Surely honey, a sweet, golden, and delightfully sticky treat, is harmless? After all, Winnie the Pooh salivated over it, ancient Egyptians embalmed their dead with it and Romans paid their taxes with it. In actuality, venom from honey producers, Apis mellifera, is toxic. Bee venom, known as apitoxin, can be deadly to predators and to the one to two percent of the human population.
Recent research has indicated that small doses of the toxic venom may be medicinally useful even if honey toxins can prove fatal. Honey: deadly?
Honey can be as poisonous as bee venom if contaminated by botulinum toxins or grayanotoxins. Botulinum contamination occurs frequently and is detected in up to 13 percent of honey products.
The bacteria Clostridium botulinum is found in most soils, in low-acid home-canned foods and indeed, in some honey products. Botulinum is sometimes referred to as “sausage poison” due to its prevalence in improperly handled meat.
Botulinum toxin is the most poisonous known substance; a dose of 0.0000001 milligram per kilogram of body weight can prove fatal.
Since infants possess far less body mass than adults, honey poses a serious threat to children under 12 months of age. This bacterium takes up residence in an infant’s immature gastrointestinal tract and spews toxins into the muscles, muddling nervous system functions.
Recent research suggests that botulism poisoning may underlie death in up to 10 percent of Sudden Infant Death Syndrome cases.
The toxic effects of botulinum arise from its molecular brutality. Imagine a train car full of thousands of people, representing neurotransmitters called acetylcholine. A train can only leave the station (the outer wall of a cell, the membrane) if it is firmly attached to the tracks. The tracks that anchor the ‘train’ are fusion proteins called SNAP-25, syntaxin and synaptobrevin.
Botulinum attacks these proteins, destroying the train tracks between the presynaptic terminal and the postsynaptic muscle. Since fewer passengers, or acetylcholine molecules, reach the neuromuscular junction, the muscles do not receive the signal to contract and the characteristic muscular weakness of botulism poisoning ensues.Victims often suffocate because the muscles involved in breathing are inhibited.
Compared to botulinum, grayanotoxin, a plant toxin from rhododendrons, laurels and azaleas, infests honey only rarely. Unprocessed honey is more likely to contain grayanotoxins than commercial honey since large production plants pool honey from many sources.
Ingestion of grayantoxins results in a temporary condition known as “honey intoxication.” This intoxication results in symptoms such as dizziness, weakness, perspiration, nausea and vomiting, and higher doses trigger low blood pressure, shock, irregular heart rhythms, convulsions and rarely, death.
The destructive effects of grayanotoxins arise from molecular recognition and forced entry onto a receptor. First, a grayanotoxin recognizes a binding site on the receptor of a sodium channel. Imagine this channel to be a ramp leading onto a highway and the receptor to be the tollbooth. If you are a sodium molecule and flash your E-Z Pass at the gated entrance, you may pass through the tollbooth onto the neuron’s axonal highway.
Grayanotoxin lacks a sodium E-Z Pass but insinuates itself on the tollbooth nonetheless. Furthermore, it prevents the gate from descending as it normally would, allowing all of the sodium molecules behind it to rush through the tollbooth unfettered by the momentary wait for the gate’s ascension.
Since these tollbooths, or sodium receptors, control the excitation level of neurons, grayanotoxin exposure results in extra excitability since the tollbooth cannot close its gate (and inactivate the channel). Neurons that cannot return to baseline excitation levels fire repetitively and, if unchecked, can result in toxicity and cell death.Excitotoxicity from grayanotoxins can prove fatal. Bee venom: helpful?
Although bee venom is potentially fatal, its components may prove helpful in enhancing memory consolidation and in restoring smooth muscle movement in Parkinson’s patients. In addition, apitherapy antidotes have also been suggested for multiple sclerosis, arthritis, bursitis, and tendinitis, among other diseases.
If apitoxin were a cosmopolitan, apamin would be the lime juice, as it is the key ingredient that puts the bite into bee venom. Yet, this same kick may endow bee venom with its therapeutic benefits.
Research suggests that small doses of apamin can affect memory. Rats exhibited improved memory consolidation and retrieval skills 24 hours after injection.
The researchers theorized that bee venom could be used to synthetically modify erroneous dopamine levels for people suffering from Parksinson’s. Dopamine comprises 1.5 percent of apitoxin and is a neurotransmitter found in the human brain. Researchers hoped that treatment with bee venom could eliminate the adverse side effects of conventional anti-Parkinsonian medication, such as L-DOPA, which often include hypotension, arrhythmias, nausea, gastrointestinal bleeding, and disturbed respiration.
Although bee venom has noticeable effects on memory improvement, no definitive studies demonstrate improvement in Parkinson’s symptoms.
Original Author: Sophia Porrino