A Pill for Time: The Promises and Perils of Rapamycin

1:12. 0:43. 0:21. Each morning, countless Americans open their New York Times app, fingers hovering over the Mini Crossword, ready to shave off mere fractions of a second from their personal best time — a daily ritual of racing against the clock, pursuing an elusive new record. Down to 0:19. Then 0:18. The thrill of watching the clock tick lower and lower.

Our obsession with time isn’t limited to daily puzzles; it extends to the ultimate race: the quest for a longer life. This pursuit is anything but new — humans have been trying to outmaneuver death since we first became aware of our own mortality. From ancient Egyptian hieroglyphs to Chinese alchemical texts, from Plato's musings to Aristotle's contemplations, the dream of extending life has echoed through millennia of human civilization. However, what took centuries of philosophical pondering to even conceptualize has now quickly become a reality through scientific advancement. In short, modern medicine has transformed the abstract theories of Plato and Aristotle into concrete gains. At the beginning of the 19th century, no country's life expectancy exceeded 40 years, but today, the global average life expectancy is estimated to be 72.6 years [3]. Although life expectancy has increased across all ages, most of our dramatic gains in average lifespan have come from technological and medical breakthroughs focused on preventing early deaths — keeping infants alive, curing infectious diseases, and making childbirth safer.

Consequently, modern medicine has been so successful in curbing death rates among the young that we've nearly exhausted all possible improvements in early-life mortality. Now, researchers must shift their focus to a new frontier: preventing deaths in old age itself. Unlike preventing early mortality, extending life in old age means confronting bodies that have accumulated decades of biological wear and tear, where cellular damage, chronic inflammation, and deteriorating systems create a maelstrom of mortality risk. In other words, each additional year of life expectancy has become increasingly harder to achieve.

This challenge has led scientists down an unexpected path as researchers have begun to focus on tackling old age from its roots: can we slow aging itself? The answer may lie in an unlikely source. Rapamycin, first discovered in the soil of Easter Island, isn't a mythical fountain of youth —but its effects may have the potential to change how we experience aging itself.

Historically, Rapamycin has been used as an oral immunosuppressant for organ transplant patients. Recent research has uncovered, however, that at low doses, rapamycin appears to reduce inflammation by inhibiting the mTOR signaling pathway, which serves as a critical regulator of aging and the body's lifespan [1]. Inspired by this discovery, scientists such as Dr. Matt Kaeberlein have started testing in animal models, with results indicating that rapamycin usage in mice can result in up to a 30% increase in lifespan [2]. Further research has proved even more successful, as shown in a trial where a one-time 3-month dosage of rapamycin in mice resulted in longer life and substantial improvements in murine heart function [2]. Due to the extensive genetic similarities between mice and humans, scientists have started to hypothesize that rapamycin may have similarly beneficial effects on human life spans.

Despite promising results in animal models, significant hurdles remain before rapamycin can be considered a viable option for improving human longevity. The long-term effects in humans are still unknown, and an optimal dosage for anti-aging purposes has yet to be established. Complicating matters further, the FDA doesn't currently recognize aging as a disease, which means that 1) drugs targeting aging specifically aren’t eligible for approval as treatments, and 2) clinical trials using rapamycin are plagued by ill-fitted regulatory constraints. Thus, leading researchers on aging and rapamycin, including Dr. Matt Kaeberlein and Dr. Eric Verdin, publicly advise against using rapamycin for life extension. The twist? They are taking it themselves, prescribed off-label [4]. 

The actions of leading longevity researchers speak louder than their words. Dr. Kaeberlein and Dr. Verdin's actions serve antithetical to their public advice. But why? For them and many others, they don't have enough years left in their lives to wait for conclusive results from long-term studies; it's now or never. So, while unapproved, is it safe to bet on rapamycin extending your life without knowing its long-term impacts?

The answer varies for each individual, but regardless of personal choice, rapamycin represents a concerning shift in our approach to longevity — the pursuit of potentially harmful quick fixes over proven routines. While exercise, nutrition, and lifestyle modifications require consistent effort, they build a foundation for comprehensive health that extends beyond mere lifespan. Rapamycin, in contrast, offers a seductive shortcut that bypasses these holistic benefits. By reducing the complex journey of healthy aging to a pill, we not only risk oversimplifying the multifaceted factors that contribute to longevity but also ignore the importance of lifestyle, environment, and social determinants of health in favor of quick pharmacological fixes.

However, the strongest argument against rapamycin’s usage lies in its potential to deepen America's already severe health disparities. Off-label prescriptions and high costs mean that even if rapamycin proves effective for human longevity, its benefits will flow primarily to the wealthy. This accessibility issue creates an unprecedented form of inequality where money doesn’t just buy better healthcare, but also more years of life itself. In an increasingly costly healthcare environment, the wealthy already enjoy longer lives due to better access to healthcare, nutrition, and healthy lifestyles. Adding rapamycin to this equation would only widen the existing life expectancy gap, fostering a society where longevity becomes a luxury good rather than a human right.

Crucially, the most urgent step isn't deciding whether to take rapamycin; rather, it is reconsidering how we view aging itself. Our current regulatory framework, which doesn't recognize aging as a disease, creates a pharmaceutical catch-22: we can't properly study anti-aging treatments because aging isn't classified as a treatable condition, yet we hesitate to classify it as such because we lack proven treatments. Breaking this cycle requires a fundamental shift in how we conceptualize and regulate aging intervention research. Only by acknowledging aging as a medical condition—rather than as an inevitable decline—can we create the regulatory framework needed to properly study, develop, and equitably distribute treatments like rapamycin.

Until then, we're left with an uncomfortable reality: a promising compound that sits in regulatory limbo, prescribed off-label by those who can afford it, while the broader implications of its use remain underexplored. Ultimately, the debate around rapamycin isn't just about a potential life-extending drug—it's a mirror reflecting our society's complex relationship with aging, inequality, and the lengths we'll go to add a few more numbers to our personal timers.

Graphic by Monica Rashkov

Reviewed by Nick Hoffmann

References

1. Abuery, A. (2024, July 1). Could a decades-old transplant drug unlock the secret to longer life? NPR. https://www.npr.org/sections/shots-health-news/2024/07/01/nx-s1-5008777/rapamycin-aging-disease-drug-humans-research

2. Kaeberlein, M. (2024, January 15). Rapamycin: The most promising life extension drug [Video]. YouTube. https://www.youtube.com/watch?v=DcxgEwQKx8Q

3. Roser, M., Ortiz-Ospina, E., & Ritchie, H. (2024). Life Expectancy. Our World in Data. https://ourworldindata.org/life-expectancy-globally

4. Whalen, J. (2024, March 15). A transplant drug shows promise for extending life. Should you take it? The Washington Post. https://www.washingtonpost.com/business/2024/03/15/rapamycin-longevity-drug/

The Scoop on Lactose Intolerance: Is It Really All About the Milk?

If you’re lactose intolerant, then you know: one scoop of ice cream is all it takes to

experience a gut-wrenching sensation. But what if lactose intolerance wasn’t solely about dairy?

New research suggests that your gut bacteria might be playing a leading role in those post-dairy

blues (Brandao Gois et al., 2020).

Let’s start with a quick refresher: lactose intolerance is usually the result of missing

lactase, the enzyme that digests lactose, the sugar in milk. Without lactase, lactose just stays in

your gut, leading to bloating, gas, and discomfort (Misselwitz et al., 2019). However, scientists

are finding that the gut microbiome, the community of trillions of bacteria in your digestive tract,

might be more involved than previously thought. One genus in particular, Bifidobacterium,

seems to be a prime suspect (Brandao Gois et al., 2020).

Bifidobacterium and other bacteria in the gut are capable of fermenting lactose. You

might think that’d help, but their “help” creates gas and byproducts that can sometimes make

lactose intolerant symptoms even worse (Misselwitz et al., 2019). In other words,

Bifidobacterium is basically acting like that overly enthusiastic friend at a karaoke party –

well-meaning, but a little too intense.

A study from the Lifelines-DEEP Dutch population cohort dove into this theory by

analyzing 959 participants. They found that people with the genetic LI variant (a particular gene

combo called G/G on SNP rs4988235) had higher Bifidobacterium populations in their gut.

Additionally, the more Bifidobacterium, the higher the frequency of GI complaints – specifically

abdominal pain, discomfort, and bloating (Brandao Gois et al., 2020). So, instead of simply

digesting lactose, these bacteria are throwing a party in your stomach (Leon, S. D., 2021).

A second study noted that Bifidobacterium actually correlates positively with dairy intake

in people with lactose intolerance but not in those without it (De Vrese et al., 2001). In other

words, the real problems seem to start when dairy enters the picture, activating these

lactose-loving bacteria, and triggering all those uncomfortable symptoms.

So what’s the takeaway? Avoiding dairy might still be your safest bet for now, but the

future might hold other options. Imagine, rather than going dairy-free, managing

Bifidobacterium levels in your gut could allow you to indulge without regretting it later.

Scientists are actively exploring gut-modifying treatments – from probiotics to dietary tweaks –

which could one day give lactose-intolerant folks a pathway to enjoy dairy without a hitch. Until

then, though, you might not want that extra scoop.

Reviewed By: Aman Meredia

Designed By: Ashley Gutierrez-Torres

References

1. Brandao Gois, M. F., Sinha, T., Spreckels, J. E., Vila, A. V., Bolte, L. A., Weersma, R. K.,

Wijmenga, C., Fu, J., Zhernakova, A., & Kurilshikov, A. (2020). Role of the gut

microbiome in mediating lactose intolerance symptoms. Gut.

2. De Vrese, M., Stegelmann, A., Richter, B., Fenselau, S., Laue, C., & Schrezenmeir, J.

(2001). Probiotics – compensation for lactase insufficiency. The American Journal of

Clinical Nutrition.

3. Foster, P. (2019, April 11). Can changing the microbiome reverse lactose intolerance?.

Department of Biology.

https://biology.indiana.edu/news-events/news/2019/foster-lactose-intolerance.html

4. Leon, S. D. (2021, June 18). Lactose intolerance: Bacteria that causes it and how to treat

it. Floré by Sun Genomics. https://flore.com/blogs/learn/lactose-intolerance-bacteria-that-causes-it-and-how-to-treat-it?srsltid=AfmBOoq-gZlTLRZ2ksgmFhYTKeTTUQ3FNjeSxvEiGs5-eFgfyrPH12o9

5. Misselwitz, B., Butter, M., Verbeke, K., Fox, M. R., & Vanner, S. J. (2019). Update on

lactose malabsorption and intolerance: Pathogenesis, diagnosis, and clinical management.

Gut and Liver.

Dancing Through Diet Culture: How Eating Disorders Impact the Health of Dancers

When Heidi Guenther, a successful 22 year old ballerina, died suddenly from a heart attack caused by a severe eating disorder, it became apparent to the public that something had to change in the world of ballet [1]. It is no secret that young dancers often develop an unhealthy relationship with food. Growing up surrounded by mirrors in an environment that encourages perfectionist tendencies and comparison to others can wreak havoc on one’s mental health. Furthermore, there is a culture of thinness in ballet that can easily influence dancers even in the healthiest, most supportive of studios. 

Compared to the general public, dancers have three times the risk of developing an eating disorder [2]. This does not only affect the mental health of ballerinas; their physical performances can also be severely hindered. Specifically, an eating disorder known as Anorexia Nervosa can cause impaired judgment, weakness, and an increased risk of injury [3]. Beyond impairing performance—whether in a young, aspiring student or a seasoned professional—eating disorders can also lead to life-threatening, long-term health consequences. Anorexia is known to damage the heart muscle, reduce bone density, lead to hair loss, and cause significant dehydration[4]. Bulimia Nervosa, another eating disorder common among dancers, can cause heart failure, tooth decay, ruptured esophagus, and peptic ulcers [5]. Anorexia, Bulimia, and other eating disorders are deadly diseases that run rampant through the dance community, impairing development and destroying careers. 

Although the tragic history of eating disorder-related trauma and deaths among dancers cannot be erased, the dance world has acknowledged this harsh reality and is now shifting toward promoting nutritional education and healthier habits. An increasing number of dancers are given the opportunity to develop their skills in nurturing environments that favor health over thinness, bringing a new strength and longevity to the world of dance.

Edited By: Jack Ringl

Designed By: Soojin Lee

References

[1] Mehren, E. and Ybarra, M.J. (1997, July 17). A Dancer’s Death Hints at ‘a Cult of Secrecy.’ Los Angeles Times. https://www.latimes.com/archives/la-xpm-1997-jul-17-ls-13399-story.html

[2] Arcelus, J., Witcomb, G. L., & Mitchell, A. (2014). Prevalence of eating disorders amongst dancers: a systemic review and meta-analysis. European eating disorders review: the journal of the Eating Disorders Association, 22(2), 92–101. https://doi.org/10.1002/erv.2271

[3] Eating Disorder Hope. Elite Athletes and Anorexia Nervosa: What Coaches, Trainers, Administrators & Parents Need to Know. https://www.eatingdisorderhope.com/blog/symptoms- eating-disorders-athletes-anorexia#:~:text=Athletes%2C%20Anorexia%20%26%20Health%20Risks&text=These%20athletes%20may%20experience%20impaired,such%20as%20anxiety%20or%20depression.

[4] National Eating Disorders Association. (2005). Health Consequences of Eating Disorders. Chapman. https://www.chapman.edu/students/health-and-safety/psychological-counseling/ _files/eating-disorder-files/4-hlth-cons.pdf

[5] National Eating Disorders Association. (2005). Health Consequences of Eating Disorders. Chapman. https://www.chapman.edu/students/health-and-safety/psychological-counseling/ _files/eating-disorder-files/4-hlth-cons.pdf