Personalized Medicine & Diabetes: The Game-Changing Breakthrough
Personalized Medicine & Diabetes: The Game-Changing Breakthrough
The concept of “personalized medicine” often seems abstract, but Stanford molecular geneticist Michael Snyder brought it vividly to life, using himself as the test subject in a groundbreaking experiment that demonstrated its potential. Snyder and a team of researchers began by sequencing his entire genome, which revealed a genetic predisposition to conditions such as high cholesterol, coronary artery disease, basal cell carcinoma (a type of skin cancer), and type 2 diabetes. Over the next two years, they tracked thousands of biological markers in his blood at regular intervals. Typically, a routine checkup examines about 20 chemical or biological markers. In contrast, Snyder’s team essentially created a dynamic, 3D molecular movie of his body’s functioning, showing how his genes, RNA, proteins, and other molecules interact during both health and illness. At the start of the study, they watched his body’s response to a cold. Later, they watched in real time how molecular changes induced by a respiratory infection pushed him into full-blown diabetes. Their findings were published in the journal Cell.
While this level of monitoring is currently too complex and expensive for everyday clinical use, it highlights the potential of personalised medicine. By identifying diseases and their molecular triggers early, it offers a glimpse of a future where healthcare will be truly tailored to the individual.
The connection between infection and diabetes
What I liked most about the study was the real-time documentation of the development of diabetes. Just before the halfway point of the study, Michael Snyder contracted a respiratory syncytial virus infection, which affects the lungs. Within about two weeks, his body’s ability to regulate blood sugar began to change. His blood sugar levels began to rise, and three months later, he was diagnosed with type 2 diabetes.
The infection activated a normal immune response, causing his body to start producing antibodies. But it also produced autoantibodies — rogue antibodies that mistakenly attack his proteins. One of these targeted a receptor on the surface of cells responsible for binding insulin, the hormone that helps glucose enter cells. When that receptor is disrupted, cells struggle to absorb sugar from the bloodstream, one of the key features of diabetes.
This part of Snyder’s story was very important to me. Six years ago, I was diagnosed with diabetes right after suffering a serious and long-lasting infection. The diagnosis was a shock: I’m lean, active, eat well, and have no history of the disease in my family.
I’d long suspected that the infection somehow triggered my diabetes, but until now, I hadn’t seen much evidence in the medical literature to support that idea. Snyder’s research may not change the way I manage the disease, but it provides valuable insights—and helps me understand why I’m living with it.
The use of advanced, data-rich biomedical technologies – such as DNA sequencing, proteomics, imaging techniques, and wireless monitoring devices – has uncovered significant variation in the development, progression, and response to treatment of diseases among individuals. This finding has raised important questions about how much this individual variation should influence decisions about the best ways to treat, monitor, or prevent disease in each person.
There is growing recognition that the biological complexity and diversity of many diseases means that treatment and prevention strategies must be tailored – or personalised – to each person’s unique biochemical composition, physiology, environmental exposures and behaviour. This approach is becoming increasingly central to modern medicine.
Several comprehensive reviews and textbooks on personalised medicine have been published, aimed at educating both medical students and practising clinicians. While the terms individual, personalised, and precision medicine are often used interchangeably (as they are here), some experts argue that subtle but meaningful differences exist between them.
Personalized medicine faces several significant challenges, particularly when it comes to gaining approval for routine use from regulatory agencies. Beyond regulatory hurdles, widespread acceptance among key health care stakeholders—clinicians, health system leaders, insurers, and patients—remains a major hurdle. At the core of many of these issues is the need to demonstrate that personalized approaches produce better outcomes than conventional treatments. This is particularly important given the often high costs of personalized treatments, such as autologous CAR-T cell transplantation for certain cancers and mutation-specific drugs such as ivacaftor for cystic fibrosis.
In this review, we explore the origins and driving motivations behind personalized medicine. We examine the developments that have shaped the field over the past few decades, identify current limitations slowing progress, and discuss what the future may hold. A major focus is on how to rigorously demonstrate that personalized medicine strategies can outperform conventional medical approaches. Additionally, we distinguish between unique challenges and examples related to three key areas: personalized disease prevention, personalized health monitoring, and personalized treatment of active disease.
Archibald Garrod and the Foundations of Personalized Medicine
The concept of personalized medicine has deep historical roots, with several milestones in Western medical history foreshadowing its emergence. While many events have contributed to this development, a few key moments reflect the core themes of personalized medicine. One of the most important early contributors was Archibald Garrod, an English physician who, more than a century ago, began investigating “inborn errors of metabolism.”
Garrod studied several rare genetic disorders with distinct physical characteristics, including alkaptonuria, albinism, cystinuria, and pentosuria. His most influential work focused on alkaptonuria. He observed that individuals with this condition, often from the same family, had different biochemical profiles than unaffected family members, particularly in their urine. From these observations, he concluded that alkaptonuria stemmed from a unique “altered course of metabolism” in affected individuals, a hypothesis that was later confirmed.
Garrod’s insights extended beyond rare diseases. Reflecting on his findings, he suggested that these disorders were extreme examples of the extensive biochemical diversity present in all humans. He wrote that “no two individuals of a species are exactly alike in physical structure [and] neither are their chemical processes exactly alike.” This idea reflected the basic concept behind personalized medicine: that individuals differ not only in appearance but also in internal biochemistry, and that these differences affect how diseases develop and manifest.
Garrod’s work emerged at a time of intense debate over the nascent field of genetics. Although a molecular understanding of genes — DNA sequences that code for proteins and regulatory functions — was still decades away, Garrod and his contemporaries often spoke of “factors” that influenced disease in ways consistent with our modern concept of the gene. These ideas were based on the earlier work of Gregor Mendel, which demonstrated that specific traits followed predictable inheritance patterns in pea plants. Subsequent research confirmed that many of the metabolic anomalies observed by Garrod were caused by genetic mutations.
This intellectual background was marked by a division between two scientific camps. “Mendelians,” including people like William Bateson and Hugo de Vries, emphasized the role of discrete, hereditary factors in shaping traits—an idea supported by both Mendel’s work and Garrod’s observations. In contrast, “biometricians,” led by Karl Pearson, focused on continuously changing characteristics such as height and questioned how these could be reconciled with the seemingly all-or-nothing inheritance patterns described by Mendelians. Garrod’s pioneering efforts helped bridge this divide by highlighting how both discrete genetic mutations and wide biochemical variability contribute to human diversity. His work laid out a foundational argument for what eventually became personalized medicine: that an individual’s unique genetic and metabolic profile plays a critical role in disease risk, progression, and treatment response.
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