The few autopsies that were ever performed on those who died of Valley Fever frequently found coccidioidomycosal absesses on the substantia nigra and in the locus coeruleus within the brainstem—both highly pigmented areas of the brain.  A high percentage of victims in one study—who were largely Hispanic— also had diabetes, which researchers thought could play a role in vascular susceptibility to the spores.  But not all fatalities had compromised health: something else was making certain individuals particularly vulnerable to this disease and, as it turned out, the US military was interested in why.

As the story goes, the US military found the fatal cases of Valley Fever compelling, but not in terms of helping victims of the disease. Instead the military reportedly researched the potential of the fungus for use as a biological weapon. One can only assume who the targets of these speculative biological weapons were intended to be. Apparently military researchers released a nearly identical but less pathogenic fungus to the Coccidioidomycosis spore in a navy depot to observe how the fungus might spread on shoes.  Bits and pieces of this incident are scattered about the web and more may be buried in books I haven’t yet read.

So to recap again from Part I of this post, here’s a history of violent racist medical abuse and punitive overdiagnoses with mental illness leading to a potentially medically-avoidant population that is also underdiagnosed and understudied for expensive-to-treat actual diseases. And don’t forget a government that was reputed to have researched methods of inducing diseases specifically among those with darker skin. Under these circumstances, was it impossible that some minorities in the US might have even higher rates of autism than whites and the authorities wouldn’t know or might not care?

Remember, I was running across this information prior to last year’s CDC report that African Americans and Hispanics have lower autism incidence and did not yet know what was true and what wasn’t (I still don’t). According to other statistics, African Americans and Hispanics certainly hadn’t been left out of other possibly vaccine-mediated epidemics like diabetes and asthma and were having greater difficulty getting adequate treatment than whites, so why would autism be different? 

This brought up the question of whether vaccine mercury had some especially fatal interaction with neuromelanin, much like what is suggested for Coccidioidomycosis. I wasn’t totally off the mark. This may very well be the case, as it is hypothetically with other toxic sources of oxidative stress. But it may take much higher exposures of certain substances to get to that point.

About twenty minutes after I posted the poll listed above on the Yahoo listserv, I came back and posted what I’d discovered in the interim from a simple Google search of “melanin + mercury”:

Thu Jan 31, 2008 2:41 pm
Answering my own post. Found this: http://tinyurl.com/2nhada

A few studies conclude that melanin is *protective* against mercury poisoning. Apparently mercury does effect melanin by displacing the copper in the cell and making the skin appear lighter (which is why it was used as a skin-lightening cream comparable in effect to
hydroquinone). This makes me think that, rather than protecting exactly, this might be a case for certain cells holding onto hg even if the substance appeared to clear from brain and organs faster in pigmented mice rather than albino mice in the study.

I see a few possible ramifications of this: for instance, how would it effect outcomes if study subjects are all darker-skinned in research on the effects of vaccine mercury? Would this effect the study of m-hg poisoning in the Seychelles and the Faroe Islands?

The link I included in the post (HERE) was the first study I ran across: Al-Saleh et al.’s “Comparison of mercury levels in various tissues of albino and pigmented mice treated with two different brands of mercury skin-lightening creams”. The study completely contradicted my original concern. The thread that followed the posting of this study lasted several days and the responses and the study itself have haunted me ever since.

In a more recent but similar study, Al-Saleh’s team also researched mercury deposits in the ovaries of the same types of lab animals—albino and pigmented mice. They conclude that skin melanin plays a protective role against mercury toxicity. Over the past five years, Iman Al-Saleh has led research for King Saud University and the King Faisal Hospital in Saudi Arabia targeting the effects of mercury on child development and human health, specifically mercury in medicine, personal care products and thimerosal. Considering my initial speculation, I was very surprised by what I was reading.

The next question was whether melanin in the brain played a protective role against cognitive injuries. For this new search, I was directed to Wikipedia’s article on melanin (HERE). Among other things, skin melanin reduces the generation of free radicals and minimizes the DNA damage which leads to cancers like melanoma.

Skin is an organ. As a rank non-scientist, I was forced to ask the most basic questions about physical systems, such as whether skin melanin does anything for organs inside the body— only to find that science hadn’t necessarily answered the most elemental questions. But the “inventing the wheel” process did lead somewhere interesting. From Wikipedia:

“The loss of pigmented neurons from specific nuclei is seen in a variety of neurodegerative diseases. In Parkinson’s disease, there is a massive loss of dopamine producing pigmented neurons in the substantia nigra. A common finding in advanced Alzheimer’s disease is almost complete loss of the norepinephrine producing pigmented neurons of the locus ceruleus.” And: “In Parkinson’s disease, a disorder that affects neuromotor functioning, there is a decreased neuromelanin in the substantia nigra as a consequence of specific dropping out of dopaminergic pigmented neurons. This results in diminished dopamine synthesis. While no correlation between race and the level of neuromelanin in the substantia nigra has been reported, the significantly lower incidence of Parkinson’s in blacks than in whites has ‘promp[ted] some to suggest that cutaneous melanin might somehow serve to protect the neuromelanin in substantia nigra from external toxins’”

The quote within the Wiki article was derived from Smith and Prayson’s study review, “Lewy Body Disease” (HERE). The Wiki article also directs the reader (HERE ).

Further studies show more evidence of neuromelanin’s neuroprotective role, but also argue that neuromelanin may only be protective to a certain degree.  Apparently when level of toxins reach a certain critical mass, the protective role can be reversed.  From L. Zecca et al.’s “Substantia nigra neuromelanin: structure, synthesis, and molecular behavior”  (HERE):  “… neuromelanin was identified as a genuine melanin with a strong chelating ability for iron and an affinity for compounds such as lipids, pesticides, and MPP+. The affinity of neuromelanin for a variety of inorganic and organic toxins is consistent with a postulated protective function for neuromelanin. Moreover, the neuronal accumulation of neuromelanin during aging and the link between its synthesis and a high cytosolic concentration of catechols suggest a protective role. However, its putative neuroprotective effects could be quenched in conditions of toxin overload”(emphasis mine).

Dr. Zecca’s review becomes more specific about neuromelanin’s “chelating” action towards iron and toxic metals: 

“Neuromelanin can sequester redox active iron ions, reducing the formation of free hydroxyl radicals. Thus, in normal subjects, neuromelanin may play a protective role by inactivating the iron ions that induce oxidative stress. The ability of neuromelanin to chelate other redox active metals such as copper, manganese, chromium, and toxic metals including cadmium, mercury, and lead strengthens the hypothesis that neuromelanin may be a high capacity storage trapping system for metal ions and, as such, may prevent neuronal damage”.

What about Dr. Zecca’s statement that neuromelanin’s “neuroprotective effects” could be breached in conditions of toxic overload?  Together with evidence from cases of Valley Fever, it’s suggested that those with more melanin in the brain (if that’s possible), or skin, or both may have a higher “tipping point” for brain injury than those with less depending on the source of oxidative stress. Operative word being “may”: the issue appears to be under-studied. 
 
Not that there might not be more to find on the subject, but I was unable to dig up much more on it. Still, the research brought up more questions: If, in fact, African American and Hispanic uptake of vaccines is not significantly lower than that of whites, yet both groups may have lower autism rates than whites, what about the issue of the quadrupled rate of autism among the Minnesota Somali? Does this also fit with the higher-but-harder tipping point model (that melanin protects but can be overwhelmed and reverse the protective role)  considering that so many Somali émigrés reported being double-vaccinated? Does the fact that African American women are not only underdiagnosed with breast cancer, but are also statistically less likely to develop it in the first place, fit within this idea of melanin’s—or another biological factor’s— systemically protective nature against certain forms of oxidative stress? Does the fact that, when African American women do develop breast cancer, it’s often more severe and lethal somehow fit with a higher-but-harder tipping point for oxidative stress as well? 

Does melanin act—to a certain degree—as a “trap” for particular toxins until such point as the cellular “trap” over-fills, causing a cascade of decidedly worse damage? 

And, back to Goodman and Gallagher’s anomalous finding of higher rates of autism among Hispanic males, would some ethnic groups’ physiological dependence on neuromelanin for defense against particular forms of oxidative stress to the brain somehow leave Hispanic male infants especially susceptible to certain vaccine toxins in the period prior to age one when all children have virtually no neuromelanin?

As I kept reading, I uncovered the fact that mercury has a particularly special relationship with melanin. Melanin and neuromelanin have a tendency to bind with “cationic” chemicals rather than “anionic” substances. Because many drugs which are illegal in general and illegal in competition sports are cationic (certain steroids), sports “doping” specialists speculate that this is why so many competition cyclists may have bleached their hair in the era when drug-monitoring was performed using head-hair. Naturally blonde, gray or colorless hair would contain less evidence of doping than darker hair, so it would follow that chemically stripping melanin from hair also stripped evidence of the illegal substances which were bound to melanin.  In other words, mercury binds to melanin in the hair and everywhere else.

Ethylmercury appears to convert to a divalent cation(ic) form once in the brain and then cannot cross back out according to Burbacher et al.  Dr. Amy Holmes discusses these findings (HERE).  But what if, once trapped in the brain, the mercury itself becomes trapped in cells and, at least until it exceeds cellular capacity, somewhat declawed?

Back to my personal concerns about race and autism, it appears that, despite my children’s Hispanic ancestry, they weren’t protected from being overwhelmed by toxins.  But Hispanic isn’t a race, it’s a culture. Despite his Argentine Indian ancestry, my husband is nearly as pale as me and freckles, probably a result of his parents’ French and Italian backgrounds. Our children didn’t inherit my Irish/Scandinavian tendency to sunburn; but they don’t tan either. Argentina, like Chile, tends to be strongly European (with even a smattering of Irish: Che Guevara-Lynch) because of the almost total decimation of Indigenous populations. My husband’s family was unusual in that they always identified with their native Indian ancestry, whereas most Argentines tended (at least in the past) to deny it. All the same, when my husband’s family was forced to leave Argentina in the wake of the military junta in 1976 and relocated to the Caribbean, they were seen as “white”. 

According to the unofficial estimate of a vaccine injury activist in Argentina, the rate of autism in the district (not the city) of Buenos Aires is astronomical—something close to a quarter million. Argentina, like other South American countries, uses a high-mercury vaccine schedule. There’s no way to confirm this number but all reports list the rates of autism in Argentina as “high” and “growing”. 

Nevertheless, the CDC reports that Hispanic children in the US have lower rates than whites and, from the sound of it, potentially lower rates than in Argentina. But which “Hispanic children”? It’s hardly as if, when polling households for incidence of autism, the CDC is going to ask, “What is your family’s percentage of Amerindian/African ancestry? How dark are your children?” And I don’t think they would even if they could. Any such correlation, if confirmed, could be explosive given the reported differences in rates.

According to some sources, white skin developed incrementally as human ancestors migrated north out of Africa because those who didn’t adapt developed, among other things, rickets from an inability to absorb vitamin D from scarcer sunlight. Lighter skin, along with the downside of more susceptibility to free radical generation from UV rays, is better able to absorb vitamin D from the sun.

The differences between ethnic groups in general are many and fascinating. Some Asians are more prone to lactose intolerance. Finns seem to have more twins than average. Ethnic Ethiopians are genetically closer to Swedes in some ways than to their own continental neighbors; and African Americans and whites may react differently to certain drugs like beta blockers. But the variances between  races—unlike American psychiatric authorities such as Frederick Goodwin might contend—have never borne out as qualitative in terms of intellect, emotions,  “degree of evolution” and general worthiness.

Another issue which motivated me to pursue this topic is the increasing “buzz” on the link between IQ and either its relationship to autism itself (the neurodiverse theory that “Einstein had autism” and that most analytical ability stems from the diagnosis—a view which I don’t subscribe to) ; or its relationship to genetic susceptibility: that higher IQ may relate to “fragile” mitochondria, increased allergies and possibly increased vulnerability to vaccine toxins (HERE and HERE).

Not that any ethnic group as a whole wants a higher rate of autism, but I’m concerned that the idea of a link between IQ and autism—if coupled clumsily with emerging data about disparity of autism rates between races— could develop a life of its own and be lent to racist “Bell Curve” concepts of differences in intellectual abilities.

It’s impossible that IQ is predicated on race; if it were to turn out that there was a difference between rates of autism among different ethnic groups, it would have to do with something quite separate from differences in intelligence. We’re apples and oranges. But apples and oranges still have some differences; and these differences, in humans, may have to do with—for better or worse— toxicology and disease susceptibility.  Nevertheless, the vaccine schedule in the US is one-size-fits-all.

There are other considerations in ethnic differences in autism rates coming from far more considered sources. At the National Autism Association conference in Fort Lauderdale last fall, Dr. Andrew Wakefield discussed the rates of autism among the Minnesota Somali, conjecturing whether the very biological factors which might make some populations from rugged areas of the world extraordinarily disease and stress resistant might also be turned to their disadvantage in the case of excess or novel toxic exposures.  He also discussed vitamin D deficiency which was found to be high among Somali mothers in Minnesota.

From where my multi-ethnic family stands, Dr. Wakefield appears to be on to something. For instance, my husband is “field tested” to be naturally resistant to malaria like many of southern Amerindian descent. Could this natural protection be somehow reversed into greater susceptibility, maybe to particular shots or to particular timing of shots and other factors?
And like Somali émigrés, prior to coming to the US, my husband was almost totally “untested” regarding any “inherent” ability to handle the current vaccine schedule. In other words, if he had passed on to our children a particularly high susceptibility to excessive vaccination, he would not show it himself: he received three vaccines as a toddler because his parents had reservations towards the growing number of “Northern” inoculations that were being pushed on children in Argentina. And, like most well-fed, middle class South Americans, my husband, his sister and everyone else they grew up with were never seriously ill. They weren’t sheltered; they travelled wherever they wanted and my husband did his graduate thesis in the poorest district of the Venezuelan outback. But everyone then knew that it was the effects of extreme poverty— having a poor diet, drinking sewage, etc.—which induced susceptibility to certain illnesses. It’s mostly in “first world” countries that we’re confused about this issue. According to reported rates of autism and vaccine uptake in Argentina, that confusion might be contagious.

All told, I have no idea whether to believe government reports that “middle class, white parents” are the ones least likely to vaccinate on the schedule in the US. Maybe this statistic is a red herring to distract anyone from noticing a correlation between lower rates of vaccination or lack of adherence to the recommended schedule among certain minorities and these groups’ consequent lower rates of autism. But if it’s true that African Americans and Hispanics really do have lower incidence without significantly lower vaccination rates, that leaves other implications: either vastly different lifestyles or different reactions to the same toxins.

Again, I don’t know what to believe, only that I’d be glad if children were spared by whatever means. I wish it could have been all our children too, but misery in this case doesn’t love company. Any more “company” and we’ll have species extinction. On the other hand, if the CDC merely underreported rates of autism among minorities as part of a cover up of lack of assistance of minority children with autism, it would be appalling but not surprising.

But if that disparity in autism incidence is real, considering government health agencies’ and mainstream medicine’s history of supporting racist policies like the Federal Violence Initiatives, etc., if differences in melanin or other forms of natural resistance among certain minorities do play a protective role against vaccine toxins, then one thing would be clear:  the epidemic probably wasn’t planned. That’s because these same “eugenitic” general authorities and often racially exploitative pharmaceutical corporations (deaths from Pfizer’s Trovan in Nigeria?) would probably never have deliberately culled white children over black and Hispanic in the US.

Medical authorities and industry may have just screwed up and are racing to disguise the potential contribution of vaccines with no real endgame in mind other than getting whatever profits (lemonade again) can be squeezed from catastrophe (lemons)—profits which just happen to be enormous enough to have inspired premeditation. Again, the $3.5 billion a year “autism drug” market; the boom in genetics funding; the industry dollars poured into autism charities and organizations which eschew research on environmental cause; and the exploding plethora of mainstream autism “experts”, some of whom might seem virtually bent on perpetuating the epidemic to keep themselves viable.  That is, if most of these folks had consciously thought of it.   

Not coincidentally, I was laughing when I saw Wired Magazine’s follow-up to the infamous “FEAR”, in which readers’ responses to Amy Wallace’s Offit-homage appeared. The edition following “FEAR” was “FAIL! Screw ups, Disasters, Misfires, Flops: Why LOSING BIG Can Be a Winning Strategy”.

Exactly. As long as the victims of these disasters are never given a voice (which, as you’d expect, they are not in the above mentioned “Wired” issue either); as long as accountability is limited to a dip in sales and not serious criminal and civil sanctions, then epic failure, injury and death can be turned into a gravy train.

What’s in the gravy? Lemonade from lemons. Apples and oranges. Consumers are all consumable “pulp” in the end and no child is safe unless we demand accountability and stand up for our right to make truly informed and individualized choices.  

Update: On the day that Part I of this article appeared, after three years in recovery, our six year old daughter had faint tan lines for the first time.


Adriana Gamondes lives in Massachusetts with her husband and recovering twins.