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Diss Factsheets

Administrative data

Description of key information

Summary of available literature

Additional information

There are extensive human data presented in the "Toxicological Summary for Dimethylethanolamine and Selected Salts, 2002".

DMAE supplementation

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 produced insomnia, muscle tenseness, and spontaneous muscle twitches.

DMAE is available as a liquid or as deanol bitartrate. The most common form of supplementation is as deanol bitartrate, 100 mg per day (Hendler and Rorvik, 2001b). Recommended doses of centrophenoxine begin with 100 mg/day (0.340 mmol/day) and gradually increase to 500 mg/day (1.700 mmol/day) (Life Extension Vitamin Supplies, Inc., undated; cited by Quackwatch, 2002). In a non-scientific study, Zs-Nagy (2002) reported that he and several colleagues have been self-medicating with centrophenoxine (500 mg/day; 1.700 mmol/day) since 1976 with no apparent evidence of adverse effects. The FDA has approved a human study of DMAE (salt form not provided), recommending daily dose of 200 mg (2.20 mmol) (LifeExtension Foundation, 1999). Doses used in clinical studies have ranged from 300 to 2000 mg/day (3.30 to 22.20 mmol/day) (Re, 1974; George et al. 1981; Penovich et al., 1978; cited by Quackwatch, 2002). Gosselin et al. (1976) reported that doses of DMAE as high as 1200 mg/day (13.46 mmol/day) produced no serious side effects. A single 2500-mg (27.80-mmol) dose taken in a suicide attempt had no adverse effect. Information regarding how the free base of DMAE was administered was not found. 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.

In psychiatric patients orally medicated with either 1.9 or 3.8 mmol (170 mg or 340 mg) Deaner for one week, plasma concentrations of Deaner were 0.25 and 0.52 μM (0.022 and 0.047 μg/mL), respectively (Ceder and Schuberth, 1977).

In humans, 33 % of an injected 1 g (10 mmol) dose of DMAE was excreted unchanged (Williams, 1959; cited by Beard and Noe, 1981). It was suggested that the remaining dose may have been demethylated to ethanolamine and entered into normal metabolic pathways.

Adverse Effects

A large number of adverse health effects were associated with DMAE in the FDA’s Special Nutritionals Adverse Event Monitoring System (SN/AEMS) Web Report (FDA CFSAN, 1998), a voluntary reporting system. Complaints associated with several DMAE-containing products included cardiovascular, neurological, and/or psychological effects. Specific attribution of adverse effects to DMAE is unlikely, as many of these products also contained Ephedra vulgaris alkaloids and other Ephedra spp. Ephedra alkaloids cause similar cardiovascular and neurological effects reported for DMAE (FDA, 1999). Similar adverse effects have been reported to support the FDA SN/AEMS by Ott and Owens (1998), Osol and Hoover (1975), and Haug and Holzgraefe (1991); and by Casey (1979), de Montigny et al. (1979), Fisman et al. (1981), and Sergio (1988) (all cited by Quackwatch, 2002).

Efficacy of DMAE in treating a variety of diseases

DMAE, thought to be a precursor for acetylcholine, has been tested for its efficacy in treating a variety of diseases possibly related to deficiencies of acetylcholine, including tardive dyskinesia, Alzheimer’s disease, amnesic disorders, age-related cognitive impairment, and Tourette’s syndrome, with mixed results (Hendler and Rorvik, 2001b). Treatment with DMAE for tardive dyskinesia, a side effect of neuroleptic medications, was associated with serious cholinergic side effects: nasal and oral secretions, dyspnea, and respiratory failure (Mehta et al., 1976; Nesse and Carroll, 1976). DMAE was used in the treatment of one patient for a low-frequency action tremor. This treatment was successful for ten years, until side effects of increasing neck pain and orofacial and respiratory dyskinesia occurred. Treatment was discontinued, and it was concluded that the dyskinesia could be attributed to the effects of DMAE (Haug and Holzgraefe, 1991). A meta-analysis of randomized controlled trials indicated that DMAE was no more effective than placebo in the treatment of tardive dyskinesia. Rather, there was a significantly increased risk of adverse events associated with the DMAE treatment (McGrath and Soares, 2000; Soares and McGrath, 1999).

Clinical trials to determine the efficacy of DMAE in treating cognitive dysfunction have, overall, resulted in negative findings. Normal or minimally impaired nondemented elders (eleven subjects) showed no benefit after 21 days of treatment with 900 mg DMAE (10.0 mmol) per day (Marsh and Linnoila, 1979). Likewise, DMAE failed to improve cognitive function in patients suffering from Alzheimer’s disease in both a double-blind, placebo-controlled trial (27 patients, dose and duration not provided) and an open-label trial (14 patients, 1.8 grams/day, duration not indicated) (Fisman et al., 1981; Ferris et al., 1977; both cited by Ott and Owen, 1998).

Treatment with a mixture of DMAE (as DMAE orotate, dose not provided) and vitamins and minerals successfully modified mental impairments of sixty volunteers (30 females, 30 males, age ranging from 40 to 65) self-reporting poor concentration and efficiency during mental exercise in a double-blind, placebo-controlled study (Dimpfel et al., 1996). Comparisons of the before and after DMAE-treatment recordings showed statistically significant changes towards decreased theta power during rest and increased absolute theta power induced by mental exercise, specifically in the frontotemporal cortex during both memory and symbol recognition tests. Similar results were observed in a randomized, parallel, placebo-control, double-blind study of 43 patients (40 to 65 years old) with poor concentration and thinking problems. Increased absolute spectral EEG power in the delta and theta frequency bands, mainly in the front-temporal cortex, were observed (Schober et al., 1994). In a double-blind clinical trial examining the effects of centrophenoxine, an ester of DMAE, in 50 patients (25 males and 25 females) suffering from organic psychosyndrome (phase DSM III, Category 1, ICD No. 229), improvements were observed in 47.6 % receiving the drug versus only 28 % observed in placebo-treated patients. Patients, all greater than 60 years of age, were dosed with Helfergin 500 tablets (two tablets, twice a day, after breakfast and lunch) containing 500 mg centrophenoxine-HCL (verum) for a total dose of two grams per day, for eight weeks, or with an identical looking placebo. Six types of evaluations, including observations by a medical doctor and psychologist, memory and performance tests, daily activity observations, and a self-rating evaluation were used to evaluate changes in performance (Pék et al, 1989). Statistical analysis for the study was made difficult due to the small numbers of individuals per treatment group and heterogeneity in the performance of the tested groups. Criteria for effectiveness of centrophenoxine were based on intra-individual improvements in at least four of the six psychometric and behavioral tests (Pék et al., 1989). Both the percentage of patients demonstrating improvements and the average percent improvement per patient were higher in the treatment than placebo group (average of 21.2 % and 9 % per patient, respectively). Of the seven patients in the placebo group demonstrating improvements, only two were described by medical doctors to have improved in health status, relative to nine out of ten patients in the treatment group (Pék et al., 1989). Negative effects were also recorded for this study. Worsening mental status was observed in one placebo-treated patient (85 years old) and five treatment patients (average age of 79.4 years). Also, three patients in the treatment group were removed from the study due to health-related issues. All three patients died within three weeks of being removed from the study. Autopsy results suggested that the deaths were not treatment-related. Three female placebo-treated patients died within six weeks of completion of the trial, with similar autopsy finds as those recorded for the deaths observed in the treatment group (Pék et al., 1989).

Other findings

In one occupational study in the manufacture of polyurethane foam insulation for refrigerators, adverse effects included disorders of the upper respiratory tract and nervous system, along with significant changes in the immune status of workers exposed to a mixture of DMAE, ethylenediamine, propylene oxide, and 4,4´-methylenediphenyl diisocyanate (Pokrovskaya et al., 1986). A spray painter developed severe respiratory symptoms, which seemed to be related to occupational exposure to a specific type of spray paint containing DMAE. Follow-on skin tests with DMAE (undiluted, and 1:10 and 1:100 dilutions in saline) in three human volunteers produced wheal and flare responses at the high dose. This was interpreted as an irritant response, and not a sign of immunotoxicity (Vallieres et al., 1977). Despite one clear case for occupational asthma form DMAE exposure, it fails to meet the current criteria for classification as a respiratory sensitizer (Davies et al., 1997).

Holmen et al. (1988) failed to demonstrate mutagenic effects as demonstrated by chromosomal aberrations, sister chromatid exchanges, or micronuclei in cultured lymphocytes from peripheral blood or mutagenic activity and thioether concentrations in the urine of workers exposed to a mixture of chemicals, including DMAE. Using a method to classify the risks associated with occupational exposures to neurotoxic chemicals obtained from four national computer-based registers, Simonsen and Lund (1992) categorized DMAE as having small risk of damaging the nervous system under normal work conditions.


DMAE in form of centrophenoxine or DMAE with choline (Vita-Gerin) is used as food supplement for mental stimulation. The efficacy of DMAE in treating of variety of disease was reported with mixed results. No benefits from DMAE treatment was reported by patients with tardive dyskinesia, cognitive dysfunction and Alzheimer's disease. Benefits from DMAE treatment were found in the studies evaluating DMAE's ability to increase theta power of concentration. Centrophenoxine showed benefits for patients with organic psychosyndrome. DMAE failed to meet criteria as a respiratory sensitizer or neurotoxic chemical. DMAE does not possess mutagenic activity in humans.