An introduction to D-lactate free probiotics

Review Article – An introduction to D-lactate free probiotics

Author – Spectrumceuticals Education, Research and Development

©Spectrumceuticals 2017 – This article, or parts thereof, may not be reproduced in any form without permission, except in the case of brief quotations embodied in critical articles and reviews.


Introduction

There has been increasing awareness about the benefits of probiotics with microorganisms which only produce the L form of lactate. This has arisen from the knowledge that humans are only able to process the L form of lactate via the pyruvate dehydrogenase enzyme.1 Thus if there is excessive production of D-lactate, the body has a limited ability to metabolise it and the subsequent build-up can lead to D-lactic acidosis.2 The symptoms can include muscle ache and pain, brain fog and fatigue.

D and L forms of lactate

Lactate, not to be confused with lactose (milk sugar), is produced through the metabolism of glucose under low oxygen (anaerobic) conditions. As with all molecules, it can be produced in two different forms: the Levo (Latin for ‘left’) or the Dextro (Latin for ‘right’). Although they each have identical chemical components, they differ in shape as mirror images of the other. The human hand is a good example of this. Although identical in composition, both hands have four fingers and a thumb, yet the left hand is different to the right. More importantly, each hand functions differently. This is also true for chemical molecules, which function differently on a three-dimensional level according to whether they have the D or the L form. The three-dimensional structure of a molecule is important in how it interacts with receptors and enzymes. If it is shaped differently it will not fit into the receptor or the enzyme and therefore there will be no chemical response. This is analogous to placing your left hand into a right-handed glove.

D lactate

D-lactate is thought to be metabolised to pyruvate instead by the enzyme D-hydroxy aciddehydrogenase (EC 1.1.99.6), which metabolises D-lactate at about one-fifth the rate that L-lactate dehydrogenase metabolises L-lactate. In humans (n _ 10) infused with 1.0 –1.3 mmol sodium DL-lactate/(kg _ h), _90% of D-lactate was metabolised and 10% excreted in the urine’. So we can say that humans have limited D-lactate metabolism (one-fifth the rate of the L form) and only 10% is renally excreted.

Neurological effects of D-lactate

The exact mechanism inducing the neurological effects of D-lactate is not known and appears to be independent of the effect of acidosis. The central nervous system has lower concentrations of the enzyme D-2-hydroxyacid dehydrogenase, which converts D-lactate into pyruvate in humans,3 thus the brain is more susceptible to the effects of D-lactate.

The lowering of intracellular pH reduces the cellular production of acetyl-CoA and ATP, which are needed for energy production in a cell.4 It is for this reason that the brain is more sensitive to the effects of D-lactate. This
is particularly true of the cerebellum, which has minimal reserves of D-2-hydroxyacid dehydrogenase, and is thus a reason why D-lactic acidosis can produce ataxia, among other symptoms.5 Gut organisms and D-lactate The presence of D-lactate is most often due to an overgrowth of bacteria in the gut or from a probiotic source which contains microorganisms which produce the D form of lactic acid.6 Researchers Sheedy et al discovered an increase in the D-lactate-acid-forming intestinal bacteria in patients with chronic fatigue. These organims were mainly enterococci and streptococci.7 It is therefore possible that this group of patients would benefit from a reduction of these bacteria and probiotics which contain bacteria which predominantly produce the L-form of lactate.

Diet

D-lactate is also present in foods fermented with lactic acid bacteria. Other natural food sources of D-lactate are apples, tomatoes, beer and wine. The diet of the individual also affects the composition of the microflora. The fermentation of carbohydrates into organic acids lowers the pH of the colon, which in turn favours the production of lactic-acid-producing organisms. Thus the reduction of carbohydrates and especially sugars in the diet may reduce the lactic-acid-producing bacteria in the bowel.8

D-lactate and autism

Increased lactic acid levels have been observed in other conditions such as autism.9 Higher levels of lactate are also associated with mitochondrial disorders, which is one of the biomarkers for these disorders.10 There is an increased prevalence of mitochondrial disorders in autism.11 Lactate has an inhibitory effect on the tricarboxylic acid cycle (TCA) in the mitochondria.12 Thus any further addition of lactic acid into a sensitive metabolic system could further reduce mitochondrial function. It is possible there are subgroups within the autism population who are more susceptible to the effects of D-lactate (e.g. those with overgrowth of streptococcus and enterococci in the gut and those with mitochondrial dysfunction).

 

Conclusion

The selection of the appropriate probiotic for each individual varies according to their specific needs. Choosing a probiotic on the basis of the content of D-lactate producing organisms is one of the considerations a practitioner will take into account when selecting the most clinically appropriate probiotic for their patient.

References

[1] Zhang DL et al, ‘D-lactic acidosis secondary to short bowel syndrome’, Postgrad Med J, 2003, 79(928):110–2.
[2] Ibid.
[3] Ibid.
[4] Ibid.
[5] Ibid.
[6] Ibid.
[7] Sheedy et al, ‘Increased D-lactic acid intestinal bacteria in patients with chronic fatigue syndrome’, In Vivo, 2009, 23(4):621–8.
[8] Zhang DL et al, ‘D-lactic acidosis secondary to short bowel syndrome’, Postgrad Med J, 2003, 79(928):110–2.
[9] Laszlo A, Horvath E et al, ‘Serum serotonin, lactate and pyruvate levels in infantile autistic children’, Clin Chim Acta, 1994, 229(1–2):205–7.
[10] Rossignol DA, Frye RE, ‘Mitochondrial dysfunction in autism spectrum disorders: a systemic review and meta-analysis’, Mol Psychiatry, 2012, 17(3):290–314.
[11] Ibid.
[12] Ibid.

©Spectrumceuticals 2017 – This article, or parts thereof, may not be reproduced in any form without permission, except in the case of brief quotations embodied in critical articles and reviews.