Common Name: Rosebay Rhododendron, Rosebay, Great-laurel – Rosebay is used as a descriptive name for several plants with characteristic rose-like blossoms. Rhododendron is one of the few plants with its genus as common name.
Scientific Name: Rhododendron maximum – The genus is a combination of the Greek words rose (rhodon) and tree (dendron), an indication of its well established association with civilizations in antiquity, “rose tree” being an apt description. Maximum is a widely used term especially in mathematics as an adjective to convey the largest in size or quantity. It is derived from the Latin magnus, meaning great or big, which, for a rhododendron, it is.
Potpourri: The lush, dense thickets of rhododendron that dominate the understory of upland elevations are testimony to an evolutionary path that produced a competitive combination of successful traits. It is one of the relatively few broad-leaved flowering plants of the angiosperm (enclosed seed) clade that is evergreen, retaining foliage year-round like the largely needle-leaved gymnosperm (naked seed) clade. The prominent rose-like blossoms that extend from the end of nearly every branch are a bouquet to attract pollinators, mostly bees, that flit from one to the other collecting nectar and pollen. With successful fertilization, an elongated, egg-shaped fruit with five cells splits open to release thousands of seeds that scatter to extend the grove ever outward. The lack of any evidence of insect damage or animal browse is a matter of chemistry. Rhododendrons, like many other members of the Ericaceae or Heath family, evolved strong chemicals to deter predation. Most animals give it a wide berth; deer supposedly are able to browse without harm but there is little evidence that they do so regularly. Rhododendron leaves can be fatally toxic to cattle and sheep. [1]
There are over one thousand species of the Rhododendron genus that extend globally across the temperate climates of the northern hemisphere. Based on fossilized pollen found in strata dating from near the end of the Cretaceous Period and fossil leaves from the beginning of the Tertiary Period, it is postulated that Rhododendrons first appeared just after the breakup of Pangaea in southeastern Asia about 50 million years ago. Speciation spread globally across a wide band of latitude during the pre-glacial epochs when a warmer climate prevailed. It is probable that the subsequent glacial cooling cycles of the current Quaternary Period resulted in the isolation of rhododendron populations in remote mountainous regions, just as Balsam Firs are isolated in elevated areas of the Appalachians. This explains the rich diversity found on the slopes of deep valleys in southeast Asia in a band extending from just east of the Himalayas through the Malaysian archipelago and the single species rhododendron diaspora to Japan, the Appalachian Mountains, and the Caucasus region of eastern Europe. [2]
While “mad honey” may also evoke marital discord, it has historical rhododendron relevance. Mesopotamia, the land between the Tigris and Euphrates rivers, is where western civilization arose from Neolithic farm villages that planted the first tentative crops. Rhododendron had spread across the Anatolian peninsula that is now Türkiye from their epicenter in the Caucasus, attracting swarms of honeybees. In 400 BCE, the soldier of fortune Xenophon led his mercenary Greek army eulogized as the “ten thousand” on a forced march of 1500 kilometers westward through hostile territory of present day Kurdistan and Armenia to the Black Sea. Lacking adequate provisions, they lived off the land, raiding bee hives for honey. As Xenophon later recorded in his chronicle Anabasis, “the soldiers who ate the honey went off their heads, and suffered from vomiting and diarrhea … so they lay there in great numbers as though the army had suffered a defeat, and great despondency prevailed.” [3] While no one died, the debilitating effects of rhododendron honey were put to nefarious use near this same location three centuries later.
Mithridates Eupator became the ruler of Pontus in 115 BCE when his mother, who had tried to kill him as a youth, was deposed in a coup d’état. To protect himself against the conspiracies inherent to governance of that era, he followed a regimen of microdoses of poison to acquire immunity over time, becoming an expert on toxins and their antidotes. Uniting the diverse population of Greeks, Persians, and Thracians along the northern tier of Asia Minor, he became a serious rival to the Romans encroaching ever eastward. In the First Mithridatic War (88-84 BCE), his navy of 400 ships and army of 290,000 took over the Black Sea and the Greek cities on its banks, putting an end to the flow of tribute money to Rome and nearly bankrupting their economy. [4] The Romans rallied in two ensuing wars that eventually drove Mithridates from power as the last major eastern threat to their burgeoning empire, but not before he had tricked them on at least one occasion with mad honey of the rhododendron. In 67 BCE, the Roman general Pompey was advancing eastward along the Black Sea coast near Trabzon to engage the Pontic forces. Mithridates, employing his mastery of poisons, placed bee hives in clay pots along their route. Three squadrons of Roman soldiers succumbed and were slaughtered in their stupor. In spite of this tactical success, the forces of Rome eventually prevailed, and Mithridates was deposed and exiled to Crimea, where he was stabbed to death by the agents of his son since poisoning was not an option. [5] The genus Eupatorium which includes the poisonous white snakeroot and the medicinal boneset is named for Mithridates Eupator in recognition of his contribution to toxicology.
Honey from rosebay rhododendron in North America is not nearly as common nor as virulent as the legendary Caucasian rhododendron of Xenophon and Mithridates. Nonetheless, the mad honey trope persists. In 1801, an account of rhododendron honey inducing nausea, muscle spasms, and blurred vision was published in the Transactions of the American Philosophical Society.[6] A report in the most venerable scholarly publication in the Americas (established in 1771 when the states yet to be united were still colonies) affords some credence to this assertion. However, there is little evidence of any significant incidence of what is sometimes euphemistically called “honey intoxication” in North America. There are several reasons for this. R. maximum is neither as toxic as R. ponticum, the plant eponymously named for Mithidates’ Pontus homeland, nor as widely dispersed. There is also the fact that honey bees are indigenous to Europe as native pollinators for many wild plants. They were introduced to the Americas for crop pollination and are largely relegated to that role, even as some have become naturalized. The few reports of mad honey illnesses in the US are at least in part attributable to an alternative medicine herbal treatment that links “sexual performance enhancement” to the consumption of bespoke beekeeper-induced rhododendron-mad honey. Of twenty one honey-related emergency room visits due to symptoms that included dizziness, nausea, vomiting, and syncope (loss of consciousness due to low blood pressure), most were men of middle age who sought to regain virility [7]―another good reason to call it mad honey.
Rhododendron maximum produces a poison named grayanotoxin which has been and is sometimes still referred to as andromedotoxin, acetylandromedol, or rhodotoxin (from the genus). While concentrated in honey, it also permeates the leaves and flowers. Grayana is an Asian Heath Family plant species from which the toxin was first extracted and analyzed. The name derives from the American botanist Asa Gray who supported Darwin’s work with the observation that many plants in eastern North America were similar to those of east Asia (like rhododendron), indicating similar evolutionary progressions. Grayanotoxin interferes with the operation of neurons by disrupting “voltage-gated sodium channels.” The effect is that the neurons that carry the signals from one part of the body to another that make everything happen … from the beating of the heart to the thinking of the brain … can no longer do so in the prescribed order with proper timing. [8] The mechanism employed by neurons to carry out their quintessential task is electrochemical. Electrical signals travel along the neuron from the dendrites at one end to the axon at the other where they pass over a gap called the synapse to the next neuron in the sequence path using sodium ions as transport. This is the main reason that electrolytes (ionic fluids) are so important and that hyponatremia (low sodium) can be fatal. It has been long been established as most likely that this ionic neural mechanism was a random (Darwinian) mutation that evolved only once, and, owing to its sensory and mobility efficacy, was replicated in every animal ever since. However, it may be much more complex than that as sea sponges, which have no neurons, and comb jellies, which do, have DNA similarities. [9] The details of evolution are still evolving.
The effects of rhododendron grayanotoxin poisoning are what one might expect considering the disruption of nerve function as its cause. Dizziness, confusion, and blurred vision are sure to follow a diminution of neuron signaling in the brain. Likewise, insidious side effects on autonomous systems take a toll; the heart beats more slowly and blood pressure can drop to induce a loss of consciousness. Since nerves do everything, a panoply of effects have been reported that range from numbness around the mouth and excessive salivation to vomiting and diarrhea. Since humans don’t as a rule eat leaves and flowers, most reported human health effects concern the consumption of toxic honey, which is brown and bitter and not golden and sweet. Since bitter is a taste sensor variant to protect against inadvertently consuming poisons, it is unclear why anyone would eat tainted honey in the first place (excepting virility which trumps reason). However, cattle, sheep, goats, and donkeys do eat rhododendron leaves and consequently fall victim to its poison. The toxic dose for cows is 0.2 percent body-weight (about one kilogram) with symptoms appearing about three hours later that last for several days. Fatalities are not uncommon in part due to the ruminating mastication of cows; chewing toxic cud can only release more poison. Domestic cats and dogs will on occasion consume the azalea type of rhododendron that is widely planted in gardens, the characteristic symptoms of gastrointestinal distress result. [10]
Plants create toxic chemicals for a reason – usually to deter animal predation. Heath Family plants are no exception. Grayanotoxin likely was an evolutionary mutation that kept herbivorous animals at bay, which it does. In some cases, a priori plant chemical defenses can be co-opted by humans to take advantage of their toxicity. This is especially true when a plant (or fungus) has evolved to ward off microbes or bacteria that are equally threats to the health of humans, becoming an antibiotic. In that grayanotoxin acts to disrupt neural activity, it would seem an unlikely candidate for medicinal use owing to its profound, disturbing effects. However, there is ample evidence that it was used by Native Americans for a variety of applications. [11] Cherokee used it both as an external poultice for rheumatic pain and as treatment for skin abrasion. This may merely have been a placebo that was thought to work, so it did. The rhododendron was apparently also used for various purposes having nothing to do with health, such as to “throw clumps of leaves into a fire and dance around it to bring cold weather.” [12] It is also reported that Native Americans made a tea from the leaves that was “taken internally in controlled doses for heart ailments.” The same guide notes “leaves toxic, ingestion may cause convulsions and coma.” [13] There has been some recent research concerning the use of rhododendron compounds for specific ailments. For example, diabetic rats treated with grayanotoxin produced more insulin, presumably due to some form of nerve stimulation. All things considered, it is probably best to avoid it altogether, in spite of any number of herbal remedies containing rhododendron extract that supposedly produce salubrious affects. [14]
Heath Family shrubs (Ericaceae) are masters of their chosen environments that include the understory of trees at higher elevations and craggy, berry bogs. They have help in the form of specialized fungal partners that envelop their roots, providing soil nutrients like phosphorus and nitrogen in exchange for the sugars generated by photosynthesis. This relationship is called mycorrhizal derived from the Greek words for fungus mykes and root rhiza, literally “fungus root.” While almost all (~90 percent) plants have mycorrhizal fungal partners, most are either in the form of fungal sheathes surrounding the outside/ecto of the root (ectomycorrhizal – mostly trees), or fungal branches that penetrate into/endo root cells (endomycorrhizal – other plants) to form little tree-like structures called arbuscules. Ericoid mycorrhizas combine the two forms in that they both surround the roots and penetrate the cells so that this effect is even more efficacious. It is now well established that trees and shrubs (like rhododendron) share and balance nutrients to maintain a healthy ecosystem through their interconnecting fungal-root networks; facetiously the “wood wide web.” [15] The effectiveness of the outer and inner “ectendomycorrhizas” of heaths in promoting interconnected communities is such that they can and do completely take over a habitat. This can be a problem when rhododendron are introduced to non-native environments. For example Rhododendron ponticum was introduced to the UK from Iberia in 1763 and has spread to crowd out native trees, covering over three percent of all woodlands. Once established, it is almost impossible to extirpate. [16]
Rhododendrons, in spite of invasive tendencies in some regions, are among the most popular horticultural plants. It is the most diverse genus of the Heath Family with more than a thousand identified species. There is a Global Conservation Consortium for Rhododendron that seeks to promote and protect all species from extinction. Their relevance to the ecosystems is of particular importance to “underpin livelihoods in regions where they protect watersheds and stabilize steep mountain slopes in the areas where some of the most significant river systems in Asia begin.” [17] The rhododendron collection at the renowned Royal Botanical Gardens at Kew is among its most cherished, with over 3,000 species of which 300 are threatened with extinction. They were in many cases discovered, named, bred, and donated by the generation of British plant hunters that plied the globe during the nineteenth century. [18] So far as is known, none of them were affected by mad honey, their virility apparently well established.
References:
1. Brown, R. and Brown, M. Woody Plants of Maryland, Port City Press, Baltimore, Maryland, 1999, pp 247-254.
2. Irving, E. and Hebda, R. “Concerning the Origin and Distribution of Rhododendrons”. Journal of the American Rhododendron Society. 1993 Volume 47 Number 3.
3. Xenophon. “4.8.19–21”. In Brownson CL (ed.). Anabasis. Perseus Hopper. Department of Classics, Tufts University. https://www.perseus.tufts.edu/hopper/text?doc=Xen.%20Anab.%204.8&lang=original
4. Durant, W. Caesar and Christ, The Story of Civilization Volume 3, Simon and Schuster, New York, 1944, pp 516-519.
5. Lane R. and Borzelleca J. “Harming and Helping Through Time: The History of Toxicology”. In Hayes AW (ed.). Principles and methods of toxicology (5th ed.). 2007, Boca Raton: Taylor & Francis.
6. Harris, M. Botanica North America, Harper-Collins, New York, 2003, pp 60-61
7. Demircan A. et al. “Mad honey sex: therapeutic misadventures from an ancient biological weapon”. Annals of Emergency Medicine. 15 August 2009 Volume 54 Number 6 pp 824–829
8. “Grayanotoxins” Bad Bug Book: Handbook of foodborne pathogenic microorganisms and natural toxins (2nd ed.). Food and Drug Administration. 2012. https://www.fda.gov/media/83271/download
9. Dunn, C. “Neurons that connect without synapses” Science 21 April 2023, Volume 280, Issue 6642, , p.241, 293.
10. Jansen S et al . “Grayanotoxin poisoning: ‘mad honey disease’ and beyond”. Cardiovascular Toxicology. 19 April 2012 Volume 12 Number 3 pp 208–215.
11. Popescu, R and Kopp, B. “The genus Rhododendron: an ethnopharmacological and toxicological review”. Journal of Ethnopharmacology Volume 2 May 2013, 147 Number 1 pp 42–62.
12. Ethnobotany database at http://naeb.brit.org/uses/search/?string=rhododendron
13. Duke, J. and Foster, S. Medicinal Plants and Herbs, Houghton-Mifflin, Boston 2000, p. 260.
14. Jansen, op. cit.
15. Kendrick, B. The Fifth Kingdom, Third Edition, Focus Publishing, Newburyport, Massachusetts, 2000, pp 257-278.
16. Simons, P. “A spectacular thug is out of control”. The Guardian. 16 April 2017
17. https://www.globalconservationconsortia.org/gcc/rhododendron/
Hiker's Notebook 