Wilson's Disease causes excessive copper levels. "The protein ATP7B is important in the vesicular pathway of hepatic copper transport into bile. The WD gene mutation leads to absence or diminished function of ATP7B, resulting in a decrease in biliary copper excretion" 
On one blog a parent said his child's uremic copper level was so high the doctor wanted to do further testing to rule out Wilson's Disease. However, this condition is usually tested for by looking at the patient's ceruloplasmin concentration, and not by genetic testing because no quick genetic test has been developed yet. Unfortunately, the ceruloplasmin test is not a reliable method for ruling out the possibility of a child being a heterozygous carrier of Wilson's Disease since, "low serum ceruloplasmin concentrations may occur in up to 20% of asymptomatic WD heterozygotes".  So 80% of the time, a child who does have one copy of this gene would still have normal ceruloplasmin levels.
When I first heard about Wilson's disease 3 years ago, I never thought that autism and Wilson's Disease could be related because Wilson's Disease (the homozygous form) is very rare and causes liver problems and Kayser-Fleischer rings in the patient's eyes. However, after I learned that many children with autism have high copper to zinc ratios I decided to research Wilson's Disease more closely, and what I learned shocked me:
1. Wilson's Disease (the homozygous form where the person has 2 copies of this gene) is rare, but "Wilson's Disease is the most common of a group of hereditary diseases that cause copper overload in the liver" 
1 out of 100 people are heterozygous carriers for Wilson's Disease.  That's almost the same percentage as the current autism rate.
2. Even though most adults who are heterozygous carriers of WD are asymptomatic, CHILDREN with only one copy of the gene were found to have reduced serum copper levels with high uremic copper levels and neurological symptoms. (Just like many children with autism.) Here's the study:
"This paper reports on a study of the heterozygous children of patients with Wilson's disease. A total of 16 children of 10 patients with the disease were followed up. Detailed biochemical, clinical and EEG tests were done. Nearly all the children were found to have reduced serum copper and caeruloplasmin levels and high rates of urine copper excretion following exposure to penicillamine. These findings were different from the results obtained in adult heterozygous carriers. Thirty per cent of the children had pathological neurological findings, and EEG abnormalities were found in 75%." 
3. Wilson's Disease IS a mitochondrial disorder that causes encephalopathy and depletes metallothionein.  And "patients with Wilson's disease have relevant glutathione depression, with low levels of reduced glutathione and cysteine and high concentrations of oxidized glutathione [just like many children with autism]. This is prevented by zinc administration, which inhibits lipid peroxidation and increases glutathione availability." 
4. This study found that Wilson's disease may involve more than just copper:
"Interaction of trace metal metabolism was studied in a patient with Wilson's dease. Atomic absorption analysis showed markedly increased urinary excretion of copper and aluminum and an increased ALUMINUM content was found in the biopsied liver by neutron activation analysis. These findings suggest a complicated pathogenetic mechanism involving other metals besides copper in the Wilson's disease." 
5. "The Wilson's disease gene (ATP7B) has been mapped to chromosome 13 (13q14.3) and is expressed primarily in the liver, kidney, and placenta. The gene codes for a P-type (cation transport enzyme) ATPase that transports copper into bile and incorporates it into ceruloplasmin. Mutations can be detected in 90% of patients. Most (60%) are homozygous for ATP7B mutations (two abnormal copies), and 30% have only one abnormal copy. 10% have no detectable mutation." 
Compare that to this finding about the placentas of children who developed autism:
"They found that the placentas from ASD children were three times more likely to have the [trophoblast] inclusions... We knew that trophoblast inclusions were increased in cases of chromosome abnormalities and genetic diseases, but we had no idea whether they would be significantly increased in cases of ASD," said Kliman. "These results are consistent with studies by others who have shown that ASD has a clear genetic basis." 
Could the trophoblast inclusions be indicative of the ATP7B gene mutation that causes Wilson's Disease?
6. Wilson's disease can cause parkinsonism and schizophrenia-like symptoms, and a family history of these disorders is believed to increase a child's risk of developing autism. Here's a report about a man who was misdiagnosed with paranoid schizophrenia (and he also suffered from parkinsonism) until it was discovered 12 years later that he really had Wilson's Disease: HERE "The clinical presentation and therapeutic response of this patient strongly suggest a link between the cerebral intoxication by copper and the psychiatric symptoms." 
7. This website even suggests treating autism by following the same steps used to treat Wilson's Disease:
"A Lesson From Wilson's Disease
-Wilson's disease is copper overload disease which disables MT
-Two-phase treatment is effective
Step 1: removal of excess Cu
Step 2: long-term maintenance using Zn therapy – in Autism need to remove all metals.
>Autism therapy requires removal of Cu and toxic metals" 
8. Another study found that "Haplotypes in AKR1A1, COMT, ATP7A and ATP7B (Where the WD gene is located) also showed association with autism." 
There have already been environmental studies linking heavy metals in pollution to autism. However, not every child in these polluted areas has autism. So wouldn't a disease that causes the body to store excessive amounts of metals be a logical genetic risk?
And even if it's not specifically the same mutation seen in heterozygous carriers for "Wilson's Disease", 300 mutations of the Wilson's Disease gene have been identified, and perhaps the ATP7B gene (or some other gene in the ATPase gene family) could give researchers a clue of what genes should be studied. Furthermore, "A normal variation in the PRNP gene can modify the course of [Wilson's Disease] disease by delaying the age of onset and affecting the type of symptoms that develop. This gene produces prion protein, which is active in the brain and other tissues and also appears to be involved in transporting copper." 
One potential problem with this theory is the incidence of autism is higher in boys than girls, but Wilson's Disease affects men and women equally. However, I don't think that should rule out heterzygous WD as a potential cause that's worth researching. It is highly possible that the genetic susceptibility could be gender neutral, and it is the triggers which are gender specific. Consider the following studies:
- A trigger that affects males: This CDC study that found that among males, increased prenatal exposure (and increased exposure from birth to 7 months) to thimerosal was associated with, "poorer performance with attention and executive functioning", but "there were no significant associations for females". Here
- A trigger that affects females: This CDC study found that "Low birth weight and preterm birth increase the risk of autism in infants by about twofold, but more so for girls than for boys. ... When the 565 boys and girls with autism were looked at separately, the boys had less than a twofold increased risk of autism if they were born at low birth weight, but the low-birth-weight girls had a threefold or higher risk". Here.
The 2 findings above could help explain the higher incidence of autism in boys than girls because the thimerosal in the flu shot is given to most pregnant women and babies over 6 months, but most babies are not born prematurely.
(And it's also possible that some other factor is causing the low zinc levels, which would also result in low metallothionein production, high copper levels, and a weakened immune system. So some research will need to be done to determine which comes first; the the excess copper storage or the low zinc levels.)
IMPORTANT: I'm NOT suggesting that children with autism have Wilson's disease (the homozygous form that causes liver problems). I'm just asking if these children could have one copy of the WD gene, which might make them more susceptible to environmental toxins (such as the metals in vaccines) than their peers. So if your child has autism, please don't worry about the problems typically seen in Wilson's Disease. This is still only a theory, and most heterozygous carriers of WD are asymptomatic. However, being a heterozygous carrier of some diseases can make you more susceptible to environmental triggers than the general population. So I'm wondering if children with one copy of the gene would have also been asymptomatic if not for all the toxins in vaccines... That would also mean that in the absence of further vaccinations, and with the addition of supplemental zinc therapy, there probably wouldn't be any further regression or worsening of health problems.