D-Lactic Acid

D-Lactate is produced by bacteria residing in the colon when carbohydrates are not completely absorbed in the small intestine. This by-product is excreted in the urine.

When large amounts are absorbed it can cause:

- metabolic acidosis (your cells throws off the chemical balance in your blood, making it more acidic),

- altered mental status (from drowsiness to coma)

- a variety of other neurologic symptoms, such as dysarthria (a speech disorder caused by muscle weakness) and ataxia (degenerative disease of the nervous system).

Although a temporal relationship has been described between elevations of plasma and urine D-lactate and the accompanying encephalopathy (brain disease, damage, or malfunction), the mechanism of neurologic manifestations has not been explained.

D-lactic acidosis is typically observed in patients with short-bowel syndrome and following jejunoileal bypass resulting in carbohydrate malabsorption.

Also, healthy children presenting with gastroenteritis may also develop the critical presentation of D-lactic acidosis.

Some possible treatment options (always consult your doctor first before starting any treatment):

- Limit simple carbohydrate intake (cakes, cookies, pie, candies, etc) as well as sugar alcohol (sorbitol, mannitol, xylitol, etc.), fructose and other highly osmolar, fermentable compounds and excess fiber.

- Carbs should be complex and modest in quantity, with small and frequent meals to avoid exposure of the gut flora to large, poorly absorbed boluses of CHO. It has also been suggested that fermented foods, such as yoghurt, sauerkraut and pickles be avoided given high preexisting concentrations of D-lactate.

- Fasting has been associated with rapid improvement in D-lactate associated encephalopathy.

- Antibiotic therapy may increase or reduce D-lactate production, depending on the gut flora selected for.

• Antimicrobial therapy should be selected with caution in patients at risk for small bowel bacterial overgrowth (SBBO) as certain antibiotics may select for lactate-producing gut flora. While it is reasonable to treat acute episodes of D-lactate toxicity with antibiotic therapy targeting Lactobacillus species, chronic preventive antibiotic therapy has not demonstrated consistent effect.

Only elevated is of concern. D-lactic acid is generally produced in minimal quantities by human cells. It comes from three sources,

1. from human methylglyoxal (MGO) pathway (assumed to be the sole source of blood D-lactate in healthy people),

2. production by gut bacteria (mostly in patients with short bowel syndrome (SBS)),

and 3. ingestion of preformed D-lactate.

The source of D-lactic acid is dependent on the situation. MGO is a precursor of glycation of proteins and DNA, resulting in advanced glycation end products (AGEs), which is associated with increased oxidative stress. MGO is predominantly detoxified by the glyoxalase system (requires glutathione), with the majority going to D-lactate.

- Only elevated is of concern. D-lactic acid is generally produced in minimal quantities by human cells. It comes from three sources,

    1. from human methylglyoxal (MGO) pathway (assumed to be the sole source of blood D-lactate in healthy people),

    2. production by gut bacteria (mostly in patients with short bowel syndrome (SBS)), and

    3. ingestion of preformed D-lactate.

- The source of D-lactic acid is dependent on the situation. MGO is a precursor of glycation of proteins and DNA, resulting in advanced glycation end products (AGEs), which is associated with increased oxidative stress. MGO is predominantly detoxified by the glyoxalase system (requires glutathione), with the majority going to D-lactate.