Part II: The Tipping Point: Questions about Autism, History, Race and Melanin
Chicago Tribune Protecting Consumers Against Natural Supplement (Again)

Part 2 Autism and Redheads - The Canaries in the Epidemic

Red canary By Teresa Conrick

In Part 1 (HERE), we learned that Autism appears to have a melanin connection with Parkinson's,  Amyotrophic Lateral Sclerosis, Alzheimer's, Melanoma, Tourette's, Dystonia and Schizophrenia.  Melanin appears to be lacking or not functioning properly thus causing quite possibly, the motor disturbances and/or neurodegeneration that is shared among these increasingly diagnosed diseases.  This may happen as those who have poor melanin then lack the ability to detoxify , ie -"the resulting melanic component serves an additional protective role through its ability to chelate and accumulate metals, including environmentally toxic metals such as mercury and lead.." HERE

decided to investigate more about autism and this melanin connection.  Though I have been in the autism world almost 15 years since Megan was diagnosed, some of this information was new to me and some I knew a little about but have learned much more.  Looking up "melanin" and "autism" together brought me to these disorders:

1-Angelman Syndrome
2-Prader-Willi Syndrome
3-Hypomelanosis of Ito
4-Rett Syndrome
5-Tuberous Sclerosis
6-Neurocutaneous Syndrome

There may be more but for the sake of making a point, I will focus on these.  Notice there is a pattern of hypomelanin and autism in each.

Angelman Syndrome

"When the OCA2 gene is also deleted from chromosome 15, a person with Angelman syndrome is likely to have light-colored hair and skin, compared to family members. This occurs because the OCA2 gene controls the protein that produces the pigment melanin, which provides color to hair, skin and eyes.  Most cases of Angelman syndrome occur even though there is no history of the disorder in the patient’s family. The syndrome often is a result of a random genetic mutation that occurs during the formation of cells early in embryonic development. The cause remains unknown in about 10 to 15 percent of Angelman syndrome cases. Angelman syndrome affects all genders, races and ethnic groups. However, the vast majority of cases in the United States involve Caucasians, according to the Angelman Syndrome Foundation." HERE

Similar to autism, individuals with Angelman Syndrome display the following behaviors: hand-flapping, little or no speech, attention deficits, hyperactivity, feeding and sleeping problems, and delays in motor development. These individuals may also engage in biting and hair pulling. Many tend to have a stiff-legged gait and jerky body movements. "
Angelman Syndrome  HERE

Key Points:   random genetic mutation (another way of saying there is not a reason and they do not know why), light-colored hair and skin

Prader-Willi Syndrome

"Cutaneous and ocular pigmentation were evaluated in 29 individuals with the Prader-Willi syndrome (PWS). Criteria for hypopigmentation included the presence of type I or II skin, the lightest skin type in the family by history, and iris translucency on globe transillumination. On the basis of these criteria, 48% of the PWS individuals were hypopigmented. The presence of hypopigmentation correlated with a small interstitial deletion on the proximal long arm of chromosome 15; however, this deletion was also found in individuals who did not meet the full criteria for hypopigmentation. Hairbulb tyrosinase activity and glutathione content, as well as urine cysteinyldopa excretion, were low in PWS individuals with and without hypopigmentation and did not separate these two groups. We conclude that hypopigmentation is found in a significant proportion of individuals with PWS and that the hypopigmentation may be associated with a deletion of the long arm of chromosome 15. The mechanism for the hypopigmentation is unknown."

Hypopigmentation in the Prader-Willi Syndrome HERE

In addition to a well-described behavioral phenotype that includes hyperphagia, obsessive-compulsive symptoms, disruptive behavior, and an increased risk for mood disorders, recent evidence also suggests that some individuals with PWS have repetitive behavior and social deficits reminiscent of autism spectrum disorders."

Autistic-like symptomatology in Prader-Willi syndrome: A review of recent findings HERE

Key Points:  hypopigmentation,  mechanism for the hypopigmentation is unknown, lightest skin type in the family by history, deletion was also found in individuals who did not meet the full criteria for hypopigmentation.

Hypomelanosis of Ito

"Hypomelanosis of Ito (HI) is a syndrome with hypopigmented whorls of skin along the Blascho lines. The old name, Incontinentia pigmentosa achromiance was probably used because HI appears to be the negative image of incontinentia pigmentosa. This disorder is inherited as an autosomal – dominant trait with variable penetrance and the implicated genes are 9q33 and q11-13, Xp11. Chromosomal mosaiscm is believed to be the reason that hypomelanosis of Ito is so varied in phenotype. Hypopigmented skin lesions appear as whorls or streaks on any part of body and tend to progress onto uninvolved areas. The cutaneous lesion is often associated with developmental and neurological abnormalities. Pyramidal tract dysfunction, mental retardation and seizures are common neurological signs. Ophtalmologic disorders are also present."

A rare case of hypomelanosis of ITO HERE

"Hypomelanosis  of ito is frequently associated with autism"

"Twenty-five children with hypomelanosis of Ito are reported: 10 of them had autism, 3 showed autistic-like features, 1 had previously shown autistic features which had subsequently faded, 2 had disintegrative psychosis. The 9 remaining children were all mentally retarded and 5 of them were more markedly retarded in their speech development. The hypothesis is considered that a dysfunction of *melatonin (* Translation error- this should be "melanin" - HERE) may favour the development of both skin depigmentation and autistic behaviour through an altered production of corticotrophin-releasing hormone and, in turn, of proopiomelanocortin. HERE

"Two girls and a boy showing autistic behaviour and fulfilling the criteria for autistic disorder, Asperger syndrome or atypical autism were diagnosed as having hypomelanosis of Ito syndrome. It is suggested that skin changes indicating underlying neurocutaneous disorders be meticulously looked for in all cases with autism and autistic-like conditions." "Hypomelanosis of Ito in three cases with autism and autistic-like conditions." HERE

Key Points: hypopigmented whorls of skin, cutaneous lesion is often associated with developmental and neurological abnormalities
Rett Syndrome

"Autopsy studies in nine girls dying between 4 and 17 years, and sural nerve and muscle biopsies from two girls aged 3 and 17 years showed:.....  mild diffuse cortical atrophy with increased amounts of neuronal lipofuscin and occasional mild gliosis, but without signs of a storage disorder; (3) underpigmentation of the zona compacta nigrae, which showed fewer well-pigmented neurons for age and fewer melanin granules per neuron.." "Neuropathology of Rett syndrome " HERE

Key Points: underpigmentation of the zona compacta nigrae, fewer melanin granules

We will focus on lipofuscin later.

Tuberous Sclerosis

"About 50% of people with TSC have learning difficulties ranging from mild to significant, and studies have reported that between 25% and 61% of affected individuals meet the diagnostic criteria for autism, with an even higher proportion showing features of a broader pervasive developmental disorder. A 2008 study reported self-injurious behavior in 10% of people with TSC. Other conditions, such as ADHD, aggression, behavioral outbursts and OCD can also occur. Lower IQ is associated with more brain involvement on MRI."

"Some form of dermatological sign will be present in 96% of individuals with TSC. Most cause no problems but are helpful in diagnosis. Some cases may cause disfigurement, necessitating treatment. The most common skin abnormalities include:

• Facial angiofibromas ( "adenoma sebaceum"): A rash of reddish spots or bumps, which appear on the nose and cheeks in a butterfly distribution. They consist of blood vessels and fibrous tissue. This socially embarrassing rash starts to appear during childhood and can be removed using dermabrasion or laser treatment.

• Ungual or subungual fibromas: Also known as Koenen's tumors, these are small fleshy tumors that grow around and under the toenails or fingernails and may need to be surgically removed if they enlarge or cause bleeding. These are very rare in childhood but common by middle age.

• Hypomelanic macules ("ash leaf spots"): White or lighter patches of skin that may appear anywhere on the body and are caused by a lack of melanin. These are usually the only visible sign of TSC at birth. In fair-skinned individuals a Wood's lamp (ultraviolet light) may be required to see them.

• Forehead plaques: Raised, discolored areas on the forehead.

• Shagreen patches: Areas of thick leathery skin that are dimpled like an orange peel, usually found on the lower back or nape of the neck.

• Other skin features are not unique to individuals with TSC, including molluscum fibrosum or skin tags, which typically occur across the back of the neck and shoulders, ''café au lait'' spots or flat brown marks, and poliosis, a tuft or patch of white hair on the scalp or eyelids." "Tuberous Sclerosis Symptoms" HERE

Key Points: Hypomelanic macules, lack of melanin, "cafe au lait" spots

Neurocutaneous Syndrome

"A 6-year-old male with apparently isolated mental delay, speech delay, attention deficit/hyperactivity disorder, epilepsy, and subtle and insignificant skin dyschromias. Investigators ruled out genetic syndromes, congenital infections, fetal deprivation, perinatal insults, intrauterine exposure to drug abuse, and postnatal events such as CNS infections as possible common causes of brain impairment. Being all further test negative, the patient exhibited an ultrastructural defect of the skin, identical to that previously described [Buoni S, Zannolli R, de Santi MM, Macucci F, Hayek J, Orsi A et al. Neurocutaneous syndrome with mental delay, autism, blockage in intracellular vesicular trafficking and melanosome defects. Eur J Neurol 2006;13:842-51], suggesting that some cell compartments, such as rough endoplasmic reticulum, lysosomes, Golgi apparatus, and the vesicular zone (racket) of Birbeck granules, sharing similar components, can be altered, resulting in a common defect in cell trafficking, associated to melanosome defects."

Key Points: ruled out genetic syndromes etc, defect in cell trafficking associated to melanosome defects

This pattern made me continue to look and question how this could happen.  Reading up on melanin, I saw that tyrosine was a precursor to melanin production, associated with melanosomes.  That flung open all new doors and like my fellow writer at Age of Autism, Adriana Gamondes, mercury was popping up with melanin.

The skin lightening issue of mercury definitely included my investigations of melanin and these neurodegenerative disorders.  I found this one first and it got my interest:

"In the present study, we investigated the dermal absorption of mercury and its accumulation in the tissues of albino and pigmented mice treated with two brands of mercury containing skin-lightening creams for a period of one months at different intervals. Mercury levels were measured in a total of 133 and 144 liver, kidney and brain tissue samples of albino and pigmented mice.  Significant differences in the mercury levels were observed between the albino and pigmented mice. This emphasizes the protective role of melanin against mercury toxicity."  "Comparison of mercury levels in various tissues of albino and pigmented mice treated with two different brands of mercury skin-lightening creams."   HERE

It got more interesting:

"Inorganic mercury compounds are also widely used in skin-lightening soaps and creams, due to the ability of the mercury cation to block the production of melanin pigment in the skin."  "Elemental Mercury And Inorganic Mercury Compounds: Human Health Aspects"

And More specific:

"The pharmacologic activity of the skin-light-eners occurs as the mercury blocks the production of melanin pigment in the epithelial melanocytes, thus lightening the skin over time."  "Inorganic: the other mercury."   HERE

As Adriana reported, even the Chicago Tribune, not a fan of mercury causing autism, reported the same thing:

"Mercury, a known toxin, is banned in skin-bleaching or lightening creams. The products are used to lighten complexions, eliminate age spots or diminish freckles. Mercury is sometimes illegally added to creams because the metal blocks production of melanin, which gives skin its pigmentation. Mercury is rapidly absorbed through the skin and can cause severe health effects, including neurological and kidney damage."  "FDA widens mercury-skin lightening cream investigation" HERE

So then I decided to investigate this phenomenon in other species:

"Ovigerous females of the estuarine crab Chasmagnathus granulatus were exposed to mercury (0.1 mg/L) during the entire, early, or late embryonic development.  Particularly, hypopigmentation of body chromatophores was the abnormality that showed the highest incidence, this incidence being greater when ovigerous females were exposed to mercury either during the totality or just the first half of the egg incubation period. In contrast, the effect of mercury on the morphology and pigmentation of eyes was greater when the exposure comprised the totality or just the second half of the incubation period. These results correlate with the timing of both body pigment synthesis and eye formation during embryonic development. Although these abnormalities have been observed in the same species with other heavy metals, such as zinc and copper, the responsiveness during the early and late embryonic development was different with mercury."  "Toxicity of mercury during the embryonic development of Chasmagnathus granulatus (Brachyura, Varunidae) HERE

Could flu shots with thimerosal act in this same manner or what about living near a coal fired power plant?

"Heavy metals (As, Cd, Cu, Hg, Se, Zn) were shown to increase the incidence of albinism. Metal-induced albinism resulted from exposure of both adult fish and eggs."  "Accelerated Rate of Albinism in Channel Catfish Exposed to Metals"  HERE

Albinism was the extreme version of hypomelanin so I thought that might show a clue:

"Oculocutaneous albinism is a hypomelanotic skin disorder.  Oculocutaneous albinism is infrequently reported in association with childhood autism when compared to tuberous sclerosis and hypomelanosis of Ito.  However, Rogawski et al [11] had reported co-morbidity of oculocutaneous albinism and childhood autism in two boys and Delong [12] in a recent description of families of individuals with childhood autism had noted additional feature of oculocutaneous albinism in some families in addition to major affective disorder and special talents. Going by the observation of this present case report and the report of these two previous reports in the literature [11,12], the question arises whether childhood autism has any genetic and clinical relationship with oculocutaneous albinism.  "Childhood autism in a 13 year old boy with oculocutaneous albinism: a case report"  HERE  

This study on albinism really interested me as these were not babies born with autism:

"2 tyrosinase-positive albino boys, 1 Caucasian and 1 American Negro, manifested moderate retardation and autistic behaviour. It is postulated that the as yet unidentified metabolic defect in albinism may be responsible for the CNS disorder in these 2 boys."
"Oculocutaneous Albinism and Mental Disorder A Report of Two Autistic Boys"  HERE

Well, Yale dropped the ball as that was in 1978 and I have not seen anything since on melanin-autism from Yale. How is it that 2 boys "manifest",  kind of like regress, into  autism, both having zero melanin, and not one researcher since thought that was significant?
"Oculocutaneous Albinism and Mental Disorder A Report of Two Autistic Boys"

At this point, I want to bring up that word, lipofuscin.  It came up when looking at the autopsies of the girls who had Rett's diagnoses.  I saved it until now as it needed to be place in a certain manner and this is a good spot.  I did gasp when I looked it up initially on Wikipedia:

"Lipofuscin is the name given to finely granular yellow-brown pigment granules composed of lipid-containing residues of lysosomal digestion. It appears to be the product of the oxidation of unstaurated fatty acids and may be symptomatic of membrane damage, or damage to mitochondria and lysosomes. Aside from a large lipid content, lipofuscin is known to contain sugars and metals, including mercury, aluminum, iron, copper and zinc."

So here was another pigment, which also looked to scavenge metals, being found in autopsied bodies of those with an autism diagnosis.  Investigating this more found these:

"Impaired language function is a principle criterion for the diagnosis of autism. The present study of brain from age-matched autistic and control subjects compared brain regions associated with the production and processing of speech. Striking differences in the density of glial cells, the density of neurons and the number of lipofuscin containing neurons were observed in the autistic group compared with the control group. The autistic group exhibited significantly greater numbers of lipofuscin-containing cells in area 22 (p<0.001) and area 39 (p<0.01). The results are consistent with accelerated neuronal death in association with gliosis and lipofuscin accumulation in autism after age seven. Production of lipofuscin (a matrix of oxidized lipid and cross-linked protein more commonly associated with neurodegenerative disease) is accelerated under conditions of oxidative stress."
"A Microscopic Study of Language-Related Cortex in Autism"  HERE

That seemed very significant.  I like Wikipedia but thought I needed more verification on what lipofuscin was so again looked for more:

"The objective of our study was to investigate the toxic effects of mercury on northern pike. Liver color (absorbance at 400 nm) varied among northern pike and was positively related to liver total mercury concentration. The pigment causing variation in liver color was identified as lipofuscin, which results from lipid peroxidation of membranous organelles. An analysis of covariance revealed lipofuscin accumulation was primarily associated with mercury exposure, and this association obscured any normal accumulation from aging. We also documented decreased lipid reserves in livers and poor condition factors of northern pike with high liver total mercury concentrations."
"Mercury toxicity in livers of northern pike (Esox lucius lucius) from Isle Royale, USA" HERE

And this:

"Eighteen stranded Atlantic bottlenose dolphins (Tursiops truncatus) examined postmortem were sampled for histologic study. All cases were examined for ferric ion and lipofuscin.  Chemical analysis for mercury was conducted on 12 of the animals by atomic absorption spectrophotometry. Nine animals were found to have excessive lipofuscin in both liver and kidney.  The evidence suggests that the excessive pigment accumulation is related to toxic effects of Hg and presents as increased active liver disease.  "Liver abnormalities associated with chronic mercury accumulation in stranded Atlantic bottlenose dolphins."  HERE

and this convinced me as well:

"A male subject became exposed to metallic mercury vapor at work in 1973.  He never returned to work again and died of lung cancer in 1990.  Ultrastructurally mercury could be demonstrated by elemental x-ray analysis within lipofuscin deposits. The lipofuscin content was increased in the mercury positive nerve cells as demonstrated by a strong positive autofluorescence."  "Demonstration of mercury in the human brain and other organs 17 years after metallic mercury exposure."  HERE

At this point, I need to say that there is more but my point, I hope, is made that research in this area is deplorably LACKING and children are SUFFERING as a result.  We have seen melanin is deficient in many children receiving an autism diagnosis as well as an increase in another type of pigment, strongly suggestive of mercury exposure in both instances.  Genes do not even come close to explaining this.  True research into environmental causes, especially mercury, needs to be done.   Dan Olmsted and Mark Blaxill's book, "The Age of Autism: Mercury, Medicine, and a Manmade Epidemic," will do much to educate on this denied and disturbing issue.  I'll leave you with one more study.  This one I could not find anything other than the title.  I did try contacting the authors but to no avail. It looks like it could have been a warning sign but again, no one noticed.

Med J Aust. 1972 Dec 30;2(27):1484-6.
Melanin in the ascending reticular activating system and its possible relationship to autism. Happy,R  Collins,JK
PMID: 4655127 [PubMed - indexed for MEDLINE]

Teresa Conrick is Contributing Editor for Age of Autism.


Wayne Morellini

Hi Teresa Conrick.

I'm going write something a bit radical, and you can respond off line.

I long noticed populations from a similar latitude in the northern hemisphere shared similar traits (not that these traits are not found significantly in some other populations). I put this down to maybe having common genetic influences, but it is far from clear cut. I have since come across a website that alledges that white European people are related to a albino producing tribe in Pakistan and since occupied the steps. The page lists many different types of genetic albinism with photos. I have been sick and occupied so have not been through it to verify it, and think it's likely not to be perfect anyway. But it is well worth looking at, to investigate wherever they might be suitable to test if the issue is derived from other population genetic factors or from pigmation. The greater population, and tribe, is naturally black. The appearance, and apprently the genetics, is very European for the Dravidian population except dark, and even Nordic at that. There is also an ancient relationship to pre-Germanic language. However, I have been told of this happening when two half cast people marry to. I suspect the hyposis of the web site is not the finale answer. To me it could even be a tribe that moved into the area that produced the effect.

Please note, this person's view of white people may not agree with you, but it is a starting point. It is rather long.

These traits I have noticed, are traits of pragmatic personality and attitude. Keeness and meaness (stoic), harshness, organisation, self discipline, even to certain tribes in North America. I lack sufficient words to describe it, as it has been many years since I came up with the observation. It must be noted, a lot of this is probably based on neural chemistry and hormones, where anybody from any population that reaches such chemistry can be the same. But these are mostly based on the genetics you inherit, so whole populations have a general flavour of ratio of types of personality.

I have limited first hand experience, but find neo- mongoloid racial group oddly European in various ways, and freinds from Punjabi a bit over the top in terms of this pragmatism. I have met some people from West Africa who have keeness too, but it maybe, from recent archeology, that the race may have extended there, or it might be just the variation of genes which dominated. However, did a genetic bottle neck wondering around the Eurasian step produce the resulting attitude in the resulting European race, or was it interaction with certain races in Northern Asia, where it was picked up. There was movement and habitation to the North, around the current Russian, Mongolian border, and confrontation with certain neighbouring aggressive tribe there causing shifts, including into the Indian subcontinent again affecting current populations.

Such tests would be to see if there are differences between the albinos in the tribe and the others in the tribe, and the pure bloods among the greater population who don't have albinism. Then purebloods from African populations with similar pragmatic intent in general (isolating out those with it personally as a subgroup) and purebloods from other groups who generally don't share pragmatism (isolating out those with that personally as a subgroup) who spend much time outside and those who spend the vast amount of their time inside away from bright or direct light). The eyes pickup from bright light producing melatonin (related) and is linked to eye health, appart from the direct action on the skin and vitamin D. In this way we could get measurements on if it is other associated traits leading to the pragmatic personality, pigmation, or just how much time one spends in the sun.

It is a question like, did the Red Canary in the coal mine because he was Red, or because he was in the coal mine.

I apologise if the above has offended anybody racially, it is not meant to be that way, it is just in a pursuit of finding out the truth.

D Carlson

Dear Ms. Conrick - you should contact Judy Converse, author of "When Your Doctor is Wrong". Her son is a redhead and we talked about this theory years ago when anesthesia dosing protocols were changed for redheads - they are much more sensitive to chemicals similar to sun exposure. Jenny McCarthy's son is quite fair. I found some haplotype research that indicated special susceptibility to chemical exposure can be expected. if there is a way to do a haplotype study of red-haired kids with autism, I think it would tip the scales. Result might be that red-haired parent(s) view the vaccine schedule with a more conservative approach for offspring. This might prevent some cases.


Thanks for your last blog.
Thanks for mentioning tectonite, a type of iron ore only found in Minn.
Iron like all metals right now are in short supply. People can get a good price for recycled metals. And iron production in Minn is UP!

Sorry but that makes more sense to me than a heavy metal - a very heavy metal like mercury even in vapor form, traveling great distances from China's smoking coal furnaces.


Hmmm... just the thing for an Autism Speaks grant.

Theresa Cedillo

Thank you Teresa for these educational and very impressive articles.

Teresa Conrick

Hi Libby. Thanks for your comment. I am curious about carotene/carrots. Is there any research?

Also, interesting about Scandinavians in Minnesota. This also is a big player:

Source: Park Rapid Enterprise (MN); 2/18/2009

Mercury rising in Minnesota fish

In a surprise development, mercury levels in Minnesota fish have been rising -- likely due to coal burned in China and India.

By: John Myers , Duluth News Tribune

The amount of toxic mercury in Minnesota walleye and northern pike has been going up since the mid 1990s, the Minnesota Pollution Control Agency reported today.

The unexpected increase in mercury was found in an analysis of 25 years of fish from 825 Minnesota lakes by the PCA and published last week in the journal Environmental Science & Technology.

The increase surprised scientists because mercury levels in fish had been slowly but steadily declining in recent decades.

"It’s surprising. We didn’t expect to see it going up at all," said Bruce Monson, PCA scientists who discovered the trend.

While mercury levels in fish declined 37 percent from 1982 to 1992, they spiked back up 15 percent from 1996 to 2006, Monson said. Other studies that looked at the entire period didn’t pick up on the recent increase.

Scientists say the mercury spike may come from a decade of global economic growth that saw a massive increase in coal-generated electricity in places like China and India. Emissions from those power plants, including mercury, can circle the globe and fall into Minnesota lakes.

Monson said global climate change also may be increasing mercury levels as water levels show greater fluctuation through increased drought and flood cycles. That fluctuation can pull more methyl mercury of the environment.

Similar increases in mercury in fish were found in Lake Ontario from 1999-2003, PCA officials said, indicating the problem of increasing mercury is not limited to Minnesota.

State officials say they won’t change fish consumption advisories for people who eat fish because the guidelines already are broad enough to be protective even at the higher mercury levels.

The news comes just a day after the Obama administration reversed years of U.S. policy and called for an international treaty on mercury, calling it the world’s gravest chemical problem. Some 6,000 tons of mercury enter the environment each year, much of it settling in oceans and lakes, contaminating big fish like tuna, walleye and pike.

"The group of states that have been active in mercury emission reductions has been calling for an international agreement since 2003, so this is great news," said Ned Brooks, the PCA’s mercury coordinator.

Mercury is a natural substance and is emitted into the atmosphere when many things are burned, especially coal at electric power plants. It also can come from burning products and garbage that contain mercury and naturally from volcanoes and evaporation from oceans.

Minnesota taconite plants also are a major source of mercury when ore pellets are hardened in giant furnaces.

Mercury falls back to the ground and in some cases becomes toxic, called methyl mercury, when it falls into waterways. That mercury then moves up the food chain from small organisms to fish and then animals that eat fish, including loons, otters and humans.

Exposure to high levels of mercury over a long period can cause severe neurological disorders, even death. Mercury also can cause major developmental problems in fetuses and small children.

The PCA and federal authorities have issued advisories for people to limit the number and size of fish meals they eat, especially women and children. Smaller fish usually have less mercury.

Minnesota has taken major steps to remove mercury form products and from incinerators. And last year the state became a national leader on the issue when it reached a landmark agreement with most major industries that emit mercury to lower their pollution to levels that would keep Minnesota fish safe to eat.

Minnesota industries agreeing to cut mercury over the next 20 years include power plants, taconite plants, dentists and even funeral homes which emit mercury when humans with dental work are cremated.

But because more than half of the mercury that falls in Minnesota lakes is from outside the region, including as far away as China, national and even international laws are needed to curb the problem, state officials said.


Might this be one reason the autism rate in Minnesota is so high? The area was settled primarily by Scandinavians.

When I lived abroad, I fell in love with "French Tanning Pills" because they prevented me from sunburning. They were very high in carotene. We now know that carrots chelate mercury.

Donna K

Wow--this is really impressive and I can't wait to read more. Thank you, Teresa, for delving into this.


So, then, one could take it a step further and do some searching on "aluminum and melanin" and come up with all sorts of very interesting sounding connections, also. Not in a detracting from mercury kind of way, but in an "enhancing the hypothesis" kind of way. Can it be taken a further step to account for the darker pigmented population, maybe having marginally different outward manifestation but similar internal consequences.


crikey, Teresa, my daughter is quite raven haired and thank God I didn't give her a damn thing (vaccine-wise) after age 4. By then I clued in that they were over-killing. We are akso of Irish/Scottish descent.


Tuberous Sclerosis includes "Other skin features are not unique to individuals with TSC."

So, skin things are hard to dignose.

For instance the white patch in a black headed young man - I have known four, all intelligent, well mannered, handsome, no problems with health

The "molluscum fibrosum or skin tags, which typically occur across the back of the neck and shoulders "cafe' au lait" creamed coffee color spots or flat brown marks. Well My husband has them. Very pronouced and noticable. When we were young he explained to me that they were from several severe sunburns as he surfed the waves of Southern California.

Maybe, but I also noticed my son had them around 8 or 9 years old just like his father shortly after a severe sunburn from our back yard pool. Only my son's have faded. So this skin stuff - I could easily see how it is not researched or if it is why it could be confusing.

liver spots - well lipofiscin - a new word to learn. wonder how it fits into the mito dysfunction stuff. You know between you and Adriana my head hurts - and then on top of that professor Hartman under the next article of your two - whew! But it is interesting stuff to think on.


Teresa, this is an excellent summary of the hordes of science that has been done on melanin, mercury, autism and autism co diagnoses with melanin disorders. But never has anyone tried to connect the dots. It is about time that all of the monies being devoted to autism research take a look at this under a much bigger microscope!

As you know one of my geneticist's theories of my son is mosaiscm. We may find out next year with a skin biopsy but I find it utterly frustrating when he becomes entirely positive about a chromosomal dysfunction but says it's genetic evolution. Nothing I did, or was environment involved, just happened. He has absolutely no basis for that argument and all of his genetic tests have come out finding zero. He had reactions to every vaccine and his had full dose thimerosal and certain "color" variations arrived later, molluscum arrived later as well. My genetic line from my paternal grandfather to my maternal grandmother and mother have had tremendous environmental heavy metal insults. Mercury and our ignorant/dangerous use of it is destroying the human genome and endangering all of it's offspring.

Laura Cox

These articles are so interesting. I think you are really on to something. Regarding lipofiscin granules, my son's mito muscle biopsy noted the presence of lipofuscin granules and the lab tech said "unusual to see lipofiscin granules at such a young age (10)". From my research they are a waste product of the cells and are normally eliminated. They are also responsible for "liver spots" we see on our hands as we age. While my son's mito dysfunction does not meet the full criteria of mito disease, they are definately functioning well below normal levels. Just did our pre-challenge heavy metal toxicity and he came back for very high Cd exposure as well as some Hg and others. Will be doing the post-challenge today.
We are of Northern European descent ( English, Irish, German, Scandinavian, etc...), fair skinned and light blue and green eyes. I never really tan and gave up trying years ago. Mostly I burn, peel and then end up with a "ruddy" reddish tan, but still paler than most.

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