1P LSD first debuted online as a research chemical in 2015. It has been sold as a designer psychedelic drug ever since. Little is known about its invention as academic literature about the substance does not exist prior to its debut online. Due to the lack of analytical, chemical, and pharmacological data on 1P LSD,1p lsd for sale. Conclusive scientific evidence is lacking on its properties, behavior, and risks. However, it is assumed that 1P LSD functions similarly to LSD. According to user accounts, its subjective effects are almost identical.
1P LSD is considered an analogue to LSD. An analogue is a substance that is structurally and functionally similar to the original substance. It was created by modifying the molecular structure of LSD, probably in an attempt to produce a novel derivative of LSD that would technically fall into a legal loophole in many countries. 1P LSD is also a homologue of ALD-52, which means that a molecular chain was added to its parent molecule.
The United States does not control 1P LSD on the federal level. However, it could be considered an analogue, which would make it illegal under the Federal Analogue Act.
What You Will Learn About 1P LSD
1P LSD is a psychedelic substance of the lysergamide class and is considered an analogue of LSD and homologue of ALD-52. It also could be a “prodrug” of LSD.
The legality of 1P LSD varies from country to country. However, it is illegal in 13 countries.
Because it is so closely related to LSD, it is considered relatively safe to use. However, there are increased risks if you have a pre-existing medical condition, heart condition, or are on certain kinds of medications.
1P LSD first appeared online in 2015 as a designer drug. We don’t know who first created it, although some speculate that it was Alexander Shulgin.
What is 1P LSD?
1P LSD is short for 1-propionyl-lysergic acid diethylamide. As an analogue of LSD and homologue of ALD-52, it is classified as a psychedelic substance of the lysergamide class. 1P LSD is made by adding a propionyl group to the nitrogen molecule of LSD’s indole. In other words, it is the same substance as LSD with an additional chemical chain. Recently, it has become available as a research chemical in the form of blotters and powdered material. Typically, it takes 45-90 minutes to begin to feel the effects and lasts anywhere between 8-12 hours,1p lsd for sale.
Though 1P LSD functions similarly to LSD, too little research exists to make definitive claims. However, due to its chemical similarities, it functions as a serotonergic substance. It binds to the 5-HT serotonin receptors in the brain or body. The way LSD binds to the 5-HT2A receptor, in particular, causes a cross-activation of the 5-HT2A receptor heteromer. In other words, this relationship produces long-lasting psychedelic effects. 1P-LSD probably binds with the monoamine receptors responsible for dopamine and norepinephrine but, again, little data exists to back up these claims.
A study from 2015 indicated that 1P-LSD shows 38% the potency of LSD in mice, though the drug did exhibit LSD-like behavior. There is a theory that 1P-LSD may act as a prodrug for LSD, which would mean that it turns into LSD once metabolized in the body. However, more studies need to be conducted in order to determine how 1P-LSD functions and if it is capable of producing its own psychedelic effects.
1P LSD & LSD: What’s the Difference?
Subjectively speaking, users claim that the effects are more or less identical. However, a recent study investigated the similarities and differences in mice. Researchers found that 1P LSD shows 38% of the potency of LSD. This could indicate that 1P LSD is a prodrug, which means that it metabolizes into LSD in the body. The process could make 1P LSD weaker in comparison as well as slower to take effect. According to users, however, this does not seem to accurately reflect their experiences,1p lsd for sale .
1P LSD: has three more carbons and one more oxygen in its molecular structure than LSD has.
Legalities: LSD is an illegal drug in most countries. 1P LSD is a research chemical and is legal.
Effects: 1P LSD may be more stimulating and fast-paced in regard to its physical and cognitive effects. However, overall, the average user expresses that they cannot tell the difference.
Benefits & Risks
Concerning the risks and benefits of 1P LSD, know how much you’re taking and what kind of experience you are looking for. If you’re new to psychedelics, doing it alone might not be advisable. An unfavorable set and setting could potentiate a series of issues.
If you’re taking medications or have a pre-existing condition, particularly those defined as cardiovascular or mental, then consult a trained physician or expert before taking any substance. There is a risk of vasoconstriction in the heart, and psychosis for bipolar disorder and schizophrenia,1p lsd for sale. Furthermore, mixing certain pharmaceutical drugs may counter-interact with 1P LSD as well. Benzodiazepine tends to lower the effectiveness of lysergic acid diethylamide and any other psychedelic substance. Mixing certain antidepressants with LSD can result in serotonin syndrome due to an overload of serotonin in the central nervous system.
Other concerns include HPPD and PTSD. HPPD, or hallucinogen persisting perception disorder, is a disorder where users see “visual snow” long after the trip has ended. This can disrupt an individual’s ability to perform regular tasks due to the distraction caused by visual snow. In more extreme cases HPPD can result in severe hallucinations for prolonged periods of time.
All these factors indicate the need for preparation and forethought to reduce the risks of taking 1P LSD.
Aside from that, the risks of 1P LSD are technically unknown. Since science governs the area of medicine, when we speak about a substance we cannot make definite claims about them unless backed up by science. Personal accounts, even if there are thousands, cannot technically be credited as factual. However, 1P LSD appears to function like LSD, which would make it a relatively low-risk drug since scientific evidence on LSD shows that there are minimal adverse effects.
Top Reported Benefits
Recently, a resurged interest in LSD has led scientists to reconsider the studies that were conducted in the 50s and 60s. Those investigations primarily focused on treating depression, post-traumatic stress disorder, drug dependency, and reducing anxiety in end-of-life patients. Since the effects are similar to LSD, it might be able to address these issues and their associated symptoms.
Ketamine: Also called “Special K,” this animal tranquilizer is sometimes used as a recreational drug by attendees at dance raves and other events. The drug may also effectively combat the symptoms of depression.What to know about ketamine .
Since it suppresses breathing much less than most other available anesthetics, ketamine is used in medicine as an anesthetic; however, due to the hallucinations it may cause, it is not typically used as a primary anesthetic, although it is the anesthetic of choice when reliable ventilation equipment is not available.What to know about ketamine .
Ketamine is frequently used in severely injured people and appears to be safe in this group. A 2011 clinical practice guideline supports the use of ketamine as a dissociative sedative in emergency medicine. It is the drug of choice for people in traumatic shock who are at risk of hypotension. low blood pressure is harmful in people with severe head injury and ketamine is least likely to cause low blood pressure, often even able to prevent it.
The effect of ketamine on the respiratory and circulatory systems is different from that of other anesthetics. When used at anesthetic doses, it will usually stimulate rather than depress the circulatory system. It is sometimes possible to perform ketamine anesthesia without protective measures to the airways. Ketamine is considered relatively safe because protective airway reflexes are preserved.
Ketamine is used as a bronchodilator in the treatment of severe asthma.However, evidence of clinical benefit is limited.What to know about ketamine .
Pain management what to know about ketamine .
Ketamine may be used for postoperative pain management. Low doses of ketamine may reduce morphine use, nausea, and vomiting after surgery.
Ketamine has similar efficacy to opioids in a hospital emergency department setting for management of acute pain and for control of procedural pain.
It may also be used as an intravenous analgesic with opiates to manage otherwise intractable pain, particularly if this pain is neuropathic. It has the added benefit of counteracting spinal sensitization or wind-up phenomena experienced with chronic pain. At these doses, the psychotropic side effects are less apparent and well managed with benzodiazepines. Ketamine is an analgesic that is most effective when used alongside a low-dose opioid; because, while it does have analgesic effects by itself, the doses required for adequate pain relief when it is used as the sole analgesic agent are considerably higher and far more likely to produce disorienting side effects. A review article in 2013 concluded, “despite limitations in the breadth and depth of data available, there is evidence that ketamine may be a viable option for treatment-refractory cancer pain”.
Low-dose ketamine is sometimes used in the treatment of complex regional pain syndrome (CRPS). A 2013 systematic review found only low-quality evidence to support the use of ketamine for CRPS.
Ketamine has been found to be a rapid-acting antidepressant in depression. It also may be effective in decreasing suicidal ideation, although based on lower quality evidence. The antidepressant effects of ketamine were first shown in small studies in 2000 and 2006. They have since been demonstrated and characterized in subsequent studies. A single low, sub-anesthetic dose of ketamine given via intravenous infusion may produce antidepressant effects within four hours in people with depression. These antidepressant effects may persist for up to several weeks following a single infusion. This is in contrast to conventional antidepressants like selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs), which generally require at least several weeks for their benefits to occur and become maximal. Moreover, based on the available preliminary evidence, the magnitude of the antidepressant effects of ketamine appears to be more than double that of conventional antidepressants. On the basis of these findings, a 2017 review described ketamine as the single most important advance in the treatment of depression in over 50 years. It has sparked interest in NMDA receptor antagonists for depression, and has shifted the direction of antidepressant research and development.What to know about ketamine .
Ketamine has not been approved for use as an antidepressant, but its active enantiomer, esketamine, has been. Esketamine was developed as a nasal spray for treatment-resistant depression and is approved for use in the United States. While there is evidence to support the effectiveness of ketamine in treating depression, there is a lack of consensus on optimal dosing and the effects and safety of long-term therapy. Ketamine can produce euphoria and dissociativehallucinogen effects at higher doses, and thus has an abuse potential. Moreover, ketamine has been associated with cognitive deficits, urotoxicity, hepatotoxicity, and other complications in some individuals with long-term use. These undesirable effects may serve to limit the use of ketamine for depression. Dozens of “ketamine clinics” have opened across the United States, where intravenous ketamine is used off-label to treat people with depression. What to know about ketamine .
The use of ketamine is cautioned against in cases of:
Conditions worsened by an increase in blood pressure or heart rate, such as angina, stroke, poorly controlled high blood pressure. Ketamine increases both heart rate and blood pressure.
Psychiatric disorders: Ketamine can cause hallucinations, and therefore may exacerbate the symptoms of certain psychiatric disorders.
Penetrating eye injury: Can increase risk of loss of eye contents, due to increased IOP.
Acute porphyria: Ketamine is considered porphyrinogenic, that is, it may provoke an attack of acute porphyria, a disease of the nervous system, in susceptible people.
Side effects What to know about ketamine .
When administered by trained medical professionals, ketamine is generally safe for those people who are critically ill. Even in these cases, there are known side effects that include one or more of the following:
Central nervous system: Ketamine is traditionally avoided in people with or at risk of intracranial hypertension (ICP) due to concerns about ketamine causing increased intracranial pressure. It does not increase ICP more than opioids.
At anesthetic doses, 10–20% of people experience adverse reactions that occur during emergence from anesthesia, reactions that can manifest as seriously as hallucinations and delirium. These reactions may be less common in some subpopulations, and when administered intramuscularly, and can occur up to 24 hours postoperatively; the chance of this occurring can be reduced by minimizing stimulation to the person during recovery and pretreating with a benzodiazepine, alongside a lower dose of ketamine. People who experience severe reactions may require treatment with a small dose of a short- or ultrashort-acting barbiturate.
Tonic–clonic movements are reported at higher anesthetic doses in greater than 10% of people.
Effects of ketamine on Zebrafish development. Green areas indicate neurons, and increasing doses of ketamine reduced growth of neurons from the spinal cord.
In 1989, psychiatry professor John Olney reported ketamine caused irreversible changes, known as Olney’s lesions, in two small areas of the rat brain. However, the rat brain has significant differences in metabolism from the human brain; therefore such changes may not occur in humans.
The first large-scale, longitudinal study of ketamine users found current frequent (averaging 20 days/month) ketamine users had increased depression and impaired memory by several measures, including verbal, short-term memory, and visual memory. Current infrequent (averaging 3.25 days/month) ketamine users and former ketamine users were not found to differ from controls in memory, attention, and psychological well-being tests. This suggests the infrequent use of ketamine does not cause cognitive deficits, and that any deficits that might occur may be reversible when ketamine use is discontinued. However, abstinent, frequent, and infrequent users all scored higher than controls on a test of delusional symptoms.
Short-term exposure of cultures of GABAergicneurons to ketamine at high concentrations led to a significant loss of differentiated cells in one study, and noncell-death-inducing concentrations of ketamine (10 μg/ml) may still initiate long-term alterations of dendritic arbor in differentiated neurons. The same study also demonstrated chronic (>24 h) administration of ketamine at concentrations as low as 0.01 μg/ml can interfere with the maintenance of dendritic arbor architecture. These results raise the possibility that chronic exposure to low, subanesthetic concentrations of ketamine, while not affecting cell survival, could still impair neuronal maintenance and development.
More recent studies of ketamine-induced neurotoxicity have focused on primates in an attempt to use a more accurate model than rodents. One such study administered daily ketamine doses consistent with typical recreational doses (1 mg/kg IV) to adolescent cynomolgus monkeys for varying periods of time. Decreased locomotor activity and indicators of increased cell death in the prefrontal cortex were detected in monkeys given daily injections for six months, but not those given daily injections for one month. A study conducted on rhesus monkeys found a 24-hour intravenous infusion of ketamine caused signs of brain damage in five-day-old but not 35-day-old animals.
Some neonatal experts do not recommend the use of ketamine as an anesthetic agent in human neonates because of the potential adverse effects it may have on the developing brain. These neurodegenerative changes in early development have been seen with other drugs that share the same mechanism of action of NMDA receptor antagonism as ketamine.
The acute effects of ketamine cause cognitive impairment, including reductions in vigilance, verbal fluency, short-term memory, and executive function, as well as schizophrenia-like perceptual changes.
A 2011 systematic review examined 110 reports of irritative urinary tract symptoms from ketamine recreational use. Urinary tract symptoms have been collectively referred as “ketamine-induced ulcerative cystitis” or “ketamine-induced vesicopathy”, and they include urge incontinence, decreased bladder compliance, decreased bladder volume, detrusor overactivity, and painful blood in urine. Bilateral hydronephrosis and renal papillary necrosis have also been reported in some cases. The pathogenesis of papillary necrosis has been investigated in mice, and mononuclear inflammatory infiltration in the renal papilla resulting from ketamine dependence has been suggested as a possible mechanism.What to know about ketamine .
The time of onset of lower urinary tract symptoms varies depending, in part, on the severity and chronicity of ketamine use; however, it is unclear whether the severity and chronicity of ketamine use correspond linearly to the presentation of these symptoms. All reported cases where the user consumed greater than 5 g/day reported symptoms of the lower urinary tract. Urinary tract symptoms appear to be most common in daily ketamine users who have used the drug recreationally for an extended period of time. These symptoms have presented in only one case of medical use of ketamine. However, following dose reduction, the symptoms remitted.
Management of these symptoms primarily involves ketamine cessation, for which compliance is low. Other treatments have been used, including antibiotics, NSAIDs, steroids, anticholinergics, and cystodistension. Both hyaluronic acid instillation and combined pentosan polysulfate and ketamine cessation have been shown to provide relief in some people, but in the latter case, it is unclear whether relief resulted from ketamine cessation, administration of pentosan polysulfate, or both. Further follow-up is required to fully assess the efficacy of these treatments.
In case reports of three people treated with esketamine for relief of chronic pain, liver enzyme abnormalities occurred following repeat treatment with ketamine infusions, with the liver enzyme values returning below the upper reference limit of normal range on cessation of the drug. The result suggests liver enzymes must be monitored during such treatment.
Radar plot showing relative physical harm, social harm, and dependence of ketamine
Ketamine’s potential for dependence has been established in various operant conditioning paradigms, including conditioned place preference and self-administration; further, rats demonstrate locomotor sensitization following repeated exposure to ketamine. Increased subjective feelings of ‘high’ have been observed in healthy human volunteers exposed to ketamine. Additionally, the rapid onset of effects following smoking, insufflation, and/or intramuscular injection is thought to increase the drug’s recreational use potential. The short duration of effects promotes bingeing; tolerance can develop; and withdrawal symptoms, including anxiety, shaking, and palpitations, may be present in some daily users following cessation of use.What to know about ketamine .
Ketamine can cause a variety of urinary tract problems that are more likely to occur with heavier and/or higher dosed use, especially in those not watching for a healthy lifestyle, according to a UK study.