A multistate outbreak of cyclosporiasis, possibly linked to contaminated lettuce, is currently working its way across the U.S. It’s a parasitic infection that does its damage by inflaming the gut and causing severe diarrhea. Illnesses like this are a reminder that diseases with little else in common are often connected by one underlying process: inflammation. Not long ago, the COVID-19 pandemic graphically demonstrated what can happen when inflammation spirals out of control in the form of cytokine storms. At the other end of the spectrum, hepatitis, literally inflammation of the liver, continues to exact a heavy toll worldwide, prompting annual World Hepatitis Day observances each July 28. Swollen broken arms, rashes, sprains, and countless other relatively less severe everyday instances are all forms of inflammation.

What is inflammation?

The word “inflammation” has its origins in Latin, and implies setting fire. In biology, inflammation is the body’s response to injury or infection, often producing the swelling, redness, and pain we readily recognize. For example, measles rashes are the result of discrete sites of inflammation. Children who contract measles can also experience cerebral inflammation, sometimes years after the initial infection. In Ebola virus disease, inflammation can become widespread throughout the body. Malaria causes inflammation of the liver and other organs, while some cancers, including stomach and liver cancers, have been linked to long-standing inflammation. Even muscle injury and repair are associated with inflammation. Have you ever noticed what a sprained ankle looks like?

In western medicine, the history of inflammation dates back centuries. In fact, Hippocrates is credited with introducing the word “edema” in the 5th century, to describe swelling. He described inflammation as an essential component of the healing cycle when there was injured tissue. But it is only since the last century that research has yielded a better understanding of the body’s immune system, and how it mounts an inflammatory response. Those insights have led to a burgeoning arsenal of medications to treat inflammation, whether it accompanies an injury, arthritis, or infectious disease.

This week marks the 138th birth anniversary of Selman Waksman, the microbiologist whose systematic hunt through soil microbes gave us streptomycin. Discovered in 1943, it was the first real weapon against the chronic and grinding inflammatory disease tuberculosis. Yet tuberculosis is only one example of a recurring theme in medicine: understanding inflammation often opens the door to better treatments.

One size does not fit all

Despite a few shared characteristics, inflammation in each disease can be fairly unique, which means treating all types of inflammation requires a large toolbox. This is underscored by the fact that inflammation often occurs in a much later step in a disease; or there is a low level of inflammation that is sometimes not easily detectable and that might be the reason for a disease. Pink eye, or conjunctivitis, is an example of the former — a virus or bacterium establishes itself in the eye and the body’s immune system detects the invader and mounts an assault to annihilate the invader. Put very simply, this war manifests as an inflammation.

Key facilitators of inflammation

In those instances where inflammation can be reduced by over-the-counter medications like ibuprofen or other non-steroidal anti inflammatory drugs (NSAIDs), the mechanism of action of the drugs is relatively straightforward, although overuse of NSAIDs can sometimes be deleterious.

NSAIDs reduce inflammation by binding to the cyclooxygenase enzymes COX-1 and COX-2. These closely related enzymes perform similar but distinct roles throughout the body. While COX-1 is found in most tissues, COX-2 has a more restricted distribution. Together they help produce prostaglandins, molecules that can promote inflammation but also help maintain the integrity of tissues such as the stomach lining.

Tissues in which COX-1 and COX-2 are found. From The Human Protein Atlas

Biochemical pathway maps outdo subway maps

In a 2016 study, Gallotti and colleagues looked at the representation of transportation on city maps. They concluded among other things, (a) that New York City subway maps were perhaps the most complicated maps, and (b) “Multimodal transportation systems in large cities have thus already exceeded human cognitive limits and, consequently, the traditional view of navigation in cities has to be revised substantially”

Maintaining a robust signalling system in the complex New York subway system is no small feat. Now, add several orders of complexity to that and you have the complex map of biochemical pathways that keep you fit in the best of times, and make you sick in the worst. The complexity of biochemical pathways compared to the most complex transportation maps that “exceed human cognitive limits” is nothing short of awe-inspiring. For several decades, researchers have taken on the challenge of dissecting these biochemical pathways to develop tools to address situations where the pathways are disrupted.

A bird’s-eye view of a NYC subway map (L) and a biochemical pathways map (R) with circled area zoomed in below

Zoom and awe

The enzymes that catalyze the synthesis of prostaglandins inhabit a tiny portion of the biochemical pathways map, yet play a key role in wellness.

Zooming in on prostaglandin biosynthesis

Noting the level of complexity, it is easier to appreciate why inflammation is such an important process, and why fine-tuning cyclooxygenases is critical. Equally important are attempts to fine-tune the steps that precede the action of cyclooxygenases. Of course, all without disrupting the numerous other processes that feed into or out of these steps. It’s like working on a Jenga game that is inconceivably complicated — move one piece a smidgen incorrectly, and the entire stack crashes.

Viewing these images of the biochemical pathways also makes it easier to appreciate that although a drug can inhibit a cyclooxygenase and thus reduce inflammation, too much of it can be counterproductive, because prostaglandins have been shown to play a role in some normal biological processes including maintenance of some tissues such as the lining of the stomach and intestines.

Prostaglandins, and therefore COX enzymes, influence many biochemical pathways

Gout — inflammation’s poster child

Gout is the most common form of inflammatory arthritis, and its incidence is increasing across the globe. It is caused by the deposition of uric acid crystals in and around the joints. When dietary intake of some purine-rich foods is high, the biochemical pathway that breaks down purines has to work overtime. In susceptible individuals, this results in an accumulation of uric acid crystals formed by the enzyme xanthine oxidase (XO)’s action in the penultimate step in the breakdown of purines. Uric acid accumulation initiates an inflammatory response resulting in the characteristic pain and inflammation unique to gout.

In the 1950s, right about the time when there was a flurry of activity as the structure of DNA was being sorted out, researchers like Gertrude Elion and George Hitchings pioneered what became known as rational drug design — deliberately targeting specific biochemical pathways, rather than the trial-and-error approach that had defined drug discovery until then. Studying purine metabolism in an effort to treat cancers (two of the four nucleic acids in DNA are purines; the other two are pyrimidines), their first success under this new approach was 6-mercaptopurine (6-MP) in 1950, which treated childhood leukemia and is still in use today, alongside its close cousin 6-thioguanine (6-TG). But in the course of these studies, they also discovered allopurinol, a drug that binds to XO, preventing it from catalyzing the formation of uric acid crystals, and thus reducing the chances of a gout attack. More than sixty years after its approval, it remains a mainstay of treatment — allopurinol is still one of the most widely prescribed drugs in the U.S., with over 14 million prescriptions filled in 2023 alone.

Taming an unruly fire

The long arm of inflammation thus reaches beyond the minor swelling and irritation resulting from a paper-cut to chronic diseases like arthritis. It’s worth remembering, too, that most non-communicable diseases—cancers, diabetes, cardiovascular disease among them—have chronic inflammation implicated somewhere in their pathology. In fact, as we learn more about diseases, we are likely to find that inflammation rears its head in some form or other in almost all of them.

From food-borne parasites and viral hepatitis to arthritis, cancer, and a simple broken arm, inflammation remains one of biology’s most universal responses, and one of medicine’s greatest challenges. Because of the complexity and interconnectedness of biochemical pathways, we will need to have exquisitely refined and targeted ways to intercept or temper the process of inflammation while keeping the rest of the pathways intact.

This piece originally appeared on Medium in 2019 under the same title. It has been substantially revised and updated for 2026.

In November 2024, Mylan recalled levothyroxine tablets in all eleven strengths it manufactures. Some of the pills tested too weak, others too strong (Mylan Pharmaceuticals Inc. recall notice, November 19, 2024).

Unfortunately, potency problems with levothyroxine have surfaced periodically over the years. I learned how sensitive this drug can be more than twenty years ago when my son’s prescription was switched from Synthroid to a generic product made by a different manufacturer. The dose on the label never changed, but his thyroid levels did.

Levothyroxine is hardly a niche medication. About 1 in 20 people over the age of 12 (roughly 5% of the US population) have hypothyroidism: their thyroid doesn’t make enough hormone (American Thyroid Association). About 1 in 2,000 children are born with the congenital form of hypothyroidism, which is why every infant in the US is screened for it at birth (Cherella & Wassner, International Journal of Pediatric Endocrinology).

The butterfly shaped thyroid gland, tucked into the base of your neck, produces T3, T4, and calcitonin.

This article is about T4, or thyroxine, which, once activated, influences the development and function of nearly every organ in the body. When levels run low, the fix is usually simple: a daily pill of levothyroxine, to compensate for what your thyroid isn’t producing. It’s one of the most commonly prescribed drugs in the US, year after year. An estimated 22 million patients filled a levothyroxine prescription in 2024 alone (FDA). The best-known brand is Synthroid, made by Abbott, but there are close to a dozen other manufacturers making generic versions. (The history of Synthroid’s FDA approval process is a fascinating story in its own right, involving years of controversy over clinical studies and corporate conduct.)

When we swapped my son’s Synthroid for a generic version, the thinking was that a 25-microgram tablet was a 25-microgram tablet regardless of who made it. But we had a rude awakening because his system reacted adversely to the change. We had to get his thyroid levels rechecked and his dose adjusted before things settled after a couple of months.

At 25 micrograms, about one-hundredth the weight of a mustard seed, there is very little room for error.

At the time, I chalked it up to storage and handling both at the pharmacy that distributed the medication and at home. Open bottles exposed to air, pills degrading slowly on a shelf are some of the consequences of pharmacies redistributing bulk supplies of drugs in the US, an almost unheard of practice in more than 80% of the world.

But it turns out there’s a more precise explanation for why levothyroxine is so sensitive. It’s one the FDA itself has now built into how it regulates the drug.

Why this one is different

Levothyroxine is what the FDA calls a narrow therapeutic index (NTI) drug: one where the gap between “not enough” and “too much” is small enough that minor differences in dose or blood concentration can cause real clinical problems. The FDA formally applied this designation to levothyroxine in the early 2010s. Since then, generic levothyroxine has been held to a noticeably higher bar than most other drugs, requiring a rigorous back-and-forth comparison (a.k.a. replicated crossover bioequivalence studies) and tighter acceptance ranges. As of 2009, potency also has to stay within 95% to 105% of the labeled dose for the entire shelf life of the tablet, not just on the day it’s manufactured.

“Generally, thyroid hormone replacement medications need to be dosed very carefully. A dose that is too high or low may not produce the intended effect, may increase the symptoms of hypothyroidism or may cause side effects. This means a doctor needs to monitor a patient’s thyroid hormone levels closely and adjust their medication dose precisely to keep their levels in the right range.” From FDA’s Actions to Address Unapproved Thyroid Medications

In 2015, the FDA went further and convened a standing NTI Drug Working Group specifically to sort out which drugs deserve this scrutiny and how to regulate them consistently. As of January 2024, there were 33 approved drug products across 14 active ingredients on that list (Anim Anno et al., The AAPS Journal). Levothyroxine is among them, alongside drugs like warfarin and certain anti-seizure and anti-rejection medications, where a small miss can mean a seizure, a clot, or an organ rejection rather than just an off day.

The FDA counts 33 separate drug products on this list because several of these medications come in multiple forms, tablet, capsule, extended-release, chewable, and so on, each of which is evaluated separately. Below are the 14 active ingredients behind those 33 products.

My observations from more than two decades ago when my son’s levothyroxine manufacturer changed, make perfect sense in light of the drug having a narrow therapeutic index. Levothyroxine is not a drug where “generic” can be trusted to mean “interchangeable” without a second thought. And the 2024 Mylan recall is a reminder that even with the tighter standards, potency failures still happen. Not because the system is broken, but because manufacturing a pill to within a few percentage points of a target, batch after batch, is genuinely hard. That’s exactly why a system to catch it when it doesn’t work has to exist.

Storage and expiration dates matter more than people think

Most of us treat storage instructions and expiration dates as fine print. For any of these 33 drug products, that’s a mistake, because potency doesn’t hold steady on its own. It depends on how the drug is stored.

A 2022 open-access study on levothyroxine (Chun, AAPS Open) tracked tablets stored in ordinary pharmacy bottles versus sealed blister packs, under conditions meant to mimic normal daily use at 28°C (82°F) and 65% relative humidity. Bottled tablets, opened once a day the way a patient would, started at just over 101% of labeled potency. By day 105 they had dropped to 93.9%, below the FDA’s required 95% to 105% range. Blister-packaged tablets, sealed until the moment of use, stayed steady near 100% the entire time. The same study found that a couple of days of hot, humid shipping conditions alone measurably increased moisture content and disintegration time in bottled tablets. None of the conditions tested were extreme: a bathroom cabinet, a car in summer, a mailbox on a warm afternoon can all get warmer and more humid than that.

An expiration date only holds if the storage conditions behind it were also met. A pill that’s been stored under incorrect conditions can fall out of specifications well before the date printed on the label, and for an NTI drug, that difference isn’t trivial. The same logic applies across the other 13 active ingredients on the FDA’s list: anticonvulsants, immunosuppressants, and blood thinners all carry the same requirement to hold within a narrow potency band for their full shelf life, which means they’re all vulnerable to the same kind of quiet degradation if they’re stored incorrectly.

There’s a second layer to this that most patients never think about. In the US, a prescription rarely arrives the way the manufacturer packaged it (illustrated in map above). Most tablets ship to pharmacies in bulk, 500- or 1,000-count bottles, and a pharmacist or pharmacy technician counts out however many pills the prescription calls for and drops them into a small amber vial. The same levothyroxine study noted this directly (Chun, AAPS Open): manufacturers ship the drug in large bulk bottles that pharmacies then open and redistribute into smaller patient-facing containers, and that repackaging step itself can introduce moisture exposure before the medication ever reaches the patient; blister packs on the other hand retain their potency. The study also pointed out that this is largely a US practice.

Regulators have quietly acknowledged the risk in this practice. Because a repackaged pill is no longer in the container the manufacturer actually used for testing stability, the FDA’s own guidance requires shortened expiration dating for repackaged solid oral drugs (FDA, “Expiration Dating of Unit-Dose Repackaged Solid Oral Dosage Form Drug Products,” 2020), capping it at whichever comes first: six months from the date of repackaging, 25% of the time remaining until the manufacturer’s original expiration date, or the manufacturer’s date itself.

In other words, the system already assumes that pulling a pill out of its original packaging degrades its shelf life. That assumption gets applied quietly, on the back end, by pharmacies following FDA and USP rules. It rarely gets explained to the patient standing at the counter, who has no way of knowing whether the tablets in their vial came straight from a sealed blister pack or were counted out of a bulk bottle that had already been opened and closed dozens of times that day.

It’s worth noting the irony here that non-prescription medications in the US are always sold in original manufacturer packaging.

Being an informed consumer

If it’s a generic drug or a headache, substitutions are less of a concern. If it’s something with a narrow margin (a thyroid medication, a blood thinner, an anti-seizure drug), asking the pharmacist to stick with the same manufacturer if at all possible is an avenue, while also paying attention to the refill labels regarding storage and other information. If a switch is unavoidable, following up with a physician is vital.

None of this is a knock on generics as a category. They’re essential, and for the vast majority of medications they work exactly as promised, keeping costs down without any real tradeoff. But for medications with a narrow therapeutic index (NTI), the manufacturer, the packaging, the storage conditions, and even a seemingly minor substitution can matter more than most patients realize. It’s a case for knowing which of your prescriptions belong to that sensitive NTI category, and handling those differently.

The information here is for educational purposes only and should not be taken in lieu of professional medical advice. Always consult a licensed healthcare provider before making any changes to your medication.

My maternal great grandmothers were named for precious things – diamonds and gold. I met Hirabai, named for diamonds, several times as a child, and never met Sonabai, named for gold. But thanks to things Sonabai left behind, I have a better sense of who she was than who Hirabai was.

Hirabai Ajinkya, my mother’s maternal grandmother, was frail, almost wraith-like. I saw her a few times a year when I’d tag along with my grandmother to visit. I don’t recall having a conversation with her . After a greeting upon arrival, I usually wandered around the house on Hughes Road and returned only when I was told it was time to leave.

Even though Sonabai Kothare, my mother’s paternal grandmother, died well before I was born, she always seemed present. I heard lots of stories about her. But more importantly, in the house in which she’d lived in Girgaon, I was surrounded by things she’d touched and changed during her life.

A beautifully embroidered tiger head. Exquisitely painted glass panes on three-paneled units that could be used as stylish room dividers. I remember spending hours wondering how on earth the eyes of the people painted on those panels followed me no matter where I stood in the room.

These and other objects provided a sensory portrait of Sonabai.

So you can imagine my joy when in 2012, my aunt, Tej, gifted me a bound collection of Sonabai’s watercolour paintings. It had been bequeathed to my aunt, and I was lucky that she thought I would be a good steward of it.

Holding the collection that I was seeing for the first time felt like I was directly communing with this not-too-distant ancestor, fragments of whose DNA I carried and have passed on to my children.

The 75-year-old album has yellowed with time and become fragile. The numerous holes in the book made it clear that it had been a feast for some sort of arthropod, so before its condition worsened I decided to photograph every page myself. I made bound copies of the photographs for my mother and each of my aunts.

There are more than 30 watercolor paintings in the book – some incomplete or abandoned, others extremely detailed, completed and signed. Of the little I know about art, I have learnt that a human form is challenging to depict in almost every medium, so it is particularly interesting that almost two-thirds of the paintings have one or more humans in them.

I wonder if all those human figures say something about the woman I’ve heard described as strong and determined.

Sonabai Kothare was part of the Pathare Prabhu community that purportedly settled in Bombay in the mid-to-late thirteenth century. It is a shrinking community that historically engaged in education, the arts, and business. Perhaps as a consequence of being close to the sea, the community is also known for its deep love for seafood .

I’ve been leaning on my mum and my aunts to share stories about Sonabai. So far, a common thread in their stories has been this woman’s fiery temper, her culinary expertise, her support for the arts and her overall elan. While I did not have the good fortune to experience her culinary expertise nor witness her panache, I’ve seen hints of that fiery temper in her descendants.

As far as I know, Sonabai was not a formally trained painter but to my lay eye, she seems to have brought some of the rigor of a professional artist to her paintings, all of which were signed “SBK” – Sonabai Balaji Kothare.

Several pages in the book have made me stop, stare and wonder.

One in particular brings together Sonabai’s talent and also her support for the arts about which my mother has spoken. It’s a scene where musicians are on stage, performing for the observer, as it were.

Who were these musicians? What was the woman singing? Where were they performing? The woman, and the musician to her left are both looking into the audience, but to their right; the other musician is almost looking straight up ahead. What caught their attention? The woman’s hands, especially her knuckles, are extremely detailed  –  was Sonabai trying to convey something through this detail?

All but two of the paintings in the book are untitled  –  “Sunrise” and “Sunset”. Curiously, she painted Sunset before Sunrise (note the numbers at the top left of each painting). I am willing to bet that her gustatory inclination towards fish prompted both these paintings. Sunrise is reminiscent of fisherfolk getting ready to go off on their home-to-home sale of early morning catches, while Sunset depicts fishermen returning from a day at sea.

Painting number 15 appears to be a more detailed depiction of sorting the catch of the day, probably before heading out to sell it. Based on the un-erased pencil lines in this painting, it’s entirely possible that her original intent was another scene altogether.

Sonabai didn’t limit herself to painting scenes favoring her palate. On page 24 of the book, we see a young woman dressed to the nines  – note her footwear  –  playing with a dog. What I think is impressive is that in this painting she has created a layered effect where one can see the woman’s arms and legs through the diaphanous material of her outfit.

Sonabai’s paintings strike me as deeply private – made for herself, with no audience beyond perhaps her family. I’m not sure she even intended Tej to be the keeper of this book until the moment she gave it to her. But in that gift, she preserved a version of herself for her descendants.

A recent exhibition about the Pathare Prabhus at the Chhatrapati Shivaji Maharaj Vastu Sangrahalaya in Mumbai makes an effort to document the community before its stories fade. But community histories, however carefully assembled, rarely capture the interior lives of women. Sonabai left no public record – no exhibitions, no reviews, no archive beyond what her family preserved and passed on. Her paintings are a reminder that the most intimate histories live not in museums but in families, and can be easily lost to time and arthropods.

It’s a shame I waited so long to embark on the project of learning more about this woman. Sonabai suffered from a stroke from which she never fully recovered and died in the early 1950s, a couple of years after she gave this book to her granddaughter, my aunt.

My grandfather who likely knew her better than his children did, and with whom I shared this planet until I was 31 is long gone. But thanks to my mother’s and aunts’ stories and general family lore, I do know that in addition to Sonabai’s prowess with the paintbrush and embroidery threads, she also played the dilruba.

It is the bowed stringed instrument that you can hear very clearly in the opening bars (and later too) of the Beatles Within You Without You. George Harrison’s lyrics to this song capture my sentiment “..it’s far too late/When they pass away.”

Thanks to these paintings, Sonabai Kothare has finally introduced herself to me.

Branded and generic medicines, when accessible, improve and save lives. Over the course of an approved and successful drug’s life in the public sphere, it slowly achieves a taken-for-granted status. Consider GLP-1 drugs: in December 2025, the World Health Organization issued global guidelines on the use of GLP-1 medicines in treating obesity. Global sales for GLP-1 drugs will soon overtake the sale of statins, cholesterol lowering drugs, by some estimates.

What is GLP-1?

GLP-1, or Glucagon-like peptide-1 is almost a third the size of a more commonly known peptide, oxytocin—nicknamed the love hormone. GLP-1 is a hormone released by intestinal cells after a meal, and sends a signal to the brain that you are full, while also sending a signal to the pancreas to release insulin to handle all the glucose released from the meal you’ve just ingested.

In the 1960s, researchers studying metabolism observed that levels of insulin increased significantly more in the blood if glucose was administered orally, versus if it was administered intravenously. This phenomenon, termed the "incretin effect," meant that the physical ingestion of glucose caused a vital intermediate step that dictated insulin production. Around the same era, physiologists like G.R. Hervey at the University of Leeds were mapping hunger signals, writing: “No one will dispute that whether or not an animal or man is eating at a particular moment depends upon many factors. In this sense, control of food intake is highly multifactorial. It is, however, sometimes valuable to isolate a single factor from the multitude which govern real events, even though this seems to lead to a theoretical abstraction.”

Over decades of research, the intermediate step was identified as the post-prandial secretion of the peptide hormone GLP-1.

Serendipity and drug discovery

Dr. John Pisano was a biochemist who studied venoms from different sources and was broadly associated with Dr. Jerry Gardner’s research group at the NIH. Pisano was interested in identifying and isolating substances from these venoms and studying how they affected human physiology. In the course of this work, a postdoctoral fellow in his lab, Jean-Pierre Raufman, focused on the venom from Gila monsters—his interest was piqued by the fact that they can get by on fewer than five meals a year and still remain active. Through their research they ascertained that Gila monster venom contains a substance that stimulates the secretion of pancreatic peptides and enzymes.

John Pisano died prematurely at the age of 56, from a heart attack.

When Raufman presented his research at the Bronx Veterans Administration where John Eng, an endocrinologist was present, a collaboration to identify as many peptides as possible from the Gila venom was launched. Over the course of their research they identified several bioactive peptides and labelled them exendins. Detailed characterization of exendin-4 (the fourth identified peptide) revealed that it interacted with specific receptors on cells from guinea pig and rat pancreas. This was in the early 1990s. Very quickly, they set out to find human analogs of exendin-4 and by 1992 they had honed in on GLP-1.

The weight of their discovery was not lost on these scientists and in 1993 Eng filed a patent application that was granted in 1995: the summary of the application states, “This invention encompasses pharmaceutical compositions containing exendin-3 or exendin-4, or any combination thereof, and methods for the treatment of diabetes mellitus and the prevention of hyperglycemia.” That patent expired in 2016.

Despite peer-reviewed papers and conference presentations, Eng and Raufman were unable to interest pharmaceutical/biotech companies to leverage their findings until a chance conference encounter with Andrew Young, a scientist at Amylin Pharmaceuticals. Amylin went on to license the patent from Eng and, with Eli Lilly, brought the first GLP-1 drug to market, approved by the FDA in 2005.

From discovery to patient

Between a promising molecule and a prescription lies a long process of clinical testing that depends entirely on human volunteers. In order to be an approved treatment, Exenatide had to undergo rigorous testing. The traditional testing process involves three overarching phases, and every phase requires individuals willing to accept inconvenience, uncertainty, and risk so that researchers can determine whether the treatment was safe and effective.

In Phase 1, a drug is tested for human safety by escalating doses in healthy human volunteers. In this phase, there is no real benefit to the volunteer subjects as they are healthy; they may be compensated for their time and effort. Phase 2 attempts to answer the amount of drug necessary to treat the disease, and this phase is typically randomized and double-blinded, which means neither study participant nor physician know which arm of the study an individual is in—placebo, or test. Phase 3 studies are typically multi-center and the number of participants is large in order to cover all demographics.

For a successful Phase 2, not only must the drug pass all parameters outlined in the study, but without the requisite number of participants, the data cannot be relied upon to prove success. To prove a drug works, scientists must calculate the exact minimum number of patients needed so the results aren’t dismissed as a lucky coincidence. If a trial fails to recruit this exact number, the data become too weak and blurry to prove anything to regulators. When a study falls short on participants, years of research and millions of dollars are completely wasted on a drug that might actually work.

The cost of volunteering

Every drug that reaches patients has passed through this same gauntlet, and the bottlenecks can be remarkably similar across trials. Typically, a late-stage clinical trial of a new drug (as opposed to a repurposed drug) will be spearheaded and sponsored by the entity that owns the molecule under study. In the case of the clinical trial for the first GLP-1 mimetic, the sponsor was Amylin Pharmaceuticals and Eli Lilly. If a drug is being tested for a new use, then it might be an academic institution. Irrespective of where the sponsor comes from, they are held responsible for initiating, managing, and financing the clinical trial.

Global medicine spending reached approximately 1.74 trillion USD in 2024, with the US alone projected to spend between 685-715 billion USD in 2026. The companies that benefit from this market are also the ones who sponsor clinical trials, and yet a significant stumbling block in participant recruitment can be something as mundane as travel costs and parking fees.

Participant recruitment is a major bottleneck in clinical trials. Since participants must fulfill specific requirements to be eligible to participate in a trial, the trial net has to be cast as wide as possible, involving multiple trial sites. These typically involve tapping into patient populations around teaching hospitals. But because monitoring during a trial might require frequent hospital visits, intensive testing, and strict daily routines, participants sometimes drop out of a trial over time, often for reasons that have nothing to do with their physiology.

Given the massive financial windfalls that a successful clinical trial affords a novel drug manufacturer, it behooves them to directly address these participant-level financial burdens up front. Investing in immediate travel and parking stipends is one critical strategy that can eliminate avoidable recruitment bottlenecks before they jeopardize the study.

A note of acknowledgment

Monumental medical findings, such as those generated by using the UK Biobank collections, underscore a vital reality: medical advancement is impossible without human participation. While it is easy to credit the scientists and clinicians who spearhead drug development, we must also acknowledge the patients who volunteer for clinical trials. Without these dedicated participant cohorts, clinical validation would cease, and life-saving treatments would remain confined to laboratory benches.

Today, roughly two-thirds of American adults take at least one prescription drug, each one the downstream result of someone, somewhere, volunteering for a trial. Deep gratitude is owed to every individual who has participated in a clinical trial or contributed samples to a research biobank, making today’s therapeutic triumphs possible.

Over the counter (OTC) medications like acetaminophen or ibuprofen are often the first line of defense for most of us when suffering from a headache or other pain, or a fever. Of course, over the course of the last few years many of us also leaned into testing for COVID when we’d been beset with unexplained pain and/or fever. With recent reduced levels of immunizations and concerning removal of solid scientific information from CDC web pages, it’s a good idea to be informed while also encouraging vaccine-hesitant individuals to get their shots.

So what causes pain and fever?

It’s complicated. Pain and fever are the body’s biochemical responses to assault — physical assault (e.g., a stubbed toe; a poorly considered exercise) will often cause pain at the site of the assault; and physiological assault (e.g., eating food that is too old, or contracting a pathogen) can cause pain and fever.

The complicated pathways to pain and fever have a few common biochemical components — specific enzymes and other proteins and lipids (fats). These are primarily the cyclooxygenase enzymes COX-1 and COX-2, the proteins they interact with, and lipids that are substrates for these enzymes.

Here’s a map of the metabolic pathways and processes, giving a bird’s-eye view of how they work together (unfortunately, the interactive website is being updated to make it easier to use). If it looks complicated, that’s because it is — but it also shows just how complex drug development can be.

Put simply, arachidonic acid (AA, ArA, ARA) is one of the central players in your pain and fever discomfort, and ironically, also in your well-being. AA is a fatty acid and a member of the polyunsaturated family of fatty acids and is found in a variety of foods.

This pictorial representation of the AA involved pathways highlights the complexity of the problem — and why pain and fever medications can lead to undesirable side effects. It is the reason that research on targeted pain medication has never slowed down. It is also one reason classes of pain medication have been abused by manufacturers.

OTC analgesics (painkillers) and antipyretics (fever-killers) have been around since aspirin was first marketed by Bayer in 1899. They fall into two broad categories — nonsteroidal anti-inflammatory drugs (NSAIDs; ibuprofen, aspirin) and paracetamol (acetaminophen). The two categories have slightly different modes of action. Initially, it was thought that both act by inhibiting cyclooxygenases, the enzymes that are responsible for the production of prostaglandins from AA. However, more recent studies have shown that acetaminophen likely has an additional independent mode of action. The data suggest that acetaminophen’s primary mode of action is via the central nervous system, and through this mode it has the ability to increase the threshold of pain perception (while the pain is not killed, the amount of pain that one can endure is higher). Further, acetaminophen also appears to target the heat-regulating area of the brain (hypothalamus), thus helping to reduce elevated body temperatures.

What’s an NSAID?

Ibuprofen (trade names Advil, from GlaxoSmithKline, and Motrin, from Johnson & Johnson), aspirin, and naproxen (trade name Aleve, from Bayer) are examples of NSAIDs. In addition to reducing pain and fever, they can reduce inflammation to some extent, in a manner that has fewer side effects than treating with steroids. The operative word here is “fewer” — NSAIDs come with their own level of risk from extended use, and unresolved symptoms after brief use should always be referred to a clinician. It is worth noting here, that muscle pain is primarily a consequence of inflammation of muscle tissue.

NSAIDs act by inhibiting the enzymes cyclooxygenase 1 and 2 (COX-1, and COX-2), that are responsible for converting AA (arachidonic acid) to prostaglandins, and other pain provoking molecules. While COX-1 is constitutively expressed (always found in the body), COX-2 is found during inflammation. Since COX-1 plays a role in maintaining mucous membranes in the stomach, it is not uncommon that NSAIDs can cause gastric problems.

And acetaminophen a.k.a. paracetamol?

Like NSAIDs, acetaminophen has antipyretic and analgesic action, but lacks anti-inflammatory properties of NSAIDs. While acetaminophen does seem to regulate the activity of cyclooxygenases, the mechanism is not the same as that of NSAIDs. In fact, some studies have suggested that when the body metabolizes acetaminophen, one of the products (N-arachidonoylphenolamine), activates a distinct pathway in the brain that creates an analgesic effect.

Two for the price of one

In 2020, the FDA approved GSK’s OTC combination of ibuprofen and acetaminophen — Advil Dual — to be consumed in no more than six caplets in 24 hours. The effective drug concentrations are 250 mg acetaminophen and 125 mg ibuprofen in each caplet, a combination that has been independently recommended by clinicians for several years. For those individuals who show no side effects to either drug, this is probably the best case scenario as multiple pathways are targeted by the combination, likely resulting in a better outcome.

At a moment when public health guidance is increasingly questioned or selectively ignored, understanding how these systems actually work matters more than ever. The cellular (“inside”) story of pain and fever is complicated. OTC medications work because they intersect with the same biochemical pathways that produce pain and fever — which explains both their effectiveness and their risks. Used thoughtfully and for short durations, NSAIDs and acetaminophen remain valuable tools; symptoms that persist or worsen are signals worth evaluating rather than simply suppressing.

A year later, while she hasn’t regained the mobility and independence she had before her fall, she continues to exhibit moments of brilliance — thanks to the excellent care my siblings arrange for her. A physiotherapist works with her around three times a week, a nurse is present during the day, and a qualified caregiver stays through the night. Since her fall last year, there hasn’t been a single 24-hour period when she’s been without a family member within twenty feet of her — most often, it’s one of my siblings.

And yet, despite all the care and attention she receives, she continues to get UTIs from time to time. Some flares are worse than others, and each recurrence takes a heavier toll on her recovery.

Possible Reasons for Frequent UTIs

When bacteria enter any part of the urinary system they result in a UTI, no matter an individual’s age. The situation is confounded in older adults who have weakened immune systems, especially those who are bedridden and use adult diapers. Unlike younger individuals who may experience classic symptoms like burning during urination or frequent urges to urinate, seniors often show atypical signs such as confusion, agitation, or sudden behavioral changes. If left untreated, a UTI can escalate to more serious conditions like kidney damage or sepsis, the latter often being fatal.

For people in my mother’s situation, unless utmost hygiene is exercised in her care, the likelihood of them having UTIs is significantly higher. The constellation of probable UTI contributors are hopelessly against them. Unable to exercise personal hygiene these individuals are completely dependent on their caregivers.

Treating and Keeping UTIs at Bay

Thanks to the array of antibiotics available these days, UTIs can be treated more effectively than they were a few decades ago. But by the very nature of the mechanisms of their action, antibiotics lead to significant debilitation which taxes an already worn out person, making recovery that much harder.

Common sense measures are also available, perhaps the simplest among them being enhanced hydration, increasing mobility, more frequent diaper changes, and exercising heightened hygiene protocols.

The last two are fully reliant on caregivers.

Threading the Needle with Caregivers

Professional caregivers don’t like being told their hygiene protocols are inadequate — any more than a seasoned chef likes being told their signature dish needs more salt. But experience is a powerful teacher, and visuals amplify credibility.

I spoke to my mother’s professional caregivers. I first had them describe their cleaning protocols, including cleaning various things that they might typically use when changing a diaper. They repeatedly underscored the fact that everything was rinsed with Dettol after use.

Dettol is a widely used antiseptic in more than 100 countries and was the brainchild of a British company in the 1930s. While alternate antiseptics exist, Dettol is widely trusted and is a household, easily recognized name. For many, wiping something down with Dettol is a close equivalent of sterilizing it.

There’s Always Room for Improvement

If Dettol was doing the adequate job the caregivers believed it was, I told them we could check that out. Armed with Petri dishes and sterile swabs, I swabbed the items they said they typically used for diaper changes and spotted them on a dish. The caregivers helped me create a reference sheet that listed each spot. A positive control was my saliva - saliva is always rich with our oral microbiome, a negative control was an aliquot of water that had come to a rolling boil - a process which is meant to kill all bacteria. I let them know that since we didn’t have a 37 C incubator, we would simply have to let the dish be incubated at room temperature for a little longer.

To their utter surprise, they were mortified when they saw the results 24 h later! In this limited, small home experiment, some bacteria thrived despite Dettol.

We quickly implemented a new protocol that involved a different antiseptic, and also included an additional scrubbing step. Overall, we prioritized solving the problem over isolating each variable — that could come later.

Ten days after implementing the new protocol, once again to their utter surprise, but this time it was filled with joy - there was a significant reduction in contamination!

What’s in an Antiseptic/Disinfectant?

A quick PubMed search reveals scores of peer-reviewed publications evaluating a variety of antiseptics in clinical and laboratory settings. Some of the studies are observational, others are more intentional.

In my home conducted n=1 home experiment, the antiseptics used were Dettol and Savlon. Savlon appears to have been more effective, but with the caveat that there was an additional step of scrubbing included.

Let’s look under the metaphorical hood of both these disinfectants to see if my results hold any water and merit a controlled study. The primary components of Dettol are chloroxylenol, terpineol and alcohol; the primary components of Savlon are cetrimide and chlorhexidine gluconate. It is worth noting that the experiment did not include non-antiseptic treated materials, so while Dettol might have controlled the proliferation of some bacteria, switching to Savlon and also including scrubbing appears to have been more effective

While I haven’t found studies that compare the efficacy of the two products side-by-side, comparisons of their components are available in the scientific literature. Based on those publications, it appears that the components of Savlon lend the product the capacity to have a more sustained effect than Dettol.

Implications of This Home Experiment

Before considering the implications, it is important to note that this exploration was not done in a controlled setting and thus cannot endorse a particular disinfectant, nor does it confirm or contest the existing rigorous scientific literature in the field of disinfectants and antiseptics.

The primary goal of this simple experiment was to demonstrate to my mother’s caregivers that small changes can have large effects. While adding an additional scrubbing step (rather than simply rinsing with disinfectant as had been the practice) might have helped, switching to a theoretically more effective disinfectant (from Dettol to Savlon) reduced the bacterial counts profoundly. A collateral win was the opportunity for science communication. Neither caregiver has studied microbiology, and while they will have received training in standard procedures of hygiene, this experiment demonstrated to them the impact of small variables — and how science-based choices can lead to better health outcomes.

This exercise is a reminder that exploring science isn’t just for lab settings — it’s an opportunity to enhance everyday care, especially when lives depend on it. The Petri dish showed there were bacteria, and it sparked a new understanding for the caregivers. Seeing the results firsthand was more convincing than any explanation I could have provided. It wasn’t about assigning blame; it was about working together to find the cause. Experience taught the lesson, and the visuals sealed it.

Acknowledgement: The caregivers referenced in this article—Ms. Yashoda Sonawne and Ms. Santoshi Surwase—are employees of Aajicare.

Disclaimer: The products mentioned here are described only in the context of a personal anecdote. This account is intended for educational storytelling, not product comparison, endorsement, or critique. It does not substitute for medical, clinical, or regulatory guidance. Please consult qualified professionals for any health-related decisions.

There’s a dangerous comfort in pretending that what we don’t measure doesn’t exist. It absolves us of responsibility. If we don’t monitor the air, we can’t be blamed for what’s in it. If we don’t count the particles, we don’t have to regulate them. But reality doesn’t wait for instrumentation.

Over the course of a typical human life, we take in more than 400 million liters of air—enough to fill 175 Olympic swimming pools. With every breath, we’re not just drawing in oxygen and nitrogen, but also minuscule particles, trace substances, and a mix of soluble and volatile compounds. Consequently, ensuring the environment we inhabit is protected and enables good health should not be a matter of argument, but a given.

When the EPA is defunded, when environmental oversight is dismissed as bureaucratic overreach, we’re not cutting red tape—we’re deliberately blinding ourselves. The cost isn’t just scientific; it’s human. Every asthma spike, every unexplained rash, every community downwind from a factory knows this truth the hard way. Coupled with the gutting of staff and research support at all agencies under the Department of Health and Human Services, and with the sweeping federal cuts just pushed through Congress, the future of healthcare in the United States looks worse than bleak.

Community dialogues for science

At a recent Tilde Cafe event, science writer Carl Zimmer shared insights from his 2025 book Air-Borne: The Hidden History of the Life We Breathe. His talk traced the emergence of aerobiology as a scientific field—one that, remarkably, didn’t exist until a few persistent researchers began asking hard questions.

One such pioneer was Fred Campbell Meier whose curiosity about plant diseases launched a new way of thinking about air itself. His research into wheat rust led him to suspect that the atmosphere itself was a conduit for microscopic life - but to what extent was the reach of this atmosphere. In collaboration with pioneering aviators Charles Lindbergh and Amelia Earhart, Meier gathered evidence to support his hunch that even at several hundred feet above sea level, the air was rife with living entities, and that plant diseases were transmissible through air. In fact, in a 1935 paper co-authored by Meier and Lindbergh, in a section titled “HISTORY OF AIR-CONTENT STUDIES” they state “While it is generally known that bacteria, spores of higher fungi and pollen grains are present among dust particles in the atmosphere near the earth's surface, much detailed information of practical value remains to be revealed by further research. The aerial movement of pollen from certain flowering plants concerns the physician who deals with "hay fever" and related troubles. The plant pathologist and the medicopathologist are interested in obtaining facts concerning the part that air currents may play in disseminating reproductive bodies of organisms that cause specific diseases of plants and animals. Definite information of this sort is obviously an aid to a well-planned control program.”

An ecosystem in the air

We’re used to thinking of life as belonging to land and sea. But the air is teeming with microorganisms—bacteria, viruses, fungi, pollen, and even insects. Trillions of these particles move through the sky every day, often traveling thousands of miles. This realm, once dismissed as sterile or cursed, turns out to be a vibrant biosphere in its own right.

The 19th-century Irish Potato Famine offered an early lesson in airborne pathogens. At the time, many believed the blight was divine punishment—or that it emerged spontaneously from decaying crops. But more recent research points to Phytophthora infestans, a mold that likely arrived in the U.S. on air currents from Mexico. It settled on potatoes that were bound for Ireland, where the cool, damp climate provided ideal conditions for it to take hold—leading to catastrophe.

The episode illustrates a crucial principle: pathogens that remain dormant or limited in their native environments can wreak havoc when displaced—if the surrounding conditions allow it.

Immunity begins with the air

A newborn’s first breath does more than initiate respiration—it sets into motion a cascade of biochemical and immunological events that shape lifelong health. This moment marks the lungs' transition from a fluid-filled environment to direct exposure to air, and with it, the first encounter with the outside world’s microbial landscape.

When the lungs inflate, epithelial cells release molecular signals—a biochemical wake-up call to the immune system. These early alerts help shape a balanced airway environment, ready for a lifetime of exposure to foreign particles and microorganisms.

With the first breath, airborne microorganisms begin colonizing the upper and lower respiratory tracts. This initial wave of colonization lays the groundwork for the airway microbiome, influencing susceptibility to respiratory diseases and allergic responses later in life.

Like some plant pathogens, some avian and mammalian pathogens are also carried through the air. Outbreaks of diseases like measles, tuberculosis, and COVID are all mediated by airborne transmission.

In 2025, more than fifty years after a reliable vaccine for measles was developed, 35 of 50 states in the US have reported measles cases that are far in excess of any in recent history. Similarly, while scientists have dedicated their careers towards understanding and developing tools to fight other airborne diseases, decision-makers seem hell bent in throwing caution to the winds, ignoring the importance of monitoring air quality and the implementation of key processes to maintain it at healthy levels.

Breathing connects to the gut microbiome

Intriguingly, what infants breathe can even influence the gut microbiome. Airborne microbes may influence the gastrointestinal tract by triggering systemic immune pathways that modulate gut colonization. Because the gut microbiome plays a central role in training the immune system, these early exposures are critical for shaping the body's defenses. A recent study from Harvard has shown that the gut microbiome is tightly tied to the air we breathe. Work from Australia also prompts us to consider the volatile nutrients that are carried in air and the negative impacts of poor air quality on those nutrients, and thus on overall health.

Trillions in transit

By some estimates, at any given moment there are trillions of microbes swirling around us. While not all of them cause disease, it behooves us to have an effective agency that ensures the air we breathe is clean, and an agency that ensures healthcare is not hamstrung by politics. The sweeping legislative Big Buggy Bill that was just passed by the House and Senate is estimated to add $3.4 trillion to the deficit over 10 years. Had it been an honest effort by our elected officials, we could have had a truly Big Beautiful Bill—one that preserved testable science, good governance, and public health instead of gutting them.

On a personal note, it was precisely the story of the invisible that drew me to study microbiology. My sister had a copy of Roger Stanier’s General Microbiology and I read the introduction describing how Antonie van Leeuwenhoek’s and Louis Pasteur’s work had revealed the busy invisible world around us — how could I possibly ignore the wonders of it!

Language as a System

Language is not just a tool for communication—it’s a system, shaped by time, culture, and cognition. Like any system, it reflects the assumptions and priorities of the societies that use it. Linguistics, like physics or biology, seeks to uncover the hidden rules that govern complex language systems. Just as astronomers analyze planetary motion or biologists map genetic codes, linguists analyze the structure of language—its syntax, semantics, and phonology—to understand how humans communicate. Pronouns, ubiquitous yet often overlooked, offer a particularly rich entry point into this exploration.

The Endurance of Pronouns

Pronouns are among the most stable elements of language. We use them constantly, often without noticing. Yet these small words carry significant weight. They are ancient, evolving, and deeply embedded in how we understand ourselves and others. And in recent years, they’ve become a focal point in broader conversations about identity, inclusion, and change.

Words, Concepts, and Meaning

A foundational idea in the philosophy of language—dating back to Aristotle—is that words don’t connect directly to the world. They connect to concepts: mental representations shaped by experience and culture. When we say “coffee,” we might mean the beans, a steaming cup, or even the ritual of our morning brew. The word doesn’t pin down a single thing—it gestures toward a whole category, a shared understanding. Language often works this way: words can refer to individual things, but they also activate broader concepts. Pronouns are a particularly interesting case—not only do they refer, they also reflect the structure of language and the assumptions we bring to it.

Pronouns as Social Mirrors

Pronouns reveal how we categorize people, how we relate to them, and how we position ourselves in relation to others. They are not fixed labels. “They” might refer to a group of friends, a single person whose gender is unknown, or even a pair of scissors. Their meaning is fluid, context-dependent, and culturally loaded.

This fluidity is precisely what makes pronouns both powerful and controversial. In English, we distinguish “he” from “him,” “I” from “we,” but other languages draw lines we don’t—between formal and informal “you,” or between inclusive and exclusive “we.” What feels natural in one language may be invisible in another. Grammar, it turns out, is not neutral. It encodes history, power, and social norms.

Interestingly, the use of plural pronouns in singular contexts in English—particularly “they/them” for individuals—has a precedent in many other languages. In most Indian languages, plural forms are routinely used to refer to a single person as a mark of respect. This practice, known as honorific plural, treats grammatical plurality not as a matter of number, but of social dignity. So while some English speakers view singular “they” as a grammatical stretch, it actually aligns with a long-standing global linguistic pattern—one that uses plurality to elevate, not confuse.

Why Change Feels Hard (but Happens Anyway)

Changes to pronoun usage can feel disorienting, in part because pronouns are so deeply embedded in everyday speech. They are high-frequency words, and shifts in their use require broad social adoption. It’s not unlike changing the design of traffic lights—everyone is affected, and consistency matters.

But pronouns are also like glaciers: ancient, slow-moving, and seemingly immovable—until they shift. And when they do, they reshape the landscape. Neopronouns like “ze” or “hir” follow familiar linguistic patterns (we turned “Google” into a verb, after all), but they haven’t yet reached the same level of usage or familiarity.

Yet language does change. English speakers once said “thou” and “ye”; now we say “you.” The singular “they” is not a new invention but a re-extension of a form that has existed for centuries. What’s new is the awareness of what it means—using language not just to describe the world, but to shape it in more inclusive ways.

Beyond Grammar

At its core, pronoun use and pronoun choice aren’t just grammatical issues—they’re about whether language can evolve to reflect a broader, more inclusive understanding of identity.

And this is where the conversation becomes most urgent. Because linguistic debates are never just about words. They are about people. They are about the concepts we hold, the categories we create, and the world we want to build.

*This piece is my take on a Tilde Cafe hosted talk by Professor Claire Bowern from the Department of Linguistics at Yale University.

The unjust detention of Columbia University graduate student Mahmoud Khalil—a legal green card holder—over his support for Palestinian rights is a disgraceful violation of fundamental freedoms. History warns us where this road leads. During the McCarthy era, thousands of Americans were surveilled, interrogated, and blacklisted—not for any crime, but for suspected political affiliations. Today, we are witnessing a new Red Scare, where pro-Palestinian activism is framed as a national security threat, and individuals are targeted not for their actions, but for their beliefs.

Being pro-Palestine does not equate to being a terrorist, supporting Hamas, or being anti-U.S. Of course, no one is saying that criticizing Israel’s actions will get you labeled an extremist—except that is exactly what’s happening. Just yesterday, a postdoctoral researcher, Badar Khan Suri, at Georgetown University was detained by ICE for the same reason. Suri, an Indian national, is accused of disseminating pro-Hamas propaganda and promoting antisemitism on social media.

These are not isolated incidents. Across the country, students, academics, and activists who speak out in support of Palestinian rights are being targeted, harassed, and, in some cases, criminalized. University administrations have suspended student groups, issued disciplinary threats, and canceled events. Legal observers have noted an unprecedented crackdown on political expression, particularly against those advocating for Palestinian lives. What began as academic ostracization has escalated into direct government intervention, with immigration authorities weaponized against those who dissent.

We have been reduced to a climate where judges fear for their safety, and legal scholars warn that this is how constitutional crises begin. When the government starts deciding which political opinions are acceptable and weaponizes law enforcement to detain, intimidate, and deport immigrants for their beliefs, it is a direct attack on the First Amendment, due process, and the very foundation of democracy. This is a dangerous erosion of democratic principles—punishing dissent, suppressing free speech, and criminalizing protests are tactics used by authoritarian regimes, and the U.S. is heading down that path.

This is not the first time in American history that dissent has been met with state-sanctioned repression. During World War I, the Espionage and Sedition Acts were used to imprison even US-born citizens critical of the war effort, including labor leader Eugene V. Debs, whose only crime was giving an anti-war speech. Debs was born in Terre Haute, Indiana – in the heartland of the United States. In the 1960s, the FBI targeted Black civil rights leaders, Muslim activists, and anti-war organizers, branding them as threats to national security. Now, in 2025, we are witnessing a new iteration of this playbook—where the government suppresses opposition not with outright bans, but through intimidation, surveillance, and selective prosecution.

This moment signals an alarming shift in the balance of power, where the government, under the guise of "national security," can strip people of their freedoms simply for refusing to remain silent in the face of human rights violations. If this precedent is allowed to stand, what comes next? Will any form of political dissent be grounds for revoking legal resident status? Will U.S. citizens face similar retaliation for challenging state policy? This is how democracies collapse—not all at once, but through a slow erosion of rights, justified by fear and constant threats.

Oppression thrives when people are too afraid to resist, and that is exactly the goal of these escalating attacks on political speech and civil liberties. But the suppression of dissent is just one piece of a larger pattern of repression. A government that stifles dissent is a government that will continue to erode the rights of those it deems expendable.

We are at a breaking point. We must expose and reject government overreach that seeks to punish dissent under the guise of “national security” and hold elected officials accountable for upholding civil liberties, free speech, and the right to political advocacy without fear of retaliation.

We cannot afford to stand by while fundamental rights are dismantled in real time. Because if we allow this to continue, the next political prisoner could be any one of us.

And if we don’t speak up now, who will?

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From decoding our genes to saving forests to rewriting the rules of physics, these women scientists working on every continent are proof that discovery knows no borders. Here’s your world tour of brilliance.

Africa

1. Wangari Maathai (Kenya) – Environmental Science

She was awarded the Nobel Peace Prize in 2004 for her environmental and political activism. She founded the Green Belt Movement, which has planted over 50 million trees to combat deforestation and promote sustainable development.

2. Quarraisha Abdool Karim (South Africa) – Epidemiology

She is an infectious diseases epidemiologist whose landmark research on HIV prevention has empowered women with methods to control their own health.

Asia

3. Tu Youyou (China) – Pharmaceutical Chemistry

Discovered artemisinin, a groundbreaking antimalarial drug that has saved millions of lives worldwide. Her work, which earned her the 2015 Nobel Prize in Physiology or Medicine, revolutionized the treatment of malaria and highlighted the value of traditional Chinese medicine in modern science.

4. Kamal Ranadive (India) – Cancer Biology

Her research focused on the links between cancers and viruses, contributing significantly to laying the groundwork for the field.

North America

5. Katherine Johnson (USA) – Mathematics & Aerospace Engineering

Her mathematical calculations were critical to the success of the first U.S. crewed spaceflights, including John Glenn's orbital mission. Her work at NASA broke barriers for African American women in STEM and earned her the Presidential Medal of Freedom in 2015.

6. Donna Strickland (Canada) – Physics

Her innovation in laser technology allows for extremely short and intense pulses of light, enabling applications like corrective eye surgeries and precision industrial manufacturing.

South America

7. Mayana Zatz (Brazil) – Genetics & Molecular Biology

Her groundbreaking work in muscular dystrophy has extended to advocating for patients' rights and advancing genetic research in Brazil.

8. Eugenia del Pino (Ecuador) – Developmental Biology

She is a renowned developmental biologist whose research on the embryonic development of marsupial and poison arrow frogs has significantly advanced the field of developmental biology

Europe

9. Marie Curie (Poland/France) – Physics & Chemistry

Her notebooks are still radioactive! She was the first person to win Nobel Prizes in two different sciences.

10. Emmanuelle Charpentier (France) – Biochemistry & Genetics

She co-invented CRISPR, the gene-editing tool that has been rewriting the field of medicine for treating diseases.

Australia

11. Fiona Wood (Australia) – Medicine

Her work transformed care of burn victims – she developed spray-on skin for burns, saving many lives after the Bali bombings.

12. Elizabeth Blackburn (Australia/USA) – Molecular Biology

She discovered how chromosomes are protected by telomeres and the enzyme telomerase. Her groundbreaking work has significantly advanced our understanding of cellular aging and cancer.

Antarctica

(researchers working there)

13. Katharine Giles (UK) – Climate Science

Before her tragic death in 2013 she mapped how melting sea ice disrupts polar oceans.

14. Christina Hulbe (New Zealand) – Glaciology

Her research focuses on polar glaciology, studying how and why polar ice sheets change over time, with a particular emphasis on the Ross Ice Shelf. Her work is crucial as we navigate the ongoing climate crisis.

Courageous innovators

These scientists asked bold questions, challenged old ideas, and opened doors for others. It’s impossible to list all the pioneering women scientists, but these fourteen stories show why diversity matters and how science grows stronger when more voices are part of the work.

The best way to honor women scientists is to keep their work visible — not only during Women’s History Month, but whenever we talk about science and who has the freedom to shape it. Let’s all Stand Up for Science.

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Adding to the confusion, media reports have often conflated rare earth elements with the broader category of critical raw materials. In 2022, Ukraine’s Deputy Environmental Minister said 5% of the world’s critical raw materials lie within Ukraine, which covers just 0.4% of Earth’s surface. Many news outlets mistakenly applied this figure to rare earth elements specifically—a textbook example of scientific nuance getting flattened into a convenient headline.

To clarify, rare earth elements are just a subset of the 50 critical raw materials listed by the US Geological Survey. Of those, 16 are rare earths (only promethium is absent), and their importance stretches far beyond today’s headlines.

Periodic table to the rescue

The fact that President Trump was pushing to secure these resources is worth noting. To understand why, we need to step back and follow the fascinating history of the periodic table, and how it shaped the technology we rely on today.

For centuries, humans tried to organize naturally occurring elements in a manner that was logical. In the sixteenth century, Theophrastus Bombastus von Hohenheim, or Paracelsus, outlined the tria prima based on the prevailing influence of alchemy. He presented a triangle with vertices represented by mercury, sulphur, and salt, believing all of life could be reduced to a combination of these three parts. Parcelsus's tria prima could perhaps be viewed as the crudest attempt at a periodic table of elements.

Chemistry began to emerge as a distinct science, separate from alchemy, thanks to Robert Boyle's work in the late seventeenth century. Over the next 100 years, substantial efforts were made to organize the elements. Antoine-Laurent Lavoisier defined elements as being substances that cannot be broken into simpler entities. Based on his definition, he considered 33 substances to be elements and published the book Traité élémentaire de chimie in 1789 to spread his thesis. (Here is a 1789 English translation by Robert Kerr - some of the points Lavoisier makes in the preface are brilliant and timeless). Through his calculations, he predicted the existence of silicon—which was discovered 40 years later. Thanks to subsequent refined techniques, we now know that ten of the 33 entities he called "elements" are not elements.

Dmitry Ivanovich Mendeleyev, or Dmitri Mendeleev, was born almost 40 years after Lavoisier's publication. By this time, John Dalton had published A New System of Chemical Philosophy (1808), listing 20 elements with their atomic weights. Fast forward another 50 years when at an international conference of chemists, it was decided that hydrogen which was known to be the lightest element be given a weight of 1, and the weight of all other elements would be ascribed based on how many times heavier they were than hydrogen. Soon after, British chemist John Newlands noticed a repeating pattern in atomic weights—what he called a "law of octaves," likening it to music. Elements seemed to fall into groups of 7, repeating every 8th element. But this pattern didn't hold beyond a point, and his work was ridiculed. Other chemists continued to work on this problem, and unaware of each others' work, Mendeleev and Julius Lothar Meyer came up with their own versions of how the elements are organized.

On March 6, 1869, Dmitri Mendeleev presented the first periodic table to the Russian Chemical Society. His table, titled “The Dependence between the Properties of the Atomic Weights of the Elements”, was a triumph of scientific intuition. By organizing elements according to atomic weight and chemical behavior, Mendeleev revealed a hidden order in nature—and even predicted the existence of elements not yet discovered.

Less than a decade later, on March 7, 1876, Alexander Graham Bell was awarded a patent for the telephone—a device whose success depended on the chemical properties of the materials used to make it. Bell’s early phone was simple, relying mainly on iron, copper, and zinc.

Every improvement since—from rotary dials to touchscreens—has been shaped by the discovery and application of new materials, a process made vastly more efficient thanks to the periodic table. Broadly speaking, our ability to predict the properties of materials—rather than just experimenting blindly—owes everything to Mendeleev’s work. In fact, most of the advances we see in almost every facet of life—from your favorite mobile device to the discovery of new drugs—are made more efficient thanks to the periodic table.

Mendeleev's contribution was most remarkable in the table he outlined because he left gaps for elements that had not been discovered at the time, but were predicted to be found based on his calculations. The elegance of Mendeleev's work is also underscored by the fact that as we learnt more about atoms in the twentieth century, those findings in no way disturbed Mendeleev's periodic table of elements. In 1869, when Mendeleev published his periodic table, only 60 elements were known. Today, we have 118 elements (including natural, and synthesized) in the periodic table, and Mendeleev's organization remains largely intact.

Rare earth elements

Scientists knew some elements were still missing, but isolating them was another story—especially the rare earths, which stubbornly refused to stand out. They occupied an awkward middle ground: not precious like gold, not workhorse metals like iron, just oddballs hiding in plain sight.

There are seventeen rare earth elements (REEs) neatly visualized in the periodic table. If you aren’t familiar with the periodic table, the rows are called periods, and columns are called groups. Elements are represented by one or two letters, mostly based on greek or latin names. Without getting too deep into the table, the image below shows the seventeen REEs - from group 3 - scandium (Sc), yttrium (Y), and the lanthanides with lanthanum (La) being a placeholder below yttrium, for the entire family commonly called lanthanides or lanthanoids.

Even the name “rare earths” is misleading. The term dates back to the late 18th century and they aren’t particularly rare (some are more common than copper, and together, almost 200 times more abundant than gold). Unlike many other elements, they don’t cluster into rich, convenient veins and are instead, scattered thinly across the earth’s crust, making extraction a chemically difficult process—a challenge that delayed their large-scale use until the 20th century.

While not rare, these elements aren’t uniformly distributed—China holds the largest reserves, dictated by specific geological environments. Importantly, for these elements to be useful, they must go through a complex purification process—and today, China handles most of the world’s production, leaving the US 100% reliant on imported rare earths. In 2017, the US Department of Energy presented a report to Congress, discussing the future of alternate avenues to secure necessary amounts of rare earths. According to the 2024 report from the US Geological Survey, the China holds almost 40% of the global reserves. It’s worth noting that minable concentrations of rare earths are much lower than their overall abundance in Earth’s crust.

Why is there such a demand for rare earths?

That Congressional report includes a useful summary highlighting at least one key application for each of the seventeen rare earths. It becomes clear from this summary that there is almost nothing you do or use daily is untouched by rare earths.

As we grapple with the complexities of our modern world, the critical role of rare earth elements in shaping the geopolitical landscape cannot be overstated. The competition for these vital resources has forged new alliances and intensified existing rivalries, underscoring the interconnectedness of science, technology, and global diplomacy. By understanding both the history and the current geopolitics surrounding rare earth elements, we gain a clearer sense of their significance—and the challenges ahead. Ultimately, our ability to innovate and collaborate across borders will determine how we navigate this ever-evolving landscape and ensure a sustainable and prosperous future for all.

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