An interesting case of cardiotoxicity due to bufotoxin toad toxin

Next, she engaged in body scan meditation, a specific form of mindfulness practice. This involved deep breathing and mind–body awareness, aimed at relaxation. The subject then inhaled 50 mg of vaporized bufotoxin, derived from the Sonoran Desert Toad (Incilius alvarius), slowly and consistently. This was estimated to contain 10–15 mg of 5-MeO-DMT 20–30% of total dried weight (38).

Modern research in toad medicines

5-MeO-DMT can, therefore, be challenging to navigate, with reports of fear, extreme anxiety, and paranoia (29). Users also describe perceptual isolation, seeing “all white” or “all black” (30). This contrasts to classic psychedelics, like N,N-DMT and LSD, that produce highly detailed, complex mental imagery.

Toad venom bufadienolides and bufotoxins: An updated review

• Right after she stabbed the frog, she got a spray of aerosol from the frog’s skin on her face.
• The medicinal parts of toads mainly include their venom, skin, and clothing.
• Alternatively, toads might not store the bufagenins but rather produce them upon gland discharge by enzymatically cutting the side chain off of the bufotoxins18,19.
• Next, she engaged in body scan meditation, a specific form of mindfulness practice.
• Altogether, one potential explanation for these results is that chemical pollutants in anthropogenic habitats may enhance the production of bufadienolides, which may be either a non-adaptive constraint or an adaptive response.
• IOP pressure was 14 mmHg in the right eye and 15 mmHg in the left eye and Descemet membrane folds, as well as corneal oedema, were in remission.

It was observed that the original toxic drug ingredients are mainly toad toxins and ester soluble constituents. Bufotoxins are a family of toxic steroid lactones or substituted tryptamines of which some are toxic. They occur in the parotoid glands, skin, and poison of many toads (Bufonidae family) and other amphibians, and in some plants and mushrooms.123 The exact composition varies greatly with the specific source of the toxin. Every year, patients with toad poisoning are referred and consulted to the Ramathibodi Poison Center (RPC). The present study was performed to describe and clarify the clinical characteristics and outcomes of patients with toad poisoning in Thailand.

Toad venom as raw materials for drugs

No ventricular tachycardia or ventricular fibrillation were detected in any of the patients. Structurally, bufotenine is an indole hallucinogen that is capable of blocking the action of serotonin, which is the indole amine transmitter of nerve impulses and can be found in normal brain tissue (and in toad poison). Bufotenine also functions as a powerful constrictor of blood vessels, causing a rise in blood pressure.

Angel of human health: current research updates in toad medicine

For example, vaporization induces effects within ~10–15 s and peak experiences within ~2–5 min, resolving within ~25–30 min (6, 22, 23). Conversely, insufflation has a slower onset of action, due to delayed absorption, inducing effects within ~3–4 min and peak experiences within ~35–40 min, resolving within ~60–70 min (24). Irrespective of route, 5-MeO-DMT produces diverse subjective effects, including visual and auditory hallucinations, distorted time perception, and memory impairment (4). It also occasions peak mystical experiences comparable to high-dose psilocybin (25). Ego dissolution, a complete loss of self-identity, is frequently reported, as are profound near-death experiences (22, 25–28).

PTSD checklist for DSM-5

• The subject further endorsed a complete mystical experience, hypothesized to underly 5-MeO-DMT’s therapeutic activity.
• Here, in accordance with CARE (CAse REport) guidelines (31), we present the first real-world, longitudinal case study on 5-MeO-DMT for post-traumatic stress disorder (PTSD).
• Similarly, the juveniles originating from urban habitats showed neither the larger parotoids nor the higher concentration of bufagenins and lower concentration of bufotoxins that we found in their parents.
• The effect of RBG, in toad venom, on cardiac function is stronger, followed by BL and CBG.
• The concentration of dehydrogenation toad tryptamine is higher in the toad skin, while it is low in toad venom.
• In this case study, a single dose of vaporized toad bufotoxin, containing 5-MeO-DMT, led to clinically significant improvements in PTSD, with next-day effects.

The onset of night terrors was not considered bufotoxin effects on humans a ‘serious adverse event’, as its association with 5-MeO-DMT could not be definitively concluded. It neither was life-threatening, required intervention or hospitalization, resulted in persistent or significant disability, nor led to the subject’s death. Animals’ chemical defences are especially under-studied in this context. Like plants, many animal species rely on defensive chemicals or toxins for protection from their natural enemies such as predators, parasites and competitors9. Chemical defence may have important consequences for life-history evolution and ecology, as chemically protected animals can live longer10 and occupy a larger niche space11.

In this case, our urban toads may have had a faster machinery for this process, allowing them to respond more rapidly to a predator attack (i.e. a human squeezing their parotoids). Clarifying the avenues by which anthropogenic environments affect toad chemical defences will take more detailed studies on their toxin physiology. The parotoid is by far the largest toxin gland in toads, and larger parotoids contain more toxins12,18. Thus, our finding that adult toads had larger parotoids in urban and agricultural habitats than in natural habitats suggests that the total amount of stored toxins was higher in the animals captured from anthropogenic habitats.

Also, we cannot rule out that some similarity in habitat effects between the two age groups might have been masked by the minor differences in the methods applied to adults and juveniles to measure parotoids and sample toxins. This similarity in retention-time effects indicates that the disparity between adult and juvenile habitat differences in toxin composition is unlikely to be a methodological artefact (for more details, see Supplementary Results 2.3). Thus, had the same differences by habitat of origin been present in juveniles as in adults, it is likely that we would have been able to detect them (note that we did find differences between the offspring of toads from natural and anthropogenic habitats in several traits other than toxicity27). Therefore, our findings suggest that phenotypic plasticity at the level of individuals may play an important role in the enhanced chemical defences of toads living in anthropogenic habitats. It is possible that anthropogenic environments exert complex selection forces on toads’ chemical defences because of spatio-temporal heterogeneity in pollution27 and predation risk44, which should then favour the evolution and maintenance of phenotypic plasticity9.