This would allow researchers to control for covariates, like age and gender, while examining potential underlying mechanisms, such as mystical experiences. The longitudinal nature of this case study serves as its primary strength, with repeated observations collected over a 1-year period. Findings are more robust, given the subject’s treatment resistance and disease chronicity, the complexity of this clinical population, and the limitation in available effective, evidence-based interventions.
Further, the presence of psychiatric comorbidities, the lack of polypharmacy or medication washout, and the naturalistic setting better reflect patients in the real world. The use of well-validated measures, capturing both subject- and clinician-reported changes, is an additional strength. Guided by the facilitator, she first set an intention for the experience. “I want to understand and accept the roots of my trauma.” This was designed to help navigate potentially difficult psychedelic states and material, by re-centering the subject’s attention.
- We carried out a retrospective study of patients with toad poisoning from the Ramathibodi Poison Center Toxic Exposure Surveillance System during a 5-year period (2012–2016).
- Slit lamp examination showed conjunctival hyperaemia and signs of ocular hypotonia.
- Therefore, there should be more scientific and economic value for toad medicines that will guarantee the prosperity of the biosphere on earth, and hence, safeguard the health of humans.
- At this age they are large enough (ca. 4 g) for measuring parotoid size (ca. 7.5 mm long and 2.5 mm wide) and their gonads are developed enough for sex identification.
- We hand-collected toads at each pond at the start of the spawning season, between 16 and 28 March 2017.
- Although we have no data on predator densities at our study sites, ample literature shows that generally both urban and agricultural environments differ from natural habitats in the composition of predator fauna44,45.
Toads phenotypically adjust their chemical defences to anthropogenic habitat change
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.
Other activity
- These results parallel the earlier experimental findings on toad tadpoles that herbicide exposure increases their bufadienolide content26.
- Furthermore, higher toxicity of toads may negatively affect other species too.
- In particular, she exhibited disruptive trauma- and stress-related psychopathology, with symptoms considerably impairing her behavior and function.
- Zhao Dazhou et al 20 did a comparative study on toad diene lactone compounds and their concentration in the toad venom and the toad skin, and found that both contain the same diene lactone composition that mainly includes four indole alkaloids.
- Meta-analytic means with 95% confidence intervals (CI) express the standardized differences between natural and anthropogenic habitats in bufadienolide concentrations (amount of each compound per unit dry mass of toxin sample).
- An adult common toad, with the length and width of the left parotoid gland shown by yellow lines.
- Bufadienolides, naturally found in toad venoms having steroid-like structures, reveal antiproliferative effects at low doses.
Cardiac glycoside poisoning can occur from ingestion of various plants and animal toxins, and the venom gland of cane toad (Bufo marinus) contains large quantities of cardiac glycosides. Toad venom, a constituent of an aphrodisiac, was considered responsible for the development of clinical manifestations and death in this patient. Digoxin specific Fab fragment has been reported to be beneficial in the treatment of toad venom poisoning. This report alerts physicians to the need to be aware of a new community toxic exposure, as prompt treatment with digoxin specific Fab fragment may be life saving.
The chemical composition of toad skin
The issues related to extraction, identification, and quantification are separated into another section. The common toad, or European toad (Bufo bufo), is an amphibian found in almost all of Europe (with the exception of Iceland, Ireland, and some Mediterranean islands) and in parts of North Asia and North-west Africa. It can live up to 50 years in captivity, and its age is counted by growth rings on their phalanges 1. It has green-gray-brown skin covered with lumps that produce bufadienolides.
Toad Poisoning: Clinical Characteristics and Outcomes
The clinician observed the subject for a total of 5 h after her 5-MeO-DMT experience, and conducted follow-ups via phone 24, 36, and 72 h later, before switching to once a month. A bufotoxin effects on humans total of 36 patients from 24 RPC telephone consultations were included; patient characteristics are summarized in Table 1. No patients were excluded from the study; that is, none of the patients had coingested other drugs or substances with toads. All patients had ingested toads as food, except four patients; one child accidentally ingested toad skin secretion when she caught an alive toad, another child caught an alive toad and then bit the toad. For the other 2 patients, one ingested dried meat of one toad as a health supplement, and the other patient deliberately ingested toad pickled eggs after arguing with her spouse as the intentional ingestion.
The main composition of dry toad, toad skin and toad clothing compared to toad venom is basically the same; however, the difference in the concentration of the components is large. Thus, the differences in pharmacological functions and clinical applications of the varied toad medicines are very distinct. However, the antidote might not be required in all instances of toad poisoning, especially for ingesting the animal itself rather than the processed or dried toxin. Further study and more patient data are needed to determine the specific indications for and doses of DsFab for toad poisoning. At the first presentation, 34 patients reported GI symptoms including nausea, vomiting, and abdominal pain -after ingestion. The other two patients did not have GI symptoms noted in their records; one presented with cardiac arrest and the other had agitation with severe bradycardia and developed cardiac arrest shortly after arrival in the emergency room (ER).
This scenario is supported by our results that bufagenins, the typically more toxic compounds19,23, were present in higher concentrations in the parotoid secretion of adult toads from urban as well as agricultural habitats, compared to their counterparts from natural habitats. This difference was particularly prominent for urban habitats (i.e. almost twice as large effect size as for agricultural habitats), where the increase in bufagenins seems to have come at the expense of bufotoxins. It is thus possible that urban toads invest more heavily into producing and storing higher amounts of the more potent compounds even at the price of having to deal with higher autotoxicity18. 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.