Progress towards new treatments for tuberculosis

Boosting the body's own disease-fighting immune pathway could provide answers in the desperate search for new treatments for tuberculosis.

Tuberculosis still represents an enormous global disease burden and is one of the top 10 causes of death worldwide.

Led by WEHI's Dr. Michael Stutz and Professor Marc Pellegrini and published in Immunity, the study uncovered how cells infected with tuberculosis bacteria can die, and that using new medicines to enhance particular forms of cell death decreased the severity of the disease in a preclinical model.

Fighting antibiotic resistance

Tuberculosis is caused by bacteria that infect the lungs, spreading from person to person through the air. A challenge in the fight against tuberculosis is that the bacteria that cause the disease have developed resistance to most antibiotic treatments, leading to a need for new treatment approaches.

Tuberculosis bacteria grow within immune cells in the lungs. One of the ways that cells protect against these 'intracellular' pathogens is to undergo a form of cell death called apoptosis—destroying the cell as well as the microbes within it.

Using preclinical models, researchers sequentially deleted key apoptosis effectors, to demonstrate their roles in controlling tuberculosis infections. This demonstrated that a proportion of tuberculosis-infected cells could die by apoptosis—opening up new opportunities for controlling the disease.

Using host-directed therapies to reduce disease burden

Dr. Stutz said researchers then tested new drugs that force cells to die. This revealed that a drug-like compound that inhibits cell death-regulatory proteins called IAPs could promote death of the infected cells.

"When we treated our infection models with this compound, we were able to significantly reduce the amount of tuberculosis disease," he said.

"The longer the treatment was used, the greater the reduction of disease."

The research team was able to replicate these results using various different IAP inhibitors.

"Excitingly, many of these compounds are already in clinical trials for other types of diseases and have proven to be safe and well-tolerated by patients," Dr. Stutz said.

"We predict that if these compounds were progressed for treating tuberculosis, they would be most effective if used alongside existing antibiotic treatments."

Opening the door to new treatment methods

Professor Marc Pellegrini said until now, antibiotics were the only treatment for tuberculosis, which were limited in their application due to increasing antibiotic resistance.

"Unlike antibiotics, which directly kill bacteria, IAP inhibitors kill the cells that the tuberculosis bacteria need to survive," he said.

"The beauty of using a host-directed therapy is that it doesn't directly target the microbe, it targets a host process. By targeting the host rather than the microbe, the chances of resistance developing are incredibly low."

The team hope the research will lead to better treatments for tuberculosis.

"This research increases our understanding of the types of immune responses that are beneficial to us, and this is an important step towards new treatments for tuberculosis, very few of which have been developed in the last 40 years," Dr. Stutz said.

"We have demonstrated that host-directed therapies are viable for infections such as tuberculosis, which is particularly important in the era of extensive antibiotic resistance."

https://www.sciencedirect.com/science/article/abs/pii/S1074761321002533?via%3Dihub

Oral Transglutaminase 2 Inhibitor Beneficial in Celiac Disease

For patients with celiac disease, treatment with a selective oral transglutaminase 2 inhibitor (ZED1227) attenuates gluten-induced duodenal mucosal damage, according to a study published in the July 1 issue of the New England Journal of Medicine.

Detlef Schuppan, M.D., Ph.D., from the Johannes Gutenberg University in Mainz, Germany, and colleagues conducted a proof-of-concept trial of a six-week treatment with ZED1227 at three dose levels versus placebo among adults with well-controlled celiac disease who underwent a daily gluten challenge. The primary end point of attenuation of gluten-induced mucosal damage was assessed among 35, 39, 38, and 30 patients assigned to 10-mg, 50-mg, and 100-mg ZED1227 and placebo, respectively.

The researchers found that at all three dose levels, ZED1227 treatment attenuated gluten-induced duodenal mucosal injury. From baseline to week six, the mean ratio of villus height to crypt depth estimated difference from placebo was 0.44, 0.49, and 0.48 in the 10-, 50-, and 100-mg groups, respectively. For the change in intraepithelial lymphocyte density, the estimated differences from placebo were −2.7, −4.2, and −9.6 cells per 100 epithelial cells, respectively, for 10-, 50-, and 100-mg ZED1227. Symptom and quality-of-life scores may have been improved with use of the 100-mg dose.

"Although this trial is very encouraging, whether treatment with ZED1227, and more generally transglutaminase 2 inhibition, in patients with celiac disease will be efficient in real life and during long-term gluten exposure remains to be determined," writes the author of an accompanying editorial.

https://www.medchemexpress.com/zed-1227.html

Oral Transglutaminase 2 Inhibitor Beneficial in Celiac Disease  

Bayer Wins Approval for CKD Drug ......

The U.S. Food and Drug Administration (FDA) greenlit Bayer’s Kerendia (finerenone) to reduce the progression of chronic kidney disease associated with type 2 diabetes. The first nonsteroidal mineralocorticoid receptor antagonist (MRA) is approved for adults with chronic kidney disease associated with type 2 diabetes. 

Kerendia was explicitly approved to reduce the risk of kidney failure, heart attack, heart failure hospitalization, and cardiovascular death in adult patients with chronic kidney disease associated with type 2 diabetes. Although there are guideline directed therapies for CKD, many patients with chronic kidney disease associated with type 2 diabetes are at risk for disease progression and cardiovascular events. 

Amit Sharma, Vice President of Cardiovascular and Renal at Bayer, expressed excitement at bringing this new treatment for patients with CKD associated with type 2 diabetes. 

Kerendia acts by blocking the overactivation of the mineralocorticoid receptor, which contributes to fibrosis and inflammation. Those can then contribute to permanent structural kidney damage. 

“Chronic kidney disease associated with type 2 diabetes can have such a debilitating impact on patients’ lives. Unfortunately, this disease is far reaching, as up to 40 percent of all patients with type 2 diabetes develop chronic kidney disease,” Kevin Longino, chief executive officer of the National Kidney Foundation and a kidney transplant patient, said in a statement. “It is important for physicians and patients to have new treatment options that can slow chronic kidney disease progression.”

The FDA approved Kerendia based on data from the Phase III FIDELIO-DKD study. The trial demonstrated positive kidney and cardiovascular outcomes in patients with CKD associated with type 2 diabetes. 

Trial findings were published in the New England Journal of Medicine in 2020. Type 2 diabetes is the leading cause of end-stage kidney disease, when patients may need dialysis or a kidney transplant to stay alive. It is estimated that about 40% of all type 2 diabetes patients will develop chronic kidney disease. 

George Bakris, the lead study investigator for the FIDELIO-DKD study, said the patient populations included in the Phase IIII study were at risk of disease progression despite being on the current standard of care treatment to control blood pressure and blood glucose. The approval of Kerendia provides physicians with a treatment option that can give kidney protection, he said. 

Bayer expects Kerendia to be available for patients by the end of the month. The company is seeking approval in Europe. Kerendia was approved under both Fast Track and Priority Review designations. 

https://en.wikipedia.org/wiki/Finerenone

Drug could be promising new option against eczema

In continuation of my update on Upadacitinib

 

 

A pill called upadacitinib, already approved for treating rheumatoid arthritis, might also ease another common immunological condition—eczema.

In two phase 3 clinical trials, patients with moderate to severe eczema showed rapid and significant improvements after taking the drug, said researchers at Mount Sinai in New York City.

The clinical trials were funded by the dug's maker, AbbVie Inc., and included nearly 1,700 patients with the inflammatory skin condition.

"The results of these trials ... were so incredible that by week 16, most patients with moderate to severe atopic dermatitis [eczema] either had a 90% disease clearance, or even 100% disease clearance," study first author Dr. Emma Guttman-Yassky said in a Mount Sinai news release. She's professor and chair of the department of dermatology at Mount Sinai's Icahn School of Medicine, in New York City.

"We achieved extremely high clearance rates that are bringing us closer to the amazing clearance rates that we see in psoriasis," Guttman-Yassky noted.

According to the National Eczema Association, "people with eczema tend to have an over-reactive immune system that when triggered by a substance outside or inside the body, responds by producing inflammation. It is this inflammation that causes the red, itchy and painful skin symptoms common to most types of eczema."

Eczema affects more that 31 million American adults and between 10 to 20% of children, the study authors noted.

The two new clinical trials involved a total of almost 1,700 patients and took place between 2018 and 2020.

Besides the rapid disease clearance noted in patients, "the itch improvements already started to be significant within days from the beginning of the trials, and the maximum clinical efficacy was obtained early, at week 4, and maintained to week 16," Guttman-Yassky said.

The drug was well tolerated by patients who received the two highest doses of the drug—15 milligrams and 30 milligrams—and no significant safety risks were seen, she added.

Upadacitinib is already approved and marketed for use against rheumatoid arthritis under the brand name Rinvoq. It works by blocking what are known as multiple cytokine-signaling pathways—parts of the immune system that can malfunction and cause eczema.

According to Guttman-Yassky, other eczema therapies exist, but most come with certain drawbacks.

While injectable biologic drugs are highly successful in treating eczema patients who don't respond to or can't use topical creams, their use cannot be stopped and restarted at will, because the potential creation of anti-drug antibodies will shorten the half-life of the drugs, she explained.

However, "patients were able to start and restart [upadacitinib] at any time, allowing for flexibility, which cannot be achieved with biologics," Guttman-Yassky, said. "And, biologics, which are injectable agents that target specific lymphocytes that are 'misbehaving' or are up-regulated in atopic dermatitis, do not suppress the entire immune system as other immunosuppressants tend to do."

Dr. Michele Green is a dermatologist at Lenox Hill Hospital in New York City who wasn't involved in the new study.

She called the findings "important."

Upadacitinib is the first drug in its class "to be effectively used for patients with significant improvement of pruritus [itch] within several days of treatment and clearance of their disease within several weeks," Green noted.

"It is also significant since adolescents were included in this study and I believe an oral treatment is much more appealing to treating adolescents than current injectable biologics," she added.

 

 https://pubchem.ncbi.nlm.nih.gov/compound/Upadacitinib#section=2D-Structure

 

Drug commonly used as antidepressant helps fight cancer in mice

A class of drug called monoamine oxidase inhibitors is commonly prescribed to treat depression; the medications work by boosting levels of serotonin, the brain's "happiness hormone."

A new study by UCLA researchers suggests that those drugs, commonly known as MAOIs, might have another health benefit: helping the immune system attack cancer. Their findings are reported in two papers, which are published in the journals Science Immunology and Nature Communications.

"MAOIs had not been linked to the immune system's response to cancer before," said Lili Yang, senior author of the study and a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA. "What's especially exciting is that this is a very well-studied and safe class of drug, so repurposing it for cancer isn't as challenging as developing a completely new drug would be."

Recent advances in understanding how the human immune system naturally seeks out and destroys cancer cells, as well as how tumors try to evade that response, has led to new cancer immunotherapies—drugs that boost the immune system's activity to try to fight cancer.

In an effort to develop new cancer immunotherapies, Yang and her colleagues compared immune cells from melanoma tumors in mice to immune cells from cancer-free animals. Immune cells that had infiltrated tumors had much higher activity of a gene called monoamine oxidase A, or MAOA. MAOA's corresponding protein, called MAO-A, controls levels of serotonin and is targeted by MAOI drugs.

"For a long time, people have theorized about the cross-talk between the nervous system and the immune system and the similarities between the two," said Yang, who is also a UCLA associate professor of microbiology, immunology and molecular genetics and a member of the UCLA Jonsson Comprehensive Cancer Center. "So it was exciting to find that MAOA was so active in these tumor-infiltrating immune cells."

Next, the researchers studied mice that didn't produce MAO-A protein in immune cells. The scientists found that those mice were better at controlling the growth of melanoma and colon tumors. They also found that normal mice became more capable of fighting those cancers when treated with MAOIs.

Digging in to the effects of MAO-A on the immune system, the researchers discovered that T cells—the immune cells that target cancer cells for destruction—produce MAO-A when they recognize tumors, which diminishes their ability to fight cancer.

That discovery places MAO-A among a growing list of molecules known as immune checkpoints, which are molecules produced as part of a normal immune response to prevent T cells from overreacting or attacking healthy tissue in the body. Cancer has been known to exploit the activity of other previously identified immune checkpoints to evade attack by the immune system.

In the Science Immunology paper, the scientists report that MAOIs help block the function of MAO-A, which helps T cells overcome the immune checkpoint and more effectively fight the cancer.

But the drugs also have a second role in the immune system, Yang found. Rogue immune cells known as tumor-associated macrophages often help tumors evade the immune system by preventing anti-tumor cells including T cells from mounting an effective attack. High levels of those immunosuppressive tumor-associated macrophages in a tumor have been associated with poorer prognoses for people with some types of cancer.

But the researchers discovered that MAOIs block immunosuppressive tumor-associated macrophages, effectively breaking down one line of defense that tumors have against the human immune system. That finding is reported in the Nature Communications paper.

"It turns out that MAOIs seem to both directly help T cells do their job, and stop tumor-associated macrophages from putting the brakes on T cells," Yang said.

Combining MAOIs with existing immunotherapies

Yang said she suspects that MAOIs may work well in concert with a type of cancer immunotherapies called immune checkpoint blockade therapies, most of which work by targeting immune checkpoint molecules on the surface of immune cells. That's because MAOIs work on MAO-A proteins, which are inside cells and function differently from other known immune checkpoint molecules.

Studies in mice showed that any of three existing MAOIs—phenelzine, clorgyline or mocolobemide—either on their own or in combination with a form of immune checkpoint blockade therapy known as PD-1 blockers, could stop or slow the growth of colon cancer and melanoma.

Although they haven't tested the drugs in humans, the researchers analyzed clinical data from people with melanoma, colon, lung, cervical and pancreatic cancer; they found that people with higher levels of MAOA gene expression in their tumors had, on average, shorter survival times. That suggests that targeting MAOA with MAOIs could potentially help treat a broad range of cancers.

Yang and her collaborators are already planning additional studies to test the effectiveness of MAOIs in boosting human immune cells' response to various cancers.

Yang said MAOIs could potentially act on both the brain and immune cells in patients with cancer, who are up to four times as likely as the general population to experience depression.

"We suspect that repurposing MAOIs for cancer immunotherapy may provide patients with dual antidepressant and antitumor benefits," she said.

The experimental combination therapy in the study was used in preclinical tests only and has not been studied in humans or approved by the Food and Drug Administration as safe and effective for use in humans. The newly identified therapeutic strategy is covered by a patent application filed by the UCLA Technology Development Group on behalf of the Regents of the University of California, with Yang, Xi Wang and Yu-Chen Wang as co-inventors.

Drug commonly used as antidepressant helps fight cancer in mice

Cancer drug shows potential against pseudo SARS-CoV-2 in lab tests

In continuation of my update on Lenalidomide

Despite the effectiveness of COVID-19 vaccines, treatments are still needed to combat this disease, which has killed millions of people and still kills thousands each day across the world. Scientists at the UNC School of Medicine conducted lab experiments showing how the cancer drug lenalidomide disrupts a cellular pathway in human cells so that pseudo-viruses derived from SARS-CoV-2—the virus that causes COVID-19—cannot enter cells to cause infection.

The research, published in a letter to the journal Signal Transduction and Targeted Therapy, shows the potential of an existing FDA-approved drug to help doctors treat the sickest COVID-19 patients.

The labs of Pengda Liu, Ph.D., and Guochun Jiang, Ph.D., both assistant professors in the UNC Department of Biochemistry and Biophysics, conducted this work. Liu is a member of the UNC Lineberger Comprehensive Cancer Center, and Jiang is a member of the UNC HIV Cure Center.

SARS-CoV-2, a novel coronavirus and the causative agent of COVID-19, has caused a global social and economic disruption, and there are still thousands of cases and death each day in the United States and around the world. Treatments to prevent severe illness and death are still needed.

In this research letter, the UNC team reported that a protein called E3 ligase SPOP recognizes and protects the human cell surface receptor ACE2, which is the protein SARS-CoV-2 latches onto in order to gain entry into cells to cause infection. Another protein called CK1 kinase triggers this recognition and protection of ACE2.

The researchers used the cancer drug lenalidomide to inhibit CK1 kinase activity in cell cultures and showed a substantial reduction in ACE2 protein levels in kidney cancer cells. Researchers used SARS-CoV-2 S protein conditioned pseudoviruses in vitro and found lenalidomide treatment reduced the effect of this infection on kidney-derived cells.

"We hope that our identification and tests for the efficacy of inactivating the SPOP/CKI signaling in reducing ACE2 protein expression to attenuate SARS-CoV-2 infection provides a timely investigation into new therapeutic directions to combat COVID-19," Liu said.

A next step could be to use animal models to see if the drug blocks real SARS-CoV-2.

https://en.wikipedia.org/wiki/Lenalidomide

Cancer drug shows potential against pseudo SARS-CoV-2 in lab tests

Melatonin shown to protect kidney damage caused by obesity with diabetes

In continuation of my update on Melatonin

Scientists from the University of Granada (UGR), the Hospital Universitario La Paz (Madrid), and the University of Texas (U.S.) have taken an important step in the fight against kidney damage and its progression toward kidney failure, which is closely related to diabesity (obesity with type 2 diabetes) and its complications.

Specifically, in two new studies recently published in the Journal of Clinical Medicine and Pharmaceuticals, researchers have developed an obese and diabetic rodent model and have shown that melatonin protects from kidney damage caused by diabesity.

The scientists have shown that chronic administration of melatonin at doses (10 mg/kg body weight/day) prevents mitochondrial and endoplasmic reticulum disruption, which play a critical role in the development and pathogenesis of kidney cell (nephron) damage, and its progression to renal failure.

Thus, it has been shown that melatonin prevents the impairment of the function and dynamics of cellular mitochondria, decreasing the increased production of oxygen free radicals (responsible for oxidative stress). It also prevents pathological alteration in the function of the endoplasmic reticulum (another cell cytoplasmic organelle), which, in conditions of abnormally high oxidative stress, is related to an increase in programmed cell death (of the nephron) leading to the loss of renal functionality, as a preliminary step to the development of renal failure and the need for hemodialysis or transplantation.

The studies coordinated by the UGR show the efficacy of melatonin in halting the progression of renal damage mediated by mitochondrial damage and excess endoplasmic reticulum stress.

As the lead author of this study, Ahmad Agil, a researcher at the Department of Pharmacology of the UGR, says, "Kidney damage is caused by metabolic complications of obesity, such as diabetes, hypertension, blood lipid disorders or fatty liver disease. Given that the prevalence of these pathologies (collectively recognized as metabolic syndrome) continues to increase, kidney damage and its progression over time to kidney failure has become a health problem that affects millions of people worldwide, with a great socioeconomic cost, requiring hemodialysis facilities and/or kidney transplant services, with the corresponding compatibility studies required."

The importance of the work lies not only in the efficacy of melatonin in counteracting the two proposed mechanisms of renal damage (based on the alteration of mitochondrial function and dynamics and the function of the endoplasmic reticulum (ER)), but they also propose an alternative preventive treatment that would improve this renal function with a well-studied drug with a very high safety profile such as melatonin, which is a drug that in the EU must be prescribed by a doctor and is already administered in the treatment of insomnia.

The new findings have also been associated with an improvement in glomerular filtration rate and renal damage of the nephron, manifested in a decrease in creatinine clearance levels (the best marker of renal function), proteinuria, and in the improvement of renal structure, observed after histopathological study of the kidney.

These results are in line with those previously published by these researchers in the last 10 years, demonstrating that the pharmacological administration of melatonin constitutes another new strategy in the therapeutic approach to diabesity (central obesity and its type 2 diabetes) and its complications (such as hepatic steatosis, hypertension, lipid alteration, etc.).

"Our main challenge is the application of melatonin and other strategies such as intermittent fasting in the field of medicine, especially to address the possibility of a treatment perspective for the aforementioned pathologies (diabesity and its complications) that involve an increase in oxidative stress, and mitochondrial damage and associated meta-inflammation (inflammation of metabolic origin)," Agil says.

According to the results, melatonin could help treat kidney damage, which establishes the need to develop new clinical trials to test its effectiveness in humans. The next step is to investigate how it helps in the maintenance of mitochondrial and endoplasmic reticulum homeostasis, and to a greater extent, if melatonin therapy would allow delaying or stopping progressive renal damage by promoting its chronic pharmacological use in kidney repair and regeneration.

https://en.wikipedia.org/wiki/Melatonin

Melatonin shown to protect kidney damage caused by obesity with diabetes

FDA Approves Roszet (rosuvastatin and ezetimibe) to Reduce LDL-C in Hyperlipidemia and Homozygous Familial Hypercholesterolemia

Althera Pharmaceuticals, a company focused on heart health, announced the FDA approval of Roszet (rosuvastatin and ezetimibe) tablets, as an adjunct to diet, for treatment of elevated low-density lipoprotein cholesterol (LDL-C) in adult patients with primary non-familial hyperlipidemia and in adult patients with homozygous familial hypercholesterolemia. Roszet contains rosuvastatin, a powerful statin for LDL-C reduction, and ezetimibe, an efficacious cholesterol absorption inhibitor. The two components work through distinct but complimentary mechanisms to give Roszet the power to significantly lower LDL-C.

  

“The optimal LDL-C levels in guidelines across the world have been shifting lower and now many patients need to get their LDL-C below 70 mg/dL,” said Dr. Christie Ballantyne, Chief of Cardiology and Cardiovascular Research at Baylor College of Medicine. “These levels can be quite difficult to achieve with just a statin on top of diet and exercise. Rosuvastatin and ezetimibe have been extensively studied in combination therapy and have been shown to significantly reduce LDL cholesterol beyond the statin alone. Combination therapy has been widely used in hypertension to achieve lower blood pressure targets. This new therapy provides a high efficacy statin plus ezetimibe in a single once daily pill which is a powerful new option to help get patients to the desirable LDL goal without increasing pill burden or requiring addition of injectable therapies”

"With Roszet’s approval in the U.S., we reaffirm our commitment to improving cholesterol treatment options for physicians and patients," said Sanjeev Agarwal, CEO of Althera Pharmaceuticals. "We are on a mission to positively impact patients’ health. By making this highly effective medicine available and affordable, we hope to improve the long-term health of patients, including those with prior cardiovascular disease.”

While a patient's out-of-pocket costs will vary depending on insurance status, the Roszet Savings Program aims to reduce co-pays to as little as $20 per month for eligible patients with commercial insurance coverage. Althera is continuing to work with all stakeholders to ensure that Roszet is affordable and accessible to all. Please visit http://www.roszet.com for more information and updates about the Roszet Savings Program and eligibility.

Availability

Roszet will be available in pharmacies in June 2021.

Roszet Indications, Dosage and Other Select Information

Roszet is indicated, as an adjunct to diet, in adults with primary non-familial hyperlipidemia to reduce low-density lipoprotein cholesterol (LDL-C), and alone or as an adjunct to other LDL-C lowering therapies in adults with homozygous familial hypercholesterolemia (HoFH) to reduce LDL-C.

Roszet is available as a once-daily tablet with rosuvastatin/ezetimibe dosages of 5 mg/10 mg, 10 mg/10 mg, 20 mg/10 mg and 40 mg/10 mg.

https://en.wikipedia.org/wiki/Ezetimibe

https://en.wikipedia.org/wiki/Rosuvastatin

FDA Approves Qelbree (viloxazine) for the Treatment of ADHD

Supernus Pharmaceuticals, Inc., a biopharmaceutical company focused on developing and commercializing products for the treatment of central nervous system (CNS) diseases,  announced that the U.S. Food and Drug Administration (FDA) has approved Qelbree (viloxazine extended-release capsules) for the treatment of attention-deficit hyperactivity disorder (ADHD) in pediatric patients 6 to 17 years of age.

“Based on the efficacy demonstrated in the clinical program, we believe Qelbree offers a unique new alternative for the treatment of ADHD,” said Jack A. Khattar, President and Chief Executive Officer of Supernus Pharmaceuticals. “Qelbree provides prescribing physicians and patients living with ADHD a therapy that is not a controlled substance with proven efficacy and a tolerable safety profile. We are grateful to the patients, families and their care givers who participated in and supported our research.”

“ADHD is one of the most common mental health issues in the U.S.,” said Andrew J. Cutler, M.D., Clinical Associate Professor of Psychiatry at SUNY Upstate Medical University, and Chief Medical Officer, Neuroscience Education Institute. “The right treatment is key for children and adolescents, as they grow and navigate school and social relationships. This approval offers a novel once a day sprinkleable non-stimulant that can be a great option for children and adolescents with ADHD.”

The approval of Qelbree is supported by data from an extensive development program consisting of four Phase III clinical trials that studied more than 1000 pediatric patients from the age of 6 to 17 years. In December 2020, the Company announced positive results from a Phase III trial in adult patients with ADHD and plans to submit a supplemental New Drug Application to the FDA for Qelbree in adults in the second half of 2021.

https://en.wikipedia.org/wiki/Viloxazine

Eating Mushrooms Lowers Cancer Risk

In continuation of my update on the benefits of mushrooms

 

Edible mushrooms are good for health. Now, a new study revealed that consuming mushrooms on a daily basis can lower your risk of developing cancer.

Next time you make a salad, you might want to consider adding mushrooms to it. The new Penn State study was published in Advances in Nutrition.

The systematic review and meta-analysis examined 17 cancer studies published from 1966 to 2020. Analyzing data from more than 19,500 cancer patients, researchers explored the relationship between mushroom consumption and cancer risk.

Benefits of Mushrooms

Mushrooms are rich in vitamins, nutrients and antioxidants.

The team's findings show that these super foods may also help guard against cancer.

Even though shiitake, oyster, maitake and king oyster mushrooms have higher amounts of the amino acid ergothioneine than white button, cremini and portabello mushrooms, the researchers found that people who incorporated any variety of mushrooms into their daily diets had a lower risk of cancer.

According to the findings, individuals who ate 18 grams of mushrooms daily had a 45% lower risk of cancer compared to those who did not eat mushrooms.

"Mushrooms are the highest dietary source of ergothioneine, which is a unique and potent antioxidant and cellular protector," said Djibril M. Ba, a graduate student in epidemiology at Penn State College of Medicine. 

Fight Cancer with Mushrooms

When specific cancers were examined, the researchers noted the strongest associations for breast cancer as individuals who regularly ate mushrooms had a significantly lower risk of breast cancer.

Ba explained that this could be because most of the studies did not include other forms of cancer. Moving forward, this research could be helpful in further exploring the protective effects that mushrooms have and helping to establish healthier diets that prevent cancer.

"Overall, these findings provide important evidence for the protective effects of mushrooms against cancer," said coauthor John Richie, a Penn State Cancer Institute researcher and professor of public health sciences and pharmacology.

"Future studies are needed to better pinpoint the mechanisms involved and specific cancers that may be impacted."

Eating Mushrooms Lowers Cancer Risk