Can honey protect your brain? Study reviews its potential against Alzheimer’s

From chestnut to manuka, honey varieties demonstrate neuroprotective power in lab studies against Alzheimer’s disease, but scientists stress that only human trials can reveal real-world benefits.

Effects of different honey types on the main molecular features of Alzheimer disease. Arrows’ design reflects the strength of the evidence. Abbreviations: AA = arachidonic acid; Aβ= amyloid beta; APP= amyloid precursor protein; AChE = acetylcholinesterase; COX-2 = cyclooxygenase-2; PGE₂ = prostaglandin E₂.

In a recent study in the journal Nutrients, researchers conducted a comprehensive review to elucidate the impacts of honey consumption on neurological outcomes, specifically regarding Alzheimer’s disease (AD). The study synthesized the findings from 27 relevant original research articles investigating honey’s association with AD and the mechanisms underlying these interactions.

Review findings suggest that honey’s rich blend of bioactive compounds helps combat oxidative stress, inflammation, and protein aggregation in laboratory models, suggesting potent anti-AD effects. Intriguingly, different honey varieties were found to exhibit significant differences in both their bioactive profiles and neuroprotective effects.

Unfortunately, while these results are promising, the review highlights a stark dearth of human clinical evidence and emphasizes that these trials are needed before standardized dosing or quality guidelines can be proposed, even though some animal-to-human dose conversions suggest that experimental exposures may be relevant.

Background

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by the gradual erosion of memory, thinking skills, and the ability to carry out simple routine tasks. It has been identified as the leading cause of dementia worldwide, and despite decades of research on the condition, it remains without a cure. Current interventions involve delaying disease progression and managing specific symptoms.

At the molecular level, the disease is characterized by two key processes that degrade cognitive performance: 1. The buildup of amyloid-beta (Aβ) peptides into sticky plaques outside neurons, and 2. The formation of tangled tau proteins inside neurons. These processes trigger and exacerbate cascades of chronic inflammation, mitochondrial dysfunction, and oxidative stress, progressively preventing neural connections and deteriorating neurological health.

Since current treatments offer only modest symptomatic relief and do not halt the underlying disease progression, researchers explore preventive strategies and complementary approaches, particularly those rooted in diet and other modifiable behaviors. Honey, the sweet, viscous, gold-colored substance produced by several bee species, has long been revered as a ‘superfood’, used as a nutritive supplement, medicine, and sweetener.

Honey is rich in potent plant-derived compounds (e.g., polyphenols and flavonoids), which are known for their antioxidant and anti-inflammatory properties, making it a prime candidate for neuroprotection against AD. Unfortunately, the literature investigating honey’s benefits remains limited and ungeneralizable.

About the review

The present review aims to address this knowledge gap by collating all available literature (predominantly preclinical) investigating honey’s association with neuroprotection and synthesizing their findings to summarize molecular mechanisms and identify research gaps prior to clinical translation.

The review comprised an equation-based search of PubMed, Scopus, and Web of Science for any peer-reviewed publications investigating the molecular mechanisms underpinning honey’s neurological benefits, focusing on honey’s impacts on oxidative stress, chronic or systemic inflammation, apoptosis, mitochondrial dysfunction, neurotransmitter modulation, β-amyloid accumulation, and tau hyperphosphorylation.

Notably, of the thousands of publications identified in the review’s screening process, only 27 met the review criteria after title, abstract, and full-text screening. Furthermore, all identified studies were preclinical, highlighting that, as of the review’s writing, not a single scientific study has investigated the physiological or neurological impacts of honey consumption on human participants.

The review instead identified in vitro experiments on isolated cells, studies on invertebrates such as the nematode worm Caenorhabditis elegans and the fruit fly Drosophila melanogaster, as well as experiments in rodent (murine) models of neurodegeneration. The breadth of the data collected (including the variety or type of honey used alongside its source) allowed for identifying how different types of honey—from Manuka and Tualang to Chestnut and Avocado—interact with AD pathology in the lab.

Study findings

Review findings revealed that honey fights AD’s hallmarks on multiple fronts, including oxidative stress, inflammation, and neurotransmitter modulation. In various models, treatment with honey or its extracts has been shown to significantly reduce levels of reactive oxygen species (ROS), the harmful molecules responsible for cellular damage.

In one study, chestnut-derived honey protected neuronal cells from glutamate-induced damage, preserving mitochondrial function at concentrations ranging from 500 to 750 μg/mL, thereby highlighting its antioxidative activity. Studies using C. elegans genetically engineered to produce human amyloid-beta, both Manuka and avocado honey (conc. of 100 mg/mL), significantly delayed the onset of Aβ-induced paralysis, demonstrating honey’s potent anti-inflammatory and anti-Aβ efficacy. However, in certain tauopathy worm models, honey unexpectedly worsened mobility, a paradoxical effect that the authors suggest could be linked to sugar content rather than tau-specific mechanisms.

Murine models validated these findings in mammalian in vivo systems, with Tualang honey reversing LPS-induced shifts in hippocampal Aβ1-40 and Aβ1-42 levels, and Kelulut honey reducing Aβ1-42 deposition in the dentate gyrus but not in CA1 or CA3. Additionally, certain honeys demonstrated a remarkable ability to inhibit acetylcholinesterase, the enzyme that degrades acetylcholine, a neurotransmitter central to memory; acetylcholinesterase inhibitors are standard symptomatic AD therapies.

The review also cautions that outcomes varied considerably across honey types, reflecting differences in botanical source, processing, and study design, and many of the included studies were rated as having a high or unclear risk of bias.

Conclusions

The present review emphatically highlights that, at least in laboratory settings and non-human model systems, honey is a potent neuroprotective agent. Its rich phytochemical content triggers several benefits against the molecular drivers of AD, from quelling oxidative stress and inflammation to directly interfering with the aggregation of toxic proteins.

Unfortunately, a stark lack of human-derived evidence remains, emphasizing the need for human-based clinical trials to identify optimal dosages and establish quality guidelines.