Publisher Health

Obese mice that were fed a high-fat diet and that received prednisone one time per week had improved exercise endurance, got stronger, increased their lean body mass and lost weight, reports a new Northwestern Medicine study. The mice also had increased muscle metabolism.
The once-weekly prednisone promoted nutrient uptake into the muscles.
Investigators also found these mice had increased adiponectin levels, a fat-derived hormone that appears to play an important role in protecting against diabetes and insulin resistance.
The scientists also showed mice that were already obese from eating a high-fat diet also had benefit after once-weekly prednisone, experiencing increased strength, running capacity and lower blood glucose.
“These studies were done in mice. However, if these same pathways hold true in humans, then once-weekly prednisone could benefit obesity,” said senior author Dr. Elizabeth McNally, director of the Center for Genetic Medicine at Northwestern University Feinberg School of Medicine.
McNally also is a Northwestern Medicine physician and the Elizabeth J. Ward Professor of Genetic Medicine.

The SARS-CoV-2 virus can infect specialized pacemaker cells that maintain the heart’s rhythmic beat, setting off a self-destruction process within the cells, according to a preclinical study co-led by researchers at Weill Cornell Medicine, NewYork-Presbyterian and NYU Grossman School of Medicine. The findings offer a possible explanation for the heart arrhythmias that are commonly observed in patients with SARS-CoV-2 infection.
In the study, reported Apr. 1 in Circulation Research, the researchers used an animal model as well as human stem cell-derived pacemaker cells to show that SARS-CoV-2 can readily infect pacemaker cells and trigger a process called ferroptosis, in which the cells self-destruct but also produce reactive oxygen molecules that can impact nearby cells.
“This is a surprising and apparently unique vulnerability of these cells — we looked at a variety of other human cell types that can be infected by SARS-CoV-2, including even heart muscle cells, but found signs of ferroptosis only in the pacemaker cells,” said study co-senior author Dr. Shuibing Chen, the Kilts Family Professor of Surgery and a professor of chemical biology in surgery and of chemical biology in biochemistry at Weill Cornell Medicine.
Arrhythmias including too-quick (tachycardia) and too-slow (bradycardia) heart rhythms have been noted among many COVID-19 patients, and multiple studies have linked these abnormal rhythms to worse COVID-19 outcomes. How SARS-CoV-2 infection could cause such arrhythmias has been unclear, though.
In the new study, the researchers, including co-senior author Dr. Benjamin tenOever of NYU Grossman School of Medicine, examined golden hamsters — one of the only lab animals that reliably develops COVID-19-like signs from SARS-CoV-2 infection — and found evidence that following nasal exposure the virus can infect the cells of the natural cardiac pacemaker unit, known as the sinoatrial node.
To study SARS-CoV-2’s effects on pacemaker cells in more detail and with human cells, the researchers used advanced stem cell techniques to induce human embryonic stem cells to mature into cells closely resembling sinoatrial node cells. They showed that these induced human pacemaker cells express the receptor ACE2 and other factors SARS-CoV-2 uses to get into cells and are readily infected by SARS-CoV-2. The researchers also observed large increases in inflammatory immune gene activity in the infected cells.
The team’s most surprising finding, however, was that the pacemaker cells, in response to the stress of infection, showed clear signs of a cellular self-destruct process called ferroptosis, which involves accumulation of iron and the runaway production of cell-destroying reactive oxygen molecules. The scientists were able to reverse these signs in the cells using compounds that are known to bind iron and inhibit ferroptosis.
“This finding suggests that some of the cardiac arrhythmias detected in COVID-19 patients could be caused by ferroptosis damage to the sinoatrial node,” said co-senior author Dr. Robert Schwartz, an associate professor of medicine in the Division of Gastroenterology and Hepatology at Weill Cornell Medicine and a hepatologist at NewYork-Presbyterian/Weill Cornell Medical Center.
Although in principle COVID-19 patients could be treated with ferroptosis inhibitors specifically to protect sinoatrial node cells, antiviral drugs that block the effects of SARS-CoV-2 infection in all cell types would be preferable, the researchers said.
The researchers plan to continue to use their cell and animal models to investigate sinoatrial node damage in COVID-19 — and beyond.
“There are other human sinoatrial arrhythmia syndromes we could model with our platform,” said co-senior author Dr. Todd Evans, the Peter I. Pressman M.D. Professor of Surgery and associate dean for research at Weill Cornell Medicine. “And, although physicians currently can use an artificial electronic pacemaker to replace the function of a damaged sinoatrial node, there’s the potential here to use sinoatrial cells such as we’ve developed as an alternative, cell-based pacemaker therapy.”
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A new type of cell that resides deep within human lungs and may play a key role in human lung diseases has been discovered by researchers at the Perelman School of Medicine at the University of Pennsylvania.
The researchers, who report their findings today in Nature, analyzed human lung tissue to identify the new cells, which they call respiratory airway secretory cells (RASCs). The cells line tiny airway branches, deep in the lungs, near the alveoli structures where oxygen is exchanged for carbon dioxide. The scientists showed that RASCs have stem-cell-like properties enabling them to regenerate other cells that are essential for the normal functioning of alveoli. They also found evidence that cigarette smoking and the common smoking-related ailment called chronic obstructive pulmonary disease (COPD) can disrupt the regenerative functions of RASCs — hinting that correcting this disruption could be a good way to treat COPD.
“COPD is a devastating and common disease, yet we really don’t understand the cellular biology of why or how some patients develop it. Identifying new cell types, in particular new progenitor cells, that are injured in COPD could really accelerate the development of new treatments,” said study first author Maria Basil, MD, PhD, an instructor of Pulmonary Medicine.
COPD typically features progressive damage to and loss of alveoli, exacerbated by chronic inflammation. It is estimated to affect approximately 10 percent of people in some parts of the United States and causes about 3 million deaths every year around the world. Patients often are prescribed steroid anti-inflammatory drugs and/or oxygen therapy, but these treatments can only slow the disease process rather than stop or reverse it. Progress in understanding COPD has been gradual in part because mice — the standard lab animal — have lungs that lack key features of human lungs.
In the new study, Morrisey and his team uncovered evidence of RASCs while examining gene-activity signatures of lung cells sampled from healthy human donors. They soon recognized that RASCs, which don’t exist in mouse lungs, are “secretory” cells that reside near alveoli and produce proteins needed for the fluid lining of the airway.
“With studies like this we’re starting to get a sense, at the cell-biology level, of what is really happening in this very prevalent disease,” said senior author Edward Morrisey, PhD, the Robinette Foundation Professor of Medicine, a professor of Cell and Developmental Biology, and director of the Penn-CHOP Lung Biology Institute at Penn Medicine.
Observations of gene-activity similarities between RASCs and an important progenitor cell in alveoli called AT2 cells led the team to a further discovery: RASCs, in addition to their secretory function, serve as predecessors for AT2 cells — regenerating them to maintain the AT2 population and keep alveoli healthy.
AT2 cells are known to become abnormal in COPD and other lung diseases, and the researchers found evidence that defects in RASCs might be an upstream cause of those abnormalities. In lung tissue from people with COPD, as well as from people without COPD who have a history of smoking, they observed many AT2 cells that were altered in a way that hinted at a faulty RASC-to-AT2 transformation.
More research is needed, Morrisey said, but the findings point to the possibility of future COPD treatments that work by restoring the normal RASC-to-AT2 differentiation process — or even by replenishing the normal RASC population in damaged lungs.
The research was supported by the National Institutes of Health (HL148857, HL087825, HL134745, HL132999, 5T32HL007586-35, 5R03HL135227-02, K23 HL121406, K08 HL150226, DK047967, HL152960, R35HL135816, P30DK072482, U01HL152978), the BREATH Consortium/Longfunds of the Netherlands, the Parker B. Francis Foundation, and GlaxoSmithKline.

People who reported multiple symptoms consistent with severe substance use disorder at age 18 exhibited two or more of these symptoms in adulthood, according to a new analysis of a nationwide survey in the United States. These individuals were also more likely, as adults, to use and misuse prescription medications, as well as self-treat with opioids, sedatives, or tranquillizers. Published today in JAMA Network Open, the study is funded by the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health.
While use of alcohol, cannabis, or other drugs is common among adolescents, previous studies have suggested that most teens reduce or cease drug use as they enter adulthood. However, this study indicates that adolescents with multiple symptoms of substance use disorder — indicating higher severity — do not transition out of symptomatic substance use.
“Screening adolescents for drug use is extremely important for early intervention and prevention of the development of substance use disorder,” said Nora Volkow, M.D., director of NIDA. “This is critical especially as the transition from adolescence to adulthood, when brain development is still in progress, appears to be a period of high risk for drug use initiation.” Dr. Volkow further discusses the findings and implications of this study in a related commentary.
Researchers in this study argue that key knowledge gaps currently hinder the initiation of screening, diagnosis, prevention, and treatment efforts for teens with substance use disorders. For example, previous methods evaluating persistence of substance use disorder tended to treat substance use disorder as one broad category, without looking at severity. They also failed to account for the possibility of polysubstance use, whereby individuals may use multiple drugs or switch the types of drugs they use as they grow older.
The NIDA-funded Monitoring the Future Panel study at the University of Michigan-Ann Arbor helped close this research gap by examining substance use behaviors and related attitudes among 12th graders through their adulthood in the United States. Since 1976, the study has surveyed panels of students for their drug use behaviors across three time periods: lifetime, past year, and past month. In this study, researchers looked primarily at a subgroup of 5,317 12th graders first evaluated between 1976 and 1986, who were followed with additional surveys at two-year, then five-year intervals for up to 32 years, until they reached age 50. Among the respondents, 51% were female and 78% were white.
The research team examined the relationship between substance use disorder symptom severity at age 18 and prescription drug use, prescription drug misuse, and substance use disorder symptoms up to age 50 in these individuals.
To measure severity of substance use disorder symptoms in adolescence, researchers recorded the number of substance use disorder symptoms that participants reported in response to initial survey questions. These questions were based on criteria for alcohol, cannabis, and “other drug” use disorders in the Diagnostic and Statistical Manual of Mental Disorders (DSM). The researchers categorized substance use disorder symptoms into five levels of severity: exhibiting no symptoms, one symptom, two to three symptoms, four to five symptoms, and six or more symptoms. Symptoms included, but were not limited to, substance use resulting in a failure to fulfill major role obligations and repeating substance use even when dangerous to health.
Approximately 12% of surveyed teens indicated “severe” substance use disorder, defined by this study as reporting six or more symptoms. Among this group, more than 60% exhibited at least two symptoms of substance use disorder in adulthood — an association found across alcohol, cannabis, and other drug use disorders. By comparison, roughly 54% of teens reporting two to three symptoms — indicative of “mild” substance use disorder — had two or more substance use disorder symptoms in adulthood. Higher severity of substance use disorder symptoms at age 18 also predicted higher rates of prescription drug misuse in adulthood.
Overall, more than 40% of surveyed 18-year-old individuals reported at least two substance use disorder symptoms (across all substances). More than half of the individuals who were prescribed and used opioids, sedatives, or tranquilizers as adults also reported two or more symptoms at age 18. This finding underlines the importance of strategies to increase safety and properly assess a potential history of substance use disorder symptoms when prescribing controlled medications to adults.
“Teens with substance use disorder will not necessarily mature out of their disorders, and it may be harmful to tell those with severe symptoms that they will,” said Dr. Sean Esteban McCabe, senior author of this study and director of the Center for the Study of Drugs, Alcohol, Smoking and Health at University of Michigan. “Our study shows us that severity matters when it comes to predicting risk decades later, and it’s crucial to educate and ensure that our messaging to teens with the most severe forms of substance use disorder is one that’s realistic. We want to minimize shame and sense of failure for these individuals.”
The authors note that more research is needed to uncover potential neurological mechanisms and other factors behind why adolescents with severe substance use disorder symptoms are at increased risk of drug addiction and misuse in adulthood. Characterizing possible causes of more severe substance use disorder could help improve understanding of vulnerability to chronic substance use and help make prevention and treatment strategies more effective.

How is the activity of genes regulated by the packaging of DNA? To answer this question, a technique to measure both gene expression and DNA packaging at the same time was developed by Franka Rang and Kim de Luca, researchers from the group of Jop Kind (group leader at the Hubrecht Institute and Oncode Investigator). This method, EpiDamID, determines the location of modified proteins around which the DNA is wrapped. It is important to gather information about these modifications, because they influence the accessibility of DNA, thereby affecting the gene activity. EpiDamID is therefore valuable for research into the early development of organisms. The results of the study are published in Molecular Cell on April 1, 2022.
In order to fit DNA into the nucleus of a cell, it is tightly packed around nuclear proteins: histones. Depending on the tightness of this winding, the DNA can be (in)accessible to other proteins. This therefore determines whether the process of gene expression, translation of DNA into RNA and eventually into proteins, can take place.
DNA packaging determine gene activity
The tightness of DNA winding around histones is regulated by the addition of molecular groups, so-called post-translational modifications (PTMs), to the histones. For example, if certain molecules are added to the histones, the DNA winding is loosened. This makes the DNA more accessible for certain proteins and causes the genes in this part of the DNA to become active, or expressed. Furthermore, proteins that are crucial for gene expression can directly recognize and bind the PTMs. This enables transcription: the process of DNA copying.
The regulation of gene expression, for instance through PTMs, is also known as epigenetic regulation. Since all cells in a body have the same DNA, regulation of gene expression is needed to (de)activate specific functions in individual cells. For instance, heart muscle cells have different functions than skin cells, thus require different genes to be expressed.
Analysis of single cells using EpiDamID
To understand how PTMs affect gene expression, first authors Franka Rang and Kim de Luca designed a new method to determine the location of the modifications. Using this approach, called EpiDamID, researchers can analyze single cells, whereas previous methods were only able to measure a large group of cells. Analysis on such a small scale results in knowledge on how DNA winding differs per cell, rather than information on the average DNA winding of many cells.
EpiDamID is based on DamID, a technique which is used to determine the binding location of certain DNA-binding proteins. Using EpiDamID, the binding location of specific PTMs on histone proteins can be detected in single cells. Compared to others, a great advantage of this technique is that researchers need very limited material. Furthermore, EpiDamID can be used in combination with other methods, such as microscopy, to study regulation of gene expression on different levels.
Future prospects
Following the development of this technique, the Kind group will focus on the role of PTMs from the point of view of developmental biology. Because single cells are analyzed using EpiDamID, only a limited amount of material is needed to generate enough data. This allows researchers to study the early development of organisms from its first cell divisions, when the embryo consists of only a few cells.
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Nearly half of all older adults now die with a diagnosis of dementia listed on their medical record, up 36% from two decades ago, a new study shows.
But that sharp rise may have more to do with better public awareness, more detailed medical records and Medicare billing practices than an actual rise in the condition, the researchers say.
Even so, they note, this offers a chance for more older adults to talk in advance with their families and health care providers about the kind of care they want at the end of life if they do develop Alzheimer’s disease or another form of cognitive decline.
The study, published in JAMA Health Forum by a University of Michigan team, uses data from 3.5 million people over the age of 67 who died between 2004 and 2017. It focuses on the bills their providers submitted to the traditional Medicare system in the last two years of the patients’ lives.
In 2004, about 35% of these end-of-life billing claims contained at least one mention of dementia, but by 2017 it had risen to more than 47%. Even when the researchers narrowed it down to the patients who had at least two medical claims mentioning dementia, 39% of the patients qualified, up from 25% in 2004.
The biggest jump in the percentage of people dying with a dementia diagnosis happened around the time Medicare allowed hospitals, hospices and doctors’ offices to list more diagnoses on their requests for payment.
But around this same time, the National Plan to Address Alzheimer’s Disease also went into effect, with a focus on public awareness, quality of care and more support for patients and their caregivers.
The end-of-life care that patients with dementia received changed somewhat overtime, including a drop in the percentage who died in a regular hospital bed or a ICU bed, or who had a feeding tube in their last six months. The percentage who received hospice services rose dramatically, from 36% to nearly 63%, though the authors note this is in line with a national trend toward more hospice care by the late 2010s.
“This shows we have far to go in addressing end-of-life care preferences proactively with those who are recently diagnosed, and their families,” said Julie Bynum, M.D., Ph.D., senior author of the study and a professor of geriatric medicine at Michigan Medicine. “Where once the concern may have been underdiagnosis, now we can focus on how we use dementia diagnosis rates in everything from national budget planning to adjusting how Medicare reimburses Medicare Advantage plans.”
In addition to Bynum, the study’s authors are Matthew Davis, Ph.D., of the U-M School of Nursing and Medical School, Chiang-Hua Chang, PhD of the Division of Geriatric and Palliative Medicine, and Sharon Simonton, PhD, MPH. Bynum, Davis and Chang are members of the U-M Institute for Healthcare Policy and Innovation. Bynum and Davis are leaders in the Center to Accelerate Population Research in Alzheimer’s (CAPRA)

Community health workers employed by Medicaid health plans can help low-income people who face barriers to care rely less on the emergency room, and more on outpatient care, a new study finds. The CHWs in the study worked with Medicaid participants to make a plan for their health and connect them with social and health care services in their local area.
And that may lead to better use of funding, and potentially lower costs, for the Medicaid system over the long run, the researchers say.
The new findings come from the most rigorous study of a real-world CHW program to date, a randomized controlled trial conducted by the University of Michigan Institute for Healthcare Policy and Innovation in partnership with local and state organizations and agencies. It’s published in the American Journal of Public Health.
But the study also shows the challenges involved in making the connection between CHW and high-use Medicaid participants. The findings could help Medicaid CHW programs in Michigan and beyond improve how they support and structure their efforts to bridge the gap between people and services.
“These results are really heartening, especially through the lens of success for Medicaid plans of decreasing acute care use and increasing use of ambulatory care among individuals who have not been accessing primary care,” said Michele Heisler, M.D., M.P.A., who led the project and is a professor of internal medicine at the U-M Medical School. “This is very encouraging for being able to sustain CHW programs over the long term, because of the potential to translate to cost savings. But our results also show the importance of flexibility and persistence when it comes to connecting with this patient population.”
Heisler and her IHPI colleagues conducted the study with the help of three of Michigan’s Medicaid managed care insurance plans, which since 2016 have been required to have CHW programs.

An international team of investigators, including several researchers in biological sciences from the U of A, have published a paper that reports the discovery of a developmental gene linked to touch in the tentacles of sea anemones as well as hearing in humans. The gene, called pou-iv (pronounced “pow four”), is important for the development of auditory cells in the human inner ear.
Cnidarians, which include jellyfish, corals and sea anemones, are the closest living relatives of animals with bilateral symmetry, such as humans and other invertebrates. As such, cnidarians are useful for studying human evolutionary history because features shared by bilateral animals and cnidarians were likely present in our last common ancestor. A feature of note is the nervous system, and both bilaterians and cnidarians use similar sets of genes in neural development.
Auditory cells in the vertebrate inner ear that pick up vibrations to enable hearing are called hair cells. While they aren’t known to be able to hear, sea anemones have similar-looking cells on their tentacles — also called hair cells — that they use to sense the movements of their prey.
In mammals, pou-iv is required for proper hair cell development, and mice that lack pou-iv are deaf. Sea anemones also have a pou-iv gene, but, prior to the research team’s work, no one had ever examined its role in anemone hair cell development.
The researchers knocked out the pou-iv gene in a sea anemone and found that it resulted in abnormal development of tentacular hair cells, removing the animals’ response to touch. They also found that pou-iv is needed to turn on the polycystin 1 gene in sea anemones, which is required for normal fluid flow sensing by vertebrate kidney cells. Taken together, this suggests that pou-iv has a very ancient role in the development of touch sensation that goes back at least as far as our last common ancestor with sea anemones.
The U of A researchers are affiliated with the Nakanishi Lab, overseen by an assistant professor of biological sciences Nagayasu Nakanishi, who was a recent recipient of an NSF CAREER award for his work on the evolution of the nervous system. He is the corresponding author on the study.
“This study is exciting because it not only opened a new field of research into how mechanosensation develops and functions in a sea anemone, which has ample potential for novel and important discoveries (to be reported in the future),” Nakanishi said, “but it also informs us that the building blocks of our sense of hearing have ancient evolutionary roots dating back hundreds of millions of years into the Precambrian.”
The paper, titled “Cnidarian hair cell development illuminates an ancient role for the class IV POU transcription factor in defining mechanoreceptor identity,” was published in eLife. Additional authors included Ethan Ozment, Arianna N. Tamvacakis and Jianhong Zhou from the U of A. Pablo Yamild Rosiles-Loeza, Esteban Elías Escobar-Hernandez and Selene L Fernandez-Valverde from The Center for Research and Advanced Studies of the National Polytechnic Institute in Irapuato, Mexico, served as co-authors.
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Researchers are rolling out a data set that provides detailed information on COVID-19 vaccine shipments and wastage across the United States, with the goal of spurring new data analysis to improve vaccination efforts in the future. The work stems from a collaboration between researchers at North Carolina State University and BuzzFeed News.
“The development and distribution of COVID-19 vaccines has been a monumental undertaking,” says Ali Hajbabaie, corresponding author of the paper and an assistant professor of civil, construction and environmental engineering at NC State. “And while it’s been a remarkable accomplishment, there are also opportunities for us to learn how to improve the vaccine supply chain. What are the logistical challenges associated with transportation and distribution of vaccines for COVID-19? How can we study this? What can we learn from it?”
“For this work, we focused on collecting data regarding vaccine shipment and wastage,” says Leila Hajibabai, co-author of the paper and an assistant professor in NC State’s Edward P. Fitts Department of Industrial and Systems Engineering. “And we’re making that data publicly available to encourage the broader research community to analyze the data so that we can learn as much from it as possible. We also want to inspire other researchers to make their data publicly available in a timely manner.”
“We did some simple analyses in this paper to highlight the potential of the data, but we think there is much more to be done, and we want to tap into the expertise of other researchers to make the most of this information,” says Hajbabaie.
The researchers collected vaccine shipment data from the Centers for Disease Control and Prevention (CDC). This data includes the type of vaccine, the amount of vaccine, and the date that each specific shipment was sent to each of 47,188 specific vaccination sites, such as clinics, hospitals, pharmacies and doctor’s offices.
The researchers also collected data from the CDC on the amount of vaccine that was spoiled and had to be disposed of by awardees. This could be because a vial was broken, because it was stored at an improper temperature, because it was past its expiration date, and so on. Awardees are large-scale entities that are responsible for overseeing specific vaccination sites. There were 92 awardees nationally, and the researchers have wastage data from 58 of them. Examples of awardees include individual states, federal entities such as the Department of Defense, federal programs such as the Veterans Health Administration, and large-scale retailers such as CVS and Walgreens. Wastage data was reported on a semi-regular basis — often daily, but not always.

The research is thin, but anecdotal experience suggests that the right dose and delivery method can make a positive difference for some people.A few weeks ago, the Ask Well column highlighted treatments for low libido in women. Afterward, several readers wanted to know if cannabis could be added to the list of potential remedies.It’s a question that is especially relevant now that the U.S. House of Representatives is poised to pass a bill legalizing marijuana at the federal level. The legislation is expected to face challenges in the Senate, but support for the full-scale legalization of cannabis is growing.Marijuana, the most commonly used drug that is federally illegal, is currently allowed for medical use in 37 states, and in 18 states for adult recreational use. According to a 2020 survey, nearly 18 percent of Americans age 12 or older had used it within the past year, and more than two-thirds of Americans support legalizing it, according to various polls.To learn more about cannabis and sex we turned to several experts, including a gynecologist who has surveyed women about their marijuana use.The bottom line: It’s hard to say with certainty that cannabis will increase desire or improve your sex life, but anecdotal evidence suggests that the right dose of cannabis can make a woman’s orgasms more satisfying and increase sex drive. This is in part because cannabis can enhance the senses and also alleviate some of the symptoms that inhibit desire, like anxiety, sleeplessness or pain. It can have positive effects for men, as well, but also several negative ones, and women should be aware of its potential downsides, too.What does the research say?Both men and women have long reported that cannabis alters their sexual experience. In an essay published in 1971, the astronomer Carl Sagan, a longtime marijuana user, wrote that cannabis “enhances the enjoyment of sex” and “gives an exquisite sensitivity.”There is very little research on cannabis and libido, however, in part because cannabis research has been notoriously difficult to fund and it remains a federally illegal drug in the United States. Most of the research that does exist relies on data from questionnaires, which are heavily skewed toward people who already use cannabis and are not representative of the general population, making it difficult to draw firm conclusions. In addition, the surveys do not provide reliable and precise information about dosage, delivery method or timing.But based on the limited evidence, the drug does seem to enhance the sexual experience among many women who already use it.“I’ve had several patients come to me and say, ‘I have low libido. Can you help me? And, oh, by the way, if I use marijuana, I can orgasm, no problem,’” said Dr. Becky K. Lynn, a sexual medicine and menopause expert and the founder of Evora Women’s Health in St. Louis. “They also tell me that low libido improves with marijuana.”Dr. Lynn, who also teaches at the Saint Louis University School of Medicine, is the lead author of a study published in 2019 that surveyed 373 women about cannabis at an obstetrics and gynecology clinic in Missouri. Of those, 34 percent reported having used marijuana before sexual activity and most of them said it resulted in an increased sex drive, improved orgasm and decreased pain.Studies have also found that some women use cannabis to help manage menopause symptoms like hot flashes, night sweats, insomnia and vaginal changes, such as dryness, all of which may contribute to lower libido when untreated.In addition, an online survey of more than 200 women and men who use cannabis found that nearly 60 percent said cannabis increased their desire for sex; almost 74 percent reported increased sexual satisfaction. But the study, which was conducted by researchers in Canada and published in The Journal of Sexual Medicine, also said that 16 percent reported sex was better in some ways and worse in others, and a little under 5 percent said it was worse.Research on cannabis use and sexual function among men is likewise sparse and can be contradictory. According to the International Society for Sexual Medicine, some men report that their sexual performance improves when they use marijuana, while others may experience problems such as less motivation for sex, erectile dysfunction, trouble reaching orgasm or premature ejaculation. Cannabis use has also been associated with reductions in sperm count, concentration, motility and viability.‘Start low and go slow’All drugs have risks and potential side effects, cannabis included.If your doctor has cleared you to try cannabis in a state where it is legal, Dr. Peter Grinspoon, a primary-care doctor at Massachusetts General Hospital Chelsea HealthCare Center and a medical-cannabis consultant, advised taking a “teeny bit” in a tincture if you’re new to it — in some cases as little as 1 milligram of THC, the main psychoactive ingredient in weed — before slowly working your way up.“At low doses, cannabis helps libido, but at high doses, it often isn’t as effective,” he said, adding that the wrong amount will lead some people to become paranoid and anxious. The drug could also inhibit orgasm, creating the opposite effect of what was intended.Dr. Lynn agreed. “Start low and go slow,” she said.How much is too much marijuana? That will vary from person to person.And because cannabis is known to impair judgment, coordination and reaction time, those who use psychoactive drugs before or during sex “must take into consideration whether people using the product and their partners can have safe and consensual sex,” said Dr. Stacy Tessler Lindau, a gynecologist at the University of Chicago Medicine and the creator of WomanLab, a website about sexual health.Given that cannabis can compromise judgment about contraception or the ability to consent, she added, women can either look to avoid products with psychoactive components or, if they wish to use them, increase safety by having sex with a trusted partner.“Sex with a stranger ideally would not involve any intoxication of anyone involved,” she said.Dr. Jordan Tishler, a former emergency medicine doctor and president of the Association of Cannabinoid Specialists, recommended trying cannabis alone for the first few times and masturbating, in order “to understand what it does to the body and sensations.”What is the best cannabis delivery method?Smoking marijuana or using oil vape pens should be avoided, because they can harm the lungs, the experts said.Dr. Lynn typically recommends tinctures, which are concentrated cannabis extracts that are taken by mouth. It is easy to measure the number of milligrams you want to use, she said.Dr. Tishler usually advises his clients to start with 5 mg of THC. Taking one puff on a cannabis flower vaporizer before having a sexual experience can work faster and more predictably than edibles or lubricants infused with THC, he said.“I teach patients to take a puff in a particular manner,” Dr. Tishler added: “a very deep, slow inhalation that allows us to estimate how much dose they are getting.”Remember that libido is complicatedThere are multiple factors that can affect someone’s sex drive and sexual function, some of which could be addressed by seeing a physician or a mental health provider.If a woman had pain with intercourse, for example, she would need to be referred to a gynecologist for a full evaluation, Dr. Grinspoon said. Cannabis could potentially help, but there would be more to investigate and consider in anyone who is experiencing uncomfortable physical symptoms.“You can be treating the symptom while looking at the underlying cause,” he said. “It’s not mutually exclusive.”