Publisher Health

Fungal pathogens have a major global impact upon human health — they are often difficult to diagnose and treat, and there is an urgent need for better diagnostics and more effective antifungal treatments. Using newly developed imaging technologies, Monash Biomedicine Discovery Institute researchers have today (21/9) revealed how Candida albicans, a common fungus, evades immune responses. According to the researchers this involves an “alien-like” shape shifting that allows the fungus to break out of immune cells.
The paper published in the journal Cell Reports, led by Professor Ana Traven and PhD student Françios Olivier, describes how Candida albicans uses a sword-like filament to engage toxin molecules and cell death pathways that damage immune cell membranes — allowing it to escape and spread.
The imaging technology, developed by Olivier in collaboration with Monash Micro-Imaging, allows for escaping fungi to be pin-pointed in real time. According to Olivier, this study was made possible by the automation of imaging analysis and increased computer processing power: “We could harness a great deal of data which provided insight into this immune escape mechanism.”
Candida is a yeast that often lives in the human digestive tract and mouth, as well as urinary and reproductive organs. Usually, it doesn’t cause disease in its host, but under certain conditions, it can switch to a harmful form. Candida albicans remains a common cause of life-threatening disease in ICU, post- surgery and cancer patients. The immune system has a particular cell type, called the macrophage, which is responsible for gobbling up invaders (bacteria, fungi, cancer cells) and triggering immune responses. Candida albicans escape macrophages by morphing into long, filament-like cells. This escape leads to spreading of the fungus. In the process is triggers immune responses that can be harmful if not kept in check.
According to Professor Traven, targeting the fungus as it is escaping “presents a promising therapeutic avenue, preventing both the spread of the infection and having the potential to dampen inflammation.” Until now, the mechanisms behind this escape have remained unclear as researchers have not been able to study this escape manoeuvre in detail. Now they can. The research team developed a live-cell imaging platform that, in real time, maps Candida’s escape from macrophages, revealing several escape mechanisms.
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Our skin forms the physical boundary between us and the outside world, yet it still holds a surprising number of secrets. Now, researchers from Japan have discovered that sensory nerve cells in our skin do more than just help us feel our way around.
In a study published this month in Cell Reports, a research group led by the Institute of Industrial Science, The University of Tokyo, has revealed that sensory neurons in human skin play an important role in pigmentation.
Pigmentation in our skin is caused in part by a group of substances known as melanin, which are produced by skin cells called melanocytes. When melanocytes are damaged or reduced in number, this leads to either increased or limited melanin production, resulting in pigmentation disorders. Typically, these melanin changes are long term, localized, and uneven — such as skin color patches. The mechanisms that underpin the maintenance and development of these patches are mostly unknown.
“Increasingly, evidence has been pointing to the possibility that the interaction between neurons and melanocytes plays a number of key roles in human skin,” says lead author of the study, Siu Yu Chow. “This includes the regulation of melanocytes by sensory neurons.”
In their study, the researchers explored the relationship between sensory neurons and melanocytes, and found that there was a greater degree of contact between them in skin color patch tissue than control tissue. When cultured with neurons, melanocytes were also found to have higher pigmentation and an increased survival rate. Melanocytes cultured in growth media that had been conditioned with sensory neurons showed increased survival, as well as longer dendrites (branch-like extensions of the cell); these effects were specific to melanocytes.
“Additionally, we identified proteins secreted by sensory neurons, including Repulsive Guidance Molecule B (RGMB),” explains Yoshiho Ikeuchi, senior author. “We discovered that melanocyte survival and darkness is promoted by RGMB.”
The study revealed that sensory neurons play a role in modulating a number of features of human melanocytes via the secretion of RGMB, which is a key factor that stimulates melanocytes.
“Our results highlight how important sensory neurons are to skin pigmentation and physiology,” says Chow.
Pigmentation disorders, including skin color patches, are common and can result in psychosocial problems; they are also often linked with health issues such as neurocutaneous diseases (diseases that affect the nervous system and skin) and melanoma. However, the effectiveness of chemical and topical treatments for these are limited. The results of this study could lead to the development of new drugs for use with current therapies by enabling the discovery of previously unknown molecules and mechanisms that include RGMB.
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The results may help explain how high-fat diets trigger inflammation, which can contribute to the development of insulin resistance, type 2 diabetes and other complications in individuals with obesity.
An invasion of inflammatory immune cells, called monocytes, into fat tissue is a hallmark of obesity, but what leads to this harmful phenomenon is unclear. Many immune cells, including monocytes, are produced in the bone marrow, which is very sensitive to environmental changes. Scientists have already shown that fat cells in the bone marrow rapidly expand in response to a high-fat diet.
“We wanted to know if bone marrow tissue was an early responder to a high-fat diet that could serve as a precursor to the inflammation observed in obesity,” says senior author Amira Klip, Senior Scientist in Cell Biology at SickKids, and Professor in the Departments of Paediatrics, Biochemistry, and Physiology at the University of Toronto, Canada. “Do high-fat diet-induced changes in the bone marrow lead to the production of the inflammatory monocytes that invade fat tissue in people with obesity?”
Klip and colleagues found that mice fed a high-fat diet begin to experience metabolic disturbances throughout their body and in the bone marrow within three weeks. Fat cells in the bone marrow multiply and take on white fat cell characteristics. Metabolic changes in the monocytes at the bone marrow cells also occur — they use less oxygen to break down sugar into energy, and lactic acid builds up in the cells and surrounding fluid. The team also found that mitochondria, cellular factories that break down sugar into energy, break apart into fragments within the monocytes and become less efficient. This process of mitochondrial fragmentation is associated with insulin resistance.
Over several weeks, the number of monocytes in the bone marrow shifts to include less of a monocyte called Ly6Clow to more of a monocyte called Ly6Chigh, the same type of monocyte that invades fat tissue in people with obesity. This accumulation of Ly6Chigh monocytes in the bone marrow starts before monocytes build up in fat tissue in the rest of the body to become inflammatory macrophages — the mature form of monocytes.
“These results show that high-fat diets can cause remodelling in bone marrow fat cells that disrupt the normal balance of monocytes, and can subsequently lead to invasive Ly6Chigh monocytes spilling into the body,” continues Klip.
The team further demonstrated that white fat tissue can spur these changes in experiments using cell samples from mice fed a high-fat diet. They also found that brown fat tissue, which is more abundant in leaner people, can cause a shift towards the non-invasive Ly6Clow monocytes.
“Our study reveals how high-fat diets trigger a cascade of inflammation in the body that involves the bone marrow,” concludes Klip. “More research is needed to understand this process further and find out if there are ways to prevent or reverse this process. It will also be important to know if the bone marrow is also an early responder to obesity in humans. Learning more could lead to new therapies for treating obesity and preventing complications such as diabetes.”
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Researchers from Tel Aviv University deciphered, for the first time, a mechanism that enables skin cancer to metastasize to the brain and managed to delay the spread of the disease by 60% to 80% using existing treatments. The encouraging study was led by Prof. Ronit Satchi-Fainaro and Ph.D. student Sabina Pozzi of the Sackler Faculty of Medicine at Tel Aviv University. The results were published in the scientific journal JCI Insight.
“In an advanced stage, 90% of melanoma (skin cancer) patients will develop brain metastases,” explains Prof. Satchi-Fainaro. “This is a puzzling statistic. We expect to see metastases in the lungs and liver, but the brain is supposed to be a protected organ. The blood-brain barrier keeps harmful substances from entering the brain, and here it supposedly doesn’t do the job — cancer cells from the skin circulate in the blood and manage to reach the brain. We asked ourselves with ‘whom’ the cancer cells ‘talk’ to in the brain to infiltrate it.”
The researchers from Tel Aviv University found that in melanoma patients with brain metastases, the cancer cells “recruit” cells called astrocytes, star-shaped cells found in the spinal cord and brain which are responsible for homeostasis, or maintaining stable conditions, in the brain.
“The astrocytes are the first to come to correct the situation in the event of a stroke or trauma, for example,” says Prof. Satchi-Fainaro, “and it is with them that the cancer cells interact, exchanging molecules and corrupting them. Moreover, the cancer cells recruit the astrocytes so that they do not inhibit the spread of the metastases. As such, they create local inflammation in the melanoma cells-astrocytes interaction areas that increase the permeability through the blood-brain barrier, as well as the division and migration of the cancer cells. The communication between them is reflected in the fact that the astrocytes begin to secrete a protein that promotes inflammation called MCP-1 (also known as CCL2), and in response to this, the cancer cells begin to express its receptors CCR2 and CCR4, which we suspected to be responsible for the destructive communication with the astrocytes.”
To test their hypothesis, Prof. Satchi-Fainaro and her team tried to inhibit the expression of the protein and its receptors in genetically-engineered lab models and in 3D models of primary melanoma and brain metastases. To this end, the researchers used both an antibody (biological molecule) and a small molecule (synthetic), designed to block the MCP-1 protein. They also employed CRISPR technology to genetically edit the cancer cells and cut out the two genes that express the two relevant receptors, CCR2 and CCR4. With each of the methods, the researchers were able to delay the spread of metastases.
“These treatments succeeded in delaying the penetration of the cancer cells into the brain and their subsequent spread throughout the brain,” says Prof. Satchi-Fainaro. “It’s important to note that melanoma metastases in the brain are very aggressive with a poor prognosis of 15 months following surgery, radiation and chemotherapy. We reached a 60% to 80% delay, depending on the stage of the intervention. We achieved the best results with the treatment conducted immediately after surgery to remove the primary melanoma, and we were able to prevent the metastases from penetrating the brain; therefore, I believe that the treatment is suitable for the clinic as a preventive measure. Both the antibody and the small molecule we used — which are primarily intended to treat sclerosis, diabetes, liver fibrosis, and cardiovascular diseases, as well as serve as a biomarker for other types of cancer — have already been tested on humans as part of clinical trials. Therefore, these treatments are considered safe, and we can try to repurpose them for melanoma.”
The research was conducted in collaboration with additional scientists and physicians from Tel Aviv University, including Prof. Adi Barzel, Dr. Asaf Madi, Prof. Iris Barshack, Prof. Eran Perlson, and Prof. Inna Slutsky. International researchers also participated in the study, including Prof. Eytan Ruppin from the US National Institutes of Health (NIH) , Prof. Henry Brem and Thomas Hyde from Johns Hopkins University-, and Prof. Helena Florindo from the University of Lisbon.
The study was funded by the European Research Council (ERC), the Melanoma Research Alliance (MRA), the Kahn Foundation, the Israel Cancer Research Fund (ICRF), and the Israel Science Foundation (ISF).
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Using equations to calculate kidney function that do not include race adjustments would result in Black patients gaining time on the transplant waitlist before their kidneys fail that matched similar durations for white patients, according to a new study led by UC San Francisco and Hennepin County Medical Center in Minneapolis.
In their study, publishing in the journal CJASN on Sept. 19, 2022, the researchers compared the length of time from waitlist eligibility to kidney failure for Black and white patients.
“The earlier a patient is waitlisted prior to kidney failure, the higher priority the patient has in getting a transplant and the more likely a patient could potentially avoid dialysis,” said first author Elaine Ku, MD, of the UCSF Division of Nephrology and of the Department of Epidemiology and Biostatistics. “Patients who avoid dialysis, or do it for a short period, generally have better outcomes than those on dialysis in the long term,” she said.
Kidney transplant waitlist eligibility is determined by a formula that calculates estimated glomerular filtration rate (eGFR). It measures creatinine, a breakdown product of muscle tissues, and factors in a patient’s age and sex. Previously, the equations for eGFR had a race adjustment that meant Black patients had a higher eGFR despite having the same creatinine level. The rationale for this is based on earlier studies that show Black people may have naturally higher levels of creatinine.
Recognizing Race as Social Construct Prompts Criteria Review
However, in recognition of race as a social construct, rather than a biological one, the American Society of Nephrology and the National Kidney Foundation last year recommended the removal of these race modifiers, which adjust kidney function upward by 16% in Blacks. The current transplant waitlist requirement for patients regardless of race is eGFR 20 ml/min, significantly lower than 90 ml/min or higher, which is considered normal.

Researchers from the Institute of Biotechnology, University of Helsinki, pioneers in identifying the first patient mutations on the NFkB1-gene, cooperated with international clinicians to identify and characterise a plethora of unreported NFKB1 variants on patients with immune system related illnesses.
In many cases, the identification of a genetic defect in a patient is of great importance for the treatment and prognosis of patients with rare diseases. NFKB1, a transcription factor, causes changes in gene expression and is activated by stress and immune related signaling pathways. Mutations in the NFkB1 have previously been linked to common variable immune deficiency (CVID).
Two new studies may bring further relief for patients with hereditary gene defect in immune system
“These studies have significantly expanded the associations of NFKB1 variants to immune system dysfunction — the connections which we first reportedin 2017, ” says research director Markku Varjosalo from the Institute of Biotechnology, University of Helsinki
Researchers identified two new NFKB1 variants in two families suffering from common variable immune deficiency. Both identified NFKB1 variants caused reduced expression of the NFKB1 protein and lead to an altered gene expression and increased inflammation response in patient cells. Interaction analysis again showed loss of interactions for one of the variants but not the other.
Another group of researchers studied a cohort of 47 NFKB1 mutations previously reported in patients, out of which 25 did not appear to behave differently from wild type NFKB1. The other 22 mutations were found to have adverse effects on NFKB1 which ranged from increased NFKB1 protein degradation, reduced DNA binding of NFKB1 to overall reduced NFKB1 function through altered protein structure: This may hint towards their likely pathogenicity. Analysis of NFKB1 variant protein interactions showed varied effects from loss of interaction with NFKB family proteins to some variants interactions appearing similar to wild type NFKB1.
“These projects are excellent examples of fruitful international multidisciplinary research collaborations between the University of Helsinki and the leading clinical research hospitals and centers in Europe. Our findings significantly deepen the understanding of the molecular mechanisms underlying NFKB1, and other autoinflammatory and autoimmune diseases associated with altered NFkB1 expression or function,” says Varjosalo.
“Also, our results yet again suggest that targeted inhibition of certain key NFkB signaling pathway components is an attractive therapeutic approach for treating these diseases which could be collectively paraphrased as diseases of NF-kB signaling.”
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Lower immunity and recurring infections are common in type 1 and type 2 diabetes. Researchers at Karolinska Institutet in Sweden now show that the immune system of people with diabetes has lower levels of the antimicrobial peptide psoriasin, which compromises the urinary bladder’s cell barrier, increasing the risk of urinary tract infection. The study is published in Nature Communications.
Diabetes results from lack of insulin and/or decreased insulin action. Insulin is a hormone that regulates glucose (sugar) and thus energy to the cells. In type 1 diabetes, the body stops producing insulin, while in type 2 diabetes, the cells have become less sensitive to insulin, which contributes to high blood glucose levels. Diabetes is a common disease that affects the health in many ways.
One effect is that it compromises the innate immune system, leaving many people with increased susceptibility to regular infections, such as urinary tract infections (UTI)s caused by E. coli bacteria. In people with diabetes, these are more likely to lead to general blood poisoning, sepsis, originating in the urinary tract.
An endogenous antibiotic
Researchers at Karolinska Institutet have now investigated whether glucose levels in people with diabetes (type 1, type 2, or prediabetes) are linked with psoriasin, an endogenous antibiotic which is a part of the innate immune system.
Using urine, urinary bladder cells and blood serum samples from patients, the researchers analysed levels of psoriasin and other peptides necessary for ensuring that the bladder mucosa remains intact and protects against infection. The findings were then verified in mice and urinary bladder cells with and without infection.
“We found that high glucose concentrations reduce the levels of the antimicrobial peptide psoriasin, while insulin has no effect,” says Annelie Brauner, professor at the Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet who led the study. “People with diabetes have lower levels of psoriasin, which weakens the cells’ protective barrier function and increases the risk of bladder infection.”
Oestrogen therapy reduced bacterial population
Professor Brauner’s research group has previously shown that treatment with oestrogen restores the protective function of bladder cells in humans and mice and thereby help to regulate the immune response to a UTI. The researchers therefore tested how oestrogen treatment affects infected cells exposed to high glucose concentrations. They found that the treatment boosted levels of psoriasin and reduced bacterial populations, indicating that the treatment may have an effect also among patients with diabetes.
“We now plan to probe deeper into the underlying mechanisms of infections in individuals with diabetes,” says the study’s lead author Soumitra Mohanty, researcher at the same department at Karolinska Institutet. “The ultimate goal is to reduce the risk of infection in this growing patient group.”
The study was conducted in collaboration with the Karolinska University Hospital, Region Stockholm, Capio and Uppsala University in Sweden and Universitätsklinikum Schleswig-Holstein in Germany. It was largely financed by the Olle Engkvist Foundation, Region Stockholm (ALF funding), the KI Research Foundation, the Swedish Society of Medicine, the Swedish Society for Medical Research (SSMF), the Clas Groschinsky Memorial Foundation, the Åke Wiberg Foundation and the Magnus Bergvall Foundation. There are no reported conflicts of interest.
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The top cardiovascular (CVD) diagnoses from U.S. emergency departments suggest that many cardiovascular emergencies are due to poorly controlled high blood pressure, according to a study of more than 20 million emergency department visits published Sept. 8 in the Journal of the American Heart Association, an open access, peer-reviewed journal of the American Heart Association.
The researchers found that 13% of all heart-related emergency department diagnoses, representing more than 2.7 million people, were for “essential” hypertension, which is high blood pressure not caused by other diseases. Most cases of high blood pressure are essential hypertension.
“These visits resulted in hospital admission less than 3% of the time and with very few deaths — less than 0.1%. This suggests that these visits were mostly related to the management of hypertension,” said lead author Mamas A. Mamas, M.D., a professor of cardiology at Keele University in Stoke-on-Trent, and a consultant cardiologist at University Hospitals of North Midlands NHS Trust, both in the UK.
For the 15 CVD conditions detailed in the study, about 30% were hypertension-related diagnoses.
The study analyzed cardiovascular diagnoses made during emergency department visits that were part of the Nationwide Emergency Department Sample from 2016-2018. The sample was 48.7% women, and the average age was 67 years. The majority were Medicare or Medicaid participants. Men in the sample were more likely to have other diseases in addition to cardiovascular disease, such as diabetes, while women had higher rates of obesity, high blood pressure and medical conditions that affect blood vessels in the brain.
The most common heart- or stroke-related diagnoses for women seen in the emergency department were high blood pressure (16% of visits), high blood pressure-related heart or kidney disease (14.1%) and atrial fibrillation (10.2%). The most common diagnoses for men were high blood pressure-related heart or kidney disease (14.7%), high blood pressure (10.8%) and heart attack (10.7%).
“Previous studies have shown sex differences in patterns of CVD among hospitalized patients,” Mamas said. “However, examining CVD encounters in the emergency department provides a more complete picture of the cardiovascular health care needs of men and women, as it captures encounters prior to hospitalization.” He also points out that previous studies of CVD emergency visits are limited to suspected heart attack visits. “Therefore, this analysis of 15 CVD conditions helps to better understand the full spectrum of acute CVD needs, including sex disparities in hospitalization and risk of death.”
The study found that outcomes from the emergency CVD visits were slightly different for men and women. Overall, women were less likely to die (3.3% of women vs 4.3% of men) or be hospitalized (49.1% of women vs 52.3% of men) after an emergency department visit for CVD. The difference may be due to women’s generally lower risk diagnoses, said Mamas, but there could be an underestimation of deaths in women.
“We did not track deaths outside of the hospital setting,” said Mamas. “Given past evidence that women are more likely to be inappropriately discharged from the emergency department, and strong evidence for the systemic undertreatment of women, further study is warranted to track outcomes beyond the emergency department visit.”
An additional limitation of the data includes potential misdiagnosis errors in cases where the final diagnosis did not match the emergency diagnosis, particularly after a hospitalization and additional bloodwork and other health information could be obtained. Furthermore, the data is limited in that it does not capture information related to severity of disease, which may make comparisons around mortality differences between different patient groups challenging.
“Our work with this large, nationally representative sample of cardiovascular emergency visits highlights differences in health care needs of men and women, which may be useful to inform planning and provision of health care services,” said Mamas. “We also encourage further research into understanding the underlying factors driving the differences in CVD patterns and outcomes between men and women.”
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ANCHORAGE — After a middle-aged woman tested positive for Covid-19 in January at her workplace in Fairbanks, public health workers sought answers to questions vital to understanding how the virus was spreading in Alaska’s rugged interior.The woman, they learned, had underlying conditions and had not been vaccinated. She had been hospitalized but had recovered. Alaska and many other states have routinely collected that kind of information about people who test positive for the virus. Part of the goal is to paint a detailed picture of how one of the worst scourges in American history evolves and continues to kill hundreds of people daily, despite determined efforts to stop it.But most of the information about the Fairbanks woman — and tens of millions more infected Americans — remains effectively lost to state and federal epidemiologists. Decades of underinvestment in public health information systems has crippled efforts to understand the pandemic, stranding crucial data in incompatible data systems so outmoded that information often must be repeatedly typed in by hand. The data failure, a salient lesson of a pandemic that has killed more than one million Americans, will be expensive and time-consuming to fix.The precise cost in needless illness and death cannot be quantified. The nation’s comparatively low vaccination rate is clearly a major factor in why the United States has recorded the highest Covid death rate among large, wealthy nations. But federal experts are certain that the lack of comprehensive, timely data has also exacted a heavy toll.“It has been very harmful to our response,” said Dr. Ashish K. Jha, who leads the White House effort to control the pandemic. “It’s made it much harder to respond quickly.”Details of the Fairbanks woman’s case were scattered among multiple state databases, none of which connect easily to the others, much less to the Centers for Disease Control and Prevention, the federal agency in charge of tracking the virus. Nine months after she fell ill, her information was largely useless to epidemiologists because it was impossible to synthesize most of it with data on the roughly 300,000 other Alaskans and the 95 million-plus other Americans who have gotten Covid.Those same antiquated data systems are now hampering the response to the monkeypox outbreak. Once again, state and federal officials are losing time trying to retrieve information from a digital pipeline riddled with huge holes and obstacles.“We can’t be in a position where we have to do this for every disease and every outbreak,” Dr. Rochelle P. Walensky, the C.D.C. director, said in an interview. “If we have to reinvent the wheel every time we have an outbreak, we will always be months behind.”A Covid Data Pipeline Riddled With Holes and ObstaclesState and local health departments have struggled to combine data from disparate sources and pass it along to the C.D.C. This flow chart shows how Covid case reports are typically handled in Alaska.

A medication for heart problems and high blood pressure may also be effective for treating alcohol use disorder, according to a new study by researchers at the National Institutes of Health and their colleagues. The study presents converging evidence from experiments in mice and rats, as well as a cohort study in humans, suggesting that the medication, spironolactone, may play a role in reducing alcohol drinking. The research was led by scientists at the National Institute on Drug Abuse (NIDA) and the National Institute on Alcohol Abuse and Alcoholism (NIAAA), both parts NIH, and Yale School of Medicine, New Haven, Connecticut. A report of the new findings is published in Molecular Psychiatry.
“Combining findings across three species and different types of research studies, and then seeing similarities in those data, gives us confidence that we are onto something potentially important scientifically and clinically. These findings support further study of spironolactone as a potential treatment for alcohol use disorder, a medical condition that affects millions of people in the U.S” said Lorenzo Leggio, M.D., Ph.D., chief of the Clinical Psychoneuroendocrinology and Neuropsychopharmacology Section, a joint laboratory of NIDA and NIAAA, and one of the senior authors.
Currently there are three medications approved for alcohol use disorder in the United States, and they are an effective and important aid in the treatment of people with this condition. Given the diverse biological processes that contribute to alcohol use disorder, new medications are needed to provide a broader spectrum of treatment options. Scientists are working to develop a larger menu of pharmaceutical treatments that could be tailored to individual needs.
Previous research has shown that mineralocorticoid receptors, which are located throughout the brain and other organs and help regulate fluid and electrolyte balance in the body, might play a role in alcohol use and craving. Preclinical research suggests that higher mineralocorticoid receptor signaling contributes to increased alcohol consumption. The current study sought to expand this line of research by testing spironolactone, a medication with multiple actions, including blocking mineralocorticoid receptors. Spironolactone is used in clinical practice as a diuretic and to treat conditions like heart problems and high blood pressure.
In experiments conducted in mouse and rat models of excessive alcohol drinking, NIAAA and NIDA researchers led by co-senior author Leandro Vendruscolo, Pharm.D., Ph.D., from NIDA found that increasing doses of spironolactone decreased alcohol consumption in male and female animals, without causing movement or coordination problems, and without affecting their food or water intake.
In a parallel study that was part of this team’s collaborative efforts, researchers led by co-senior author Amy C. Justice, M.D., Ph.D., of the Yale School of Medicine, examined health records of a large sample of people from the U.S. Veterans Affairs healthcare system to assess potential changes in alcohol drinking after spironolactone was prescribed for its current clinical indications (e.g., heart problems, high blood pressure). They found a significant association between spironolactone treatment and reduction in self-reported alcohol consumption, as measured by the Alcohol Use Disorders Identification Test-Consumption, a screening tool. Of note, the largest effects were observed among those who reported hazardous/heavy episodic alcohol consumption before starting spironolactone treatment.
“These are very encouraging findings,” said NIAAA Director George F. Koob, Ph.D., a co-author of the study. “Taken together, the present study argues for conducting randomized, controlled studies of spironolactone in people with alcohol use disorder to further assess its safety and potential efficacy in this population, as well as additional work to understand how spironolactone may reduce alcohol drinking.”
“Just like for any other medical condition, people with substance use disorders deserve to have a range of treatment options available to them, and this study is an exciting step in our effort to expand medications for people with alcohol use disorder,” said Nora Volkow, M.D., director of NIDA. “In addition, we must address the stigma and other barriers that prevent many people with alcohol use disorder from accessing the treatments we already have available.”