Honey is often praised for a range of health benefits, from soothing a sore throat and helping you get to sleep to healing woulds and lowering risk factors for diabetes and heart disease.

Honey’s acidity has the potential to prevent bacterial growth, while its density and stickiness generates osmotic pressure (in the same way as quicksand) which restrain bacteria.

Other compounds in honey contribute anti-inflammatory and antioxidant effects.

But do the claims about honey for specific health problems and injuries stack up to science? Let’s check what the evidence says.

First, what’s in honey?

Honey contains up to 20% water. The remaining 80% is made of simple sugars: monasaccharides that we rapidly digest. Fructose (32-28%) and glucose (26-31%) are the main ones, followed by small amounts of sucrose and others.

This can increase blood sugar levels to varying degrees. The glycemic index (GI) measures how fast blood sugars rise after eating or drinking. The GI of different Australian honeys ranges from 35 (low) to 72 (high), though most food labels don’t contain GI information.

Honey also has traces of vitamins (A, B1, B2, B6, C), minerals (potassium, magnesium, iron, zinc), amino acids (protein) and enzymes from plant, bee and insect secretions.

Nutrients vary depending on where the honeybees collected pollen, the time of honey harvest and how long it has been stored.

Can honey heal wounds?

A 2015 Cochrane review update assessed the effects of honey in treating acute burns, lacerations and chronic wounds, compared to topical treatments or other dressings.

It found high-quality evidence that honey dressings healed second-degree burns 4–5 days faster than conventional dressings. There was moderate-quality evidence that wounds infected after surgery healed faster with honey.

A 2020 review evaluated antimicrobial activity of Manuka and medical-grade honeys against a range of multi-drug resistant bacterial species. It found all honeys were effective against most species and could be considered for use in antibiotic-resistant infections.

Only sterilised medical-grade honey that has been processed to remove contaminants, and meets safety and antibacterial standards, should be used, with guidance from your doctor.

Does honey help adults sleep?

Research on the effects of honey on sleep is limited.

One trial compared sleep quality of 68 adults admitted to hospital. Half were given a mixture of milk (150mL) and honey (30g) twice a day, and half were not.

Those in the honey-mixture group said they slept better after day three. But these results could be biased, because participants were aware they were getting honey-milk and drinking it can be associated with feeling of comfort.

Can it soothe sore throats and coughs, or help kids sleep?

Five studies in children have compared honey mixtures to over-the-counter cough medicines or no medication. Each study linked honey to better sleep and less severe coughs in children.

But before you rush out to stock up on honey, there are major limitations related to the honey used. The quantity and type of honey given varies across the studies, with no certainty about which components are present. So the results need to be interpreted with caution.

Chemical analysis of some honey varieties found traces of the “feel-good” brain chemical serotonin and the hormone melatonin, which affects sleep and circadian rhythm. But the researchers concluded the small amounts detected were more likely to affect activity of the bees, rather than affecting human behaviour.

What about for diabetes, heart disease and cancer care?

For diabetes, a 2023 review of 48 clinical trials found honey had some positive effects on a range of risk factors, including glucose tolerance and wound healing. However, the honey dose and type weren’t standardised, so the researchers concluded that honey could be used in addition to, but not instead of, regular medications.

For heart disease, a 2022 analysis combining findings from trials evaluated the impact of honey on blood fats. It found no effect on several risk factors for heart disease: total cholesterol, triglycerides (another type of blood fat), low-density lipoprotein (LDL or bad) cholesterol or high-density lipoprotein (HDL or good) cholesterol.

However a 2025 meta-analysis of propolis (bee glue) did find significant reductions in triglycerides, LDL (bad) cholesterol, fasting blood sugars, insulin and systolic blood pressure (the top number on a reading). But given most propolis supplement trials have only lasted a few months and supplements are expensive, that money is likely better spent on healthy foods.

For cancer patients, a 2023 review found honey alleviated ulceration and inflammation in the mouth following chemotherapy or radiotherapy, and it reduced some of the toxic effects of chemotherapy.

Can it affect your mind?

Some honeys have psychotropic, or mind-altering effects. “Mad honey” comes from plant nectar of Rhododendron species and naturally contains grayanotoxins, which have pharmacological and toxic effects.

These include nausea, dizziness, low blood pressure, severe bradycardia (an abnormally slow heart rate), neurological complications and even life-threatening cardiac arrhythmia (irregular heart beat).

It’s illegal to import or sell “mad honey” in Australia but Nepal and Turkey have historically used it for medicinal and psychoactive properties.

Who shouldn’t have honey?

Although commercial honey is pasteurised, the process does not kill spores of the bacteria Clostridium botulinum. This is why babies under one year and immunocompromised people shouldn’t have honey.

Clare Collins, Laureate Professor in Nutrition and Dietetics, University of Newcastle

This article is republished from The Conversation under a Creative Commons license. Read the original article.

A form of Parkinson’s disease caused by mutations in a gene known as PINK1 has long been labelled rare. But our research shows it’s anything but – at least for some populations.

Our meta-analysis revealed that people in specific Polynesian communities have a much higher rate of PINK1-linked Parkinson’s than expected. This finding reshapes not only our understanding of who is most at risk, but also how soon symptoms may appear and what that might mean for treatment and testing.

Parkinson’s disease is often thought of as a single condition. In reality, it is better understood as a group of syndromes caused by different factors – genetic, environmental or a combination of both.

These varying causes lead to differences in disease patterns, progression and subsequent diagnosis. Recognising this distinction is crucial as it paves the way for targeted interventions and may even help prevent the disease altogether.

Why we focus on PINK1-linked Parkinson’s

We became interested in this gene after a 2021 study highlighted five people of Samoan and Tongan descent living in New Zealand who shared the same PINK1 mutation.

Previously, this mutation had been spotted only in a few more distant places –Malaysia, Guam and the Philippines. The fact it appeared in people from Samoan and Tongan backgrounds suggested a historical connection dating back to early Polynesian migrations.

One person in 1,300 West Polynesians carries this mutation. This is a frequency well above what scientists usually classify as rare (below one in 2,200). This discovery means we may be overlooking entire communities in Parkinson’s research if we continue to assume PINK1-linked cases are uncommon.

Traditional understanding says PINK1-linked Parkinson’s is both rare and typically strikes younger people, mostly in their 30s or 40s, if they inherit two faulty copies of the gene. In other words, it’s considered a recessive condition, needing two matching puzzle pieces before the disease can unfold.

Our work challenges this view. We show that even one defective PINK1 gene can cause Parkinson’s at an average age of 43, much earlier than the typical onset after 65. That’s a significant departure from the standard belief that only people with two defective gene copies are at risk.

Why this matters for people with the disease

It’s not just genetics that challenge long-held views. Historically, PINK1-linked Parkinson’s was thought to lack some of the classic features of the disease, such as toxic clumps of alpha-synuclein protein.

In typical Parkinson’s, alpha-synuclein builds up in the brain, forming sticky clumps known as Lewy bodies. Our results, contrary to prior beliefs, show that alpha-synuclein pathology is present in 87.5% of PINK1 cases. This finding opens up a promising new avenue for future treatment development.

The biggest concern is early onset. PINK1-linked Parkinson’s can begin as early as 11 years old, although a more common starting point is around the mid-30s. This early onset means living longer with the disease, which can profoundly affect education, work opportunities and family life.

Current treatments (such as levodopa, a precursor of dopamine) help manage symptoms, but they’re not designed to address the root cause. If we know someone has a PINK1 mutation, scientists and clinicians can explore therapies for specific genetic pathways, potentially delivering relief beyond symptom management.

Sex differences add a layer of complexity

In Parkinson’s, generally, men are at higher risk and tend to develop symptoms earlier. However, our findings suggest the opposite pattern for PINK1-linked cases. Particularly, women with two defective copies of the gene experience onset earlier than men.

This highlights the need to consider sex-related factors in Parkinson’s research. Overlooking them risks missing key elements of the disease.

Genetic testing could be a game-changer for PINK1-linked Parkinson’s. Because it often appears earlier, doctors may not recognise it immediately, especially if they are more familiar with the common, later-onset form of Parkinson’s.

Early genetic testing could lead to a faster, more accurate diagnosis, allowing treatment to begin when interventions are most effective. It would help families understand how the disease is inherited, enabling relatives to get tested.

In some cases, where appropriate and culturally acceptable, embryo screening may be considered to prevent the passing of the faulty gene.

Knowing you have a PINK1 mutation could also make finding the right treatment more efficient. Instead of a lengthy trial-and-error process with different medications, doctors could use emerging therapies designed to target the underlying PINK1 mutation rather than relying on general Parkinson’s treatments meant for the broader population.

Addressing research gaps

These findings underscore how crucial it is to include diverse populations in health research.

Many communities, such as those in Samoa, Tonga and other Pacific nations, have had little to no involvement in global Parkinson’s genetics studies. This has created gaps in knowledge and real-world consequences for people who may not receive timely or accurate diagnoses.

Researchers, funding bodies and policymakers must prioritise projects beyond the usual focus on European or industrialised countries to ensure research findings and treatments are relevant to all affected populations.

To better diagnose and treat Parkinson’s, we need a more inclusive approach. Recognising that PINK1-linked Parkinson’s is not as rare as previously thought – and that genetics, sex differences and cultural factors all play a role – allows us to improve care for everyone.

By expanding genetic testing, refining treatments and ensuring research reflects the full spectrum of Parkinson’s, we can move closer to more precise diagnoses, targeted therapies and better support systems for all.

Victor Dieriks, Research Fellow in Health Sciences, University of Auckland, Waipapa Taumata Rau and Eden Paige Yin, PhD candidate in Health Sciences, University of Auckland, Waipapa Taumata Rau

This article is republished from The Conversation under a Creative Commons license. Read the original article.