Lysergic Acid Diethylamide in Pregnancy and Breastfeeding
Fetal Risk Summary
Lysergic acid diethylamide (LSD, lysergide) is a chemical used for its hallucinogenic properties. The drug does not have a legal indication in the United States. Illicitly obtained LSD is commonly adulterated with a variety of other chemicals (e.g., amphetamines) (1,2). In some cases, doses sold illicitly as LSD may contain little or none of the chemical; as a result, the actual amount of LSD ingested cannot be determined (1). In addition, persons consuming the hallucinogen often consume multiple abuse drugs simultaneously, such as marijuana, opiates, alcohol, amphetamines, STP (dimethyloxyamphetamine, or DOM, a synthetic hallucinogen), barbiturates, cocaine, and other prescription and nonprescription substances. Further complicating the situation are the lifestyles that some of these persons live, which are often not conducive to good fetal health. As a consequence, the effects of pure LSD on the human fetus can only be evaluated by examining those cases in which the chemical was administered under strict medical supervision. These cases, however, are few in number. Most data are composed of sample populations who ingested the chemical in an unsupervised environment. Correct interpretation of this latter material is extremely difficult and, although cited in this monograph, must be viewed cautiously.
The passage of LSD across the human placenta has not been studied. The molecular weight of the chemical, approximately 323, is low enough, however, that rapid passage to the fetus should be expected. LSD has been shown to cross the placenta in mice with early 1st trimester fetal levels averaging 5 times the levels measured in late gestation (3).
Concerns with fetal exposure to LSD have primarily focused on chromosomal damage (both chromatid-type and chromosome-type abnormalities), an increased risk of spontaneous abortions, and congenital malformations. These topics are discussed in the sections below.
A 1967 report was the first to claim that the use of LSD could cause chromosomal abnormalities in human leukocytes (4). Because these abnormalities could potentially result in carcinogenic, mutagenic, and teratogenic effects in current or future generations, at least 25 studies were published in the next 7 years. These studies were the subject of three reviews published in the 1970s with all three arriving at similar conclusions (2,5,6). First, in the majority of studies, the addition of LSD to cells in vitro caused chromosomal breakage, but a dose-response relationship was not always apparent. The clinical relevance of the in vitro studies was questionable because pure LSD was used, usually with much higher levels than could be achieved in humans, and the in vitro systems lacked the normal protective mechanisms of metabolism and excretion that are present in the body. Second, only a slight transitory increase in chromosomal breaks was seen in a small percentage (14%) of the subjects administered pure LSD. A much higher percentage of persons (49%) consuming illicit LSD was observed to have chromosomal damage. The abnormalities in this latter group were probably related to the effects of multiple drug abuse and not to LSD alone. Four prospective studies found no definitive evidence that LSD damages lymphocyte chromosomes in vitro (2). Third, there was no evidence that the chromosomal defects observed in illicit LSD users were expressed as an increased incidence of leukemias or other neoplasia. Fourth, mutagenic changes were only observed in experimental organisms (e.g., Drosophila) when massive doses (2,00010,000 g/ml) were used. Because of this, LSD was believed to be a weak mutagen, but mutagenicity was thought to be unlikely after exposure to any concentration used by humans (5). Finally, the reviewers found no compelling evidence for a teratogenic effect of LSD, either in animals or humans.
A 1974 investigation involving 50 psychiatric patients, who had been treated for varying intervals under controlled conditions with pure LSD, provided further confirmation that the chemical does not cause chromosomal damage (7). Chromosomal analyses of these patients were compared with those of 50 nonexposed controls matched for age, sex, and marital status. The analysis was blinded so that the investigators did not know the origin of the samples. No significant difference between the groups in chromosomal abnormalities was observed. In another 1974 Reference (not included in the previously cited reviews), involving only two subjects, no evidence of chromosomal damage was found in their normal offspring (8). The two women had been treated medically with pure LSD before pregnancy. Thus, the predominance of evidence indicates that LSD does not induce chromosomal aberrations, and even if it did, it has no clinical significance to the fetus.
The question of whether fetal wastage could be induced by LSD exposure was investigated in a study published in 1970 (9). This investigation involved 148 pregnancies (81 patients) in which either the father (N=60) or the mother (N=21) had ingested LSD. In 12 pregnancies, exposure occurred both before and during pregnancy. In the 136 pregnancies in which the exposure occurred only before conception, 118 involved the administration of pure LSD (the medical group) and 18 involved both medical and illicit LSD exposure (the combined group). The spontaneous abortion rates for these two populations were 14% (17 of 118) and 28% (5 of 18), respectively. In 83 of the pregnancies, only the father had been exposed to LSD. Excluding these, the incidences of fetal loss for the medical and combined groups are 26% (11 of 43) and 40% (4 of 10), respectively. In the 12 pregnancies in which LSD was consumed both before and during gestation, 3 were in the medical group and 9 were in the combined group. The frequency of spontaneous abortions in these cases was 33% (1 of 3) and 56% (5 of 9). In the combined sample, however, one woman accounted for five abortions and one liveborn infant. If she is excluded, the incidence of fetal wastage in the combined group is zero.
In the medical group, the number of women (12 of 46; 26%) with fetal wastage is high. However, 25 of these pregnancies occurred in women undergoing psychotherapy, and 21 occurred in an experimental setting (9). The number of spontaneous abortions in the psychotherapy group (N=9) (36%) was more than twice the incidence in the experimental sample (N=3) (14%). The authors speculated that the greater frequency of fetal wastage in the women undergoing psychotherapy may have been caused by the greater emotional stress that often accompanies such therapy. The increased rate in the combined sample (9 of 19; 47%) was probably caused by the use of multiple abuse drugs, other nondrug factors, and the inclusion of one woman with five abortions and one live birth. Exclusion of this latter patient decreases the combined sample incidence to 31% (4 of 13). Thus, although other studies examining the incidence of spontaneous abortions in LSD-exposed women have not been located, it appears unlikely that pure LSD administered in a controlled condition is an abortifacient. The increased rate of fetal wastage that was observed in the 1970 study was probably caused by a combination of factors, rather than only to the ingestion of LSD.
A number of case reports have described LSD use in pregnancies ending with poor outcomes since the first report in 1967 of an exposed infant with major malformations (10,11,12,13,14,15,16,17,18,19,20,21,22,23,24 and 25). All of these reports, however, are biased in the respect that malformed infants exposed in utero to LSD are much more likely to be reported than exposed normal infants and are also more frequently reported than nonexposed malformed infants (2). Most of the reports either involved multiple drug exposures, including abuse drugs, or other drug exposures could probably be deduced because of the illicit nature of LSD. With these cautions, the reports are briefly described below.
The first mention of an anomaly observed in an infant exposed in utero to LSD appeared in a 1967 editorial (10). The editorial, citing a report in a lay publication, briefly described a case of LSD exposure in a pregnancy that ended in a malformed infant with megacolon. Apparently, details of this case have never been published in the medical literature.
The first case report in the medical literature also appeared in 1967 and involved a female infant with unilateral fibular aplastic syndrome (11,12). The mother had taken LSD 4 times between the 25th and 98th days of gestation with one dose occurring during the time of most active lower limb differentiation (11). Defects in the infant, which were characteristic of the syndrome, included absence of the fibula and lateral rays of the foot, anterior bowing of the shortened tibia, shortening of the femur, and dislocated hip. A second case involving limb defects and LSD exposure was published in 1968 (13). The infant, with a right terminal transverse acheiria defect (absence of the hand), was the offspring of a woman who had taken LSD both before and during early gestation. She had also smoked marijuana throughout the pregnancy and had taken a combination product containing dicyclomine, doxylamine, and pyridoxine for 1st trimester nausea. Another infant with a terminal transverse deficit, also exposed to LSD and marijuana, was described in 1969 (14). The defect involved portions of the fingers on the left hand, syndactyly of the right hand with shortened fingers, and talipes equinovarus of the left foot. Two of these same authors described another exposed infant with amputation deformities of the third finger of the right hand and the third toe of the left foot (15). A critique of these latter three case histories concluded that the defects in the infants could have been caused by amniotic band syndrome (26). Limb defects and intrauterine growth retardation were observed in an offspring of a malnourished mother who had used LSD, marijuana, methadone, and cigarettes during gestation (16). The anomalies consisted of partial adactyly of the hands and feet, syndactyly of the remaining fingers, and defective formation of the legs and forearms. In a study of 140 women using LSD and marijuana followed up through 148 pregnancies, 8 of 83 liveborn infants had major defects, as did 4 of 14 embryos examined after induced abortion (17). The incidence of defects in this sample was 8.1% (12 of 148) and may have been higher if the other abortuses had been examined. Only one of the liveborn infants had a limb defect (absence of both feet) combined with spina bifida occulta and hemangiomas. Defects in the other 7 infants were: myelomeningocele with hydrocephalus in 3 babies (1 with clubfoot); tetralogy of Fallot; hydrocephalus; right kidney neuroblastoma; and hydrocephalus and congestive heart failure. A limb defect was one of several anomalies found in a male infant whose mother ingested LSD both before and during gestation (18). The abnormalities included absent left arm, syndactyly, anencephaly with ectopic placenta, cleft lip and palate, coloboma of the iris, cataract, and corneal opacity with vascularization. At least one author thought the limb and cranial defects in this latter case may have been caused by amniotic band syndrome (27). This opinion was contested by the original authors, who stated that the limb defects were true aplasia and not an amputation deformity (28). Similarly, they claimed that the cranial anomaly was not a form of encephalocele, which an amniotic band could have caused, but a true anencephaly (28). Congenital anomalies were observed in 11 of 120 liveborn infants in a previously cited study that examined the effects of LSD on spontaneous abortions and other pregnancy outcomes (9). Nine of the 11 infants had limb defects that were, in most cases, easily correctable with either special shoes or casts. None of the 11 cases appears to be related to LSD exposure. The defects were (the number of cases and possible causes are shown in parentheses): turned-in feet (6 cases, 4 familial, 2 unknown); crimped ureter (1 case, familial); tibial rotation (2 cases, 2 familial); pyloric stenosis (1 case, possibly genetic); bone deformity of legs and deafness (1 case, postrubella syndrome) (9).
Other infants with ocular defects, in addition to the case mentioned immediately above, have been described. A mother who ingested LSD, marijuana, meprobamate, amphetamines, and hydrochlorothiazide throughout pregnancy delivered an infant with generalized hypotonia, a high-pitched cry, brachycephaly with widely separated sutures, bilateral cephalohematomas, a right eye smaller than the left and with a cataract, and overlapping second and third toes (19). Two other cases of ocular defects were published in 1978 and 1980 (20,21). In one case, a premature female infant was delivered from a 16-year-old mother who had consumed LSD, cocaine, and heroin during the 1st trimester (20). The infant, who died 1 hour after birth, had microphthalmos, intraocular cartilage, cataract, persistent hyperplastic primary vitreous, and retinal dysplasia. A hypoplastic left lung and a defect in the diaphragm were also noted. The second case involved another premature female infant born to a mother enrolled in a methadone program who also used LSD (21). The infant had left anophthalmia but no other defects.
Various other malformations have been reported after in utero LSD exposure (22,23,24 and 25). Complete exstrophy of the bladder, epispadias, widely separated pubic rami, and bilateral inguinal hernias were observed in a newborn exposed to LSD, marijuana, and mephentermine (22). The mother had consumed LSD 1215 times during an interval extending from 2 months before conception to 2.5 months into pregnancy. A mother, who ingested LSD at the time of conception, produced a female infant with multiple defects including a short neck, left hemithorax smaller than the right, protuberant abdomen because of a severe thoracolumbar lordosis, a thoracolumbar rachischisis, craniolacunia, long fingers, clubfeet, and defects of the urinary tract and brain (23). The infant died at 41 days of age. Other drug exposures consisted of cigarettes, an estrogen preparation (type not specified) that was used unsuccessfully to induce menstruation, and medroxyprogesterone for 1st trimester bleeding. Because the case resembled a previously described cluster of unusual defects (i.e., spondylothoracic dysplasia, Jarcho-Levin syndrome), which is caused by an autosomal recessive mode of inheritance, the authors could not exclude this mechanism. In a case of a female infant with multiple anomalies compatible with trisomy 13 with D/D translocation, the mother had last used LSD 9 months before conception (24). She had also used marijuana, barbiturates, and amphetamines throughout gestation and, presumably, before conception. The authors theorized that the defect may have been caused by LSD-induced damage to maternal germ cells before fertilization. A 1971 study evaluated 47 infants born to parents who had used LSD (25). Maternal use of the drug could be documented in only 30 of the cases and multiple other abuse drugs were consumed. Abnormalities observed in 8 (17%) of the infants were transient hearing loss and ventricular septal defect, cortical blindness, tracheoesophageal fistula, congenital heart disease (type not specified), congenital neuroblastoma, spastic diplegia, and seizure disorders in 2 infants.
Two other case reports involving the combined use of LSD and marijuana with resulting adverse fetal outcomes do not appear to have any relationship to either drug (29,30). One of these involved a report of six infants with persistent ductus arteriosus, one of whom was exposed to LSD and marijuana during early gestation (29). The history of maternal drug use was coincidental. The second case described an infant who died at 2.5 months of age of a bilateral in utero cerebral vascular accident and resulting porencephaly (30). The mother had used LSD, marijuana, alcohol, and other abuse drugs, including cocaine. This latter drug was thought to be the causative agent.
In contrast to the above reports, a large body of research has been published describing the maternal (and paternal) ingestion of LSD without apparent fetal consequences (1,7,8 and 9,31,32,33,34,35 and 36). A number of reviews have also examined the teratogenic potential of the chemical and have concluded that a causal relationship between congenital malformations and LSD does not exist (2,5,6,37,38,39,40,41,42,43,44 and 45). (See Reference 6 for an excellent critique of the early investigations in laboratory animals.) In summary, the available data indicate that pure LSD does not cause chromosomal abnormalities, spontaneous abortions, or congenital malformations. There have been no cases published of fetal anomalies when only pure LSD was administered under medical supervision. Early descriptions of congenital abnormalities involved patients who had used or were using illicit LSD and are believed to be examples of reporting bias, the effects of multiple drugs, or other nondrug factors. However, long-term follow-up of exposed infants has never been reported. This is an area that warrants additional research.
Breast Feeding Summary
No reports have been located concerning the passage of lysergic acid diethylamide into breast milk. However, because the drug has a relatively low molecular weight (approximately 323), which should allow its passage into milk, and because its psychotomimetic effects are produced at extremely low concentrations, the use of LSD during lactation is contraindicated.
- Warren RJ, Rimoin DL, Sly WS. LSD exposure in utero. Pediatrics 1970;45:4669.
- Matsuyama SS, Jarvik LF. Cytogenetic effects of psychoactive drugs. Mod Probl Pharmacopsychiatry 1975;10:99132.
- Idanpaan-Heikkila JE, Schoolar JC. LSD: Autoradiographic study on the placental transfer and tissue distribution in mice. Science 1969;164:12957.
- Cohen MM, Marinello MJ, Back N. Chromosomal damage in human leukocytes induced by lysergic acid diethylamide. Science 1967;155:14179.
- Dishotsky NI, Loughman WD, Mogar RE, Lipscomb WR. LSD and genetic damage: Is LSD chromosome damaging, carcinogenic, mutagenic, or teratogenic? Science 1971;172:43140.
- Long SY. Does LSD induce chromosomal damage and malformations? A review of the literature. Teratology 1972;6:7590.
- Robinson JT, Chitham RG, Greenwood RM, Taylor JW. Chromosome aberrations and LSD: a controlled study in 50 psychiatric patients. Br J Psychiatry 1974;125:23844.
- Fernandez J, Brennan T, Masterson J, Power M. Cytogenetic studies in the offspring of LSD users. Br J Psychiatry 1974;124:2968.
- McGlothlin WH, Sparkes RS, Arnold DO. Effect of LSD on human pregnancy. JAMA 1970;212:14837.
- Anonymous. Hallucinogen and teratogen? Lancet 1967;2:5045.
- Zellweger H, McDonald JS, Abbo G. Is lysergic-acid diethylamide a teratogen? Lancet 1967;2:10668.
- Zellweger H, McDonald JS, Abbo G. Is lysergide a teratogen? Lancet 1967;2:1306.
- Hecht F, Beals RK, Lees MH, Jolly H, Roberts P. Lysergic-acid-diethylamide and cannabis as possible teratogens in man. Lancet 1968;2:1087.
- Carakushansky G, Neu RL, Gardner LI. Lysergide and cannabis as possible teratogens in man. Lancet 1969;1:1501.
- Assemany SR, Neu RL, Gardner LI. Deformities in a child whose mother took L.S.D. Lancet 1970;1:1290.
- Jeanbart P, Berard MJ. A propos d'un cas personnel de malformations congenitales possiblement dues au LSD-25: revue de la litterature. Union Med Can 1971;100:91929.
- Jacobson CB, Berlin CM. Possible reproductive detriment in LSD users. JAMA 1972;222:136773.
- Apple DJ, Bennett TO. Multiple systemic and ocular malformations associated with maternal LSD usage. Arch Ophthalmol 1974;92:3013.
- Bogdanoff B, Rorke LB, Yanoff M, Warren WS. Brain and eye abnormalities: possible sequelae to prenatal use of multiple drugs including LSD. Am J Dis Child 1972;123:1458.
- Chan CC, Fishman M, Egbert PR. Multiple ocular anomalies associated with maternal LSD ingestion. Arch Ophthalmol 1978;96:2824.
- Margolis S, Martin L. Anophthalmia in an infant of parents using LSD. Ann Ophthalmol 1980;12:137881.
- Gelehrter TD. Lysergic acid diethylamide (LSD) and exstrophy of the bladder. J Pediatr 1970;77:10656.
- Eller JL, Morton JM. Bizarre deformities in offspring of user of lysergic acid diethylamide. N Engl J Med 1970;283:3957.
- Hsu LY, Strauss L, Hirschhorn K. Chromosome abnormality in offspring of LSD user: D trisomy with D/D translocation. JAMA 1970;211:98790.
- Dumars KW Jr. Parental drug usage: effect upon chromosomes of progeny. Pediatrics 1971;47:103741.
- Blanc WA, Mattison DR, Kane R, Chauhan P. L.S.D., intrauterine amputations, and amniotic-band syndrome. Lancet 1971;2:1589.
- Holmes LB. Ocular malformations associated with maternal LSD usage. Arch Ophthalmol 1975;93:1061.
- Apple DJ. Ocular malformations associated with maternal LSD usage (in reply). Arch Ophthalmol 1975;93:1061.
- Brown R, Pickering D. Persistent transitional circulation. Arch Dis Child 1974;49:8835.
- Tenorio GM, Nazvi M, Bickers GH, Hubbird RH. Intrauterine stroke and maternal polydrug abuse. Clin Pediatr 1988;27:5657.
- Cohen MM, Hirschhorn K, Frosch WA. In vivo and in vitro chromosomal damage induced by LSD-25. N Engl J Med 1967;277:10439.
- Sato H, Pergament E. Is lysergide a teratogen? Lancet 1968;1:63940.
- Egozcue J, Irwin S, Maruffo CA. Chromosomal damage in LSD users. JAMA 1968;204:2148.
- Cohen MM, Hirschhorn K, Verbo S, Frosch WA, Groeschel MM. The effect of LSD-25 on the chromosomes of children exposed in utero. Pediatr Res 1968;2:48692.
- Hulten M, Lindsten J, Lidberg L, Ekelund H. Studies on mitotic and meiotic chromosomes in subjects exposed to LSD. Ann Genet (Paris) 1968;11:20110.
- Aase JM, Laestadius N, Smith DW. Children of mothers who took L.S.D. in pregnancy. Lancet 1970;2:1001.
- Hoffer A. Effect of LSD on chromosomes. Can Med Assoc J 1968;98:466.
- Smart RG, Bateman K. The chromosomal and teratogenic effects of lysergic acid diethylamide: a review of the current literature. Can Med Assoc J 1968;99:80510.
- Rennert OM. Drug-induced somatic alterations. Clin Obstet Gynecol 1975;18:18598.
- Glass L, Evans HE. Perinatal drug abuse. Pediatr Ann 1979;8:8492.
- VanBlerk GA, Majerus TC, Myers RAM. Teratogenic potential of some psychopharmacologic drugs: a brief review. Int J Gynaecol Obstet 1980;17:399402.
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- Stern L. In vivo assessment of the teratogenic potential of drugs in humans. Obstet Gynecol 1981;58:3S8S.
- Lee CC, Chiang CN. Maternal-fetal transfer of abused substances: pharmacokinetic and pharmacodynamic data. Natl Inst Drug Abuse Res Monogr Ser 1985;60:11047.
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Questions and Answers
What is Lysergic acid diethylamide (LSD) used for?, What is What is Lysergic acid diethylamide (LSD) used for, I know it is a common drug also known as acid which is a really strong hullucinogen. However does it have any actual purpose in society or is it just used to get high on an have crazy trips.
It was thought to be a new tool in the CIA's arsenal and was used in experiments to determine if it could be used as a novel 'truth' serum. The Sunshine act has revealed to interested parties the unclassified results of these disastrous tests. Beware of reports telling of religious experiences and mind expanding trips. Dosage varies among individuals and purity of this illegal drug has caused many cases of psychosis.
Have you ever tried Lysergic acid diethylamide when you were younger?, Lysergic acid diethylamide (LSD)
I have done LSD many times and every time it was great! First time I was 13 and was a little scary but still as cool. Just watch that now a days people use strychnine instead.
Do you trip on Lysergic ACID Diethylamide?, What was your best trip like? What was your worst trip like? Did LSD change your life as it does for myself and millions of others? If I take a cross country trip, where are some relaxing places with good vibes and beautiful views that I should stop at to smoke a bowl/drop acid?
I tripped, but never actually hallucinated. It got me through one of the worst times of my life, but I gave it up because it made me feel so good that I could easily have become psychologically addicted.
Best place: anywhere near a stream. My personal best: on a large fallen trunk across a small stream near Racine, Wisconsin.
What does the first "d" in d-lysergic acid diethylamide mean?, I've been trying to find this out. It's probably something completely obvious to somebody who knows chemistry, but unfortunately, I do not fall under that category. I tried googling for it, and even taking a different approach by researching a possible chemical prefix (if those exist) of the letter "d", and I didn't find anything that way. So, I figured I'd ask on here. :)
D = Diastereomer
This is a sort of mirror image that is slightly twisted.
Read the wiki link for more...
What do you know/think about lysergic acid diethylamide?, I respectfully ask that you summarize what you know about LSD. Personal opinions are welcome, but I would appreciate it if responses were unbiased (prejudice against OR in favor of) and thoughtful.
Also, please do not give me a link to erowid or wikipedia. I am aware that they have a wealth of information, but I am most interested in what people know and think about the substance.
It is a dangerous drug that can cause permanent damage and result in mental illness like schizophrenia. That being said as a child of the 70's I must admit that I did a tab one night(cause I was dumb) and it was actually horrible. I flicked the ash off my cigarette and it looked like ants were pouring out of the ashtray. I went to the bedroom to lay down and close my eyes and I thought the bed had swallowed me. I went to the fridge to get some water and all the condiments like mustard, mayo, and ketchup seemed to be dripping thought the selves and onto the floor. Once was all it took for me and I am forever grateful(especially since I am a nurse and have seen the effects first hand) that I didn't have any permanent damage of any kind.
Whats the natural source of Lysergic acid diethylamide (LSD)?, Whats the natural source of Lysergic acid diethylamide (LSD), what products are used in making and processing LSD?
fyi I don't plan on making it just need it for a paper for chemistry
LSD does not occur naturally.
Only LSA and ergotamine . Both can be turned into LSD.
Albert Hoffman did LSD from ergotamine.
Ergotamine is in Ergot.
You cant make LSD without lab equipment ( very expensive one)
Ergot is a poison. And if ingested will cause hallucinations and awful pain. Somehow ergot closes the blood vessels and it causes loss of limbs(even in minimal doses)
Outbreaks of ergot fungus plagued Europe many times and were associated with witchcraft.
How do I make d-lysergic acid diethylamide?,
Seriously, don't. And it is not because I am opposed to LSD. (I am.)
Even if I gave you the procedure, it is not like a recipe. It has to be followed very carefully and skilfully or there will be impurities.
A chemist, like me, is the only person who should try something like this. And a chemist would not have to ask how to do it.
It's not like cooking up some soup. The impurities that will certainly could poison you or drive you crazy.
Is Their Any way To Make LSD (Lysergic acid diethylamide) with common household items ?, is thier any way to Make LSD or acid without using any crazy chemicals, jsut simple household items ?
No. Why would you think that would be possible?
Here's one way to make it: http://www.erowid.org/library/books_onli...
Why should LSD (Lysergic acid diethylamide, or "acid") be made legal in the USA?,
All drugs should be legal. Nobody should have the right to tell me what I can and cannot put into my body. You should be able to buy LSD at your local pharmacy. One trip per customer.
Of course, conservatives and republicans simply couldn't allow the general population to actually think that we are all "one", and that love is the answer. That would be a nightmare for them.