Update on Urine Mycotoxin Testing

Occasionally, I receive emails from individuals who have read my prior blog post on urine mycotoxin testing. Often, these are from people who disagree with my position on the use of this testing.

When evaluating patients for chronic inflammatory response syndrome (CIRS), historically—and according to the Shoemaker Protocol—the use of urine mycotoxin testing has been discouraged. The primary reason is that, until recent years, available tests largely focused on food-based mycotoxins (such as ochratoxin, verrucarin, zearalenone, roridin, sterigmatocystin, and aflatoxin).

More recently, newer tests have become available that attempt to evaluate for mycotoxins associated with water-damaged buildings (WDB) rather than food sources.

I am now seeing more patients who bring in results from these newer mycotoxin tests. In some cases, the results can be mildly helpful—particularly when the mycotoxins identified in the patient correlate with those found in environmental testing of the home. However, it is critical to understand that abnormal urinary mycotoxin results do not eliminate the need for proper evaluation of the home, workplace, or school environment as well as the patient themselves.

These newer tests attempt to detect a broader range of mycotoxins associated with WDB exposure. For example:

• Satratoxin and isosatratoxin are trichothecene mycotoxins often produced by Stachybotrys chartarum and other WDB-associated molds. Their presence may be significant, particularly if the same toxins are identified in a building the patient occupies.

• Gliotoxin is produced by Aspergillus fumigatus, another organism commonly associated with water-damaged environments.

• Mycophenolic Acid is a mycotoxin produced by Penicillium fungi and occurs in WDB, moldy foods, and grains. If tested and elevated, it is not possible to know the source.

Despite these advancements, urine mycotoxin testing remains limited compared to environmental testing.

Tests such as ERMI and HERTSMI-2 use PCR-based methods to detect and quantify mold DNA within a building. For example, ERMI evaluates 36 different mold species, providing a much broader and more comprehensive environmental assessment.

In contrast, current urine mycotoxin tests for WDB-related exposure typically evaluate only one or two relevant toxins. I recently reviewed a lab report that grouped all trichothecene mycotoxins together. This presents a problem, as trichothecenes can be derived from both food sources (e.g., roridin) and WDB molds (e.g., satratoxin). Without specific differentiation, it is not possible to determine the true source of exposure.

Example of a newer mycotoxin test marketed as a Mycotoxin Building Panel. Notice the "TRICHO" or the trichothecene group includes several trichothecene mycotoxins, which may be from grain-based foods or a WBD. There is no differentiation for what makes up the "Present" and high level. The majority of mycotoxins tested on this report are from food sources.

Returning to the principles of the Shoemaker Protocol, it remains more practical and clinically sound to:

1. Evaluate the environment (home, workplace, school) for WDB-associated molds and bacteria

2. Assess the patient for the characteristic inflammatory patterns showing reactivity and genetic predisposition associated with CIRS

   
   

It is important to recognize that approximately 50% of buildings in the United States may have some degree of water damage, while about 24% of the population has a genetic predisposition to develop CIRS. However, most individuals within that 24% will not go on to develop illness.

Conversely, roughly 75% of the population is not genetically susceptible, meaning it would not be appropriate to diagnose or treat these individuals for CIRS based solely on urine mycotoxin testing. Knowing that half of all buildings in the US are considered WDB, it would be expected that half of the people testing as controls would likely have elevated WDB mycotoxins.

Bottom line: Urine mycotoxin testing may provide supportive information, but it should not be used to diagnose CIRS or to guide treatment. Environmental evaluation and clinical correlation remain the foundation of appropriate care.

To learn more about food-based mycotoxins, please see the related post.