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Toxicological information

Exposure related observations in humans: other data

Administrative data

Endpoint:
exposure-related observations in humans: other data
Type of information:
other: review
Adequacy of study:
key study
Study period:
2002
Reliability:
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
other: Acceptable wel-documented publication which meets basic scientific principles.

Data source

Reference
Reference Type:
review article or handbook
Title:
Unnamed
Year:
2002

Materials and methods

Type of study / information:
human data
Endpoint addressed:
basic toxicokinetics
Test guideline
Qualifier:
no guideline required
GLP compliance:
no

Test material

Constituent 1
Chemical structure
Reference substance name:
2-dimethylaminoethanol
EC Number:
203-542-8
EC Name:
2-dimethylaminoethanol
Cas Number:
108-01-0
Molecular formula:
C4H11NO
IUPAC Name:
2-(dimethylamino)ethanol
Details on test material:
not applicable

Method

Details on study design:
not applicable
Exposure assessment:
measured

Results and discussion

Results:
1. Pfeiffer et al., 1959. 10 to 20 mg of DMAE tartrate orally- mild mental stimulation.
2. Gosselin et al., 1976. 1200 mg/day - no serious side effects.
3. Hendler and Rorvik, 2001. a) The common form of supplementation is as deanol bitartrate, 100 mg per day. b) DMAE is contraindicated during pregnancy. c) Treatment with DMAE for tardive dyskinesia resulted in a side effect associated with cholinergic side effect.
4. Dimpfel et al., 1996; PEK et al., 1986. Improvement of concentration and thinking capacity.

Applicant's summary and conclusion

Conclusions:
DMAE has been tested for its efficacy in treating of variety of diseases. There are benefits and no benefits from DMAE treatment reported.
Executive summary:

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 has been tested for its efficacy in treating a variety of diseases possibly related to deficiencies of acetylcholine with mixed results. Three reported no benefit from DMAE treatment (tardive dyskinesia; cognitive dysfunction; Alzheimer’s disease). Benefits from DMAE treatment were found in other studies evaluating DMAE’s ability to increase theta power or concentration. Centrophenoxine showed benefits for patients with organic psychosyndrome. DMAE supplementation is contraindicated during pregnancy, lactation, and for treatment of people with symptoms of schizophrenia and clonic-tonic seizure disorders. DMAE antagonizes the depressant effects of barbiturates. A large number of adverse health effects were associated with DMAE, including 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. Treatment with DMAE for tardive dyskinesia was associated with serious cholinergic side effects (nasal and oral secretions, dyspnea, and respiratory failure). Adverse effects were observed in one occupational study (manufacture of polyurethane foam insulation for refrigerators) and included disorders of the upper respiratory tract and nervous system, along with significant changes in the immune status. Workers were exposed to a mixture of DMAE, ethylenediamine, propylene oxide, and 4,4´-methylenediphenyl diisocyanate. Severe respiratory symptoms were observed in a single painter exposed to spray paint containing DMAE. Wheal and flare responses occurred after exposure of human volunteers to DMAE (undiluted, and 1:10 and 1:100 dilutions in saline) but were interpreted as an irritant response. DMAE failed to meet the current criteria for classification as a respiratory sensitizer.

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