Acetaminophen, which also goes by names like paracetamol or Tylenol, is a common over-the-counter pain reliever and fever reducer. It is often prescribed during pregnancy to help with mild to moderate pain. Recently, there has been a lot of discourse about its safety. Claims have been made suggesting that taking acetaminophen during pregnancy may increase the likelihood of autism in children.

A large study from Denmark adds clarity to this debate, finding no increased risk of autism in children exposed to acetaminophen before birth. These results were consistent across both the general population analysis and sibling-matched comparisons, and did not vary with the timing or dosage of exposure. The findings are published in JAMA Pediatrics.

Risk or no risk

Public concern over whether taking acetaminophen during pregnancy could increase autism risk quickly moved into the spotlight—dominating news channels, newspapers, and social media. The debate became so intense that in September 2025, the U.S. Food and Drug Administration advised clinicians to consider limiting its use for routine low-grade fevers during pregnancy.

Yet the scientific evidence remained conflicted—some studies have reported a small risk, while others have found no link at all. A large study from Sweden initially reported a slight rise in autism risk when analyzing the general population. However, when the same researchers compared siblings within the same families—a method that accounts for shared genetic and environmental factors—the apparent link disappeared.

A sibling-matched analysis is a research method that scientists use to compare siblings from the same family to better understand how a particular exposure affects an outcome. Since siblings share many of the same genes and a common home environment, this approach helps account for hidden factors that might otherwise influence the results.

In search of more definitive evidence, the researchers carried out a nationwide cohort study in Denmark. They examined all children born from single pregnancies between 1997 and 2022, using official national health records to follow more than 1.5 million children over time. The analysis focused only on children who were alive at age one and excluded cases with missing data or conditions already known to be linked to autism.

The researchers found that taking acetaminophen during pregnancy is not linked to an increased risk of autism in children. The findings were the same for the general population and siblings comparisons. The adjusted hazard ratio—a measure of relative risk between two groups—was close to 1, indicating no increased risk.

The study closely examined both the amount of medication taken—low, medium, or high—and the stage of pregnancy during which it was used, covering each trimester. Across all these variations, the team found no evidence of an increased risk.

These findings could help ease anxiety among parents while also giving medical practitioners the evidence they need to clearly explain to patients and support their informed decision-making.

Air pollution is associated with increased migraine activity, according to a study published in Neurology. Both short-term and cumulative exposure to air pollution as well as climate factors such as heat and humidity were associated with increased migraine activity.

The study does not prove that air pollution causes migraine attacks; it only shows an association.

“These results help us to better understand how and when migraine attacks occur,” said study author Ido Peles, MD, of Ben-Gurion University of the Negev in Be’er Sheva, Israel.

“They suggest that for people who have a susceptibility to migraine to begin with, environmental factors may play two roles: intermediate-term factors such as heat and humidity may modify the risk for attacks, while short-term factors such as spikes in pollution levels may trigger attacks.”

How the long-term study was done

The study involved 7,032 people with migraine who lived in Be’er Sheva in the Negev desert and were followed for an average of 10 years.

Researchers looked at daily exposure to air pollution from traffic, industry and dust storms, as well as weather conditions. Then they looked at how often and when people had to visit the hospital or a primary care office with an acute migraine and compared that to the pollution and weather conditions that day and up to seven days earlier, since pollution effects may take a few days to affect the body.

They also looked at cumulative exposure to air pollution and migraines. As another measure of migraine activity, researchers checked pharmacy records to see how many doses of the migraine medications, called triptans, participants needed.

What the migraine data revealed

During the study, 2,215 people, or 32%, had at least one visit to the hospital or clinic for acute migraine. A total of 47% of the people had purchased triptan medications during the study, with average use at two tablets per month and 2.3% of people using 10 or more tablets per month.

The researchers found an association between air pollution and visits to the hospital or clinic for migraine.

On the day with the highest number of visits to the hospital or clinic, air pollution levels were elevated compared to the average amount over the study period. On that day, the level of particulate matter 10, or PM₁₀, which includes dust, was 119.9 microns per square meter (µm/m³), compared to an average of 57.9 during the study.

For PM2.5, which includes particles from motor vehicle exhaust and the burning of fuels from power plants and other industries, the level on that day was 27.3 µm/m3, compared to an average of 22.3 during the study. For nitrogen dioxide, or NO2, a gas mostly from traffic emissions, the level on that day was 11.2 parts per billion, compared to an average of 8.7.

The day with the fewest visits to the hospital or clinic also had lower than average pollution levels.

Pollution types and relative risks

After adjusting for other factors that could affect the risk of migraine attacks, such as sex and socioeconomic status, researchers found that people with short-term exposure to high levels of NO₂ were 41% more likely to go to the hospital or clinic for migraine than people not exposed to high levels.

People exposed to high levels of solar radiation, or ultraviolet (UV) rays from the sun, were 23% more likely to seek help for migraine than those not exposed to high levels.

People with cumulative exposure to high levels of NO₂ were 10% more likely to have high use of migraine drugs than people without cumulative exposure to high levels. People with cumulative exposure to high levels of PM_2.5 were 9% more likely to have high use of the drugs.

Researchers found that climate conditions played a role in the effects of pollution. High temperatures and low humidity amplified the effect of NO2, while cold and humid conditions intensified the effect of PM2.5.

Implications for care and prevention

“These findings highlight opportunities for anticipating what care will be needed,” Peles said. “As climate change intensifies the frequency of heat waves, dust storms and pollution episodes, we will need to integrate these environmental risk factors into our guidance for people with migraine.

“When high-risk exposure periods are in the forecast, doctors can advise people to limit their outdoor activity and use air filters, take short-term preventative medications and start using their migraine drugs at the first sign of a problem to ward off attacks.”

Study limitations and who it reflects

A limitation of the study is that exposure to air pollution was measured by monitoring stations and did not take into account individual behaviors such as amount of time spent indoors, use of air conditioning or air filters, type of job and daily activities.

In addition, since the information on migraine activity was gathered through hospital and clinic visits and pharmacy data, the findings mainly reflect people with severe migraine and may not be applicable to people with milder episodes of migraine or those they manage on their own.

If scientists could shrink themselves to microscopic size and take a journey through the human body—like the submarine crew in the 1966 science fiction classic “Fantastic Voyage”—one of their first stops would no doubt be the liver. The unique structure of our largest internal organ comprises small, hexagonal functional units called lobules, each carrying out more than 500 functions simultaneously. Studies from the 1970s and 1980s revealed that liver cells divide these many tasks among themselves according to their location within each subunit; however, the technology available at the time provided only a blurred picture of this division of labor.

A new high‑resolution liver atlas

In a new study published in Nature, scientists from the Weizmann Institute of Science, together with colleagues at Sheba Medical Center and the Mayo Clinic, present the first genetic atlas of a healthy human liver at a resolution of 2 microns. The findings show that the division of labor in the human liver differs from that of other mammals and is more extensive than previously recognized, helping explain why certain regions of the liver are particularly vulnerable to fatty liver disease.

In recent years, technological advances have made it possible to identify which genes are active in each individual cell while also mapping the cells’ precise spatial positions within the tissue. Still, a comprehensive map of functional division in the human liver remained elusive, largely due to the difficulty of obtaining tissue samples from healthy donors.

Leveraging living liver donations

Researchers in Prof. Shalev Itzkovitz’s group at the Weizmann Institute realized that the solution could come from altruistic living liver donation. Because the liver has a remarkable capacity for regeneration, healthy individuals can donate a substantial portion of their livers to patients in need.

With the help of Prof. Ido Nachmany and Prof. Niv Pencovich from the Department of General Surgery and Transplantation at Sheba Medical Center, and Dr. Timucin Taner from the Mayo Clinic in Minnesota, the researchers obtained eight liver samples from healthy donors and constructed a gene expression atlas of the human liver.

“Thousands of genes were found to be active at different levels in liver cells across various locations, pointing to a far more precise and complex internal organization than previously thought,” says Itzkovitz. “Instead of the coarse division into three functional zones that has been accepted for decades, the atlas reveals eight regions with distinct roles. This precise mapping now enables any laboratory worldwide to dive deep into the liver and investigate why different regions are susceptible to different diseases.

“Metabolic diseases, for example, tend to originate in the center of the lobule, whereas viral and autoimmune inflammations primarily appear at its periphery. Likewise, liver cancer and metastases from other cancers have their preferred locations. The key to understanding these patterns lies in the detailed genetic data we have collected.”

How human livers differ from animals

To enable comparison with other species, Itzkovitz’s laboratory also mapped healthy livers in mice, as well as in larger mammals—pigs and cows—whose metabolic rates and lobule sizes are similar to those of humans. In all mammals, blood flows through the lobule from the periphery to the center, supplying oxygen and nutrients to cells along the way. As a result, the periphery is characterized by abundance of resources, while the center experiences relative scarcity.

In all the mammals studied except humans, these depleted conditions at the center of the lobule resulted in relatively lower cellular activity. In humans, however, the core of the lobule was found to carry out numerous functions, including synthesizing fats from excess energy, producing glucose from non-carbohydrate sources during fasting, filtering toxins and secreting bile to aid digestion.

Another striking difference between the human liver and those of other mammals concerns glucose storage. The liver functions as the body’s “fuel tank,” efficiently absorbing sugars during meals and releasing them in a controlled manner between meals. The study found that in humans, glucose uptake occurs mainly in the centers of the lobules, rather than at their periphery, unlike in mice.

The double‑edged nature of efficiency

“This division of labor is both a blessing and a curse,” Itzkovitz explains. “It allows the liver to store carbohydrates efficiently: Cells at the center of the lobule absorb and store glucose directly from the blood, while cells at the periphery convert lactate into glucose, further contributing to the energy reserves used during fasting. However, this efficient system was not designed for a modern diet rich in fats and carbohydrates, which may help explain why we tend to accumulate excess fat in the liver and develop liver fibrosis.”

To cope with cellular wear and tear and prevent disease, a unique turnover mechanism appears to have evolved in the center of the human liver lobule. “We found that in humans, unlike in other mammals, a particular type of immune cell prefers to reside in the core of the lobule rather than guarding its periphery—the entry point of blood into the tissue,” says Dr. Oran Yakubovsky of Itzkovitz’s lab, who led the study and is also a surgical resident at Sheba Medical Center.

“Kupffer cells are specialized scavenger cells that can offer protection against infections but also engulf, break down and recycle the remains of worn-out cells. We hypothesize that in humans they ‘relocated’ to the center to cope with the increased cellular attrition occurring there.”

Linking the atlas to liver disease

In the final part of the study, the scientists demonstrated how their new atlas can be used to trace disease development. They focused on fatty liver disease associated with metabolic dysfunction—a common condition, linked to obesity and diabetes, in which fat accumulates in the liver and may lead to inflammation and fibrosis.

Comparing healthy liver cells with those that had begun to accumulate fat revealed a protective response: Cells that started to “gain weight” switched off genes involved in fat production and uptake while activating genes associated with fat breakdown. However, the human liver has a limitation that reduces the efficiency of this process: Fat accumulation also leads to decreased production of certain components of the mitochondria, the organelles responsible for breaking down fats.

“Based on the precise mapping of the liver, it may become possible to develop treatments that will target the genes responsible for making specific regions particularly vulnerable to certain diseases,” says Itzkovitz. “Moreover, the approach of constructing a single-cell–resolution genetic atlas from healthy donor samples can be applied to other organs that have not yet been accurately mapped in humans. It could fundamentally change how we understand the structure and function of the human body.”