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Manuka Honey Combination Therapy May Help Treat Lethal Lung Infection

The benefits of manuka honey have been used throughout the areas of New Zealand and Australia for many years. It has been said that manuka honey is four times more nutrient-dense in terms of its healing compounds compared to regular floral honey. Now, a team o

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The benefits of manuka honey have been used throughout the areas of New Zealand and Australia for many years. It has been said that manuka honey is four times more nutrient-dense in terms of its healing compounds compared to regular floral honey. Now, a team of scientists at Aston University has combined manuka honey and the drug amikacin in a lab-based nebulization formulation to treat the harmful bacterial lung infection Mycobacterium abscessus.

The findings are published in the journal Microbiology in an article entitled, “In vitro synergy between manuka honey and amikacin against Mycobacterium abscessus complex shows potential for nebulization therapy.”

“M. abscessus is an opportunistic human pathogen of increasing concern, due to its ability to cause aggressive pulmonary infections (especially in cystic fibrosis patients), as well as skin and soft tissue infections,” wrote the researchers. “M. abscessus is intrinsically drug-resistant and treatment regimens are lengthy, consisting of multiple antibiotics with severe side effects and poor patient success rates. New and novel strategies are urgently required to combat these infections. One such strategy thus far overlooked for mycobacteria is manuka honey. For millennia manuka honey has been shown to have wide-ranging medicinal properties, which have more recently been identified for its broad spectrum of antimicrobial activity. Here we demonstrate that manuka honey can be used to inhibit M. abscessus and a variety of drug-resistant clinical isolates in vitro.”

In the study, the researchers used samples of the bacteria M. abscessus taken from 16 infected cystic fibrosis (CF) patients. They then tested the antibiotic amikacin, combined with manuka honey, to discover what dosage was required to kill the bacteria.

Manuka honey has antibacterial, antiviral, anti-inflammatory, and antioxidant properties. It gets its antibacterial effects from an active ingredient called methylglyoxal (MGO). MGO is created in manuka honey by the conversion of another compound known as dihydroxyacetone (DHA). A high concentration of DHA is found in the nectar of manuka flowers. The higher the concentration of MGO, the stronger the antibacterial effects of manuka honey.

M. abscessus is a bacterial pathogen from the same family that causes tuberculosis. However, this pathogen differs by causing serious lung infections in people (particularly children) with pre-existing lung conditions, such as CF and bronchiectasis, as well as causing skin and soft tissue infections.

Patients are given a cocktail of antibiotics, consisting of 12 months or more of antimicrobial chemotherapy, and which often doesn’t result in a cure. The dosage of amikacin usually used on a patient to kill the infection is 16 micrograms per milliliter. But the researchers found that the new combination using manuka honey, required a dosage of just two micrograms per milliliter of amikacin.

“So far treatment of M. abscessus pulmonary infections can be problematic due to its drug-resistant nature,” explained Victoria Nolan, lead author and PhD researcher.

The use of this inhalation therapy of amikacin and manuka honey demonstrates great promise as an improved therapy for M. abscessus pulmonary infections, which could lead to an increase in successful treatment outcomes and reduce the burden on the patient produced by drug-associated side effects.

“By combining a totally natural ingredient such as manuka honey with amikacin, one of the most important yet toxic drugs used for treating M. abscessus, we have found a way to potentially kill off these bacteria with eight times less drug than before. This has the potential to significantly reduce amikacin-associated hearing loss and greatly improve the quality of life of so many patients—particularly those with cystic fibrosis.

“I am delighted with the outcome of this research because it paves the way for future experiments and we hope that with funding we can move towards clinical trials that could result in a change in strategy for the treatment of this debilitating infection,” concluded Jonathan Cox, PhD, senior lecturer in microbiology, Aston University.

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Related questions

01What is cystic fibrosis? A Mayo Clinic expert explains

Learn more from pulmonologist Sarah Chalmers, M.D. Cystic fibrosis (CF) is a condition passed down in families that causes damage to the lungs, digestive system and other organs in the body. CF affects the cells that make mucus, sweat and digestive juices. These fluids, also called secretions, are usually thin and slippery to protect the body's internal tubes and ducts and make them smooth pathways. But in people with CF, a changed gene causes the secretions to become sticky and thick. The secretions plug up pathways, especially in the lungs and pancreas. CF gets worse over time and needs daily care, but people with CF usually can attend school and work. They often have a better quality of life than people with CF had in past decades. Better screening and treatments mean that people with CF now may live into their mid- to late 50s or longer, and some are being diagnosed later in life.

Source: www.mayoclinic.org ↗
02What to expect from your doctor

After getting detailed information about the symptoms and your family's medical history, your healthcare professional may order tests to help with diagnosis and plan treatment. Your healthcare professional also may ask questions, such as: What symptoms are you or your child having? When did the symptoms start? Does anything make the symptoms better or worse? Has anyone in your family ever had cystic fibrosis? Has growth been average and weight been stable? Cystic fibrosis. National Heart, Lung, and Blood Institute. https://www.nhlbi.nih.gov/health/cystic-fibrosis. Accessed Aug. 8, 2024. Bronchiectasis. National Heart, Lung, and Blood Institute. https://www.nhlbi.nih.gov/health/bronchiectasis. Accessed Aug. 8, 2024. FAQs: Cystic fibrosis: Prenatal screening and diagnosis. American College of Obstetricians and Gynecologists. https://www.acog.org/womens-health/faqs/cystic-fibrosis-prenatal-screening-and-diagnosis. Accessed Aug. 8, 2024. Ferri FF. Cystic fibrosis. In: Ferri's Clinical Advisor 2025. Elsevier; 2025. https://www.clinicalkey.com. Accessed Aug. 8, 2024. Kliegman RM, et al., eds. Cystic fibrosis. In: Nelson Textbook of Pediatrics. 22nd ed. Elsevier; 2025. https://www.clinicalkey.com. Accessed Aug. 8, 2024. Kellerman RD, et al. Cystic fibrosis. In: Conn's Current Therapy 2024. Elsevier; 2024. https://www.clinicalkey.com. Accessed Aug. 8, 2024. Lockwood CJ, et al., eds. Respiratory diseases in pregnancy. In: Creasy and Resnik's Maternal-Fetal Medicine: Principles and Practice. 9th ed. Elsevier; 2023. https://www.clinicalkey.com. Accessed Aug. 8, 2024. Ong T, et al. Cystic fibrosis: A review. JAMA. 2023; doi:10.1001/jama.2023.8120. Rubin R. Tackling the misconception that cystic fibrosis is a "white people's disease." JAMA. 2021; doi:10.1001/jama.2021.5086. Care centers. Cystic Fibrosis Foundation. https://www.cff.org/managing-cf/care-centers. Accessed Aug. 8, 2024. Trikafta (prescribing information). Vertex Pharmaceuticals Inc.; 2023. https://www.trikafta.com/. Accessed Aug. 8, 2024. Symdeko (prescribing information). Vertex Pharmaceuticals Inc.; 2023. https://www.symdeko.com/. Accessed Aug. 8, 2024. Orkambi (prescribing information). Vertex Pharmaceuticals Inc.; 2023. https://www.orkambi.com/. Accessed Aug. 8, 2024. Kalydeco (prescribing information). Vertex Pharmaceuticals Inc.; 2023. https://www.kalydeco.com/. Accessed Aug. 8, 2024. Pilewski JM. Update on lung transplantation for cystic fibrosis. Clinics in Chest Medicine. 2022; doi:10.1016/j.ccm.2022.07.002. Fridell JA, et al. Pancreas transplantation for cystic fibrosis: A frequently missed opportunity. Clinical Transplantation. 2021; doi:10.1111/ctr.14371. Wadsworth LE, et al. Non-invasive ventilation is associated with long-term improvements in lung function and gas exchange in cystic fibrosis adults with hypercapnic respiratory failure. Journal of Cystic Fibrosis. 2021; doi:10.1016/j.jcf.2021.05.011. Allscripts EPSi. Mayo Clinic. Medical review (expert opinion). Mayo Clinic. Oct. 18, 2024.

Source: www.mayoclinic.org ↗
03What Is Cystic Fibrosis?

Cystic fibrosis (CF) is a genetic disorder, which means you get it from your parents at birth. It affects your lungs, pancreas, and other organs. CF changes the way chloride (salt) moves through the cells of your body. This causes the mucus (which should be thin and slippery) in various organs to become thick and sticky. Over time, this thick mucus builds up inside your airways, making it hard to breathe. The mucus traps germs and leads to infections and inflammation. It can also cause severe, long-term damage to the lungs and lead to respiratory failure (inability to breathe normally) and death. In the pancreas, the thick mucus caused by CF prevents the release of digestive enzymes when you eat. This leads to malnutrition and poor growth. CF can also cause liver disease, reproductive problems, and cystic fibrosis-related diabetes (CFRD). More than 40,000 people in the U.S. live with CF. Doctors diagnose about 1,000 new cases each year. Today, more than half of the CF population is aged 18 or older, and new treatments have expanded the life expectancy by decades.

Source: www.webmd.com ↗
04What Types of Drug Interactions Can Happen?

Your body uses special enzymes called CYP450 to break down certain medicines. When you have long-term illness, your body may produce more or less of these enzymes, which can change how some medicines work. Some medicines and foods may affect the levels of these enzymes, which could impact how Alyftrek works in your body. Avoid CYP3A Inducers: Some medicines called CYP3A inducers (e.g. carbamazepine or rifampin ) can lower the amount of Alyftrek in your body, making it less effective. Be Cautious with CYP3A inhibitors: CYP3A inhibitors (e.g. erythromycin or itraconazole ) can increase the levels of Alyftrek in the body, which may raise the risk of side effects. If you are taking one of these medicines, your health care provider may adjust your Alyftrek dose. Avoid grapefruit products: Grapefruit and grapefruit juice can also increase the amount of Alyftrek in the body, so it is best to avoid them while on this medicine. Alyftrek can also affect how other medicines work in your body. P-gp and BCRP substrates: Alyftrek may increase the levels of certain medicines that rely on P-gp (P-glycoprotein) and BCRP (breast cancer resistance protein) in the body. This could lead to stronger effects or more side effects from those medicines. Your health care provider may monitor you more closely if you are taking one of these medicines. CYP2C9 substrates (e.g., warfarin): Alyftrek may interfere with CYP2C9 substrates, such as warfarin , a blood thinner. If you take warfarin, your doctor may need to check your blood clotting levels more often. Always tell your health care provider about any prescription or over-the-counter (OTC) medicines, vitamins/minerals, herbal products, and other supplements you are using or have recently taken. This will help make sure your medicines work well together.

Source: www.webmd.com ↗
05Is there anything else I need to know about a sweat test?

In rare cases, conditions other than CF may result in high chloride levels on a sweat test. These conditions include hypothyroidism , nephrogenic diabetes insipidus , and Addison disease .

Source: medlineplus.gov ↗
Research context

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Research and Statistics: Who Has Cystic Fibrosis?

About 40,000 people are living with cystic fibrosis in the United States, and there are approximately 105,000 people with CF worldwide. (3) More than 75 percent of people with the disease are diagnosed by age 2, and more than half of all people living with cystic fibrosis are 18 or older. CF occurs predominantly in white populations, at a rate of 1 in 2,500 births. Between 2 and 5 percent of white people are carriers of the CFTR gene variant but have no overt clinical signs of disease. The disease is less common among African Americans, occurring at the much lower frequency of approximately 1 out of 17,000 births. (15) CF gene variants are most prevalent in persons of northern and central European ancestries or of Ashkenazi Jewish descent. They are rarely found in Native Americans, Asians, or native Africans. (16) CF is equally common among men and women, but women patients fare significantly worse than male patients with the disease. The median survival age for female CF patients is about three years younger than it is for men, but the reasons for the poorer survival rates among women are not completely understood. (17)

Source: everydayhealth.com ↗
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Peptide Therapy Guide Editorial Team

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