The Myth of Autism

by Dr. Michael J. Goldberg, Elyse Goldberg, Dr. Ismael Mena

  In medical school there was no discussion of entities in adults of chronic fatigue syndrome, fibromyalgia or in children of mixed ADHD, quiet ADHD, or of an epidemic of “autism.” As discussed, the appearance of these entities makes sense when looked at together.

  It is worth noting that classically autoimmune diseases are more common in women than men, and while “autism” is now in girls and boys, the fact that it is more common in boys than girls may support discussions that boys, before their hormonal changes, may be more susceptible to immune dysfunctions/stress. Perhaps children and adults have been honest when they said they didn’t feel good, couldn’t think straight, that their brains felt foggy—it turns out that in medical history the mysterious idea of chronic fatigue or CFIDS goes back to at least the 1500s. There have been epidemics throughout history (one documented by the father of English medicine Thomas Siddenhaum in the 1680s) of a mysterious ailment, fatigue, mental dysfunction with a flulike presentation—but unlike today, these presumed outbreaks were reported and then would disappear for long periods of time. Of course with no objective data, no ability to determine the cause of these epidemics, the result was hysteria rather than scientific investigation.

  In 1934, Dr. Sandy Gilliam described an outbreak of an unusual fatiguing illness that was then termed “atypical poliomyelitis.” Two particular outbreaks that were investigated by Dr. D. A. Henderson at the CDC and Dr. Alexis Shelokov at the NIH led to the term “epidemic neuromyasthenia,” which has been the preferred term for outbreaks of fatigue since they reviewed this problem in the New England Journal of Medicine back in 1957.

  The problem began somewhere in the late 1950s and early 1960s, accelerating dramatically by the 1970s and 1980s. Worldwide outbreaks of this strange phenomenon began to occur, but unlike in the past, they keep recurring, instead of stopping. One of the outbreaks in Japan, in 1984, was termed the “low NK syndrome.” Symptoms were a general dullness, with no identifiable bacterial or viral agent evident.

  If one applies our emerging understanding of complex immunology and virology, it appears that a medically based epidemic may be occurring—and we have ignored this for at least twenty-six years now.

  As far back as an NIH-sponsored research conference in Boston in October 1998, it was acknowledged that some of these “psychosomatic” adults might really have something medically wrong with them. Some of them showed low NK cells, evidence of an immune stress that could lead to chronic viral activation, mitochondrial dysfunction, and unfortunately an increased risk for cancer. At that conference was the recognition that some of these patients were found to have evidence of an “activated” HHV6. Twelve years later, these finding are still being challenged and investigated. Over the years it has remained easier for many in the NIH and our academic institutions to “debate” and challenge viral or immune findings (they are not the same, they are not consistent on everyone), rather than focus on explaining and understanding how they might really be playing a key role in the pathogenesis of these disorders. The reasons or explanations for this become harder and harder to understand or remotely justify at a time of crisis like this.

  Historically these outbreaks have led to an inquiry and investigation by the NIH’s National Institute of Allergy and Infectious Disease and the CDC’s Viral Exanthems and Herpesvirus Branch. But unfortunately, CFS/ CFIDS was not classified as a possible immune or viral disease, and, sadly, high-powered experts concluded these symptoms were psychosomatic. I do not believe we would be missing the medical reality of this misnamed epidemic of “autism” today, if CDC experts, when called in to investigate this outbreak, had been constructive, leading the way on a progressive, logical course to understanding, prevention, and likely treatment. Instead, after first mistakenly dubbing it Epstein-Barr syndrome, due to elevated viral titers, embarrassed, many of the researchers went on personal vendettas, encouraging the press to use the term “yuppie flu,” and implying this was not a serious medical illness in these adults (mostly women). It is worth noting that CFS is no longer considered an infectious disease. While perhaps not an acute, fast-moving infectious disease like the flu, a cold, measles, or polio, there is no question that we are looking at a slow but insidious immune/viral phenomenon we might have stopped or corrected by now if we had focused resources on understanding, getting answers.

  One of the major reasons for the misdirection of the medical system can be traced back to the confusion over the patients presenting during the Lake Tahoe outbreak starting in August/September of 1984. As noted, high-level investigators/researchers disregarded the importance of elevated viral titers. By focusing on psychosomatic causes and ignoring the evidence of viruses and markers for probable immune dysfunction in these adults, we veered off course more than twenty-six years ago.

  Back in medical school, we were all taught that evidence for an acute viral infection meant what was called an IgG titer rose, changed fourfold (i.e., 1:20 becomes 1:80 (borderline), 1:40 became 1:160, 1:80 became 1:320, etc.). While not definitive, when symptoms of an illness were present and a viral titer changed fourfold or more, that was considered suggestive, very suspicious evidence for that virus. Even then, without a brain biopsy or a technique that evolved to what we call a positive PCR probe, the titers were suggestive, even convincing, but not definitive proof (the brief appearance of any positive IgM titer was very suspicious, often felt to be hard evidence of an active virus—now even that is often ignored as a “false positive”). However, as noted, in 1984 for very complex reasons, when at first these adults and later children appeared with constantly high elevated titers, titers that in medical school we were taught represented presumed evidence of that virus, they were ignored. So instead of what should have been the start of a medical investigation into why these adults had these acutely elevated Epstein-Barr or other viral titers but now on a chronic, long-term basis, mainstream researchers and “medicine” decided (and began to teach) that these titers meant nothing.

  Now, instead of twenty-six years devoted to understanding this new disease phenomenon, definitive protocols, and new medications to help, we first discredited adults by calling all their complaints psychosomatic, and now we are somehow selling a completely illogical, unscientific idea that everything in these children is developmental. No.

  A recent article from Stanford University illustrates how extreme this has become. A Dr. Montoya and his associates argued that if we were taught that it was significant if viral titers went up fourfold, shouldn’t it be significant if with therapy the titers went down fourfold? He treated twelve adult, chronically ill CFS/CFIDS patients with elevated herpes-6 (HHV-6) and Epstein-Barr virus (EBV) titers. Each patient had to have four or more of the following neurocognitive symptoms (parents, think of your children): impaired cognitive functioning, slowed processing speed, sleep disturbance, short-term memory deficit, fatigue, and symptoms consistent with depression. After six months with an agent called Valganciclovir (an antiherpes antiviral, but not safe for routine use), nine out of twelve (75 percent) of the patients experienced near resolution of their symptoms, resumed daily home and/or work functions—something they had been unable to do for years.

  In a world that denies meaning to these titers in adults and children, the researchers showed a significant drop in both their EBV VCA IgG titers (1:2560 > 1:640) and their HHV-6 IgG titers (1:1280 > 1:320).

  Key researchers I’ve been involved with, who are openly pleased with “the Dr. Montoya article” acknowledged they could never have received funding or approval in the current research atmosphere. Only because he was so powerful, so “big,” was he able to do it. After twenty-six years of this, isn’t it time the prevailing attitudes changed?

  3

  CHANGING LETTERS: ADD? ADHD? MIXED ADHD? QUIET ADD?

  IN THE EARLY TO MID 1980S, the varying labels of ADHD (ADD with hyperactivity, ADD without hyperactivity, ADHD, etc.) were being applied to describe the newly dysfunctional children appearing in my practice and around the country. Wit
h no imaging and no application of new tools to understand the brain, the radical differences with the new ADHD (now the majority in pediatrics) have not been understood—leading to likely medication errors in these children. Making judgments, even educated ones, based on symptomatology, without closer evaluation of real function in the brain, in my opinion, should not be allowed in the twenty-first century. We now have the tools. We have a responsibility to use them. From NeuroSPECT work (see later discussion in this book and article references), the old-fashioned hyper-ADHD child (bright, alert, with increased blood flow to the frontal lobes and normal temporal lobes and rest of brain) is quite different from the new mixed or quiet ADHDs (where each has components of temporal lobe hypoperfusion, and usually has components of “spaciness,” “zoniness,” cognitive dysfunctions, anxiety, oppositional behaviors, or depression).

  With this insight, the obvious idea is that this is not the same as whatever was happening with the possible 5–10 percent of children, usually boys, who were considered the old-fashioned hyper-ADD child. As noted, that child was bright, intelligent, and alert—if you could get them in their seats. Significantly, there was no discussion in medical school of these children having cognitive or executive dysfunction. Subsequently, on NeuroSPECT scans, they had hyperperfusion in their frontal lobes and a generally healthy rest of the brain. When the mixed, quiet, and multiple other variants of ADHD began to appear, it was immediately obvious—since most of them had components of temporal lobe dysfunction, temporal lobe hypoperfusion—something else must be going on.

  Against this background of an autism epidemic, attention deficits now represents not only the most common developmental problem in school-age children but has also changed dramatically. Where it was once thought that ADD affected school-age children, who were expected to outgrow their “ADD” issues by puberty, it is now recognized that between 50 to 70 percent of children with attention deficits diagnosed between six and twelve years of age continue to manifest troublesome symptoms throughout adolescence and beyond. With the term ADHD now routinely applied to adults and children, and with multiple variants discussed, perhaps it is time to recognize that this has nothing to do with the original work about ADD/ADHD. An increasing number of ADHD children are now being diagnosed with Tourette’s syndrome. Tourette is now viewed as “immune” related. I not only believe that none of this is coincidental but also that the only way to understand it is the overwhelming fact we have an unrecognized medical epidemic. This is not compatible with the idea of suddenly better awareness, or as noted, an “epidemic” of previous developmental or psychological categories of dysfunction.

  Supporting the conclusion that this is a new medical epidemic are observations by researchers over the last three decades that continue to emphasize the contribution of weaknesses in higher-order cognitive functions (i.e., thinking and reasoning processes) to the school failure of many learning-disabled children. Children have appeared in large numbers with deficits in “metacognitive” skills (i.e., being able to access acquired knowledge when needed, knowing how to apply learned skills). These children are unable to focus their attention on the salient features of tasks. They cannot effectively devise strategies to get them done. These children are often described as “passive” learners. It was immediately obvious that when I was taught that an ADD child (referred to as hyper-ADD) was inherently very intelligent, very bright, “they just could not be kept in their seats,” it was clearly a different era, and those children presented with different symptoms than they have now. Children now present with cognitive issues, and these children are appearing in larger and larger numbers. These symptoms, these ADHD variants that were not even recognized in the 1970s, are now the vast majority. We are also, to our great detriment as a society, continuing to focus on all the “other” reasons why schools are failing, grades are falling, IQs are dropping, without any recognition that these children are having an outright “cognitive dysfunction” from a disease. How long do we fail, and how long do we allow these children to fail, before we say enough is enough?

  With the rapidly enlarging group of children that do not fit “classic” autistic profiles, the number of ADHD variants, and other multiple labels being used to categorize, define our children, it is time to step back, and return these children to the medical world. With the increased recognition and understanding of immune-dysregulatory phenomenon, it is time to realize these issues in children are not secondary to some strange, previously misunderstand developmental or psychological issues, but we have a real medical epiphenomenon. Whether this epiphenomenon is caused by a retrovirus, a regular virus, a genetic disposition (very probable), environmental changes (very probable), ozone layer issues, or multiple other factors insinuated or looked at over the years impacting our immune systems, once in effect we have a process being controlled by the body’s own “innate” neuroimmune system (supported by multiple peer-reviewed articles), and it’s time we understood that and dealt with that appropriately and effectively as medical physicians.

  Additional support for the immune system linkage, not as a secondary factor but as a true primary pathophysiologic explanation for this disease/ disorder, is the recognition that within this group of patients a common denominator is a large number of allergies or intolerances. Around 25 percent of healthy children now have chronic illnesses including allergies, migraines, diabetes, and more, while it has been also recognized that many children with complex medical disorders show allergies and immune issues. Commonly, within the family histories one often finds eczema, migraines (especially in mothers), hay fever, asthma, and/or some other “autoimmune” disease such as thyroiditis, lupus, or rheumatoid arthritis. As I point out to parents frequently, this supports the primary pathophysiology of the immune system, immune-related issues, not something being developmental or genetic. What one does not see within these families is a routine history of true genetic or developmental disorders.

  How is it that nobody has recognized or linked the lowering of IQ over the last twenty years per ERIC (Educational Resource Information Center) databases to the likelihood of a medical, cognitive, and physical epidemic?

  As noted elsewhere, the key is the recognition that these new type of children with ADHD, Tourette’s syndrome, and other variants of LD (learning disorders) really had a common denominator of temporal lobe hypoperfusion, linked, one could argue, by the new idea we were proposing called NIDS.

  Going beyond just the study of symptoms and intelligent but subjective ideas and approximations, this gave a logical, objective insight to understand these disorders and, most important, look at real treatment goals for these children. (Again, the fact that our medical system is still pursuing subjective treatment and medications for these children should be intolerable to all parents of children afflicted with these disorders.)

  While I was generally opposed to the use of stimulant medications for something we called hyper ADD, and though I was never comfortable with not understanding how they worked, it turns out in some situations they might have helped that child with “classic” hyper ADD. That said, the chances of helping the new “mixed” or quiet type of ADD via these methods are not only extremely low, in theory they may be causing long-term harm. Based on NeuroSPECT, as noted, the original class ADD child had too much function, with increased blood flow in their frontal lobes. While I remain generally opposed to their use, one could argue that stimulant medications, with their now recognized vasoconstrictive action (just like cocaine and amphetamines), had a limited place in the treatment of those type of children. One was potentially decreasing blood flow to those hot frontal lobes with, one hopes, minimal negative effects to the key temporal lobes. The problem is that even today, it is difficult to conceive of long-term “cocaine use” (i.e., the effects of ritalin or amphetamine-based medications today) ever being healthy for the brain. In fact, while I was in medical school these “upper” stimulant medications that calmed hyperactive children down were not recommended with teenagers
or adults. We were warned not to use them in teenagers or adults. How is it that they are routinely being used in adolescents and adults today? Instead of using stimulant medications as prescription uppers for a seemingly tired brain, perhaps it’s time we asked why these patients are tired and why they have trouble staying focused. If we did, maybe we would understand that we are looking at a medically based disorder, not the developmental disorder of decades ago. Like autism, and now autism spectrum disorder, we have expanded almost exponentially the labels (based on combinations of symptoms) rather than look at a true medical, physiologically based disorder or problem.

  The problem was soon quite obvious. Approaching the expanding categories of ADHD in a knee-jerk manner, we are using stimulant medications (although some experts are finally beginning to change) for these new kinds of ADDs, just like the hyper-ADDs. In these children, one could first argue theoretically, using a vasoconstrictor (which causes a narrowing of the arteries), like a stimulant medication, particularly without an SSRI or other support for the temporal lobes, could very likely result in a net ongoing education dysfunction, and even a lowering of IQ potential, by further slowing down or delaying already-decreased temporal lobe functions.

  Sadly, these concerns are probably no longer idle or just theoretical, because if you look at the statistics around this country, there is now a recognized lowering of the IQ potential of children across many grade levels. How many adolescents (perhaps at that age still more boys than girls) are not really healthy, not energetic or sharp enough to really push themselves to excel? How many are part of our growing rate of high school dropouts? If they make it to college, how many of these young adults are unable to function in a college environment, after going through high school on stimulant medications, perhaps seeming to do okay, but likely missing many key cognitive tools they were supposed to have developed further or better? The good and the bad here is that with many years of insight and good scientific studies, we now know the brain is more pliable than we imagined—able to develop years beyond old ideas, old time lines. It is just as correct to say that we are not born with a five- or ten-year-old brain. We have known for years that the brain is like a muscle. As we mature, as we use it, we develop new tracks, we refine connections to become more efficient, faster, etc. Beyond just not functioning right, it has become apparent that we are missing key maturation and development points when an area is shut down, not functioning correctly. So only by directing appropriate therapies can we realistically hope to allow these areas to reopen, regain potential ability, and function in a healthier manner. Only then, for so many of these interconnected cognitive disorders, do you have any real expectation, potential chance, or possible true goal of restoring function and higher developmental abilities. Everything happening makes sense if we look at this as an illness and apply hard science.