Sallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger

НазваниеSallie Bernard* Albert Enayati, B. S., Ch. E., M. S. M. E. Heidi Roger
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In addition to the above case studies, we have collected preliminary data on three autistic children who have not undergone chelation. These children also exhibit elevated levels of mercury.

Data on Non-Chelated ASD Children



Mercury level and source of sample

2 ½ yrs.


Heavy metal hair analysis 5.6ppm (ref.range 0-2)

4 ½ yrs.


Hair analysis 1.2ug/g (ref. <0.4) PRBC 18.4 (ref <9)

5 yrs.


Hair analysis 1.8 ppm PRBC 18.3 (ref.<9)


Several observations from these case studies deserve mention. One is that all of the children experienced a regressive form of autism. Other findings are that (i) low levels of mercury in hair may be associated with large amounts of mercury excretion on provocation and (ii) initial levels of provoked mercury may not be as high as subsequent ones. Mercury in the hair will only reflect a current or recent exposure of approximately one year or the body's active detoxification of mercury. This was evident in a child with non-detectable levels of mercury in the hair and positive levels on provocation.

In the case studies there is also a trend of higher numbers for mercury in younger children (20 month hair sample of 4.8 ppm and 2 ½ year hair sample of 5.6 ppm). This may be related to the fact that the testing was performed closer to the time of exposure. Hair levels of mercury greater than 5.0 ppm are considered diagnostic for mercury poisoning (Applied Toxicology, 1992). Among the majority of these case studies much more modest elevations of mercury, if detected at all, were associated with high levels of provoked mercury.

There are no standards for provoked levels of mercury in children in the context of behavioral disorders. Therefore, we surveyed a large number of physicians treating adults with chronic health problems diagnosed as secondary to mercury. These clinicians advise that tolerable limits may vary according to the general health of the patient and associated health problems. All consulted agreed that in adults excretion of 50 mcg of mercury per gm creatine after intravenous DMPS challenge is worrisome. We submit that the concern level for children should be even more stringent. High levels of mercury are demonstrated in some children without a history of fish consumption, amalgam burden, or known environmental exposure, suggesting the role of vaccines as a contribution to body burden.

The families who submitted these case histories wanted to tell their stories because their children are noticeably improved after treatment for mercury. Whether this improvement was sudden or gradual, the parents are convinced that lessening the mercury and heavy metal burden has helped their child. They ask us to request support for much needed research in this area.


How reasonable is it to claim that the most common form of autism, where there is normal development and then regression, could be caused by mercury poisoning? There are several reasons to believe that this process has indeed occurred.

Diagnostic Criteria Are Met

Medical literature demonstrates that mercury can induce autism-spectrum traits, and this association extends to mercury’s localization within specific brain nuclei. In attempting to address “the totality of the syndrome” (Bailey et al, 1996), we have shown that every major characteristic of autism has been exhibited in at least several cases of documented mercury poisoning, and that every major area of biological and neurological impairment implicated in ASD has been observed with Hg exposure. Recently, government-directed studies have revealed that the amount of mercury given to infants receiving vaccinations exceeds safety levels. The timing of mercury administration via vaccines coincides with the onset of autistic symptoms. Case reports of autistic children with measurable mercury levels in hair, blood, and urine indicate a history of mercury exposure along with inadequate detoxification. Thus the standard criteria for a diagnosis of mercury poisoning in autism, as outlined at the beginning of this paper, are met. In other words, mercury toxicity is a significant contributing factor or primary etiological factor in many or most cases of autism.

Unique Form Would be Expected, Implicates Vaccinal Thimerosal

Symptoms manifested in mercury poisoning are diverse and vary by the interaction of variables such as type of mercury, age of patient, method of exposure, and so forth. Thus, although it could be argued that in all the thousands of cases of past Hg poisonings, no instance of autism could be found, such an argument fails to take into account the possibility of unique expression. It would be comparable to saying that, because in all the cases of Minamata disease no instance of acrodynia could be found, then acrodynia could not be caused by mercury poisoning. Since there are no case reports or systematic studies in the literature of the effects of intermittent bolus doses of injected ethylmercury on “susceptible” infants and toddlers, it would be reasonable to expect that symptoms arising from this form of mercury poisoning would present as a novel disease. In fact, given the high neurotoxicity of organic mercury, its known psychological effects, and the age at which it has been given in vaccines, it would almost be a given that the “novel disease” would present as a neurodevelopmental disorder like autism.

Conversely, the fact that autism meets the diagnostic criteria for mercury poisoning, yet has never been described as a mercury-induced disease, requires that the disorder must arise from a mode of mercury administration which has not been studied before. This would rule out other known sources of Hg like fish consumption or occupational mercury hazards, as these have been well characterized. It is possible that another under-investigated mercury route, such as maternal Hg exposures (e.g., from vaccinations, thimerosal-containing RhoGam injections during pregnancy, or dental fillings) or infant exposures to thimerosal-containing eardrops or eyedrops, might be a factor, and this cannot be ruled out.

Historical Precedent Exists

There is a precedent for large scale, undetected mercury poisoning of infants and toddlers in the syndrome that came to be known as acrodynia or pink disease. For over 50 years, tens of thousands of children suffered the bewildering, debilitating, and often life-long effects of this disease before its mercury etiology was established, as Ann Dally relates in The Rise and Fall of Pink Disease (1997, excerpts):

"Acrodynia is a serious disease that was common, at least in children’s clinics, during the first half of the present (20th) century. Reports abound of children too miserable to acknowledge their mothers, such as the child who kept repeating, “I am so sad.” One unhappy mother was quoted as saying, “My child behaves like a mad dog.” In most cases the condition improved spontaneously, but was often regarded as chronic. Mortality varied from 5.5% to 33.3% and was usually about 7%. Most physicians who speculated on the causes of pink disease believed in either the infective or the nutritional theory. No one seems to have suggested that it might be due to poisoning. It was a tradition to advise student doctors to treat cases of difficult teething with the mercury powders that were eventually to be revealed as the cause of the disease. The ill-effects of mercury on the mouth had been known at least since the time of Paraclesus, but it was not until 1922 that the pediatrician, John Zahorsky, commented on the similarity between pink disease and mercury poisoning. He dismissed rather than pursued his new idea of possible mercury poisoning and suggested a theory that was more in tune with current fashion. Most doctors, even those skilled in the use of calomel, associated mercury poisoning with adults (syphilis, industrial poisoning, hatters shakes) rather than with infants. By 1935 the disease was seen in every children’s out-patient clinic.

The mystery began to be solved in 1945 by Dr. Josef Warkany, of the Cincinnati Children’s Hospital. He and his assistant found large amounts of mercury in the urine of a child with pink disease. They did not publish their findings until 1948, but it is noteworthy that the news seems not to have spread through the small and tightly knit pediatric world, where everyone knew everyone else. It was probably because the idea was unfashionable and contrary to the conventional wisdom. The theory that mercury poisoning caused pink disease was gradually accepted, but against resistance, particularly by older men and those in powerful positions. Mercury was withdrawn from most teething powders after 1954, initially through voluntary action by the manufacturers because of adverse publicity and probably in the hope of avoiding statutory prohibition. Pink disease almost disappeared. Later in the decade the theory was widely accepted and soon pink disease was no longer part of the usual pediatric out-patient clinic."

Thus, like acrodynia before it, autism may in fact be “just another” epidemic of mercury poisoning, this time caused by childhood vaccinal mercury rather than infant teething powders.

Barriers Preventing Earlier Discovery Are Removed

The priorities and methods of research experts in the autism and mercury fields have prevented the association between mercurialism and ASD to be recognized until recently.

The effects on humans of mercury-containing medicinals and home remedies used to be studied quite regularly by medical researchers (Warkany and Hubbard, 1953); but since, aside from vaccinal thimerosal, such products have declined dramatically in number since the 1950s and 1960s, most mercury researchers today focus on biochemical studies or environmental sources like fish and coal plants. Some mercury experts seem surprised to learn that Hg is present in infant vaccines (authors’ personal experience), and as recently as 1997, when the EPA released its massive review of extant mercury research, vaccines were not even mentioned as a potential source. Thus it is not surprising that mercury experts have never investigated thimerosal as they have, say, contaminated whale meat consumption in the Faroes Islands or Hg exposure among Amazonian goldminers.

Likewise, it is not surprising that neither mercury experts nor autism professionals have ever investigated autism as a possible disease of mercury exposure. Since its discovery by Kanner, autism has been characterized in almost exclusively psychological terms. The descriptions have been such that the symptoms would be essentially unrecognizable as manifestations of poisoning to any mercury expert not looking closely. A perfect example is Kanner himself, who recorded feeding problems and vomiting in infants and concluded: “Our patients, anxious to keep the outside world away, indicated this by the refusal of food.” Bruno Bettleheim, who dominated autism discourse in the 1950s and 1960s and blamed the entire disorder on “refrigerator mothers” who forced the withdrawal of the child, asserted, "the source of the anxiety is not an organic impairment but the child's evaluation of his life as being utterly destructive" (1967, reported in ARI Newsletter). In 1987, Robert Sternberg would propose a “unified theoretical perspective on autism” by defining the disorder in terms of a “triarchic theory of intelligence,” and in the same publication Lorna Wing and Anthony Attwood would write:

“Sometimes young autistic children will stand in a dejected posture, with tears streaming down their faces, as if they suddenly felt their helplessness in the face of a world they cannot understand."

Even as recently as 1995, a typical slate of articles in the dominant Journal of Autism and Developmental Disorders (April 1995) would consist of eight psychological pieces (example: “Generativity in the Play of Young People with Autism”) and one biomedical one (on biopterin). Thus biomedical research in autism existed, but it was mostly relegated to the margins as psychology held center stage, and the symptomatic characteristics of autism continued to be presented in accord with psychological biases.

In the latter part of the 1990s, the situation on both sides changed. Congressional mandate led to the public quantification of the cumulative amount of mercury in vaccines, raising interest in understanding its effects. Parent organizations like CAN and NAAR, working with the NIH and other researchers, engineered an autism research agenda which is more heavily focused on underlying physiological mechanisms of the disease. With parents already suspecting a vaccine-autism link, the environment was right for investigations focused on the link between vaccinal mercury and autism.


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