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Your body makes almost no D-lactate on its own. The tiny amounts that normally circulate in your blood come from background metabolism of a waste product called methylglyoxal, and the levels are so low they barely register on standard lab equipment. When D-lactate rises into the detectable range, it almost always means one thing: bacteria in your colon are fermenting carbohydrates that should have been absorbed higher up in your digestive tract. That fermentation produces D-lactate, which spills into your bloodstream and, at high enough concentrations, can poison your brain.
What makes this test uniquely valuable is that standard lactate tests cannot detect it. Routine lactate assays measure only L-lactate, the version your own muscles and organs produce during normal metabolism. D-lactate is the mirror-image molecule, and it requires a separate, specialized assay. A person can be severely acidotic with dangerously high D-lactate levels while their routine lactate reading comes back completely normal.
D-lactate and L-lactate share the same chemical formula but are three-dimensional mirror images of each other, the way your left and right hands share the same structure but cannot be superimposed. This difference in shape means they are handled by entirely different enzymes in your body. L-lactate is a normal byproduct of how your cells burn sugar for energy, and your body recycles it efficiently. D-lactate, by contrast, is metabolized by a separate enzyme called D-lactate dehydrogenase (LDHD), and your body clears it much more slowly.
In healthy people, the main source of circulating D-lactate is your gut bacteria. Certain species, particularly Lactobacillus, produce D-lactate when they ferment sugars and starches. Normally, this stays contained in the colon at low levels. Problems arise when large amounts of unabsorbed carbohydrates reach the colon and fuel a surge in bacterial D-lactate production that overwhelms your body's ability to clear it.
D-lactic acidosis is a distinct metabolic emergency that occurs almost exclusively in people with short bowel syndrome (a condition where a large portion of the small intestine has been surgically removed or is non-functional) or in people who have had older types of weight-loss surgery that bypass part of the intestine. A systematic review of the medical literature identified 98 reported cases, with about 21% of people with short bowel syndrome experiencing at least one episode. The condition is considered common in this population but frequently missed.
The syndrome requires several conditions to align: carbohydrates must be poorly absorbed in the small intestine, D-lactate-producing bacteria must be present in the colon, carbohydrate intake must be high enough to fuel significant fermentation, colonic transit must be slow enough to allow absorption of the D-lactate produced, and the person's capacity to metabolize D-lactate must be insufficient to keep up. Contrary to an older belief that humans cannot metabolize D-lactate at all, current evidence shows that healthy people can clear it at meaningful rates. This means impaired metabolism is likely a prerequisite for the condition to develop, not just excessive production.
The hallmark presentation is episodic encephalopathy, a medical term for a temporary disruption of brain function. People with D-lactic acidosis become confused, develop slurred speech, lose coordination, and often appear intoxicated. The neurological symptoms are a direct toxic effect of D-lactate on the brain, distinct from the effects of L-lactate. Severe cases can require mechanical ventilation. The metabolic picture shows a high anion gap (a calculated marker of acid buildup in the blood), low bicarbonate, but normal L-lactate and negative ketones. This combination of findings is the diagnostic signature.
A case-control study of children with intestinal failure found that a history of midgut volvulus (a dangerous twisting of the intestine) carried 17 times the odds of developing D-lactic acidosis. Intestinal lengthening procedures were also a strong risk factor. Among children who developed D-lactic acidosis, anion gap acidosis on blood work was a consistent finding. In pediatric short bowel syndrome, risk was associated with the underlying cause and the type of surgical reconstruction, not simply the length of remaining intestine.
While short bowel syndrome is the most studied context, D-lactate elevation has been observed in several other settings. Propylene glycol, a compound found in some intravenous medications, food additives, and antifreeze, is metabolized to D-lactate and can cause accumulation in people receiving large doses. D-lactate has also been found elevated in diabetic ketoacidosis, where one study measured average levels of 3.82 mmol/L in affected individuals compared to 0.25 mmol/L in controls, with a strong correlation (r=0.686) to the anion gap.
An emerging line of research has examined D-lactate as a potential marker for bacterial infection in the bloodstream. Because bacteria, not human cells, produce D-lactate, a rise in blood levels could theoretically signal bacteremia. One study found that a plasma D-lactate level above 131 micromoles per liter had 100% specificity and positive predictive value for bacteremia, meaning that every person above that threshold truly had bacteria in their blood. However, the sensitivity was only 31%, meaning the test missed most cases. This limits its standalone diagnostic value but suggests it could be useful as a confirmatory signal.
D-lactate has also been studied as a marker for acute intestinal ischemia (loss of blood flow to the gut), but the results have been disappointing. The largest study, involving 2,958 patients, found poor diagnostic performance for detecting intestinal tissue death, with only 26% sensitivity and a statistical accuracy measure (AUC) of just 0.588. A separate study found D-lactate could not reliably distinguish intestinal ischemia from other causes of abdominal pain.
One study examined the connection between D-lactic acidosis and small intestinal bacterial overgrowth (SIBO, a condition where excessive bacteria colonize the upper intestine) in people with brain fog, gas, and bloating who had normal gut anatomy. Among those evaluated, D-lactic acidosis was present in 77% of patients who had brain fogginess, compared to 25% of those without brain fogginess. SIBO was also more common in the brain fog group (68% versus 28%). This suggests that even without short bowel syndrome, bacterial overgrowth may produce enough D-lactate to cause neurological symptoms in some people.
D-lactate does not have standardized clinical reference ranges endorsed by major guidelines. The values below are drawn from published laboratory validation studies. Different labs use different assay methods, and results can vary between platforms, so the most reliable approach is to compare your results within the same lab over time.
| Tier | Approximate Range | What It Suggests |
|---|---|---|
| Normal | Below 0.25 mmol/L | No significant bacterial D-lactate production detected. Consistent with normal gut function. |
| Elevated | 0.25 to 0.5 mmol/L | Mild elevation that may reflect increased colonic fermentation. Warrants clinical correlation and repeat testing. |
| High | Above 0.5 mmol/L | Clearly abnormal. In a person with short bowel syndrome or malabsorption, this level is consistent with D-lactic acidosis risk. |
| Critical | Above 3.0 mmol/L | Associated with D-lactic acidosis and encephalopathy. This level typically produces neurological symptoms and requires urgent evaluation. |
These tiers are drawn from published research. Your lab may use different assays and cutpoints. One pediatric reference study found a 95th percentile of just 19 micromoles per liter (0.019 mmol/L) in a non-diseased population, with no differences between boys and girls. Another lab established an upper reference limit of 0.05 mmol/L. The gap between these values and the clinical cutpoints above reflects the enormous range between "statistically normal" and "causing symptoms." Compare your results within the same lab over time for the most meaningful trend.
D-lactate levels can swing dramatically in a single day. One case documented plasma levels fluctuating between 0.5 and 3.1 mmol/L within hours, and urinary levels ranging from 1.1 to 52.8 mmol/L. This extreme variability means a single normal reading does not guarantee that D-lactate is not spiking at other times, particularly after meals.
For people with short bowel syndrome or known malabsorption, serial measurements correlated with symptoms are far more informative than isolated values. If you are monitoring D-lactate to evaluate dietary management or antibiotic therapy, consider testing during or shortly after a symptomatic episode, and again when you feel well, to establish your personal range. If your levels are consistently below 0.25 mmol/L and you have no symptoms, annual monitoring during routine follow-up is reasonable. If you are making dietary changes to reduce carbohydrate fermentation, retesting 4 to 8 weeks after the change can show whether the intervention is working.
For people without short bowel syndrome who are testing D-lactate as part of a gut health investigation (for example, evaluating SIBO-related brain fog), a baseline value provides a starting reference point. If it comes back elevated, retesting after treatment gives you concrete evidence of whether your gut bacterial balance has shifted.
D-lactate levels can be distorted by several factors unrelated to the condition you are trying to evaluate.
In healthy adults with normal gut anatomy, D-lactate levels are remarkably stable at near-zero concentrations. Exercise, time of day, and typical dietary variation do not meaningfully change the reading, because D-lactate is not a product of human muscle metabolism. The confounders above matter primarily for people who already have a reason to produce or accumulate excess D-lactate.
Evidence-backed interventions that affect your D-Lactate level
D-Lactate is best interpreted alongside these tests.