Reprinted from Life Enhancement, Issue #25
ver hear the expression "the lights are on but nobody's home"? Ever have a conversation with someone and you felt like they were in the Fifty Percent Club - they were only half present, the other half being who-knows-where?
On the other hand, you've probably also had the experience of meeting a person who seemed to be fully there, fully present. That's presence of mind. When you are in that state yourself, it's a state of excellence. It's not a feeling, it's a high level of responsiveness to your environment.
Some of the published studies on the naturally-occurring nutrient DMAE (dimethylaminoethanol) call this state vigilance and they have elaborate operational definitions and methods of testing for it. In these studies DMAE has been shown to support the vigilance mechanisms. We asked what vigilance really means and we looked at the testing methods. We found that it boils down to this elusive excellence we're calling presence of mind.
Brain Function Maintenance
DMAE is normally present in small amounts in our brains. When supplemental amounts are used, the brain-function support effects are remarkable. DMAE is a naturally-occurring nutrient found in seafood such as anchovies and sardines.1 Perhaps this explains why fish has often been called brain food.
Throughout the scientific literature, DMAE has been reported as helping to elevate mood, improve memory and learning, heighten intelligence, increase physical energy and, in laboratory animals, extend the life span. It is used by many people for its mild, safe, stimulant effect, and yet DMAE also makes it easier for most people to get to sleep and to have more lucid dreams.2 Many people report less fatigue in the day and sounder sleep at night, as well as needing less sleep when taking DMAE.
The stimulant effect of DMAE is significantly different from that produced by coffee, amphetamines, or other stimulant drugs: DMAE does not have a drug-like quick pick-up and quick come-down. People who take DMAE have reported that after three to four weeks they feel a mild stimulation continually, without side effects. Also, when DMAE is discontinued, no depression or letdown occurs.
DMAE may be thought of as a nootropic substance. More than 20 years ago the concept of a nootropic emerged from studying the unusual pharmacology of certain drugs, especially piracetam (which, upon confirmation, was extended to clinical applications). What is it that characterizes the essence of the nootropic effect?
1) The direct functional activation of the higher integrative brain mechanisms that help maintain normal, healthy cortical vigilance;
2) a telencephalic functional selectivity; and
3) a particular efficiency in restoring deficient higher nervous system activity.3
What is especially interesting is that the nootropic concept doesn't deal with subcortical events such as those involving the reticular or limbic systems. It deals with cortical events, meaning those that have a direct impact on consciousness.
Although the neurochemistry of nootropic mechanisms is not clearly understood, we do know that nootropic activity enhances certain characteristics of membranes, such as their stability, permeability, strength, stress resistance, and assimilability. It is also thought that serotonin mechanisms are involved.
Simply put, the goal of the search for nootropic essence is that of finding and exploiting more selective nootropic agents. DMAE, with its ability to help maintain brain functions, thus perhaps supports cognitive efficiency. It may compensate for various neuropsychologic deficits ranging from cognitive processes to aging itself.
Riker Laboratories developed a prescription drug called Deaner (also called Deanol). This substance is the p-acetamidobenzoate salt of DMAE and has very similar effects. Riker marketed its DMAE-like product for learning problems, underachievement, shortened attention span, hyperactivity, reading and speech difficulties, impaired motor coordination, and behavior problems in children. This drug is no longer available in the U.S. due to the "vigilance" of the FDA, which demanded that Riker retest Deaner's efficacy, in accordance with new and, purportedly, higher FDA standards. Riker apparently decided that they could not afford the tens of millions of dollars that would be required to maintain its right to continue selling the product. Thus Deaner has become an "orphan drug."
DMAE probably works by accelerating the brain's synthesis and turnover of the neurotransmitter acetylcholine, which in turn plays a key role in maintaining mental ability as well as supporting healthy memory in aging adults. It has also been suggested that DMAE may work, in part, by inhibiting choline metabolism in peripheral tissues, causing free choline to accumulate in blood, enter the brain, and stimulate cholinergic receptors.5,6
Mood and Vigilance
In a French double-blind, crossover study designed to measure the impact of DMAE on vigilance and mood, four subjects categorized as anxiety ridden, and four subjects used as controls, were given 1200 mg/day of DMAE for five days. The subjects then had their EEG and inter-hemispheric coherence measured. In the subjects given DMAE, a significant and progressive synchronization of the two hemispheres was noted. This synchronization was correlated with improved neuromotor control, enhancement of behavioral tasks, increased verbal memory, and better control in anxious and rhythmic reactivity.7
Learning, Behavior, and IQ
DMAE has proven to be a valuable and safe alternative for certain learning and behavior problems such as Attention Deficit Disorder (ADD) and hyperkinesia (usually the providence of children but also known to affect adults). Unfortunately, amphetamine or amphetamine-like drugs are often used to deal with these problems. In one study, consisting of 25 girls and 83 boys, conducted by Dr. Carl Pfeiffer of the Brain-Bio Center in Princeton, New Jersey, DMAE was found to result in enhanced behavior in 2/3 of the boys and 3/4 of the girls. Hyperactivity was greatly lessened as attention span was lengthened, irritability was decreased, scholastic ability improved, and, in some cases, IQ was elevated.8
Similar results were found when 500 mg of DMAE was given to 74 children with learning problems, including many who were hyperactive. These subjects were screened for neurological or psychiatric illnesses beforehand. DMAE was given in a double-blind fashion for 3 months. Testing was done before and after treatment for behavior, reaction time, and a series of standard psychometric parameters. Not only was there significant improvement overall but DMAE was shown to improve performance in children with learning and behavior disorders.9
Fatigue, Depression, Confusion
In one of Dr. Pfeiffer's earliest studies on 100 subjects, he demonstrated that DMAE can help alleviate chronic fatigue and mild depression through its effects on physical energy and motivation. He also noted personality improvements and help with insomnia.10 It is important to note that the subjects did not develop any dependency on DMAE, as often occurs with many drugs used for fatigue and insomnia.
In another study, doses of 400 to 800 mg were given daily to 52 patients with a variety of different central nervous system problems, the result of which was significant diminishment of their conditions.11
Richard Hochschild has studied the influence of DMAE on the mean and maximum life spans of fruit flies and mice.12-14 He found that in mice of a strain that normally lives a shorter period than most species, DMAE extended the mean life span by 30% and the maximum life span by up to 27%. The same was not found to be the case in longer living strains of mice, however. But, in another study, 40% of a long-lived strain had survived to the end of the study versus only 10% of untreated mice.
In a study using rats, DMAE has been found to diminish the level of water-insoluble, cross-linked, protein fractions that normally increase with age in brain cortical tissue and liver. This cross-linking of proteins is believed to be caused by hydroxyl free radicals during several metabolic processes. DMAE actually caused the reversal of this phenomenon in old rats. The RNA in the brain cortex of these rats ultimately reached the level of young adult members of the species.
Other studies have shown that DMAE decreases the accumulation of age pigment (lipofuscin) in the brain and heart muscle of a variety of lab animals.16-18 At least one study shows that this may be the result of enhanced levels of antioxidant enzymes in the brain.19
Tardive dyskinesia is a movement disorder thought to arise from dopamine receptor supersensitivity brought on by long-term neuroleptic-induced receptor blockade. In a succession of studies, DMAE has been found to exercise a favorable effect on the chronic dyskinesias following prolonged use of neuroleptics. It also proved helpful with other extrapyramidal manifestations and on motor restlessness (akathisia).20
The Dose-Response Curve
In memory research, scientists often do what is known as a dose-response study. Memory is tested at several different dosage levels and the results are then plotted on a graph. As the dosage increases, memory improves - but only up to a point: as you increase the dosage further, you find memory dropping off.
DMAE is no exception to this rule. DMAE improves retention test performance but, as with most substances that support memory function, after the optimum dose is reached, performance declines.
When combined with certain drugs or nutrients, the optimum dose levels may be much lower. When DMAE is combined with cholinergic drugs, there is a striking reduction in the optimal dose for enhanced retention.21
Precautions: Overdosage can produce insomnia, dull headaches, or tenseness in muscles (especially those of the jaws, neck, and legs). These side effects disappear if the dosage is lowered slightly. No serious adverse effects have ever been reported with DMAE. Patients with certain types of epilepsy should be closely monitored by a physician. DMAE should not be used by people who are manic because it can deepen the depressive phase.
- Honegger C, Honegger R. Occurrence and quantitative determination of 2-dimethyl-aminoethanol in animal tissue extracts. Nature. 1959;184:550-552.
- Sergio W. Use of DMAE (2-dimethylaminoethanol) in the induction of lucid dreams. Med Hypotheses. 1988;26:255-257.
- Giurgea CE. The nootropic concept and its prospective implications. Drug Dev Res. 1982;2:441-446.
- Anderson K, Anderson L. Orphan Drugs. Los Angeles, CA: The Body Press, 1987:69.
- Haubrich DR, Gerber NH, Pflueger AB. DEANOL affects choline metabolism in peripheral tissues of mice. Neuropsychopharmacol. J. Neurochem. 1981;37:476-482.
- Millington WR, McCall AL, Wurtman RJ. DEANOL acetamidobenzoate inhibits the blood brain barrier transport of choline. Ann Neurol. 1978;4:302-306.
- Caille E.-J. Study concerning the bisorcate demanol effects upon quantified EEG, cortical vigilance and mood. Comparative double-blind, cross-over balanced design versus pirisudanol. Psychol Med. 1986;18:2069-2086.
- Pfeiffer CC, et al. Stimulant effect of 2-dimethyl-l-aminoethanol: possible precursor of brain acetylcholine. Science. 1957;126:610-611.
- Lewis JA, Young R. Deanol and methylphenidate in minimal brain dysfunction. Clin Pharmacol Ther. 1975;17:534-540.
- Pfeiffer CC. Parasympathetic neurohumors. Possible precursors and effect on behavior. International Review of Neurobiology. 1959:195-244.
- Destram H. Presse Medical. 1961;69:1999.
- Hochschild R. Effect of dimethylaminoethyl p chlorophenoxyacetate on the life span
of male Swiss Webster albino mice. Exp Geront. 1973;8:177-183.Also 1971;6:133 and
- Zs-Nagy I, Nagy K. On the role of cross-linking of cellular proteins in aging. Mech Ageing Dev. 1980;14:245-251.
- Nandi K. J Gerontol. 1968;23:82.
- Riga S, Riga D. Brain Research. 1974;72:265.
- Dylewski DP, et al. Neurobiol Aging 1983;4:89.
- Roy D et al. Experimental Gerontol. 1983;18:185.
- Lambert PA, Wolff PH, De Maximy B, Ghenim A. Dimethylaminoethanol in the treatment of late dyskinesia induced by neuroleptic drugs. Ann Med Psychol. 1978;136:625-629.
- Flood JF, Smith GE, Cherkin A. Memory retention: Potentiation of cholinergic drug combinations in mice. Neurobiol. Aging 1983;4:37-43.
- Saccar CL. Drug therapy in the treatment of minimal brain dysfunction. Am J Hosp Pharm. 1978;35:544-552.