That is what mainstream sources would tell you, certainly. However, Arthur provides a lot of evidence that this isn't in fact the truth. To understand how we have been misled, we need to look into the work of Dr. William E. Morton, professor of occupational and environmental medicine at Oregon Health Sciences University. Again, from Chapter 10 of Arthur Firstenberg's "Invisible Rainbow" book. I've bolded a few sentences that I thought were particularly relevant: *** Because of the way it was discovered, and the lack of synthetic chemicals in the environment at that time, porphyria became known as a rare disease that was triggered in genetically susceptible people by certain drugs, such as sulfonal and barbiturates, which these patients had to avoid. It was not until another century had passed, in the early 1990s, that Dr. William E. Morton, professor of occupational and environmental medicine at Oregon Health Sciences University, realized that because ordinary synthetic chemicals were far more widespread in the modern environment than pharmaceuticals, they had to be the most common triggers of porphyric attacks. Morton proposed that the controversial disease called multiple chemical sensitivity (MCS) was in most cases identical with one or more forms of porphyria. And when he began testing his MCS patients he found that, indeed, 90 percent of them were deficient in one or more porphyrin enzymes. He then investigated a number of their family trees, looking for the same trait, and succeeded in demonstrating a genetic basis for MCS—something no one had attempted before because MCS had never before been connected to a testable biological marker.3 Morton also found that most people with electrical sensitivity had porphyrin enzyme deficiencies, and that electrical and chemical sensitivities appeared to be manifestations of the same disease. Porphyria, Morton showed, is not the extremely rare illness it is currently thought to be, but has to affect at least five to ten percent of the world’s population.4 Morton was courageous, because the rare-disease world of por-phyria had come to be dominated by a handful of clinicians who controlled virtually all research and scholarship in their small, inbred field. They tended to diagnose porphyria only during acute attacks with severe neurological symptoms and to exclude cases of milder, smoldering illness. They generally would not make the diagnosis unless porphyrin excretion in urine or stool was at least five to ten times normal. “This makes no sense,” wrote Morton in 1995, “and would be analogous to restricting the diagnosis of diabetes mellitus to those who have ketoacidosis or restricting the diagnosis of coronary artery disease to those who have myocardial infarction.”5 The higher numbers reported by Morton agree with the numbers reported over a century ago—the proportion of the population that became ill when they took the sleeping medication sulfonal. They are consistent with the finding, in the 1960s, of “mauve factor,” a lavender-staining chemical, not only in the urine of patients diagnosed with porphyria, but in the urine of five to ten percent of the general population.6 Mauve factor was eventually identified as a breakdown product of porphobilinogen, one of the porphyrin precursors.7 Morton also found, in agreement with recent reports from England, the Netherlands, Germany, and Russia, that persistent neurological problems occur during the chronic, smoldering phase of every type of porphyria—even those types which were previously supposed to cause only skin lesions.8 *** Source: Firstenberg, Arthur. The Invisible Rainbow . Chelsea Green Publishing. Kindle Edition.