

EQ can help prevent emotions affecting clinical decisions. This self-awareness can be critical in ensuring each patient is treated with respect & dignity and is provided the highest quality care, thereby covering two of the six core NHS values.5 

Leadership and Teamwork – To be a physician is to lead6

In addition to clinical responsibilities, physicians serve as leaders and advocates and medicine involves leadership responsibilities at various levels i.e. individual, community, and societal levels. 

EQ accounts for 67% of the abilities needed for leaders and mattered twice as much as IQ. 7 Besides leadership, teamwork is essential for best patient outcomes and high EQ individuals create better connected and motivated teams. A lack of EQ, a source of failure as a leader, results in being overly defensive, resolving conflict poorly, and not connecting well with your team.8 

Despite the unfocused attention towards leadership, it can make an important difference in better clinical outcomes, experiences, increased empathy, and financial sustainability; not only this, but it also affects physician well-being. EQ and higher levels of leadership can help make physicians more resilient to the stresses of professional burnout and result in greater professional satisfaction. Overall, higher EQ increases both influence and change and helps physicians become the type of leader that others want to follow.

Conclusion: What is important – EQ or IQ? 

Let us picture it: High IQ but can’t get along with others? Or high EQ but unable to make the correct diagnosis? Without the other, achieving success would be a huge struggle. 

Instead of focusing on one aspect of intelligence, the greatest benefit may lie in learning to improve the less dominant one.

A successful doctor cannot have one but not the other. Instead of focusing on one aspect of intelligence, the greatest benefit will come from striving to learn the one lacking. 

Doctors with EQ besides IQ demonstrate greater influence, deliver positive results and create leaders. In the future, new technologies based on Artificial Intelligence and surgical robots will enhance technical expertise, but not the ability to emulate emotions, making EQ more valuable than ever. 

EQ can also be enhanced9 and IQ can be increased10, so what does this mean? 

Multiple aspects of intelligence are all essential to the growth in the field of medicine. The perfect balance of the qualities which lie in both is what makes not only ‘good’, but a ‘great’ doctor. 

Asmita Anand, Youth Medical Journal 2021



7Goleman, D. (1998). Working With Emotional Intelligence. New York, NY. Bantum Books