The Autoimmune Epidemic: Bodies Gone Haywire in a World Out of Balance--and the Cutting-Edge Science that Promises Hope (No Series) (22 page)

But Pollard, who has been a faculty member at Scripps since 1992 and has since added a great deal of scientific understanding to the way mercury stimulates this two-step autoimmune response, is perhaps best known for showing how a slight difference in genetic code can dramatically change mercury’s impact on the immune system, causing it to induce an autoimmune response swiftly, more moderately—or even not at all.

Because researchers would never expose human beings with differing genetic profiles to mercury on purpose in order to see exactly what genes might help some people avoid disease, mice are used instead. As it turns out, mice provide a clear lens through which scientists can view how different degrees of genetic susceptibility contribute to mercury-induced autoimmunity. Over the course of several studies Pollard and his Swedish collaborators have exposed strains of mice with different genetic susceptibility to autoimmune disease to inorganic mercury. The mice in their experiments displayed varied degrees of autoimmune responses to mercury depending upon their genetic backgrounds. A few strains that were not genetically susceptible to lupus were resistant to developing mercury-induced autoimmunity, while a number of other strains that were genetically susceptible to lupus developed a disease closely resembling lupus in humans.

But the salient question was: How did these exposures in mice relate to the amount of mercury that average Americans are exposed to in their day-to-day lives?

In order to replicate in lab mice what everyday contact with mercury in our environment might translate to for humans, Pollard and his colleagues had to figure out the average level of mercury—the mercury body burden—that most Americans are carrying in their tissues and bloodstreams. His team looked at data showing the standard amount of mercury that has accumulated, over time, in the kidneys of healthy people who did not have a history of occupational exposure to mercury and who died in accidents or from other non-disease-related causes. It turns out that the average level of inorganic mercury in healthy people’s kidneys is about 0.5 micrograms for every gram of kidney tissue. Pollard’s lab set that level as a guideline for dosing lab mice with mercury so they could build up a load in their kidneys analogous to that which most humans are unknowingly walking around with. They then exposed groups of lupus-prone female mice, known as BXSB mice, to doses of mercury that they thought might produce a similar burden of mercury in their kidneys.

Just as the investigators had found with the other lupus strains of mice, not only did mercury exposure make the disease occur earlier in these BXSB mice, but the greater the dose of mercury the earlier the disease appeared. After thirty-eight weeks of slow, continuous exposure, one group of female BXSB mice developed a level of mercury in their kidneys equivalent to that of a typical human exposure. This group of mice, and groups with higher levels of exposure, showed accelerated development of autoimmunity, while mice given a lower dose of mercury developed disease at a rate similar to the control mice, which were exposed merely to a saline solution. Pollard and his colleagues concluded that “environmentally relevant tissue levels of mercury”—meaning levels analogous to that which many Americans have in their bodies—“could be associated with exacerbations of autoimmune disease in genetically susceptible individuals.”

Genetics is therefore key to understanding how mercury influences autoimmunity. To see how this works, let’s imagine that we have in front of us a group of ten mice, each with a different genetic susceptibility to lupus, and a train with ten boxcars that each mouse must race through. Before attempting to make it through the train, each mouse is first exposed to a dose of mercury that’s analogous to what many of us carry in our bodies right now from a combination of mercury amalgam dental fillings, fish consumption, and the amount of mercury we absorb from other foods, water, and the atmosphere around us. When a mouse possessing a high genetic susceptibility to autoimmunity gets exposed to a low dose of mercury, it develops the autoimmune disease lupus quite quickly. We might visualize this mouse as falling ill before it even gets through the very first boxcar of the train. Other mouse strains, however, which possess more genetic resistance to lupus, might only get sick after they’ve made it as far as the third or fifth boxcar—they’ve lasted that much longer before succumbing because they possess a bit more genetic resistance. And then there is that one lucky mouse strain that packs so much genetic resistance to autoimmune disease that it flies through to boxcar ten and still feels quite plucky—even though it has been exposed to the same amount of mercury in the same doses as all the other mice who developed autoimmune disease.

In this sense, different strains of mice are a good substitute for researchers to work with when considering the myriad possible different genetic subsets that make people who have been exposed to heavy metals vary in their susceptibility to autoimmune disease. Others, possessing fewer susceptible variants of genes, are less prone. Some people, like the mouse who gets to the tenth box, are remarkably resistant regardless of what you throw at them.

“The mice in our experiment are sort of like humans going through life, building up mercury exposure,” says Pollard. “This long-term chronic exposure to mercury can set autoimmune disease in motion—and certainly, for those who already suffer from autoimmunity, make disease more severe over one person’s lifetime.”

LOOPING BACK TO VACCINES

Even as the evidence pointing to the harmful effects of mercury mount, the Institute of Medicine announced in May 2004 that it had reviewed earlier studies asking whether thimerosal in vaccines could be linked to the tenfold increase in childhood autism spanning from the early 1980s through the late 1990s—and concluded that there was no link. Nevertheless, in the United States, thousands of parents of autistic children and those with certain learning disabilities are going to the mat to demand a deeper investigation into whether thimerosal has had any role in their children’s disabilities. They cite alleged evidence that the CDC covered up critical information that, throughout the 1990s, federal health officials had inadvertently nearly tripled the amount of ethyl mercury being injected into some babies during a critical period of brain development. This was at a time when new thimerosal-containing vaccines were added to the list of a child’s required shots in unprecedented numbers. By 1999, a baby who received all recommended vaccines at her two-month checkup might well have been injected with up to 118 times the EPA’s safety limit for daily exposure to mercury.

Recent research from the University of California, Davis shows that extremely small levels of thimerosal can alter the normal activity and function of critical immune cells by stimulating the production of cytokines—the body’s signaling proteins that can whip up the immune cells to trigger a full-blown immune response. By inciting immune cells at the wrong time, the cytokines lead the immune system to turn on the body itself. Researchers believe that the genetic background of some individuals may render them especially susceptible to the effects of thimerosal.

Meanwhile, in Sweden, where researchers may feel freer to write the inciting word “thimerosal” on a grant application, Mike Pollard’s close collaborators in the Division of Molecular and Immunological Pathology at Linköping University are looking closely at whether mercury in the form of thimerosal (an organic mercury) might induce the same autoimmune conditions observed in mice after exposure to inorganic mercury (inorganic mercury being the type Pollard used in his studies). Their findings, published in 2006, indicate that thimerosal does induce a systemic autoimmune response similar to that seen with inorganic mercury itself. Another recent study caused a stir within the scientific community by finding that even the low level of mercury used in vaccines preserved with thimerosal can trigger irregularities in immune-system cells in test-tube experiments. Even so, if there is an interplay with mercury, top scientists in the autoimmune-mercury field caution that there is probably no one single environmental trigger that is causing autism, just as there is no one single gene that is causing it. Any environmental role that mercury plays in autism may well be due to cumulative effects of mercury—including heightened exposure in the womb because of the way in which mercury concentrates in fetal cord blood—combined with specific viral hits, which also may occur in utero. And, just as in mice, each child’s unique genetic makeup will make it easier or harder for mercury, in combination with many other factors, to wreak its damage.

THE AUTISM-AUTOIMMUNE CONNECTION

Although we are a long way from understanding the interplay of these triggers in the rapidly rising rates of autism across the industrialized world—including the United States, Japan, England, Sweden, Denmark, and France—one of the more stunning recent findings about the syndrome is that autism may in fact have an autoimmune component. In what researchers believe is a major new discovery about the origins of autism, scientists recently detected aberrant antibodies in the blood of kids in families with a pattern of autism and in mothers with more than one autistic child. The working hypothesis is that these antibodies are actually raised against proteins in the fetal brain; indeed, researchers have found that autistic brains have chronic inflammation, a sign of immune activity. A number of scientists are now investigating whether autism might conceivably be attributed to the formation of autoantibodies against the central nervous system in genetically susceptible individuals. All of which begs the question: Are researchers about to determine that autism is also—at least in some cases—autoimmune in nature? If so, are the triggers similar to those with other autoimmune diseases? Would it then seem at all surprising if mercury were one of them, given what we know about mercury as a trigger for autoimmunity in general?

As for the role of thimerosal in autoimmunity, when I ask one researcher, who prefers to go unnamed, whether thimerosal exposure from vaccines might bear any responsibility in today’s rising rates of autoimmune disease, she is decidedly candid. She reminds me that at the same time that we are “pricking up” the immune cells to be reactive by administering a vaccine, we are also introducing that foreign antigen in a bath of mercury. For some patients, this is a potential double whammy. Think of it: in the old days, only a certain percentage of kids got mumps. Some of them suffered life-altering consequences or died, which underscores the need for the mumps vaccine. Now, however, every child gets exposed to the foreign antigen of the mumps virus (and the many other diseases we vaccinate against) via vaccines, with many of them exposed to that foreign viral protein sequence at the same moment in time that they are exposed to foreign ethyl mercury. Now, says this expert, “you have a child patient who doesn’t get measles or mumps—but they do get an autoimmune disease. Only we may not see that relationship in broad epidemiological terms, because we haven’t been looking for it.” In correcting one problem, we may have been creating another.

Some worry that our exposure to mercury from fallout from the atmosphere, intake from foods, and exposure from vaccines and dental amalgam has reached such a level that it may be contributing across the board to today’s international rise in autoimmune-disease rates—creating one widespread, global cluster, if you will. A cluster so widespread that we are all but blind to the connection.

THE HYGIENE HYPOTHESIS

The idea that our immune systems are so barraged by an onslaught of viral hits and vaccines, so vulnerable to an environment dirty with mercury, TCE, dioxin, and a hundred other known autogens that it’s sparking an autoimmune crisis, doesn’t pass muster with everyone. In fact, according to scientific proponents of what’s termed “the hygiene hypothesis,” the root cause of rising rates of autoimmunity stems not from the fact that we are living in too dirty a world, but, rather, from the fact that we are living too clean.

The too-clean theory is based on the argument that in the same century that we’ve seen a considerable rise in the prevalence of allergies and autoimmune disease, we’ve seen a dramatic decline in many previously common childhood infections such as rubella, mumps, measles, and diphtheria. That leads many scientists to argue that a lack of exposure to viruses and the swill of bacteria that most of our ancestors were exposed to living
sans
vaccines or modern hygiene means children’s immune systems are no longer forced to build up the necessary immune defenses they need. In a world of well-vacuumed homes, scrubbed bathrooms and kitchens, and more time spent in minivans than mucking about through woods, forests, and farmland, coupled with massive vaccination campaigns that prevent full-fledged infection from many childhood diseases, children’s immune systems are, in a sense, overprotected.

If a child’s immune system were a military academy, you might think of invading pathogens (be they bacteria or viruses) as sergeants providing a comprehensive set of military drills. Academy trainees need a certain number of drills to learn how to perform against a wide array of attacks. Each time they experience a practice exercise, their ability to respond with accuracy and precision is enhanced. But an underdrilled immune system may result in too few key immune cells becoming educated enough to know how to recognize and fight back against different attacks in an effective manner.

Hence, believe the too-clean theorists, the true culprit behind rising rates of autoimmune disease may be the fact that we simply don’t have enough disease and germ-laden dirt challenging our immune systems as children. Because we’ve been so well vaccinated, our homes are kept largely free of dust, dirt, and disease, and we lather up with antibacterial soaps, our immune systems haven’t had to do enough battle to become seasoned fighters. And that makes our immune cells a bit like dangerously underchallenged teenagers who are loose on the street just looking for something, anything, to occupy themselves. So when a foreign virus invades, our immune system overreacts, kick-starting a hyper-driven response, provoking everything from allergies to allergy-induced asthma to autoimmunity.