Summary And Conclusion
Two-thirds of the existing in vitro studies have reported some degree of increased chromosomal breakage following exposure to illicit or pure LSD. With one exception, these changes were observed with concentrations of LSD and durations of exposure that far exceeded the dosages commonly used in humans. In none of the studies was there a clear dosage-response relationship. Since similar findings have been reported with many commonly used substances, including artificial sweeteners, aspirin, caffeine, phenothiazine tranquillizers and antibiotics, there is no reason why LSD should be singled out and put in a special category. There is no justification for referring to the structural changes of the chromosomes as "chromosomal damage"; their functional relevance and relation to heredity remains to be established. In addition, the fact that the in vitro experiments bypass the excretory and detoxifying systems present in the integral organism casts doubt on the overall relcvanee of the in vitro results.
In the in vivo chromosomal studies, the majority of positive findings was reported in persons who had been exposed to illicit, "alleged" LSD. Dishotsky et al. (28) in their excellent synoptic review of the chromosomal studies made in the past, summarized the existing evidence in the in vivo papers as follows; "In twenty-one in vivo chromosomal studies, a total of 310 subjects were reported. Of these, 126 were treated with pure LSD; the other 184 were exposed to illicit, alleged LSD. Only 18 of 126 (14.3 percent) of the subjects in the pure LSD group were reported to have chromosomal aberration frequencies above mean control rates. In contrast, 89 of 184 (48.9 percent) of the subjects in the illicit LSD group had elevated aberration frequencies. Of all the subjects reported to have chromosomal damage, only 18 of 108 (16.7 percent) were exposed to pure LSD. The frequency of individuals with chromosomal damage reported among illicit drug users was nearly triple that associated with the use of pharmacologically pure LSD." These findings indicate that chromosomal aberrations when found were related to the more general effects of drug abuse and not to LSD per se; it is highly improbable that pure LSD ingested in moderate dosages produces chromosomal aberrations in the white blood cells.
The positive findings in some of the chromosomal studies using human leucocytes were interpreted as indicating genetic damage and danger to future generations. To be of direct genetic relevance, however, the chromosomal damage would have to be demonstrated in the germinal cells, the sperms and ova, or their precursor cells. Several existing studies of the effect of LSD on the meiotic chromosomes have been inconclusive despite the use of excessive dosages. The mutation studies in Drosophila melanogaster indicate no mutagenic effect from 0.28 to 500 micrograms of LSD per cc and a definite mutagenic effect from 2,000-10,000 micrograms of LSD per cc. The fact that truly astronomic dosages have to be used to induce mutations in Drosophila shows LSD as a rather weak mutagen that is unlikely to be mutagenic in any concentration used by human subjects.
In some of the early studies, LSD was implicated as a potential cause of congenital malformations, abortions and fetal wastage. The original reports of teratogenic effects in hamsters, rats and mice have not been confirmed by later studies. The experiments in rodents indicated a rather wide range of individual strain and species susceptibility to the effect? of LSD. It is highly questionable whether and to what extent the results of such investigations can be extrapolated to the situation in humans. There have been six individual cases reported of malformed children born to parents who have used illicit LSD. Only one team of workers reported an increased frequency of congenital malformations in the offspring of illicit LSD users. In regard to the high frequency of unexplained "spontaneous" birth defects and the wide-spread abuse of LSD, the above observations may be coincidental. The increased occurrence of malformations in the LSD users reported in one of the studies may be explained by many other variables characterizing this group, and there is no logical reason to implicate LSD as the single or most important factor. At the present time there is no clear evidence that pure LSD is teratogenic in humans. However, in view of the high vulnerability of the developing fetus to a great variety of substances and conditions, the administration of LSD is contraindicated for the gestation period.
There is no clinical or experimental data demonstrating that LSD has carcinogenic properties, as suggested by some of the early studies. No increase in the incidence of tumors among LSD users has ever been detected. Case reports of leukemia and malignant tumors in the population of LSD users have been exceedingly rare. In the three existing case reports of leukemia, there has been no proof or even indication of a causal relationship, and the association of leukemia with LSD use may have been merely a coincidence.
As this review shows, no convincing experimental or clinical evidence exists to prove that the commonly used dosages of pure LSD produce genetic mutations, congenita) malformations or malignant growths. As far as illicit LSD is concerned, the situation is much more complex, and the results of the studies of illicit LSD users should not be considered relevant to the question of the biological dangers of LSD. Uncertainties about the dosage, and the contamination of black-market samples of psychedelic drugs by various impurities and additives contribute a very important dimension to the already serious psychological hazards associated with unsupervised self-experimentation.
There is absolutely no indication in the research data currently available that responsible experimental and therapeutic use of LSD by experienced professionals should be discontinued.
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