Is Diethylstilbestrol (DES) Still Used Today?

Diethylstilbestrol (DES) has been banned for most of the purposes it was originally prescribed for, but it has not vanished entirely. The drug is no longer given to pregnant women and has been removed from livestock feed in many countries, yet it persists in limited oncological settings, shows up as an environmental contaminant, and continues to generate health consequences in people who were exposed decades ago. The story of DES is less about whether it is “still used” and more about how a single drug’s legacy keeps unfolding across generations.

What DES Was Originally Used For

DES is a synthetic compound that mimics estrogen. It binds to estrogen receptors with roughly two to three times the affinity of the body’s own estradiol, which made it a powerful pharmacological tool when it was introduced in the late 1930s.¹ Doctors prescribed it to millions of pregnant women between the 1940s and early 1970s, believing it could prevent miscarriage, premature birth, and other complications. Estimates put the number of exposed pregnancies in the United States alone at several million.

At the same time, the agricultural industry discovered that DES accelerated weight gain in cattle, poultry, and other livestock. It became the most widely used hormone-like growth promoter in food-producing animals before regulators stepped in.² In both medicine and agriculture, DES was cheap, orally active, and effective. Those qualities made it ubiquitous, and the fallout from that ubiquity has taken decades to fully appreciate.

Why DES Was Pulled from Obstetric Use

In 1971, a landmark observation linked prenatal DES exposure to an extremely rare form of vaginal and cervical cancer, clear cell adenocarcinoma (CCA), in young women whose mothers had taken the drug during pregnancy. The cancer was so unusual in young women that the cluster was immediately suspicious. Within months, the U.S. Food and Drug Administration issued an advisory against prescribing DES to pregnant women. Other countries followed.

Subsequent decades of follow-up confirmed that the cancer risk, while real, was relatively small in absolute terms. By age 50, the cumulative risk of CCA for women exposed to DES in utero was about 1 in 750.³ The incidence peaked around age 19 and the first cases appeared as early as 1961. But CCA was only the most dramatic consequence. Exposed daughters also faced higher rates of reproductive tract abnormalities, and exposed sons showed increased risks of genital and urinary problems including undescended testes and epididymal cysts.⁴ The risks were strongest when exposure occurred early in pregnancy; for men exposed before the 11th week of gestation, the risk of undescended testes was roughly three times higher than in unexposed men.⁴

The mothers who took DES were not spared either. Long-term studies found a modestly elevated breast cancer risk among women who were prescribed the drug during pregnancy, with a relative risk of about 1.27 compared to unexposed women.⁵ The overall picture was one of harm radiating outward from a drug that had never been shown to work for its intended purpose of preventing miscarriage in the first place.

Where DES Still Appears in Cancer Treatment

Despite its toxic reputation, DES did not entirely disappear from oncology. Its powerful estrogen activity turned out to be therapeutically useful in two specific cancers, though in both cases safer alternatives have mostly replaced it.

In advanced prostate cancer, DES works by suppressing testosterone. Clinical trials demonstrated that it was as effective as surgical castration at controlling the disease, but came at a steep cardiovascular cost. Patients receiving the standard 5-milligram daily dose had significantly higher rates of fatal and nonfatal heart disease compared to placebo, and the survival benefit from reduced cancer deaths was wiped out by cardiovascular deaths.⁶ In smaller studies using lower doses, cardiovascular events still occurred in roughly 10 to 30 percent of patients, with complications including blood clots, heart attacks, and transient ischemic attacks.⁷ European trials comparing DES to other hormonal agents confirmed that cardiovascular toxicity was higher with DES than with alternative drugs, and that the first six months of treatment carried the greatest risk of severe complications.⁸

In metastatic breast cancer, DES showed response rates comparable to tamoxifen. A randomized trial of 151 postmenopausal women found that DES produced a regression rate of about 41 percent versus 33 percent for tamoxifen, and intriguingly, women on DES had significantly better overall survival at five years (35 percent versus 16 percent).⁹ But DES caused more nausea, fluid retention, vaginal bleeding, and cardiac problems, so tamoxifen became the standard first-line treatment.¹⁰ Still, the researchers noted that estrogens “remain in the armamentarium” for selected patients, meaning DES (or drugs like it) could still be pulled off the shelf when other options fail.

In practice, DES is now extremely rare in oncology. Modern hormonal therapies for prostate cancer, such as LHRH agonists and newer antiandrogens, achieve the same testosterone suppression without the cardiovascular baggage. For breast cancer, aromatase inhibitors and newer targeted agents have pushed DES even further to the margins. But “rarely used” is not the same as “never used,” and in resource-limited settings or after multiple treatment failures, DES can occasionally resurface as a last-resort option.

The Agricultural Ban and Its Limits

The use of DES as a livestock growth promoter was banned in the United States in 1979, after years of regulatory battles. The European Union banned it as well. These bans were motivated by evidence that DES residues could persist in meat and pose cancer risks to consumers.²

However, reports indicate that illegal use has not been entirely stamped out globally. DES can accelerate growth and increase protein content in animals, making it economically attractive even where it is banned. Research has documented its continued use in aquaculture and terrestrial livestock operations in some regions, which contributes to DES turning up in environmental samples including water and soil.¹¹ DES is also used as an additive in plastic production, and it can leach into the environment as plastics age, break down, and migrate.¹¹ So even in places where every intentional use has been outlawed, DES persists as a low-level environmental contaminant with endocrine-disrupting potential.

Health Effects That Outlast the Drug

One of the most unsettling aspects of the DES story is how long the health consequences continue. The women who were prescribed DES during pregnancy are now in their 80s and 90s, and many have died. Their children, the so-called “DES daughters” and “DES sons,” are in their 50s through 70s. And the effects have not stopped with them.

The range of harm in directly exposed offspring is broad. Beyond the cancer and reproductive tract anomalies already described, research has identified links to neurodevelopmental disturbances, immune system problems, and cardiovascular and pancreatic disorders.¹² There is also evidence suggesting psychiatric effects, though the findings have been difficult to interpret because of potential biases in how exposed individuals were identified and studied.¹³

In animal studies, DES exposure during fetal development disrupted the normal formation of reproductive structures. In male mice, prenatal DES delayed a critical step in reproductive tract development by about two days, which was enough to cause persistence of structures that normally disappear.¹⁴ In genetically male mice carrying a mutation that makes their cells unresponsive to androgens, DES exposure preserved female reproductive structures in a dose-dependent manner, demonstrating how profoundly the drug could override normal sexual development.¹⁵ These animal findings helped explain the anatomic abnormalities observed in humans.

The Third Generation Question

Perhaps the most troubling research frontier involves DES grandchildren. If your grandmother took DES while pregnant with your mother, could you be affected even though you were never directly exposed to the drug?

Data from the U.S. National Cancer Institute’s DES Third Generation Study found evidence of increased risk of menstrual irregularity, missed periods, preterm birth, and possibly ectopic pregnancy in women whose mothers were exposed to DES in the womb.¹⁶ A separate multigenerational study found that the elevated preterm birth rate was specific to the maternal line: grandchildren born through the maternal germline had preterm birth rates of about 15 percent whether their mother was directly exposed to DES or born after the exposure period, while those in the paternal germline showed no such pattern.¹⁷

The proposed biological explanation centers on epigenetics. When a pregnant woman took DES, the drug reached not only her fetus but also the germ cells developing inside that fetus. Those germ cells would eventually become the eggs or sperm that produced the next generation. During pregnancy, these precursor cells are especially vulnerable to chemical disruption because they are undergoing critical developmental steps and lack some of the protective mechanisms that shield DNA from permanent modification.¹⁸ Animal studies have confirmed that endocrine disruptors can produce effects that carry across generations through this mechanism.

This research is still evolving, and the evidence in humans remains suggestive rather than definitive. But the possibility that a drug taken by a grandmother could affect the reproductive health of her grandchildren is a sobering illustration of how long-lasting pharmaceutical harms can be, and it gives DES a relevance that extends well beyond the question of whether anyone is still prescribing it.

Screening Recommendations for DES-Exposed Women

Because the cancer risk for DES daughters has not disappeared with age, medical guidelines still address this population specifically. The American Society of Colposcopy and Cervical Pathology recommends that women who were exposed to DES in utero receive annual screening for clear cell adenocarcinoma through cytology (Pap smears) until the age of 65. After 65, screening can be discontinued if the woman otherwise meets standard criteria for stopping cervical cancer screening.¹⁹

This guideline represents one of the clearest ways DES remains medically relevant today. DES daughters are now mostly in their 50s and 60s, meaning a significant number are still within the recommended screening window. Yet adherence to screening has been uneven. Research has identified various factors that lead DES-exposed women to skip regular Pap smears, which is concerning given that screening remains one of the main tools for catching any late-appearing tumors.²⁰ Some women may not even know they were exposed, since their mothers’ medical records from the 1950s and 1960s are often incomplete or lost.

DES as an Environmental Contaminant

Even where human and agricultural uses have been banned, DES does not simply vanish from the environment. It turns up in water, soil, and sediment at low levels. Some of this comes from illegal agricultural use, but another source is the plastics industry: DES functions as an additive in certain plastic manufacturing processes, and it leaches out as those plastics weather and fragment.¹¹

Laboratory studies on aquatic organisms have shown that even low concentrations of DES can disrupt endocrine function and impair reproduction. This places DES within the broader category of endocrine-disrupting chemicals that researchers worry about in waterways worldwide. The concentrations found in typical environmental samples are far below those that caused harm in humans taking therapeutic doses, but the concern is about chronic, low-level exposure in wildlife populations and the potential for compounding effects when DES mixes with other endocrine disruptors in polluted water.

The environmental dimension adds a layer to the “is it still used” question that most people do not think about. DES was designed to be biologically potent at tiny doses, and that same potency makes even trace environmental concentrations worth monitoring. For aquatic species living in contaminated water, the drug’s legacy is not historical at all.

Why DES Matters Beyond Its Own Story

DES became a cautionary case study in pharmacology, toxicology, and regulatory science. It was the first clearly documented instance of a transplacental carcinogen in humans: a substance taken by a pregnant woman that caused cancer in her child years later. That discovery reshaped how regulators think about drug safety during pregnancy and helped establish the precautionary frameworks used for drug approval today.

The multigenerational findings have broadened the lesson further. The idea that a chemical exposure could alter gene expression patterns through epigenetic changes and pass those alterations to a generation that was never directly exposed has implications for how we evaluate all endocrine-disrupting chemicals, from pesticides to plasticizers to compounds in personal care products. DES was, in a sense, the original proof of concept for these concerns. Animal models involving DES continue to be used in laboratories studying how endocrine disruptors affect development, precisely because the drug’s effects are so well characterized and so potent.¹²

For the families directly affected, the practical reality is that DES is still very much part of their lives. DES daughters continue to need specialized screening. Third-generation women may carry reproductive risks they did not know were connected to a pill their grandmother swallowed. And for researchers studying endocrine disruption, DES remains the reference compound against which other synthetic estrogens are measured, its binding affinities and developmental effects serving as the benchmark for understanding how estrogen-mimicking chemicals behave in living systems.²¹