The top scientists driving circadian anything

The names you will be hearing in science as we head into an era of circadian X

May 14, 2026

I’m just now coming down from the high of my first Society for Research on Biological Rhythms (SRBR) conference, held on the beautiful Amelia Island and attended by top scientists and clinicians in the field of circadian science. We spent 5 research-packed days together at roundtables, panels, poster sessions, and coffee networking. As a newcomer to the tight-knit community of circadian science, I felt like I had entered an Olympic event as a mere mortal. So I can distill the information and not invoke too much eyeball glaze from my readers, this is Part I of II in a short series, so be sure to check out Part II when you're finished here.

A thread running through the work of leading scientists in circadian science helps explain why circadian medicine is generating so much momentum right now. It is that timing is a dimension of health that traditional medicine has largely ignored. When we eat, when we sleep, when we take a drug, when we exercise, and when we are exposed to light. These are not incidental variables, as the science is now showing.

What the 2026 SRBR meeting made clear to me is that the field is passing through an inflection point. Circadian science is now mature enough that the translational question is no longer whether timing matters, but rather how we measure it, how we intervene on it, and how we build systems that make it accessible in clinical care.

The leading scientists attending this year’s conference are bringing three complementary solutions to that challenge: population-level phase measurement, cardiovascular precision medicine, and behavioral interventions people can actually implement.

From our Nobel Laureate to the pioneer in longevity, here are the top researchers from SRBR you should know, what they’ve been talking about, and how they are leading the charge in circadian science.

1. Michael Rosbash. 2017 Nobel Laureate

Who He Is Michael Rosbash is a professor and Howard Hughes Medical Institute investigator at Brandeis University, and the 2017 Nobel Laureate in Physiology or Medicine, an honor shared with Jeffrey Hall and Michael Young, “for their discoveries of molecular mechanisms controlling the circadian rhythm.” Sitting in the same room with a person of such contribution was, for me, like being near the red carpet with one of your all-time favorite rock stars.

What He Built Rosbash’s contribution is foundational in the most literal sense: without his work, the field of circadian medicine as we know it wouldn’t exist. In 1984, his lab (alongside Hall) cloned the first clock gene, period. Then, in 1990, following the discovery by postdoctoral fellow Paul Hardin that the period protein oscillated in a 24-hour cycle, Rosbash and Hall proposed the Transcription-Translation Negative Feedback Loop (TTFL), the core conceptual model that explains how biological clocks keep time at the molecular level. This model, now confirmed across species from fungi to humans, explains how a set of proteins essentially “count” 24 hours by building up and breaking down in a self-sustaining loop. In 1998, his lab went on to discover the cycle gene, the clock gene, and the cryptochrome photoreceptor. Without his work, circadian anything would not be where it is today.

What He Discussed at SRBR 2026 Rosbash chaired and spoke in the Saturday session titled “What is Ready — or Almost Ready — for Prime Time, and What Is Not?” I thought this was a deliberately provocative framing, asking the field’s leadership to draw honest lines between what circadian science has proven and what remains aspirational. With so much commercial and clinical interest now flowing into chronobiology, the risk of overpromising is real, and a conversation I believe the field needs. That he was chosen to anchor this session is also telling. He also spoke Tuesday evening in “Where Should Circadian Biology Go Next? A Community Conversation,” And this was one of SRBR’s closing, open-floor dialogue about the field’s future direction.

Current Focus At 81, Rosbash remains a working scientist, not a figurehead, and I was struck by his willingness to publicly ask “what is not ready?” His active research at Brandeis explores RNA processing and transcriptional regulation in the context of circadian clocks.

2. Charles Czeisler. Defined How Light Controls the Human Clock

Who He Is Charles Czeisler is the Professor of Sleep Medicine at Harvard Medical School, Chief of the Division of Sleep and Circadian Disorders at Brigham and Women’s Hospital, and arguably the single most influential figure in translating circadian biology into human clinical practice. He has been researching this field for over 40 years.

What He Built Czeisler’s career is defined by a series of landmark human studies. He was among the first to rigorously characterize the intrinsic period of the human circadian clock (approximately 24.2 hours, not exactly 24) and the precise mechanisms by which light resets it. His lab demonstrated that the wavelength, duration, timing, and intensity of light independently affect circadian phase (work that later helped explain why blue-rich evening light from screens is so disruptive to sleep). He investigated how blind individuals without vision can still retain circadian responsiveness to light through melanopsin-containing retinal ganglion cells, a finding that reshaped understanding of non-visual photoreception in humans.

Beyond basic science, Czeisler has been the field’s most prominent voice on public health implications: he conducted influential studies on the consequences of physician sleep deprivation during residency, helped reform hospital work-hour policies, and has worked extensively on shift work, jet lag, and occupational safety. In 2023, together with Elizabeth Klerman, he organized a Harvard seminar on whether daylight saving time should be abolished (a policy question with genuine circadian biology underpinning it, and a very passionate topic at the SRBR this year). His lab’s most recent work includes circadian proteomics (mapping how the blood proteome oscillates over 24 hours) and the development of tools to estimate circadian phase from wearable data. This work is a critical step toward clinical deployment.

What He Discussed at SRBR 2026 Czeisler delivered a keynote on sleep and circadian rhythms in clinical practice. His speech set the proverbial stage for the conference’s opening day. He also participated in a panel discussion on what it would look like for circadian rhythms to be routinely assessed and treated as part of standard medical care.

Current Focus His lab is actively working on wearable-based circadian phase estimation using melanopic irradiance (spectral light data), work that could eventually let clinicians or patients alike, assess their internal clock state at home without expensive laboratory protocols. He is also continuing research on the effects of sleep restriction on glucose metabolism, cardiovascular risk, and immune function.

3. Frank Scheer. Bridging clock and clinic work

Who He Is Frank Scheer is a Professor of Medicine at Harvard Medical School and Director of the Medical Chronobiology Program at Brigham and Women’s Hospital. He is consistently among the most-cited researchers in human circadian physiology, with NIH funding that has run continuously since 2005 (which, I have learned, is an incredible feat in and of itself). I use so much of his studies in my own research, and getting to meet him was definitely a rock start moment for me.

What He Built Scheer’s lab occupies a really cool space between circadian science and chronic disease. His long-term research integrates our circadian system with cardiovascular, metabolic, and pulmonary regulation in living humans and documents how our internal clock governs daily fluctuations in blood pressure, heart rate, platelet aggregation, and vulnerability to cardiac events. The evidence provides biological explanations for the well-known morning peak in heart attacks and strokes. His work has also extended into chrono-nutrition: a landmark 2023 report he co-organized, published, and synthesized evidence on how the timing of meals affects cardiometabolic outcomes independent of what is eaten. Of note, one of the most thorough treatments of the topic to date was published by Sheer this year title “Unlocking the Potential of Circadian Biology for Cardiovascular Health”.

What He Discussed at SRBR 2026 Scheer delivered “The Distinguished SRBR Circadian Medicine Keynote” on Saturday. It was the highest-profile single lecture of Circadian Medicine Day. He also contributed to the Saturday working lunch roundtable discussions on cardiovascular therapeutics and circadian medicine.

Current Focus His team is actively investigating dinner timing and its interaction with genetic diabetes risk (a recent randomized crossover trial examined the MTNR1B type 2 diabetes risk variant and glucose tolerance), melatonin’s effects on insulin sensitivity in adipose tissue, and how natural daylight exposure shapes human metabolism. His group is also working on home-based dim-light melatonin onset (DLMO) assessment protocols, which would make it practical to measure circadian phase outside the laboratory.

4. Emily Manoogian. Leading research on time-restricted eating

Who She Is Emily Manoogian is the head of human research and staff scientist at the Salk Institute for Biological Studies in La Jolla, California, and is working in Satchidananda Panda’s lab. She has become one of the most important voices driving time-restricted eating (TRE) research from animal models into clinical human trials, with an emphasis on rigor and honest translation. Emily is not only the leader in TRE, but she is also one of the nicest and most approachable humans I have had the pleasure of conversing with.

What She Built Manoogian has been central to establishing TRE as a scientifically coherent intervention rather than a wellness trend. Her work has emphasized what makes TRE biologically distinct from generic caloric restriction: the consistency of the eating window and its alignment with circadian timing, rather than just the narrowing of the eating period itself. She has conducted and co-authored foundational clinical studies testing TRE in populations with metabolic syndrome, heart failure, and shift workers, including a 2024 UCSD study showing that a 10-hour TRE window improved cardiometabolic markers in patients with metabolic syndrome, independent of caloric reduction. She co-authored the comprehensive 2022 Endocrine Reviews paper “Time-Restricted Eating for the Prevention and Management of Metabolic Diseases,” which became a key reference for both researchers and clinicians. She has also led research on the practicalities of when to eat, advocating for earlier eating windows that align more closely with the body’s natural circadian phase.

What She Discussed at SRBR 2026 Manoogian had an unusually prominent role across multiple sessions. She delivered a talk on time-based medicine that discussed the possibility of bringing circadian timing into clinical practice and trials at Saturday’s Plenary Keynote. She co-chaired the DISRUPT study panel on Monday, the first formal presentation of results from a major clinical trial testing TRE in real-world patient populations. She also spoke on circadian-aligned nutrition and metabolic health. The DISRUPT study results session is particularly significant: it moves TRE from promising pilot data into the realm of properly powered, randomized clinical evidence which, in my person opinion, is precisely what the field needs to develop future clinical guidelines.

Current Focus Beyond DISRUPT, Manoogian is actively co-investigating TRE in bipolar disorder (examining circadian mechanisms in psychiatric conditions), and is involved in a multi-arm RCT comparing caloric restriction with and without TRE in adults at risk for type 2 diabetes. Her emphasis on studying diverse populations, including shift workers and underrepresented groups, is an important corrective to a field that has historically skewed toward healthy, affluent samples.

5. Joseph Takahashi. Longevity, and a pioneer of the clock gene

Who He Is Joseph Takahashi is the Chair in Neuroscience, Investigator Emeritus at the Howard Hughes Medical Institute, and Chair of Neuroscience at UT Southwestern Medical Center. He is one of the foundational molecular geneticists of the entire circadian field.

What He Built Takahashi’s landmark contribution was the discovery of the mammalian Clock gene in 1994. This was the first gene controlling circadian rhythms in mice and humans, and it was successfully cloned in 1997. He pioneered the use of forward genetics in the mouse, meaning he could identify clock mutants by behavior first, then work backward to find the responsible gene, a powerful discovery engine that yielded not just Clock but numerous downstream findings. His lab has demonstrated that circadian clock genes interact with virtually every major cellular pathway: metabolism, immune function, cardiovascular regulation, cell growth, cancer susceptibility, and the “hallmarks of aging.” More recently, his lab has shown that the circadian alignment of feeding under caloric restriction is a major factor in lifespan extension in mice. This finding directly links meal timing to longevity biology, elevating TRE from a metabolic intervention to a potential aging intervention.

What He Discussed at SRBR 2026 Takahashi spoke Tuesday evening in the “Where Should Circadian Biology Go Next? A Community Conversation” panel — SRBR’s open dialogue with its most senior figures. He also participated in Monday’s lunch table discussion on clocks in health span and longevity, a topic that represents his lab’s current frontier. As one of the architects of the molecular clock, his perspective on where the field should direct its energy carries unusual weight.

Current Focus: Takahashi’s lab is now explicitly targeting aging, because circadian transcriptional activity declines with age, they are testing interventions that rescue circadian amplitude, essentially strengthening the clock as it weakens with aging, as a strategy to promote health span and life span. This includes developing small-molecule drugs that could enhance clock function. His group continues to investigate how caloric restriction, feeding timing, and clock gene activity interact across the lifespan. The ambition in the field is substantial: drugs that strengthen the biological clock as we age.

One of the things that struck me most at SRBR is how specific the science is. Not specific in a dry, inaccessible way, but specific in the way that makes you realize how much invisible infrastructure goes into what eventually becomes a clinical recommendation or a drug.

The scientists I’ve highlighted in this piece are standing on an enormous body of work from dozens of institutions, hundreds of researchers, and thousands of experiments that will never make headlines. That is how research and discovery works: in layers.

Take cancer. Multiple labs are now asking not just whether the circadian clock interacts with tumor biology, but exactly how, and the answers are getting super granular.

Researchers at Scripps are mapping how circadian disruption remodels the immune environment inside lung tumors through a protein called HSF1. Texas A&M is showing that the timing of exercise changes its anti-tumor effects in breast cancer, with a single clock protein (PER1) appearing to mediate the difference.

And separate work is revealing that circadian rhythm disruption reshapes the tumor metabolome and microbiome, suppressing the immune system’s ability to fight back. None of this is a clinical guideline yet. But all of it is building the case, piece by piece.

Takahashi’s lab is targeting clock amplitude as a longevity strategy. The idea that, as we age, our clocks weaken and that strengthening them might slow downstream consequences, and researchers at Texas A&M are already screening drug compounds in a bread mold to find molecules that restore circadian amplitude in aged cells.

They found 187. Five are validated. Some extend lifespan. This is how a drug begins: not in a human, not even in a mouse, but in a fungus on a petri dish, in a lab most people will never hear of.

So here’s a spoiler alert on what everyone was talking about across the conference: where is all of this going? Science is now moving fast, so how do we get it built into the real world? You can read my thoughts on the topic in Part II.

I’m curious, for those of you in practice, where do you feel the gap between circadian research and clinical application? The clinicians in attendance were very clear in their messaging that, to get this into their clinics, there must be overwhelming evidence and indisputable proof. Do you agree?

I’d love to hear what it looks like from where you’re standing.

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