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Synonyms: 2-dimethylaminoethanol, dimethylethanolamine, deanol
This supplement has been proposed for the following purposes or treating the following conditions. Also given is the current scientific support for use (on a scale of 0-10). Note that a low rating does not necessarily indicate that a supplement does not work, just that research is either unavailable or has not demonstrated a benefit.
ADD/ADHD - 7
Learning/memory - 3
Alzheimer's - 1
Tardive dyskinesia - 1
Side effects
Reported side effects associated with DMAE use include gastrointestinal disturbances, bad body odor, drowsiness, sedation, retardation, confusion, increased blood pressure, depression, and hypomania.
DMAE may cause a decrease in the levels of some choline metabolites. Choline supplementation may help to correct this.
DMAE should be avoided under all circumstances by pregnant women.
DMAE is a naturally occuring analogue of choline. It is mareketed primarily as a memory enhancing agent and anti-aging nutrient. This article will review the presently available research on DMAE and whether or not it supports these claims.
Centrophenoxine (CPH), an established nootropic and anti-aging nutrient, is DMAE bonded to p-chlorophenoxyacetic acid (PCPA). CPH is a potent OH radical scavenger and also prevents the buildup of the age-related pigment lipofuscin. According to some research, the properties of CPH can be primarily attributed to DMAE moiety, while the PCPA just allows for better penetration of the blood brain barrier [1-2]. If this were the case, DMAE would be pharmacologically very similar to CPH, but with a higher amount needed for the same effect. However, other research contradicts this idea. For example, an in vitro study found that DMAE did not reduce age pigment accumulation, but the combination of DMAE and PCPA did [3]. Another found that PCPA had superoxide radical scavenging properties, whereas DMAE did not, although high concentrations of the substances were used [4]. Other researchers also indicate that PCPA is responsible for some of the important actions of CPH [5].
Research has also been conducted to see if DMAE shares the anti-aging properties of CPH. Like CPH, DMAE is a potent and site specific OH radical scavenger. This is due to DMAE's ability to become phosphatidyl-DMAE and replace phosphatidylcholine in nerve membranes, thus offering local protection from free radicals [1]. An in vitro study found that adding DMAE to myocytes protected from cell damage from ischemia and metabolic inhibition [6], while a study in mice found that DMAE did not change survival rate, but did reduce lipofuscin content [7]. However, a study in Japanese quail found that administration of DMAE (18 mg/kg) starting late in life actually reduced life span by twenty weeks [8]. Therefore, it is necessary to emphasize caution when applying the effects of CPH to DMAE. It also brings up a larger issue, that of possible toxicity or side effects from DMAE.
Another reputed effect of DMAE supplementation is a rise in choline and acetylcholine levels and a corresponding increase in memory ability. This is based on the assumption that DMAE is a choline precursor [1] and also crosses the blood brain barrier more effectively than choline itself [9], giving it the ability to reach the brain and then increase brain choline levels. DMAE does consistently increase levels of free choline in the brain and body, but this is not because it is a converted to choline – it is because it competitively inhibits choline kinase and choline oxidase, preventing the metabolism of choline to phosphocholine and betaine [10-12]. As mentioned above, this results in the production of phosphatidyl-DMAE. However, this is not necessarily beneficial, since it replaces phosphatidylcholine, and thus may effectively blunt some of the biological actions of phosphatidylcholine [39].
There is very little evidence that this increase in choline levels leads to a consequent rise in acetylcholine, and given that DMAE competitively inhibits choline transport, there is theoretical basis for an anticholinergic effect [10-11, 13-15]. If anything, this renders DMAE supplementation the equivalent of choline supplementation, since that also increases brain choline levels but generally fails to increase acetylcholine [16]. In an in vitro study, DMAE reduced the synthesis of acetylcholine by inhibiting high affinity choline transport, and the same researchers found no effect of DMAE on acetylcholine levels in vivo in rats [17]. In another study in which a wide range of doses of DMAE was administered to mice, there was no increase in brain acetylcholine levels except an increase in the striatum at the highest dose which appeared to be unrelated to tissue DMAE content [18].
Studies on the effects of DMAE on learning and memory have also been discouraging. In mice, DMAE improved one-week retention in mice on a T-maze active avoidance task [19]. However, trials in the healthy elderly and in people with Alzheimer's and amnestic disorders have found no positive effect on memory or cognition [20-23]. One study did report better mood after treatment, but there was no control group [23].
DMAE has also been researched in the treatment of tardive dyskinesia (a type of movement disorder). Although initial results were promising, they failed to be replicated in double-blind, placebo-controlled trials [24-30]. In two of these studies, choline was effective whereas DMAE was not [24, 29]. In one trial, symptoms were worse in the DMAE-treated group, and it was suggested that DMAE had actually interfered with cholinergic function [25].
A final use proposed for DMAE is in the treatment of childhood hyperactivity. A placebo-controlled trial in 74 children found that DMAE at 500 mg daily was as effective as methylphenidate (Ritalin) [15]. The mechanism of action for this effect is not established.
Numerous side effects from DMAE treatment have been reported in the literature. These include gastrointestinal disturbances, bad body odor, drowsiness, sedation, retardation, confusion, increased blood pressure, depression, and hypomania; some of these are causes of frequent withdrawal [20, 31-33]. Airborne DMAE is associated with a variety of adverse events (some of which have been reported in humans exposed to high concentrations in a label printing plant), primarily visual disturbances (blurry, halo, and blue-grey vision, corneal opacity, and decrements in visual acuity and contrast sensitivity) and skin irritation [34-36]. However, it is doubtful that oral supplementation will lead to these effects. DMAE also has potential teratogenic effects due to the fact that it inhibits choline uptake [10]. In one study, rat pups fed a choline-deficient diet containing DMAE died within 36 hours of birth, supporting the notion that DMAE does not function as an effective choline precursor [37]. In another experimental study, the presence of choline or acetylcholine offset developmental toxicity due to DMAE [38].
In conclusion, the scientific literature does not support many of the claims made regarding DMAE, although older research does support a possible benefit in the treatment of hyperactivity. When taken in the right amounts, there are some possible benefits related to its antioxidant effects and benefits resulting from an anticholinergic effect can even be hypothesized. Also, there is not enough research to determine the effects when DMAE and choline are taken together. It is possible that the two would just blunt one another's effects. However, it is also possible that this would offer the best of both worlds, both the antioxidant effects of DMAE but also sufficient choline metabolites to protect against any potential negative effects. Further research is clearly needed, but until then, it is unwise to use DMAE without a protective choline supplement.
This supplement has been proposed for the following purposes or treating the following conditions. Also given is the current scientific support for use (on a scale of 0-10). Note that a low rating does not necessarily indicate that a supplement does not work, just that research is either unavailable or has not demonstrated a benefit.
ADD/ADHD - 7
Learning/memory - 3
Alzheimer's - 1
Tardive dyskinesia - 1
Side effects
Reported side effects associated with DMAE use include gastrointestinal disturbances, bad body odor, drowsiness, sedation, retardation, confusion, increased blood pressure, depression, and hypomania.
DMAE may cause a decrease in the levels of some choline metabolites. Choline supplementation may help to correct this.
DMAE should be avoided under all circumstances by pregnant women.
DMAE is a naturally occuring analogue of choline. It is mareketed primarily as a memory enhancing agent and anti-aging nutrient. This article will review the presently available research on DMAE and whether or not it supports these claims.
Centrophenoxine (CPH), an established nootropic and anti-aging nutrient, is DMAE bonded to p-chlorophenoxyacetic acid (PCPA). CPH is a potent OH radical scavenger and also prevents the buildup of the age-related pigment lipofuscin. According to some research, the properties of CPH can be primarily attributed to DMAE moiety, while the PCPA just allows for better penetration of the blood brain barrier [1-2]. If this were the case, DMAE would be pharmacologically very similar to CPH, but with a higher amount needed for the same effect. However, other research contradicts this idea. For example, an in vitro study found that DMAE did not reduce age pigment accumulation, but the combination of DMAE and PCPA did [3]. Another found that PCPA had superoxide radical scavenging properties, whereas DMAE did not, although high concentrations of the substances were used [4]. Other researchers also indicate that PCPA is responsible for some of the important actions of CPH [5].
Research has also been conducted to see if DMAE shares the anti-aging properties of CPH. Like CPH, DMAE is a potent and site specific OH radical scavenger. This is due to DMAE's ability to become phosphatidyl-DMAE and replace phosphatidylcholine in nerve membranes, thus offering local protection from free radicals [1]. An in vitro study found that adding DMAE to myocytes protected from cell damage from ischemia and metabolic inhibition [6], while a study in mice found that DMAE did not change survival rate, but did reduce lipofuscin content [7]. However, a study in Japanese quail found that administration of DMAE (18 mg/kg) starting late in life actually reduced life span by twenty weeks [8]. Therefore, it is necessary to emphasize caution when applying the effects of CPH to DMAE. It also brings up a larger issue, that of possible toxicity or side effects from DMAE.
Another reputed effect of DMAE supplementation is a rise in choline and acetylcholine levels and a corresponding increase in memory ability. This is based on the assumption that DMAE is a choline precursor [1] and also crosses the blood brain barrier more effectively than choline itself [9], giving it the ability to reach the brain and then increase brain choline levels. DMAE does consistently increase levels of free choline in the brain and body, but this is not because it is a converted to choline – it is because it competitively inhibits choline kinase and choline oxidase, preventing the metabolism of choline to phosphocholine and betaine [10-12]. As mentioned above, this results in the production of phosphatidyl-DMAE. However, this is not necessarily beneficial, since it replaces phosphatidylcholine, and thus may effectively blunt some of the biological actions of phosphatidylcholine [39].
There is very little evidence that this increase in choline levels leads to a consequent rise in acetylcholine, and given that DMAE competitively inhibits choline transport, there is theoretical basis for an anticholinergic effect [10-11, 13-15]. If anything, this renders DMAE supplementation the equivalent of choline supplementation, since that also increases brain choline levels but generally fails to increase acetylcholine [16]. In an in vitro study, DMAE reduced the synthesis of acetylcholine by inhibiting high affinity choline transport, and the same researchers found no effect of DMAE on acetylcholine levels in vivo in rats [17]. In another study in which a wide range of doses of DMAE was administered to mice, there was no increase in brain acetylcholine levels except an increase in the striatum at the highest dose which appeared to be unrelated to tissue DMAE content [18].
Studies on the effects of DMAE on learning and memory have also been discouraging. In mice, DMAE improved one-week retention in mice on a T-maze active avoidance task [19]. However, trials in the healthy elderly and in people with Alzheimer's and amnestic disorders have found no positive effect on memory or cognition [20-23]. One study did report better mood after treatment, but there was no control group [23].
DMAE has also been researched in the treatment of tardive dyskinesia (a type of movement disorder). Although initial results were promising, they failed to be replicated in double-blind, placebo-controlled trials [24-30]. In two of these studies, choline was effective whereas DMAE was not [24, 29]. In one trial, symptoms were worse in the DMAE-treated group, and it was suggested that DMAE had actually interfered with cholinergic function [25].
A final use proposed for DMAE is in the treatment of childhood hyperactivity. A placebo-controlled trial in 74 children found that DMAE at 500 mg daily was as effective as methylphenidate (Ritalin) [15]. The mechanism of action for this effect is not established.
Numerous side effects from DMAE treatment have been reported in the literature. These include gastrointestinal disturbances, bad body odor, drowsiness, sedation, retardation, confusion, increased blood pressure, depression, and hypomania; some of these are causes of frequent withdrawal [20, 31-33]. Airborne DMAE is associated with a variety of adverse events (some of which have been reported in humans exposed to high concentrations in a label printing plant), primarily visual disturbances (blurry, halo, and blue-grey vision, corneal opacity, and decrements in visual acuity and contrast sensitivity) and skin irritation [34-36]. However, it is doubtful that oral supplementation will lead to these effects. DMAE also has potential teratogenic effects due to the fact that it inhibits choline uptake [10]. In one study, rat pups fed a choline-deficient diet containing DMAE died within 36 hours of birth, supporting the notion that DMAE does not function as an effective choline precursor [37]. In another experimental study, the presence of choline or acetylcholine offset developmental toxicity due to DMAE [38].
In conclusion, the scientific literature does not support many of the claims made regarding DMAE, although older research does support a possible benefit in the treatment of hyperactivity. When taken in the right amounts, there are some possible benefits related to its antioxidant effects and benefits resulting from an anticholinergic effect can even be hypothesized. Also, there is not enough research to determine the effects when DMAE and choline are taken together. It is possible that the two would just blunt one another's effects. However, it is also possible that this would offer the best of both worlds, both the antioxidant effects of DMAE but also sufficient choline metabolites to protect against any potential negative effects. Further research is clearly needed, but until then, it is unwise to use DMAE without a protective choline supplement.