Now the math: According to the National Institutes of Health, roughly 23.5 million Americans have 24 of the 80 recognized ADs (the other 56 lack sufficient research for inclusion), making the prevalence of autoimmune disease greater than cancer (9 million) and roughly equal to heart disease (22 million).

Far from politically correct, AD truly discriminates—more than 75 percent of its patients are women. Discounting accidents, homicides, and suicides, an analysis from the Department of Community Medicine at the University of Connecticut Health Center’s School of Medicine in 2000 lists AD as a the seventh-leading cause of death among females ages one to 14, the fifth-leading cause of death among females ages 15 to 44, and the seventh-leading cause of death among females ages 45 to 65.

Given these numbers, it’s easy to conclude that the national rate of AD has increased; it’s just not easy to prove. Numerous factors—our growing population, significantly improved diagnostic techniques, increased awareness, and better access to health care, especially for minorities—make the numbers behind the AD debate more difficult to pin down. While no one study shows an overall increase in the incidence of autoimmune disease in the US or internationally, other studies illustrate that certain ADs are indeed on the rise, namely Type 1 diabetes. Edwin Gale, MD at the University of Bristol in the UK, estimates the global rate of increase of Type 1 diabetes since the mid-20th century at roughly 3 percent a year. While his study focused on rates rather than causes, Gale posits that environment factors, in conjunction with an individual’s genetics, may explain the steady rise of Type 1.

Other autoimmune diseases, such as MS and lupus, lack definitive empirical studies showing overall increases in stable populations; but one look at their numbers tends to make a rather damning impression: MS rates doubled in the US among females from the 1980s to the �0s, according to the Department of Health and Human Services. And mortality rates for lupus nearly doubled from 1979 to 1998, according to the Centers for Disease Control and Prevention.

Emphasizing the complexities of AD and the study of its overall incidence rate, Glinda Cooper, PhD, a leading environmental epidemiology and AD researcher, explains, “While creating an umbrella category for autoimmune disease benefits awareness and research funding, as a generalized disease designation, it’s an oversimplification, in that there are important differences between many ADs.�While she concurs that Type 1 diabetes is on the rise—and says MS and lupus probably are, too—others, such as rheumatoid arthritis, are on the decline in the US. But, even though the RA incidence rate—the number of new cases occurring yearly in a population—has dropped, the disease most often occurs after age 50. Thus, as the baby boomers, that demographic juggernaut, reach their most RA-susceptible years, the number of cases will rise.

“We don’t know why the rates of different ADs have changed,�says Cooper, lead author of “Occupational exposures and autoimmune diseases,�a National Institute of Environmental Health Sciences (NIEHS) study, “but it’s likely that environmental factors, including infectious agents, and occupational and environmental exposures to a variety of compounds—dusts, metals, solvents—are contributing to these patterns.�Still, like most AD researchers, Cooper feels the definitive link between environmental culprits and autoimmune disease won’t be established without further study.

And yet our environment abounds with innumerable suspects, in incalculable combinations and concentrations, that interact with our genetic predispositions—and they start as soon as we’re conceived. It’s no surprise that, as with cancer, genes matter. Compared to people without autoimmune disease, AD patients tend to have more parents, siblings, or children with AD, albeit not necessarily the same AD.

Aside from the genetic hands our parents have benevolently dealt us, the possible environmental offenders encompass both natural and synthetic factors. Studies have shown that exposure to mercury, silica dust, the Epstein-Barr virus, volatile organic compounds, or stress, might precipitate autoimmune disease. Others indicate that vitamin D deficiency, cow’s milk fed to infants, or the hygiene hypothesis may play a role. Of course, no list of shady characters omits cigarette smoking and the man-made environmental estrogens, such as the infamous dichloro-diphenyl-trichloroethane (DDT), polychlorinated biphenyls (PCBs), and dioxin, along with some of the newer concerns on the block, bisphenol A (BPA), phthalates, and polybrominated diphenylethers (PBDE)—the latter trio being practically unavoidable in societies awash in plastics.

Primarily a female hormone (men have trace amounts), estrogen can also act as an immuno-enhancer. If a significant amount of environmental estrogens accumulates during fetal and infant development, it may hypersensitize the immune system, which could result in an increased susceptibility to autoimmune disease. And considering AD’s overwhelming prevalence in women, many members of the research community ponder the possible connection between environmental-estrogen exposure and AD.

Phytoestrogens, naturally occurring plant estrogens that we eat nearly everyday—in soybeans, grains, vegetables, herbs—complicate matters. Since we all typically consume phytoestrogens in quantities greater than the amount of synthetic estrogens we unwittingly ingest, many toxicologists (and Big Industry) say there’s no need for concern.

Endocrinologists, however, argue that environmental estrogens impact the endocrine system at extremely small doses—doses deemed safe by toxicologists—and are capable of modifying immune responses. While not denying the potential culpability of phytoestrogens, most endocrinologists point out that we evolved to eat plants, not to consume the synthetic hormones currently leeching into our food and water supplies from plastic containers, PVC pipes, and leaky landfills.

The lack of communication between the medical specialties only compounds disagreements between toxicologists and endocrinologists. Autoimmune patients don’t see dedicated AD doctors, they see specialists, resulting in the compartmentalization of AD—a rheumatoid arthritis patient sees a rheumatologist, an MS patient sees a neurologist. Not surprisingly, the new focus of the NIEHS calls for improving the dialogue between specialists, researchers, and patients. Welcoming that tack, an optimistic Ladd, herself a lupus patient for more than 40 years, says that her organization is satisfied with the current strategic planning of the NIEHS. “While most researchers want to focus on one aspect of environmental causation, we agree that an integrated analysis of the multiple factors that are involved in developing AD—hereditary, toxicological, endocrinological, and stress—is the best method of working toward a real understanding of associations between AD and environmental exposures.�/FONT>