Publisher Health

A recent study by University of Helsinki researchers sheds new light on the ecological adaptability of early humans at the time when they first expanded their range outside Africa, 2-1 million years ago.
The origins of human genus have long been associated with savannah and grassland environments of Africa. Due to this association, it was thought that the first human dispersal into Eurasia followed grassy corridors leading from Africa to Asia and to Europe. This link between humans and savannah-grasslands has been considered so strong that it delayed the appearance of early humans in Europe compared to Asia, as open grassy environments appeared in Europe later than in Asia. According to this view, early humans were ecologically clearly less versatile than our own species, Homo sapiens, as we have colonized almost all terrestrial environments on the planet.
“But that’s clearly not the whole story” Says the lead author Tegan Foister, a doctoral researcher in the Hominin Ecology group at the University of Helsinki. “Because we knew of some studies suggesting that early humans were living in environments other than savannah-grassland, we thought that it would be interesting to do a more systematic investigation on the environments humans are known to have occupied during this crucial time period.”
The research published in Evolutionary Anthropology is a systematic review of 121 previously published reconstructions of early human habitats and it revealed that humans, when dispersing out of Africa for the first time, started to occupy a diverse set of environments from grasslands to forests.
“We have long associated early humans with savannah-like environments outside of the African continent. However, when the research published over the past two decades is considered together, it shows humans inhabiting diverse environments early in the evolution of the genus Homo. Already one million years ago humans in Europe were occupying fully forested environments.” Foister continues.
Although the analysis shows that grasslands and savannahs were important components of early human habitats, it places humans into a wide spectrum of environments, and in many cases environments with varied vegetation composition. This suggests that commonly held believes about early humans are not entirely correct: Humans did not have that strict requirements for their habitats and they seem to have been ecologically more versatile than previously assumed.
The study also indicated regional differences in human habitat characteristics. The grasslands and savannahs show the highest prevalence among African habitats, whereas forested habitats were more prominent in Eurasia making the range of different habitats wider in Eurasia. This suggests a possibility that the first human range expansion into Eurasia was accompanied and potentially even enabled by the expansion of human ecological niche.
The research is part of University of Helsinki and Kone Foundation funded project that investigates the evolution of the human niche over the past 2 million years. Although the present study focuses on the early humans, its findings are important also to the understanding of the origins of uniquely wide niche of our own species Homo sapiens. Co-author Miikka Tallavaara, leader of the project and the Hominin Ecology group, says: “The ability of Homo sapiens to occupy most of the terrestrial ecosystems has enabled our ecological dominance and triggered the current biodiversity crisis. Our finding that human species in the Early Pleistocene were also able to thrive in multiple environment types provides an exciting target for future research into the evolutionary origins of the human plasticity and ecological success.”

A new study published in BMJ Mental Health has found that individuals with severe mental illness are almost twice as likely to report physical multimorbidity, emphasising the critical importance of addressing the intersection between mental and physical health.
The research, led by Anglia Ruskin University (ARU) in collaboration with the University of Cambridge’s Biomedical Research Centre, involved an extensive analysis of 19 different studies, encompassing data from 194,123 psychiatric patients across the world, with a comparison to 7,660,590 individuals in control groups.
Multimorbidity is when a person is affected by any combination of chronic disease with at least one other physical health condition, and the researchers found the psychiatric patients were 1.84 times more likely to report multimorbidity than the control group.
The study found that people with severe mental health issues also report physical conditions including metabolic diseases, hypertension, epilepsy, respiratory, vascular, kidney, and gastrointestinal diseases, as well as cancer.
As of 2019, nearly one billion people were living with a mental disorder, making it a leading cause of disability worldwide. According to Mind, one in four people will experience a mental health problem of some kind each year in England.
Previous research has found that a large percentage of individuals in need of mental health services lack access to effective, affordable, and quality mental healthcare, especially in low-income countries. For instance, 71% of individuals with psychosis worldwide do not receive necessary mental health services, with a vast disparity between high-income and low-income countries.
Lead author Lee Smith, Professor of Public Health at Anglia Ruskin University (ARU), said: “Mental health underpins our individual and collective abilities to make decisions, build relationships, and shape the world we live in. It is evident from our research that individuals with severe mental illness are at a significantly higher risk of experiencing physical multimorbidity.
“This complex relationship between severe mental illness and physical multimorbidity has far-reaching implications, including decreased treatment compliance, increased risk of treatment failure, increased treatment costs, relapsing disease, worsening prognosis, and reduced life expectancy.
“Poor clinical management of physical comorbidities in people with mental disorders exacerbates the issue, leading to an increased burden on individuals, their communities, and healthcare systems. A holistic approach is urgently needed to improve the physical, mental, and social outcomes of individuals dealing with severe mental illness and physical multimorbidity.”

High fiber diets, like those that include broccoli sprouts or other cruciferous vegetables, may reduce disease symptoms and improve quality of life in patients with inflammatory bowel disease (IBD), according to a study conducted in mice. The study was published in mSystems, a journal of the American Society for Microbiology.
In the study, the investigators used a popular interleukin-10-knockout (IL-10-KO) mouse model of Crohn’s to investigate the interactions between mice and their immune systems, as well as the broccoli sprout diet, microbes within the Crohn’s-afflicted gut, and how those microbes would use an inactive compound in the broccoli sprouts to make an anti-inflammatory compound in the gut. They also wanted to determine if, and by how much, a diet containing broccoli sprouts alleviates Crohn’s symptoms, given the anti-inflammatory metabolites innately present in the sprouts.
The researchers used 4 groups of IL-10-KO mice in the study. In the first round, they had younger mice enrolled at 4 weeks of age who ate their standard mouse chow the whole time, as well as mice who ate the mouse chow with raw broccoli sprouts mixed in. In the second round, they had the same 2 diet groups, but mice were enrolled at 7 weeks of age. The researchers were particularly interested in understanding the development of IBDs in early life, which is why they studied the Crohn’s mouse models at the juvenile stage (4-6 weeks old) and at the adolescence stage (7-9 weeks old) with hopes to better understand how host-diet-microbial community interactions and disease severity differ by age.
The mice were fed for 7 days to acclimate to their respective diets before the researchers triggered symptoms, and the mice stayed on their diets for the following 2 weeks while the disease progressed. To trigger symptoms, new healthy mice that host more microbes were added to the cage. Since the IL-10-KO mice in the study can’t produce IL-10, their immune systems have trouble tolerating gut microbiota, and the new microbes in the cage triggered colitis and Crohn’s symptoms. For the next 15-16 days after infection, the researchers regularly weighed the mice and collected fecal samples to assess for signs of colitis development.
At the end of the study, the researchers examined the gut tissues of the euthanized mice and microbial communities present throughout their intestines, as well as the presence of certain markers of inflammation and broccoli metabolites in the blood. The researchers wanted to know what types of microbes were living in particular parts of the gut. In other words, they wanted to understand how the broccoli sprout diet affected microbial biogeography in the Crohn’s models, since they cannot study this in humans.
DNA was extracted from the intestinal tissue samples collected from the mice and sent for sequencing to identify the bacteria present. Once the sequencing data was returned, the researchers used bioinformatics software and human ingenuity to study the gut microbial ecology of our mouse models.
“We found many exciting results from this study. First, we show that the mice that ate the broccoli sprout diet had a greater concentration of an anti-inflammatory metabolite called sulforaphane in their blood. Even though our mice were immunocompromised and had colitis, this increase in sulforaphane protected them from severe disease symptoms like weight loss, fecal blood and diarrhea,” said Lola Holcomb, lead author and a Ph.D. Candidate in the Graduate School of Biomedical Sciences and Engineering at the University of Maine. Lola is a member of a lab led by Suzanne Ishaq, Ph.D., a corresponding study author and assistant professor of animal and veterinary sciences at the University of Maine, School of Food and Agriculture, Orono, Maine.
Interestingly, the researchers found that the younger group of mice, the juveniles, responded better to the broccoli sprout diet than their adolescent counterparts did. The younger mice had milder disease symptoms and richer gut microbial communities. Furthermore, the younger mice showed stronger bacterial community similarity to each other (aka, stronger beta-diversity), and stronger adherence to location-specific community composition throughout different parts of the gut.
“Simply put, we found that of the 4 groups we studied, the younger mice fed a broccoli sprout diet had the mildest disease symptoms and the most robust gut microbiota,” Holcomb said.
The researchers say that broccoli sprouts, which are easily grown and found in grocery stores, could be used as a treatment strategy for patients with IBD.

A review of 15 years’ worth of data from the Vitamin D Antenatal Asthma Reduction Trial (VDAART) found that vitamin D supplementation during pregnancy was linked to reduced rates of asthma and wheezing in children compared to standard prenatal multivitamin.
A new review paper from investigators from Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system, strengthens the link between vitamin D levels during pregnancy and childhood wheezing and asthma in offspring. The researchers published their review paper in the Journal of Allergy and Clinical Immunology.
“Vitamin D deficiency is very common, especially in pregnant women who are not taking supplements,” study first author Scott T Weiss, associate director of the Channing Division of Network Medicine at Brigham Women’s Hospital and professor at Harvard Medical School, said. “Based on our findings, we would recommend that all pregnant women consider a daily intake of at least 4400 IU vitamin D3 throughout their pregnancy, starting at the time of conception.”
Vitamin D is a nutrient from sunlight exposure, diet, or supplements. It is commonly considered essential to bone health but also has a role in autoimmune and other illnesses. The review links vitamin D deficiency to childhood asthma and wheezing, a major cause of illness in young children. About 40% of kids report daily wheezing at age three. By age 6, 20% are diagnosed with asthma.
The link between childhood asthma and vitamin D has been contentious. Observational studies suggest that higher vitamin D levels during pregnancy can be protective against asthma. However, a clinical trial of vitamin D supplementation in pregnancy, called the Vitamin D Antenatal Asthma Reduction Trial (VDAART), was inconclusive when comparing the supplemented group to the non-supplement group.
“In general, the observational studies show an effect, but the clinical trials don’t because nutrient trials are very different from drug trials,” Weiss said. “In a drug trial, you’re comparing giving a drug to giving no drug. In a nutrient trial, you’re comparing more of a nutrient to less, but that baseline amount in the control group is variable.”
Understanding the role of a nutrient during pregnancy requires consideration of the nutrient dose, the timing of when dosing starts, and the baseline levels in the control group. Weiss said the original VDAART trial and analysis and other meta-analyses of vitamin D supplements during pregnancy do not consider this.

A multinational study of almost one million individuals confirms a strong and clear association between exposure to radiation from CT scans in young people and an increased risk of blood cancers. This is the main conclusion of the analyses led by the Barcelona Institute for Global Health (ISGlobal), a centre supported by the “la Caixa” Foundation, in the European-funded EPI-CT study. These results, published in Nature Medicine, highlight the importance of continuing to apply strict radiological protection measures, particularly in paediatric populations.
The benefits of computed tomography (CT) for imaging in patient management (including diagnostic efficacy, treatment planning and disease follow-up) are undisputed. However, the extensive use of this procedure in recent decades has raised concerns in the medical and scientific community about the potential cancer risks associated with exposure to ionising radiation, particularly in young patients. “The exposure associated with CT scans is considered low (less than 100 mGy), but it is still higher than for other diagnostic procedures,” says Elisabeth Cardis, Head of the Radiation Group at ISGlobal and senior author of the study. Previous studies have suggested an increased risk of cancer in in children exposed to CT scans, but they had several methodological limitations.
To address these limitations, clinicians, epidemiologists and dosimetrists from nine European countries (Belgium, Denmark, France, Germany, Netherlands, Norway, Spain, Sweden, and UK) came together to conduct a multinational, European-funded study, EPI-CT, coordinated by the International Agency for Research on Cancer (IARC).
“Implementing this large, multinational study was challenging — it involved extracting data from radiology records of 276 hospitals and linking them to population-based registries in nine countries, all while maintaining the confidentiality of the individuals’ data,” says Cardis.
A dose-dependent association
The study analysed data from almost one million people, who underwent at least one CT scan before the age of 22. The dose of radiation delivered to the bone marrow, where blood cells are produced, was estimated for each person. By linking this information to national cancer registries, EPI-CT researchers were able to identify those who developed a blood cancer over time. Individuals were followed for an average of 7.8 years, although for those who had CT scans in the early years of the technology, researchers were able to monitor cancer incidence for more than 20 years after the first scan.
The results show a clear association between the total radiation doses to the bone marrow from CT scans and the risk of developing both myeloid and lymphoid malignancies. A dose of 100 mGy multiplied the risk of developing a blood cancer by a factor of about 3. These results suggest that a typical scan today (with an average dose of about 8 mGy) increases the risk of developing these malignancies by about 16%. “In terms of absolute risk, this means that, for every 10,000 children who have a CT scan, we can expect to see about 1-2 cases of cancer in the 12 years following the examination,” says first author Magda Bosch de Basea, ISGlobal researcher at the time of the study.
The authors point out that more work is needed to ensure that doses and technical parameters are systematically and adequately collected in the clinics in real time to further improve risk estimates in the future.
Public health implications
Today, more than one million children in Europe undergo CT scans every year. Although radiation doses from CT scans have decreased substantially in recent years, the findings of this study underline the need to raise awareness among the medical community and to continue to apply strict radiation protection measures, especially in the youngest patients. “The procedure must be properly justified — taking into account possible alternatives — and optimised to ensure that doses are kept as low as possible while maintaining good image quality for the diagnosis,” Cardis explains.

Researchers at Duke University have adapted CRISPR technologies for high-throughput screening of gene function in human immune cells and discovered that a single master regulator of the genome can be used to reprogram a network of thousands of genes in T cells and greatly enhance cancer cell killing.
The master regulator is called BATF3 and is one of several genes that the researchers identified and tested for improving T-cell therapies. These targets, and the methods developed to identify, test and manipulate them, could make any of the T cell cancer therapies currently in use and under development more potent. Combined with other advances, the platform could also enable generalized, off-the-shelf versions of the therapy and expansion into other disease areas such as autoimmune disorders.
The results appear online November 9 in the journal Nature Genetics.
T-cell therapy is a decade-old approach to treating cancer. More recent versions involve reprogramming the immune system’s primary soldiers to seek and destroy cancerous cells that they might otherwise overlook. Many companies are working to enhance the technology, mostly through the use of genetic engineering techniques that instruct the T cells how to identify cancerous cells and make them more effective at destroying them.
There are currently six FDA-approved T-cell therapies for specific leukemias, lymphomas and multiple myeloma. Their approaches, however, do not currently fare well when applied to solid tumors, although there are hints of success in certain studies. Solid tumors often present large physical barriers for the T cells to overcome, and the sheer number and density of cancer cells presenting targets can lead to “T-cell exhaustion,” wearing the attackers out to the point that they are not able to mount an antitumor response.
“In some cases, T-cell therapy works like a miracle drug, but in most others, it hardly works at all,” said Charles Gersbach, the John W. Strohbehn Distinguished Professor of Biomedical Engineering at Duke. “We are looking for generic solutions that can make these cells better across the board by reprogramming their gene regulation software, rather than rewriting or damaging their genetic hardware. This demonstration is a crucial step toward overcoming a major hurdle to getting T-cell therapy to work in more patients across a greater range of cancer types.”
Gersbach and his laboratory have spent the past several years developing a method that uses a version of the gene-editing technology CRISPR-Cas9 to explore and modulate genes without cutting them. Instead, it makes changes to the structures that package and store the DNA, affecting the activity level of the accompanying genes.

A group of researchers led by the Francis Crick Institute, working with the National Physical Laboratory (NPL) and Imperial College London, have discovered that breast cancer cells expressing a cancer-driving gene heavily rely on vitamin B5 to grow and survive. The researchers are part of Cancer Grand Challenges team Rosetta, funded by Cancer Research UK.
In their research published today in Nature Metabolism, the team studied the metabolic effects of one of the major cancer-driving genes called Myc. In tumour cells where Myc is highly expressed, it disturbs normal processes, drives cell growth and also makes tumour cells dependent on certain nutrients.
These dependencies could be exploited as potential therapeutic targets, but it’s hard to appropriately identify and target metabolic dependencies in human tumours, as Myc expression can vary throughout the tumour.
The researchers developed tumours inside mice with two different types of cells, either with high or low levels of Myc. They also transplanted human breast cancer tumour tissue into mice, which also had a mixture of Myc-high and Myc-low areas.
By using a technique called mass spectrometry imaging, the researchers saw that vitamin B5 was associated with Myc-high areas of both mice and human transplanted tumours. This association was also observed in biopsies taken from patients with breast cancer.
They found that Myc increased the amount of a multivitamin transporter, which allowed more vitamin B5 to enter the cells. When the researchers made the cells produce more molecules which make up the transporter, more vitamin B5 entered the cells, even in Myc-low cells. This was enough to enable faster growth of these cells, just like Myc would normally do.
They then fed mice a vitamin B5-deficient diet, and saw that their Myc-low and Myc-high mixed tumours grew more slowly than tumours in mice who were fed a standard diet. This also happened in the human breast cancer tissue when transplanted into the mice.

A globe-spanning scientific team has compiled the most comprehensive list of genetic variants associated with prostate cancer risk — 451 in all — through a whole-genome analysis that ranks as the largest and most diverse investigation into prostate cancer genetics yet. The research, led by the USC Center for Genetic Epidemiology, the Keck School of Medicine of USC and USC Norris Comprehensive Cancer Center, and in the United Kingdom by The Institute of Cancer Research, London, included major increases in representation among men from racial and ethnic groups that have often been left out of such research, revising what is known about genetic risk for the disease.
With these findings, the researchers improved a system they developed for measuring genetic risk so that it was more effective in predicting who would or wouldn’t develop prostate cancer — even distinguishing between the likelihood of aggressive and less-serious cases among men of African descent. The finding that higher risk scores based on the 451 variants correlated with more-aggressive disease in men of African ancestry is a meaningful step toward improving early detection and making better informed decisions about screening.
The study, published in Nature Genetics, builds on 2021 research documented in the same journal that found 269 genetic variants correlating with prostate cancer risk, based on a sample of nearly 235,000 men. The new results were derived from genomic information from close to 950,000 men.
“We’re not going to learn everything there is to know about the genetics of prostate cancer by studying only white men,” said co-senior author Christopher Haiman, ScD, holder of the AFLAC Chair in Cancer Research and professor of population and public health sciences at the Keck School of Medicine. “Larger and larger studies, engaging a broader spectrum of populations, are important if we’re going to identify genetic markers of risk and develop risk prediction tools that are equally effective across populations.”
A substantial revision of what’s known about genetic risk for prostate cancer
The researchers compared genomic data from 156,319 prostate cancer patients with that of a control group totaling 788,443. From the previous study, there was an 87% increase in the number of prostate cancer cases included from men of African ancestry, 45% from Latino ethnicity, 43% from European ancestry and 26% from Asian ancestry.
Haiman and his colleagues found 187 new genetic variants associated with prostate cancer risk. They also found 150 genetic variants from earlier research that were replaced by variants in nearby spots on the DNA double helix that better correlated with prostate cancer risk through the lens of the larger, more diverse sample.

Many of the children were eligible for federal aid, experts said, but errors have been common as states “unwind” assistance from earlier in the coronavirus pandemic.At least two million low-income children have lost health insurance since the end of a federal policy that guaranteed coverage through Medicaid earlier in the Covid-19 pandemic, according to new analyses by researchers at the Georgetown Center for Children and Families and KFF, a health policy research organization.The figures, which are likely a significant undercount, represent one of the fastest and most dramatic ruptures in the American safety net since Medicaid went into law in 1965, experts say. Many of the children were qualified for federal assistance but lost it because of bureaucratic mistakes, such as missing paperwork or errors by state officials.It is not clear how many of these children have found new coverage in the more than seven months since the Medicaid rolls began shrinking, but at least one million are likely to still be uninsured, said Joan Alker, the executive director of the Georgetown center and a research professor at the university’s McCourt School of Public Policy.The trend is accelerating: In the coming weeks, she said, new state numbers will probably show that three million children have lost coverage.“This is an unprecedented situation,” Ms. Alker said. The unraveling, she added, “has the potential to increase the uninsured rate for children by the largest amount that we’ve seen in decades.”Federal researchers forecast the crisis, estimating last year that more than five million children would eventually lose their health insurance through Medicaid or the federal Children’s Health Insurance Program as states tried to redetermine eligibility, a process health experts have called “unwinding.”But the scale and speed of coverage losses among children has surprised even those who anticipated an upheaval. “This is not happening in a vacuum — states have the power to make choices,” said Senator Ron Wyden, Democrat of Oregon. “And they can either stand up for kids or they can basically walk away from them.”In Lady Lake, Fla., about 50 miles northwest of Orlando, Christina Ragsdale’s children twice lost Medicaid insurance because of what she said were state enrollment errors. Her 13-year-old son, Aaron, went without his A.D.H.D. medication at school until a family member covered the out-of-pocket costs, which ran over $1,000 for a monthlong supply, she said.“The anxiety, the panic, being overwhelmed, the frustrations in class — there are just so many moving variables when that happens and you don’t have notice,” said Ms. Ragsdale, 38, who has just finished cosmetology school.She added: “When you can’t help your kids, you feel like you’re failing.”The number of people with Medicaid coverage rose dramatically earlier in the pandemic. By 2022, researchers estimate, more than half of children in the United States were covered by Medicaid or CHIP, programs that are jointly financed by states and the federal government.More than 90 million Americans, or more than one-quarter of citizens nationwide, were enrolled in the programs. Medicaid enrollment has already declined by nearly six million people during the unwinding, according to the Georgetown center.A significant number of children who no longer qualified for Medicaid were expected to be absorbed into CHIP, which is intended to cover young Americans in families with incomes too high for Medicaid eligibility but too low for private plans.But the program has not functioned as the refuge that lawmakers and health officials had hoped it would be. Ms. Alker and her colleagues estimate that 21 states with separate CHIP programs had picked up only 87,355 children — after 1.5 million were removed from Medicaid in those states.Since respiratory illnesses circulate widely in the fall and winter, the insurance coverage losses are happening at a particularly risky time. Even small medical expenses can be prohibitively costly for families of uninsured children, while larger bills can eat up savings.Parents “are being asked to make a decision between their children’s health care and something else that is a necessity,” said Dr. Valerie Borum Smith, a pediatrician in Tyler, Texas, who treats a large number of patients on Medicaid.One child she saw went a month without therapy before his Medicaid was reinstated, she said. A mother of two children who had lost Medicaid because of a paperwork error was forced to pay out-of-pocket costs for multiple rounds of antibiotics.A sign-up event for Medicaid and the Supplemental Nutrition Assistance Program in Houston in August. Medicaid losses are likely to continue rising significantly in the coming months.Callaghan O’Hare for The New York TimesSome Republican governors have defended the unwinding, arguing that Medicaid programs are reverting to their intended shape and scope after enrollments soared earlier in the pandemic.Over 70 percent of Americans who have lost Medicaid since April did so for procedural reasons, according to KFF. Through official letters and public and private coaxing, the Biden administration has implored state officials to follow federal guidelines and help Medicaid recipients through the process of establishing their eligibility.Still, some experts say that the federal government, which can halt a state’s unwinding process, has not been aggressive enough with officials in states such as Texas, which has disenrolled more than 700,000 children from Medicaid.Some children cut off from government-sponsored insurance may have parents with incomes that are too high, or their families may have obtained coverage through plans offered by an employer. Some may have moved to other states, while others are now over 18, the age cutoff.Still, the rising rate of low-income children without insurance is alarming, especially since many of the newly uninsured likely should not be, experts and officials said in interviews.“I go to sleep at night thinking about this,” Daniel Tsai, a senior official at the Centers for Medicare and Medicaid Services, said in an interview.He added: “We should not have kids being uninsured without health care, with families worried about how to pay for medication or what to do if your kid needs to go to the emergency department.”There is some imminent relief for parents. A law passed in December will require that states preserve Medicaid and CHIP coverage for a year for all children starting in January 2024. But children first will need to establish eligibility as part of the current unwinding, Ms. Alker noted.A week or even a day without health insurance can be precarious for young children. Medicaid and CHIP allow families to visit primary care practices, pay for inhalers or to receive specialty care for developmental needs, for example.Dr. Eliza Varadi, a pediatrician in Charleston, S.C., said that without Medicaid medications her patients need for asthma and diabetes can cost hundreds of dollars. Families regularly canceled appointments at her practice after realizing their children no longer had health coverage.In Carlisle, Pa., Rhiannon Hall’s 17-year-old daughter, Kayden, went two months this year without Medicaid, leaving Ms. Hall frightened of potential medical expenses that could have suddenly swallowed her savings.Before Kayden secured a free CHIP plan, Ms. Hall, a medical records employee at a community health clinic, canceled Kayden’s urgent orthodontist appointments and a regular dental cleaning.She nearly stopped picking up her daughter’s supply of Depo-Provera shots, used to control an internal bleeding problem. “When it’s gone, you worry every day that something is going to happen,” Ms. Hall said of her daughter’s health insurance.Kerstin Foor, one of Ms. Hall’s co-workers at the clinic, has a 2-year-old daughter who went without health insurance for several weeks in July before receiving a free CHIP plan. Her daughter suffers from ear infections and allergies, and medication was unaffordable while she was uninsured.“It makes you feel like you’re not doing your part, because your child should never go without health insurance,” Ms. Foor said. “It made me feel like the worst person in the world.”

S.S.R.I.s, the most widely prescribed antidepressants, frequently cause sexual problems. Here’s what patients can do about it.Antidepressants have long been among the most widely prescribed drugs in the U.S. Their popularity only grew at the start of the coronavirus pandemic, when many people struggled with depression and anxiety. Some surveys have found a striking rise among adolescents, particularly teenage girls.For many people, the drugs can be lifesaving or can drastically improve their quality of life.But many of the most popular antidepressants, known as selective serotonin reuptake inhibitors, or S.S.R.I.s, come with sexual side effects. In many cases, the problems caused by the medications can be managed. Here’s what patients should know.A wide variety of symptoms has been reported.More than half of patients who take S.S.R.I.s report some problems having sex. They include low levels of sexual desire or arousal, erectile dysfunction, pleasureless or painful orgasms and loss of genital sensitivity.Many people also report emotional blunting after taking S.S.R.I.s. This may make negative feelings less painful but also make positive feelings less pleasurable.Don’t be shy about talking to a doctor.When S.S.R.I.s went on the market in the late 1980s, patients began telling their psychiatrists that they were having sexual problems. Initially, doctors were perplexed: As far as they knew, older antidepressants had never come with these issues. But they had been wrong.“Only in going back and looking more carefully and gathering more data did we realize that actually those serotonergic drugs, the older ones, also caused sexual dysfunction,” said Dr. Jonathan Alpert, head of the American Psychiatric Association’s research council. Doctors and patients just hadn’t been talking about it, he said.As S.S.R.I.s boomed in popularity, and social stigmas about discussions of sex eased, researchers began documenting the problem in the scientific literature. But some patients found it easier to talk about than others did. Men were much more likely to report sexual side effects to their doctors than women were, even though women are almost twice as likely to be prescribed antidepressants.“The charitable interpretation is that we simply have more treatments available for male patients, and so doctors are more likely to ask after things that they feel they can actually help with,” said Tierney Lorenz, a psychologist at the University of Nebraska-Lincoln who has studied antidepressant-induced sexual dysfunction in women. “The significantly less charitable interpretation is that we still live in a very sexist society that doesn’t believe that women should have sexual interest.”Doctors may first recommend waiting it out.For some people, the sexual side effects of S.S.R.I.s will show up almost immediately after starting the medications and then resolve on their own. So doctors may suggest waiting four to six months to see whether the patient adjusts to the drugs and the most distressing sexual effects subside.But the odds of spontaneous resolution of sexual side effects are low, happening in an estimated 10 to 20 percent of patients who report the symptoms.Other medications, including other antidepressants, can help.One common way to manage sexual side effects is to try another S.S.R.I. Research suggests that certain drugs, such as Zoloft and Celexa, come with a higher likelihood of causing sexual problems. Switching drugs, however, means enduring a trial-and-error period to try to find what works.If a patient is otherwise doing well on an S.S.R.I., a doctor may be hesitant to drastically change the drug regimen. Instead, the doctor might recommend adding an additional drug to the mix that could help counteract the sexual side effects.For example, adding the non-S.S.R.I. antidepressant Wellbutrin, which acts on norepinephrine and dopamine in the brain, has been shown to diminish sexual symptoms in many patients, Dr. Alpert said.For erectile dysfunction, doctors may also suggest adding phosphodiesterase type 5 inhibitors like Viagra, which acts on the vascular system, he said.‘Drug holidays’ can help. But be careful.Another approach that should be used cautiously and under the close supervision of a physician is temporarily stopping the S.S.R.I. or lowering the dose for 24 to 48 hours before having sex.But for many patients, this isn’t an ideal solution. Planning ahead can be annoying. And withdrawal from S.S.R.I.s can immediately cause other unpleasant symptoms, including dizziness, nausea, insomnia and anxiety. Some doctors are concerned that frequent use of drug holidays may make patients more likely to discontinue the medications altogether, which could lead to worsening mental health problems.In rare cases, sex problems can persist after stopping the drugs.A small but vocal group of patients is speaking out about sexual problems that have endured even after they stopped taking S.S.R.I.s. Some have reported low libido and numb genitals persisting for many years.Though studies are scarce, the risk appears to be low. A recent study estimated that about one in 216 men who discontinued S.S.R.I.s were subsequently prescribed medications for erectile dysfunction, a rate at least three times as high as that among the general population.But diagnosing this condition is tricky, in part because depression itself can dull sexual responses. Among unmedicated men with depression, 40 percent report a loss of sexual arousal and desire, and 20 percent struggle to reach orgasm.