Просветление⁠⁠

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5603820/
цитата:
Autonomic and Adverse Effects

LSD moderately increased blood pressure, heart rate, body temperature, and pupil size (Dolder et al, 2016; Kaelen et al, 2015; Schmid et al, 2015). The sympathomimetic effects of 100 and 200 μg doses of LSD were similar (Dolder et al, 2016, 2017) and less pronounced than those of MDMA and stimulants (Hysek et al, 2014b). Acute adverse effects up to 10–24 h after LSD administration included difficulty concentrating, headache, dizziness, lack of appetite, dry mouth, nausea, imbalance, and feeling exhausted. Headaches and exhaustion may last up to 72 h (Dolder et al, 2016; Schmid et al, 2015). No severe adverse reactions were reported in modern LSD studies (Carhart-Harris et al, 2016b; Dolder et al, 2016; Kaelen et al, 2015; Preller et al, 2017; Schmid et al, 2015). This is consistent with the view that LSD is relatively safe when used in medical settings and according to safety guidelines (Johnson et al, 2008). LSD is physically non-toxic, but there are psychological risks especially when it is used in unsupervised settings. In addition, it is important to note that many novel hallucinogens are being used and may even be sold as LSD but have a different pharmacology and possibly risk profile than LSD (Rickli et al, 2015, 2016). LSD has typically been reported to produce flashbacks. Flashbacks after LSD can be defined as episodic and short (seconds or minutes) replications of elements of previous substance-related experiences (Holland and Passie, 2011). In a web-based survey among hallucinogen users, greater past LSD use was a predictor of the probability of experiencing unusual substance-free visual experiences (Baggott et al, 2011). Clinically significant flashbacks are also defined as hallucinogen persisting perception disorder (HPPD). This disorder is considered rare and occurs almost exclusively in the context of illicit recreational use or/and in patients with anxiety disorders and it typically will have a limited course of months to a year (Halpern and Pope, 1999; Holland and Passie, 2011; Johnson et al, 2008). In controlled non-therapeutic research settings, psilocybin did not produce HPPD or flashbacks (Studerus et al, 2011). However, the prevalence and relevance of HPPD is unclear and needs to be studied (Halpern et al, 2016).

Endocrine Effects

LSD acutely increased plasma concentrations of cortisol (Strajhar et al, 2016), prolactin, oxytocin, and epinephrine (Schmid et al, 2015). LSD does not increase plasma concentrations of norepinephrine (Schmid et al, 2015), testosterone, or progesterone (Strajhar et al, 2016). The endocrine effects of LSD are consistent with those of other serotonergic substances including psilocybin, DMT, and MDMA (Hasler et al, 2004; Hysek et al, 2014b; Seibert et al, 2014; Strassman and Qualls, 1994a).

Model Psychosis

LSD (75 μg, i.v.) increased subjective ratings of cognitive disorganization and delusional thinking (Carhart-Harris et al, 2016b). Disordered cognition has been suggested to be a more fundamental characteristic of LSD’s effects than positive or negative mood (Carhart-Harris et al, 2016b). Nevertheless, the LSD experience was not dominated by unpleasant psychosis-like phenomena but rather characterized by an overall positive mood state in the majority of subjects (Carhart-Harris et al, 2016b). Investigators rated subjects as more distant from reality and happy after administration of 200 μg LSD, whereas ratings of anxiety and paranoid thinking did not increase (Schmid et al, 2015). Patients with schizophrenia present deficits in sensorimotor gating, reflected by prepulse inhibition (PPI) of the startle response. LSD acutely disrupts PPI in both animals (Halberstadt and Geyer, 2010) and healthy human subjects (Schmid et al, 2015), producing deficits in information processing that are similar to those observed in schizophrenia. Similarly, inhibitory processes are impaired in schizophrenia and in healthy subjects after administration of LSD (Schmidt et al, 2017).

Emotional Processing

LSD impaired the recognition of sad and fearful faces (Dolder et al, 2016) and enhanced emotional empathy (Dolder et al, 2016), similar to psilocybin (Kometer et al, 2012; Preller et al, 2015) and MDMA (Hysek et al, 2014a; Kuypers et al, 2017). These effects of LSD on emotion processing may be considered useful in LSD-assisted psychotherapy. However, LSD also impaired the identification of complex emotions (Dolder et al, 2016).

Functional Brain Imaging

LSD acutely decreased the functional integrity of brain networks (Figure 2a) and the separation between networks (Carhart-Harris et al, 2016c; Tagliazucchi et al, 2016) (Figure 2b). At the whole-brain level, LSD increased functional connectivity between various brain regions (Figure 3). LSD also increased measures of functional ‘brain entropy’ (ie, the predictability of resting-state fMRI time series) across many functional systems (Lebedev et al, 2016). The acute LSD-induced global increase in ‘brain entropy’ was associated with trait openness that was assessed 14 days later (Lebedev et al, 2016). LSD increased thalamocortical resting-state functional connectivity (RSFC) (Mueller et al, 2017b; Tagliazucchi et al, 2016), overall connectivity in high-level cortical regions and the thalamus, and connectivity between normally more dissociated resting-state networks (Tagliazucchi et al, 2016). These findings indicate more globally synchronized activity within the brain and a reduction of network separation while under the pharmacological effects of LSD. Similar decreases in within-network integrity (Carhart-Harris et al, 2014; Muthukumaraswamy et al, 2013) and increases in between-network connectivity (Carhart-Harris et al, 2013; Roseman et al, 2014) have been observed under psilocybin. The LSD-induced increases in global connectivity, particularly in the temporo-parietal junction and insular cortex, correlated with feelings of moderate ‘ego dissolution’ that were produced by LSD (Tagliazucchi et al, 2016). ‘Ego dissolution’ refers to a disintegration of the sense of possessing a ‘self’ or identity that is distinct from others and from the environment (Preller and Vollenweider, 2016; Tagliazucchi et al, 2016). In addition, LSD-induced RSFC between the thalamus and right fusiform gyrus and insula correlated with subjective visual and auditory alterations, respectively (Mueller et al, 2017b). Remaining to be determined is the way in which LSD-induced increases in thalamocortical connectivity may be linked to the thalamic gating of perceptions (Mueller et al, 2017b). In contrast to the higher connectivity between neural networks while under the effects of LSD, LSD globally decreased within-network RSFC (integrity) and within-network signal variance (Carhart-Harris et al, 2016c) (Figure 2a). Specifically, LSD decreased default mode network (DMN) integrity (Carhart-Harris et al, 2016c) as previously shown for psilocybin (Carhart-Harris et al, 2014), and this LSD-induced disintegration of the DMN correlated with ratings of ego dissolution (Carhart-Harris et al, 2016c; Tagliazucchi et al, 2016). Furthermore, reductions of RSFC in the DMN (ie, DMN disintegration) were associated with fewer mental spaces for the past (ie, decreased mental time travel to the past) while under the effects of LSD (Speth et al, 2016). Increases in DMN RSFC have been described in depression, and decreases in DMN RSFC that are induced by LSD may be linked to its potential antidepressant effects (Carhart-Harris et al, 2016a).

не верю чтоб у кислотников не было навязчивых состояний. видать ты плохо понимаешь что это такое, и оно у тебя и у друзей уже как обыденность, ибо ты кратко прочитал на вики статью, тут же произвел самоанализ себя и друзей, учитывая что мой коммент был оставлен 50 минут назад. ахаха
PS хотя употреблять каждую неделю и раз в год это разные вещи)