Daily Archives: February 7, 2020

Twins in School: Why We Should Rethink Classroom Placement

Twins posing for a picture on a railing.

Twins posing for a picture on a railing.

If you take a look at a typical US elementary classroom, chances are at least one of the students is a twin. In a society where women are giving birth later in life and have access to fertility treatments, twins and triplets are being born at higher and higher rates. 

Our educational system, however, has failed to address that the needs of multiples must be considered carefully. Twins have a unique bond that must be considered when children start school. When a student enters kindergarten, they are facing a drastic change in their life, and having a twin adds another aspect to that. In some cases, separation may be traumatizing, while in others separation would create a better learning environment.

Schools have failed to evaluate twin classroom placement since the modernization of western society’s educational system. According to Professor Jan Lacina of Texas Christian University, the basis forming many policies about twin classroom placement is research that was later discredited. Helen Koch performed a study following the development of twins by measuring their IQ, but she failed to do a blood test to determine if twins were monozygotic (identical) or dizygotic (fraternal)While this may seem insignificant, there is often a much stronger bond between identical twins than between fraternal twins.

Koch’s research is still the basis for many school policies regarding twins, while little new research is being conducted. New studies are key to determining what is truly best for twins in school, but often times schools are simply sticking with their outdated policies. However rare these new studies may be, they provide new insight into an often ignored subject.

A study published in Twin Research assessed 1116 pairs of twins in England and Wales to determine if separation caused issues. Both identical and fraternal twins were assessed by teachers for symptoms of ADHD and assessed with the Child Behavior Checklist Teacher Report Form, the Revised Rutter Scale for School-Age Children and the Strengths and Difficulties Questionnaire, an IQ test, and the Test Of Word Reading Efficiency. Both identical and fraternal twins were impacted by forced separation, but identical twins faced the greatest problems. Identical twins scored higher levels of withdrawal, depression, and anxiety when separated.

Another study tracking the development of twins in school was published in Twin Research and Human Genetics. Researchers studied 1505 children in the U.S., Australia, Norway, and Sweden – all of whom were either a twin or triplet – and tracked their reading levels through kindergarten, first grade, and second grade. The researchers found the difference in literacy between separated and non-separated sets to be very insignificant, especially after controlling for pre-kindergarten literacy ability. However, the lack of academic difference does not mean we can dismiss the emotional impact classroom placement can have.

Often when someone thinks of problems in school, they think of reading difficulty, poor understanding of math, or any other academic issue. However, emotions and well-being can impact a student’s mental health, as well as academic performance. Mental health and academic performance go hand-in-hand, so we cannot disregard potential issues simply because a student continues to perform well in class.

By taking a look into current research, Lynn Melby Gordon was able to see the drastic differences in what principals see as best for twins compared to kindergarten teachers, parents of twins, and twins themselves. The most often stated reason for separating twins is to allow for individual development, while the most often stated reason for keeping twins together is to keep children feeling unafraid in the new environment of kindergarten. Only 5% of parents surveyed agree that there should be a policy for every set of twins, especially as they develop. Earlier on in school, twins are more likely to want to remain with their twin than in later grades.

This difference in beliefs, especially between principles and twins, show just how difficult it can be to view something from a different perspective. Principles hold power in schools that twins don’t even have a fraction of, meaning they often believe they know what is best for every student. In order to remedy this issue, a conversation must be started with leaders in schools to emphasize the importance of evaluating every student as an individual.

Though some sets of twins are afraid of being apart from each other, others can become very competitive and want a break from each other. In Gordon’s article, some twins wanted separation to be independent, to develop one’s own identity, and simply to just get some time apart from each other.

Each set of twins is different from the next. Some rely on each other for everything, while others fight over everything. It can also be easy to forget that twins, especially identical twins, are individuals. They are not the same person and cannot be treated as such.

To best help twins in primary school, schools must have lenient policies. By solely separating or keeping twins together, schools are failing to give children their best learning environments. Each set of twins – and higher-level multiples – must be addressed individually, doing what is best for every child. A one-size-fits-all policy, for any aspect of education, will ultimately fail students.

By: C. Campbell


Coventry, W., Byrne, B., Coleman, M., Olson, R., Corley, R., Willcutt, E., & Samuelsson, S. (2009). Does Classroom Separation Affect Twins’ Reading Ability in the Early Years of School? Twin Research and Human Genetics, 12(5), 455-461. doi: 10.1375/twin.12.5.455

Lacina, J. (2010). Review of Research: School Placement and Separation of Twins: A Review of Research. Childhood Education, 86(3), 172–174. doi: 10.1080/00094056.2010.10523142

Polderman, T. J. C., Bartels, M., Verhulst, F. C., Huizink, A. C., Beijsterveldt, C. E. M. V., & Boomsma, D. I. (2009). No effect of classroom sharing on educational achievement in twins: a prospective, longitudinal cohort study. Journal of Epidemiology & Community Health, 64(01), 36–40. doi: 10.1136/jech.2009.091629

Tully, L., Moffitt, T., Caspi, A., Taylor, A., Kiernan, H., & Andreou, P. (2004). What Effect Does Classroom Separation Have on Twins’ Behavior, Progress at School, and Reading Abilities? Twin Research, 7(2), 115-124. doi: 10.1375/twin.7.2.115

Image Credit:

Pustovit, Vladimir. twins. https://www.flickr.com/photos/pustovit/15311467630/in/photolist-pk2gTd-4Gk1su-2gYtAqF-mRLfD-4tM7XE-eJ5JBZ-egoAas-GKFgVM-e2vKDs-dX4j5S-dYwoxy-geRpiS-276HoR1-e8NnLm-2EeQS-HEJQd-6MS9Co-a5tQRQ-6uvpF6-6uvpxn-2h45Lq7-27edwM9-ekD5Es-Vz99JY-5bmrL5-NPjqgB-J2Fvw-4fg68k-J2G51-J2Lui-J2Fvs-J2Luv-J2KXM-J2G55-J2HGp-J2G5y-J2HGx-J2HGc-J2HG8-J2KqF-J2Fvo-J2KqD-J2KqB-J2KqM-J2Fvf-J2KqK-J2LuD-J2G57-J2Fvy-J2Fvj

Xplaining X Inactivation

Xplaining X-Inactivation: How this untapped genetic landmine could lead to a cure for cancer

Hand holding DNA.

Have you ever thought that the human body could be the best doctor in the world? No scientist, pharmacist, or doctor could think some of the cures that the human body prescribes itself on a daily basis. The microscopic processes going on in your body as you read this are some of the most complex and sophisticated regulatory measures that exist in the world.

One process in particular, called X inactivation, involves the silencing of an entire X chromosome in a female cell. Since females have two X chromosomes and males have only one, the human body silences one X chromosome in females to make the genes equal between the sexes. How does the body achieve such a massive feat? The answer is epigenetics.

Epigenetics, the process of changing DNA’s physical shape and not its genetic information, is the main mechanism by which these X chromosomes are silenced. By changing the shape of DNA through proteins and chemicals, the human body’s genetic “on/off” switch is triggered. By adding chemicals to DNA, certain genes, such as cancerous ones, are turned off and cancer is never initiated. Conversely, chemicals can be added to turn on certain genes, such as cancer-killing genes, which enables the body to kill cancer cells after they have developed. If scientists harnessed this mechanism and created drugs that added chemicals to DNA, many illnesses would be nipped in the bud and a cure for cancer could possibly be in mainstream healthcare in the near future.

X inactivation occurs by the same processes of epigenetics: DNA modification. Put simply, the body takes chemicals that you consume through activities such as eating, drinking, or smoking and adds it to your DNA. Depending on how coiled up or spread out your DNA is, your genes will be more or less expressed. We want good genes to be more expressed and bad or mutated genes to be less expressed. An X chromosome is silenced by making it as coiled up as possible, rendering it practically useless.

DNA with various modifications.

X inactivation has inspired many scientists to study epigenetics in other contexts. Researchers have examined the mechanisms of the human body’s ability to inactivate an entire chromosome and are seeking to synthetically mimic that in pharmaceutical drugs.

Epigenetics is the human body’s way of editing your genes if things go awry. The best thing about it is that it is reversible. This key factor, as well as its versatility, is what makes epigenetic drugs, or epidrugs, the perfect medicine for serious illnesses and cancer. Epidrugs can add chemicals to your DNA and be reversed by other epidrugs that remove chemicals from your DNA.

Epidrug clinical trials are currently still in their elementary stages. Scientists have yet to figure out the correct dosage and delivery of epidrugs in regards to cancer and other serious diseases. According to medical journal Breast Cancer Research, epidrugs against breast cancer are in phase I and II trials, but are proving to be only mildly effective against reducing tumors. When used in combination with other drugs, however, the tumors were significantly reduced. 3% of patients responded to epidrugs alone, whereas 20% of patients responded to epidrugs used along with other chemotherapies. The good news is that Phase II trials are exploring ways to make epidrugs effective on their own. Scientists are studying how to make epidrugs more specific to each disease. Medical journal Cancer Management and Research reports that the International Human Epigenome Consortium (IHEC) is making an effort to sequence thousands of genomes that contain cancerous mutations. The information that the IHEC gains through mapping out as many variations in the human genome as possible contributes to the ability to make epidrugs as specific to its target as possible.

Examples of drugs that have shown success rates are Vidaza and Zebularine, as reported by scientific journal Genetics and Epigenetics. Both epidrugs use the same mechanism, in which the drug edits the DNA and turns on a certain gene. These drugs turn on genes that cause cell death, so it becomes useful in killing rapidly dividing cancer cells. The more this cancer-killing gene is expressed, the more likely it will stop cancer from spreading. Vidaza has been FDA-approved and is injected into the patient by needle. Zebularine, however, is not FDA-approved yet and is taken by mouth, which makes it the first epidrug of its kind that is administered orally. Zebularine is just one example of the many epidrugs that can lead to effective anticancer drugs in the future.

More money needs to be placed in the research of epidrugs. There are only 6 FDA-approved epidrugs, many of which have low efficacy due to their limited funding. By allotting more money into projects such as the IHEC’s efforts to sequence genomes, we can learn more about epigenetics. By studying more biological phenomena like X inactivation, scientists can add to their knowledge of epigenetics and create effective drugs that imitate the human body’s internal processes. Also, more specialized research studies need to be done on humans with varying illnesses to see the results of epidrugs in a broad range of diseases. If epidrugs are given more research and funding, then a more advance version of Zebularine can be produced and cancer could quite possibly be cured by a single pill. The future of medicine depends on unique and innovative treatments, most of which reside within the human body itself.

By: R. Ammanamanchi


Dueñas-González, Alfonso, et al. “Introduction of Epigenetic Targets in Drug Discovery and Current Status of Epi-Drugs and Epi-Probes.” Epi-Informatics, Academic Press, 25 Mar. 2016, www.sciencedirect.com/science/article/pii/B9780128028087000010.

Falahi, Fahimeh, et al. “Current and Upcoming Approaches to Exploit the Reversibility of Epigenetic Mutations in Breast Cancer.” Breast Cancer Research : BCR, BioMed Central, 29 July 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC4303227/.

Heerboth, Sarah, et al. “Use of Epigenetic Drugs in Disease: an Overview.” Genetics & Epigenetics, Libertas Academica, 27 May 2014, www.ncbi.nlm.nih.gov/pmc/articles/PMC4251063/.

Roberti, A., Valdes, A.F., Torrecillas, R. et al. Epigenetics in cancer therapy and nanomedicine. Clin Epigenet 1181 (2019). https://doi.org/10.1186/s13148-019-0675-4

Valdespino, Victor, and Patricia M Valdespino. “Potential of Epigenetic Therapies in the Management of Solid Tumors.” Cancer Management and Research, Dove Medical Press, 31 July 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4529253/.

Image Credits

  1. “Hand Holding DNA.” What Is Epigenetics?, 30 July 2018, https://www.whatisepigenetics.com/what-is-epigenetics/.
  2. “Methylated DNA .” Flickr, Flickr, 23 Aug. 2010, https://www.flickr.com/photos/ajc1/4920090582/in/photolist-8uLKvY-bk42PS-a3Xwxb-2eknUHg-nm7TGS-rzwAKk-oQpGgT-5o66kM-e6dK6V-UWdG1b-WaausU-7LzR9U-W23J6x-WaatbA-VCnAxA-UWfsFS-UZ6gbX-Bm9RGd-WaaqHQ-VCnyYy-TDkF8n-5gYb7X-Mtsp4n-VCnytA-VCp6FU-UZ6eRH-WdxMjB-UZ6e2B-VXGchs-gHkeCk-7LzR3S-xaFrRz-d1w1a9-gnZ1gz-uHzsug-nGH9aZ-dvTywo-nGYqfY-qzx5W1-eEPXa7-nEXpWs-mpgEMX-nqvuiT-nC3V6Q-7YW1A9-2in23So-hmingS-bzZ5sm-qWinea-YxsCUg.


Cytokines in Psychopathology: How the Immune System Can Induce PTSD

Artistic Rendering of a Cytokine

Artistic Rendering of a Cytokine: 11 April 2018 www.scientificanimations.com

Microscopic proteins, known as cytokines, are the master-coordinators behind a multitude of vital operations in the body. From stitching up a scraped knee, to forging an aching fever, to even activating blood assembly—cytokines are the regulatory bodies behind growth and repair, the immune system and inflammation, as well as cell division. Although these immune communicators are well versed in fighting off infection, mounting evidence has demonstrated their fluency in the nervous system’s language: including the development of mental illnesses. 

However, cytokines function in a highly sensitive regulatory harmony within our bodies. One tiny miscalculation may result in a dysfunction: an overproduction or underproduction of cytokines, particularly those that interact with immune cells, can send the body into disarray. Although cytokines are crucial to the immune response, these miniature communicators transform into harmful vandals when they overwhelm the body. And when they fail to make an appearance, their absence, too, unleashes an assortment of issues.

Pro-inflammatory cytokines, an important component of the immune system, help dispel pathogens during infection—in the short term. But when they linger in the body, smothering it with chronic inflammation, they trigger widespread dysfunction through complex biological pathways. 

Cytokines bridge the gaps in the bigger picture of the body’s functioning: they tell the immune system what substances in the body are foreign, and should be marked for destruction. They signal when cells should divide. However, if these important organizers of the body go haywire, we experience some major misdirection.  

An example of this incompetent signaling, chronic inflammation, can provoke life-threatening complications, including heart disease, diabetes, arthritis, and even cancer. Pro-inflammatory cytokines’ overabundance during chronic inflammation in cancer, for example, can induce cell production and alter cell survival for the worse. By modifying how cells divide, cytokines transform cells in ways that render them cancerous: proliferating out of control. 

Cytokines are impressively effective at altering cell-functioning, such as their potential to mutate healthy cells into ones with cancer. Although the inflammation theory of disease is well-documented and explored for a multitude of disorders, a lesser-known role of cytokines is their influence on the brain: particularly in psychological disorders. Dysfunctional cytokines can manifest in a dysfunctional mind—including disorders such as depression, anxiety, bipolar, and even PTSD. 

Cytokines can induce mental dysfunction by altering neural communication, as well as glial communication, both of which are intrinsic to mental illnesses. Although they command cell-signaling through many pathways, one route by which cytokines veer the brain towards psychopathology (a mental or behavioral disorder) is through changing neurotransmitter functioning. Neurotransmitters are chemical signals that direct neuron firing, and, in excess or deficiency, can lead to mental disorders. 

Once a cytokine’s signal reach the brain, it can influence the synthesis, release, and reuptake of neurotransmitters including serotonin, dopamine, and norepinephrine. These neurotransmitters are especially critical in the development of depression, anxiety disorders, bipolar, and schizophrenia: some of the most common mental illnesses. 

Swiergiel and colleagues have tested these theories about cytokines and psychopathology through experiments assessing cytokines’ effect on mental dysfunction through mice studies, and found that administering IL-1b (an inflammatory cytokine known as interleukin 1 beta) in mice can induce increased anxiety reactions when exploring an open field, or in a maze. 

By inducing an artificial immune dysfunction, we are able to show how real immune dysfunction can alter brain functioning. In this case, these cytokines drastically transformed how the mice responded to their environment: rendering neutral environments threatening, and foreign environments even more daunting. 

Further, in human studies, researchers such as Chang and colleagues have found elevated pro-inflammatory cytokine levels in patients with schizophrenia and those with depression, as well as reduced anti-inflammatory cytokine levels. This finding implies that an imbalance in cytokine concentrations–which can be induced by a variety of factors, including diet, environmental pollutants, obesity, or stress–can play a critical role in the development of anxiety disorders, schizophrenia, and depression.

Additionally, recent research by the Lysle Lab at UNC Chapel Hill has shown that SEFL (stress-enhanced fear learning, a rat model of PTSD) will not develop after a stressful event without the release of IL-1b from the hippocampus, a brain region that stores memories.

This evidence implies that IL-1b, an inflammatory cytokine, is essential to PTSD development.  

When taking a closer look at the role of cytokines in PTSD, we can see that IL-1b increases the hippocampal neurons’ activityaltering how the hippocampus stores memories long term. IL-1b may change memory storage by stripping contextual details from a stressful event: leaving only the event’s fear, and rendering both animals and humans hypersensitive to stress. 

IL-1b’s role in PTSD represents a major breakthrough in neuroimmunology. This evidence holds promising new treatments, focused on cytokine manipulation, to target immunologic dysfunction in psychiatric disorders.

In fact, in rat studies, Jones and colleagues have started to examine these possible treatments for PTSD. For example, these researchers have prevented the development of SEFL, in mice by inhibiting IL-1b expression through morphine injections, and through injections of IL-1ra, which is the antagonist of IL-1b. 

Antagonists bind to IL-1b receptor sites, and prevent IL-1b from acting upon the brain. Evidence that IL-1b inhibition is associated with lower risk of PTSD is also echoed on the battlefield: studies show that soldiers that are administered morphine (which inhibits IL-1b) 48 hours to 72 hours after trauma have lower rates of PTSD.  

These findings demonstrate that IL-1b signaling is crucial to SEFL development, and therefore, should be a target of new PTSD treatments. Additionally, other studies have located brain regions and cell types where these cytokines are produced, finding that astrocytes primarily manufacture the cytokines implicated in SEFL. Not only does this evidence demonstrate one way astrocyte signaling may affect complex behavior, but by specifying astrocytes as IL-1b’s primary source, researchers are able to create astrocyte specific manipulations to inhibit IL-1b.

In fact, researchers can manipulate astrocytes to inhibit IL-1b with chemogenetic technologies. These technologies are valuable tools that can specifically target certain neuronal signaling, such as the way that astrocytes release cytokines, one of them being a technology called DREADD (Designer Receptors Exclusively Activated by Designer Drugs). In the Lysle Lab, researchers engineered DREADDs to specifically activate inhibitory signaling in dorsal hippocampal astrocytes, in turn, suppressing the release of IL-1b. In rats, astrocyte-specific manipulation can inhibit SEFL. 

This research gives us new insight into the complex and daunting inner workings of the human mind, and advances our understanding of psychopathology development. By understanding cytokines in anxiety, depression, and PTSD, we are one step closer to solving an issue that plagues millions of people. 

Further, this research confirms our understanding that the origins of abnormal functioning are chaotically intricate: cytokines do not just have one purpose, just as dysfunction does not have one source. We are constantly untangling the interconnected relationships between our bodily systems, as seen in the intertwinedness of the immune system and the nervous system. 

An adequate level of cytokines will help your body heal from a scrape or cold: while an overabundance may contribute to cancer or depression. Our brain’s functioning, which takes place before our eyes. is truly more unknown and misunderstood than the cosmos.

By: L. Adams


Chang, T.-T., & Yen, Y.-C. (2010). Cytokines and Major Psychiatric Disorders. Taiwanese Journal of Psychiatry, 24(4 ), 257–268.

Jones, M. E., Lebonville, C. L., Barrus, D., & Lysle, D. T. (2014). The Role of Brain Interleukin-1 in Stress-Enhanced Fear Learning. Neuropsychopharmacology, 40(5), 1289–1296. doi: 10.1038/npp.2014.317

Jones, M. E., Lebonville, C. L., Paniccia, J. E., Balentine, M. E., Reissner, K. J., & Lysle, D. T. (2018). Hippocampal interleukin-1 mediates stress-enhanced fear learning: A potential role for astrocyte-derived interleukin-1β. Brain, Behavior, and Immunity, 67, 355–363. doi: 10.1016/j.bbi.2017.09.016

Roth, B. L. (2016). DREADDs for Neuroscientists. Neuron, 89(4), 683–694. doi: 10.1016/j.neuron.2016.01.040

Swiergiel, A. H., & Dunn, A. J. (2007). Effects of interleukin-1β and lipopolysaccharide on behavior of mice in the elevated plus-maze and open field tests. Pharmacology Biochemistry and Behavior, 86(4), 651–659. doi: 10.1016/j.pbb.2007.02.010

Image Credit

“3D medical animation still of Cytokines that are important in cell signaling.” Scientific Animations, www.scientificanimations.com,11 April 2018