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 I just wanted to say thanks for such great customer service on my recent order. I didn't expect to receive it so quickly after just placing the order the other day. This was my first order with your company but will not be my last. Thanks again..Darrin L (Arvada, CO)

Dimethyl Glycine (DMG)

Dimethylglycine or DMG is a non-protein amino acid found naturally in animal and plant cells. DMG is produced in cells as an intermediate in the metabolism of choline to glycine.

There has been much confusion surrounding the history of DMG as a nutritional supplement. DMG appeared as a supplement in the 1960s under the names vitamin B15, pangamic acid and calcium pangamate. Calcium pangamate was originally a mixture of calcium gluconate and DMG. Calcium pangamate was intended as a delivery form of DMG. However, several products entered the supplement marketplace called pangamic acid or calcium pangamate, and these did not contain DMG. Some of these products contained, instead of DMG, a substance called diisopropylammonium dichloroacetate. At present, DMG supplements are available that do contain dimethylglycine.

DMG-containing calcium pangamate was popular with Russian athletes and cosmonauts because it was reputed to enhance oxygenation at the cellular level, reduce fatigue and enhance physical stamina. None of those claims, however, was ever substantiated. DMG is neither a vitamin nor an essential nutrient. DMG is also known as N, N-dimethylglycine, (dimethylamino)acetic acid and N-methylsarcosine.

DMG is a solid, water-soluble substance. DMG should not be confused with TMG (trimethylglycine or betaine). TMG is involved in the methylation of homocysteine to form methionine.


DMG is absorbed from the small intestine and from there transported by the portal circulation to the liver. DMG is metabolized in the liver to monomethylglycine or sarcosine which, in turn, is converted to glycine. Dimethylglycine dehydrogenase, a flavoprotein, is the enzyme that catalyzes the oxidative demethylation of DMG to sarcosine. The methyl group produced in this reaction returns to the one carbon pool at the level of N10-hydroxymethyl-tetrahydrofolic acid. DMG itself is formed from trimethylglycine or betaine. DMG that is not metabolized in the liver is transported by the circulatory system to various tissues in the body.


It is too early to say whether DMG might eventually be indicated as an immune enhancer or in the management of autism. It is not indicated as an anticonvulsant, in epilepsy or for any condition characterized by seizures. Nor is it indicated as an energy booster or athletic-performance enhancer.


Based on claims that DMG is a highly potent "oxygenator" of body/brain tissues, this supplement has been touted as a panacea for years.

Several studies show that DMG has no anticonvulsant value and is thus of no help in epilepsy or other conditions characterized by seizures. Persistent claims that DMG is useful in autism are thus far anecdotal.

Claims that DMG can boost energy and athletic performance have been refuted by human and animal studies. Tests on exercising thoroughbred horses found "no beneficial effects on cardiorespiratory function or lactate production." And male track athletes supplemented with DMG exhibited no significant changes in short-term maximal treadmill performance.

On the other hand, an early finding that DMG can enhance both humoral and cell-mediated immune responses has been fortified by some subsequent research. This animal research needs to be extended to humans.

Early fears that DMG might be mutagenic now appear to be unfounded.


Dimethyl Glycine (DMG)

Immunomodulating properties of dimethylglycine in humans.

Graber CD; Goust JM; Glassman AD; Kendall R; Loadholt CB. J Infect Dis 1981 Jan; 143(1): 101-5 PMID: 6163829 UI: 81169354

Dimethylglycine (DMG), a tertiary amino acid, has had wide acceptance as a nonfuel nutrient; presumably it enhances oxygen utilization by tissue and complexes free radicals. Its potential as an immunoadjuvant has also been suggested by a study of an analog of DMG, calcium pangamate. A double-blind study in 20 human volunteers showed a fourfold increase in antibody response to pneumococcal vaccine in those receiving DMG orally as compared with controls (P less than 0.01). Production of leukocyte inhibitory factor in response to concanavalin A was similar in the two groups, but those taking DMG tablets had a significantly highr mean response of leukocyte inhibition factor to streptokinase-streptodornase (P less than 0.001). The in vitro responses of lymphocytes from patients with diabetes and those with sickle cell disease to phytohemagglutinin, convanavalin A, and pokeweed mitogen were increased almost threefold after addition of DMA. These results suggest that DMG enhances both humoral and cell-mediated immune responses in humans.

N,N dimethylglycine and epilepsy.

Gascon G; Patterson B; Yearwood K; Slotnick H. Department of Neuroscience, University of North Dakota School of Medicine, Fargo. Epilepsia 1989 Jan-Feb; 30(1): 90-3 PMID: 2463912 UI: 89107126

Nineteen institutionalized patients with frequent seizures (group average two to three per day; seizure types--generalized, akinetic/myoclonic), were treated randomly with either placebo or N,N dimethylglycine (DMG) for 28 days. Dosage was 300 mg/day for the first 14 days and then 600 mg/day. Plasma levels were measured at baseline, days 2, 5, 8, 15, 22, 30, and 1 and 2 weeks after the study ended. No differences in seizure frequency were noted between placebo and DMG or between baseline and test conditions. No toxicity was noted.

Dimethylglycine and chemically related amines tested for mutagenicity under potential nitrosation conditions.

Hoorn AJ. Hazleton Biotechnologies, Veenendaal, The Netherlands. Mutat Res 1989 Apr; 222(4): 343-50 PMID: 2468082 UI: 89201299

Dimethylglycine (DMG) and the chemically related amino acids glycine, sarcosine (monomethylglycine) and betaine (trimethylglycine) were tested in Salmonella typhimurium strain TA100 after treatment with sodium nitrite under acidic conditions using a modified Ames Salmonella/microsome assay as reported by Colman et al. (1980). The increase in the number of revertants observed both with and without metabolic activation was also induced in the control mixtures without adding the amines. From the subsequent testing of the individual components of the mixtures, we concluded that non-consumed nitrite was responsible for the mutagenic responses observed in the different reaction mixtures, and not the amines themselves. There were no consistent indications of mutagenic activity of the DMG test mixture as compared to the control mixture which exhibited both consistent mutagenic activity and a toxic effect which was not increased by the addition of DMG. In fact, DMG seemed to decrease the toxicity of the control reaction solution to the Salmonella which was clearly observed at the higher doses. DMG cannot be considered mutagenic under the test conditions employed. The same can be said of the other amino acids as well.

Stimulation of the immune response by dimethylglycine, a nontoxic metabolite.

Reap EA; Lawson JW. Department of Microbiology, Clemson University, SC 29634-1909.

J Lab Clin Med 1990 Apr; 115(4): 481-6 PMID: 1691258 UI: 90217822

The immunomodulating capacities of dimethylglycine (DMG) were examined in a rabbit model. Female New Zealand white rabbits were immunized on day 0 and were given booster inoculations on day 9 with either killed influenza virus or Salmonella typhi vaccine. Experimental animals were force fed 20 mg/kg body weight of DMG daily beginning 14 days prior to the first inoculation and continuing throughout the experiment. Control animals were force fed daily only distilled water. Blood was obtained on day 0, day 9, and day 30. Hemagglutination inhibition assays showed a more than fourfold increase in mean antibody titer to influenza antigen in the DMG-treated animals (p = 0.0006) after the first inoculation, and a fourfold increase in mean titer after the booster inoculation (p = 0.1000). A standard agglutination test for Salmonella typhi O (somatic) and H (flagella) antigens was performed on all sera from animals receiving the typhoid vaccine. Mean antibody titers to the O antigen were significantly higher (more than threefold) after the first inoculation (p = 0.0302) and more than fivefold higher after the booster inoculation (p = 0.0047) in DMG-treated animals. Mean antibody titers to the H antigen were also higher in DMG-treated animals compared with controls after both the first and second inoculation. Lymphocyte transformation assays on cells taken from DMG-treated animals immunized with the influenza vaccine showed a tenfold increase in mean proliferative response (p = 0.0024). Lymphocytes from DMG- treated animals immunized with the typhoid vaccine showed a fourfold increase (mean values) in thymidine uptake (p = 0.0180). No toxicity or adverse effects were observed at any time during the experiment.

Immunologic responses in healthy random-source cats fed N,N- dimethylglycine-supplemented diets.

Weiss RC. Department of Pathobiology, College of Veterinary Medicine, Auburn University, AL 36849. Am J Vet Res 1992 May; 53(5): 829-33 PMID: 1381880 UI: 92398180

The immunomodulatory capacities of N,N-dimethylglycine (DMG) were examined in random-source cats. Blood mononuclear leukocytes of healthy adult cats that had negative results to tests for FeLV and feline immunodeficiency virus were exposed in vitro to various concentrations of DMG (10 to 1,000 micrograms/ml) and were evaluated for proliferative responses to T- or B-cell phytomitogens. Although increased, mean lymphocyte blastogenic responses to phytolectins in DMG-treated cultures did not differ significantly from responses of untreated cultures. For in vivo studies, cats were given a solution containing either 100 mg of DMG or a control solution without DMG orally at 8 AM and 6 PM for 40 consecutive days. On post-treatment day 24 and 25, mean blastogenic responses to phytolectins in DMG-treated and control cats inoculated 10 days earlier with an inactivated feline virus vaccine were similar. Cats given DMG and inoculated twice in a 3-week interval with a commercial vaccine containing inactivated feline herpesvirus-1 and feline calicivirus had significantly (P = 0.045) lower virus neutralizing serum antibody titers against feline herpesvirus-1, compared with titers of control cats, whereas feline calicivirus titers were similar in both groups. On day 25, mean serum interferon activity, induced after IV inoculation of Newcastle disease virus, was significantly (P = 0.021) lower in the DMG-treated cats. Results of this study of DMG in healthy cats failed to demonstrate enhancement of either specific or nonspecific immunity.

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