https://ntp.niehs.ni..._110002_508.pdf
9.1.1 Human Data Pfeiffer et al. (1959; cited by Beard and Noe, 1981) reported that 10 to 20 mg (0.042-0.084 mmol) of DMAE tartrate administered orally to humans, produced mild mental stimulation. At 20 mg/day (0.084 mmol), there was a gradual increase in muscle tone and perhaps an increased frequency of convulsions in susceptible individuals. Larger doses (not specified) produced insomnia, muscle tenseness, and spontaneous muscle twitches.
20mg per day is even active, so why are all these capsules loaded with atleast 100mg???
DMAE supplementation is contraindicated during pregnancy and lactation (Quackwatch, 2002; Hendler and Rorvik, 2001b). It is also contraindicated for treatment of people with symptoms of schizophrenia and clonic-tonic seizure disorders (Osol and Hoover, 1975; cited by Quackwatch, 2002). The principal contraindication to the use of DMAE cited by Gosselin et al. (1976) was grand mal epilepsy. DMAE also antagonizes the depressant effects of barbiturates.
9.1.6 Synergistic/Antagonistic Effects
Theoretically, concomitant use might decrease the effect of drugs with anticholinergic activity,
due to the potential cholinergic activity of DMAE (Cited by Quackwatch, 2002).
Several studies report interactive biological effects, either potentiation or antagonism, caused by
derivatives of DMAE, possibly due to improved penetration into tissues. DMAE (175 to 350
mg/kg [1.95 to 3.90 mmol/kg], subcutaneously) was reported to potentiate the central action of
cardiazol, strychnine, morphine, chlorpromazine, evipan, and phenobarbital in rats. Treatment
with DMAE for seven to fourteen days increased levels of chlorpromazine in the brains of rat,
relative to treatment with chlorpromazine alone (Danysz et al., 1967b). Rowell and Chiou
(1976) reported that a synthetic ester of DMAE, N,N-DMAE chloroacetate, inhibited choline
acetyltransferase in a reversible and uncompetitive fashion.
DMAE bitartrate (100 to 500 mg/kg; 0.300 to 1.5 mmol/kg, intraperitoneally), administered
simultaneously with paracetamol (acetaminophen), protected rats and mice from the hepatotoxic
effects of the latter. Mixed function oxidases that metabolize paracetamol were inhibited, and
elimination of free paracetamol and its glucuronide was enhanced (Siegers and Yones, 1979).
DMAE p-chlorophenoxyacetate, given one hour prior to pentetrazole (route not provided)
reduced the threshold for pentetrazole-induced generalized tonic-clonic crisis (species not
provided) (Thuillier, 1960).
Chicks injected intraperitoneally with Small doses of DMAE pacetamidobenzoate
(Deaner, 2 mg/kg; 0.02 mmol/kg) 15 minutes before intraperitoneal injection
of tremorine potentiated the tremorine-induced tremor response. Large doses of DMAE
(Deaner, 200 mg/kg; 2.00 mmol/kg) given two hours prior to tremorine suppressed the tremor
response completely (Bowman and Osuide, 1968).
So it can be both pro convulsive and anti convulsive.
Also seems it can potentiate anti cholinergic effects aswell as cholinergic effects.
Seems to be able to have an effect on possible aggression:
Voronina et al. (1987a,b) [Russian] reported that long-term administration [details not provided in the abstracts] of centrophenoxine and Cleregil (DMAE aceglumate) increased the “emotional reactivity” and aggressiveness in rats. Spontaneous aggressiveness and “still greater enhancement of emotional reactivity” occurred after withdrawal of the drugs. Garibova et al. (1984) reported that prolonged intraperitoneal injections of Cleregil (150 mg/kg) induced “manifestations of aggressiveness, fear and anxiety.” The rats “developed a dissociated state in which the reflex [learning in a T-maze] manifested itself only after [Cleregil] injection and did not occur without it.” Withdrawal of either centrophenoxine or Cleregil produced an “even greater enhancement of emotional reactivity and appearance of spontaneous aggressiveness” (Voronina et al., 1987b). Meszaros and Gajewska (1972) reported increased aggressiveness in mice associated with several forms of DMAE. In this report, the authors stated that several pharmacological properties of centrophenoxine may be attributed to the p-chlorophenoxyacetic acid (PCPA) moiety. Low doses of PCPA or centrophenoxine increased aggressiveness in mice, whereas high doses decreased aggressiveness. DMAE increased aggressiveness at high doses and decreased aggressiveness at low doses. The effects of centrophenoxine and PCPA were more similar to each other than with DMAE.
Would be interesting to see if long term DMAE/centro users have noticed a shift in personality
