“RAJ, I’ve seen you reference the leprosy-resistance before, but I still don’t see what parallel you are trying to make. Most genes are inherited as alleles from both parents, and resistance/susceptibility/tolerance factors to some things can be heritable. So what’s the point? Autism is not an infectious disease, unlike leprosy”

Let me try and be clearer. Leprosy is a Gold Standard model for a gene-environment interaction model. When you compare side by side decades of genetic research in leprosy and autism and note the sartling similarity between the published data what it suggests is that the genetic theorists in autism, because of their inherent bias towards genetic explanations, may have resulted in misinterpreting the meaning of what genetic research in autism is telling us.

The polygenic theorists have promulgated for decades the notion that there is no environmental component involved in the etiolgy of autism based on making hypothetical assumptions. This may have led to making false assumptions and misleading conclusions about the meaning of the genetic research in autism.

The environmental component in autism is much more complex than is found in leprosy which has a single environmental pathogen. In autism there is a multitude of environmental insults that have been identified and accepted by most autism researchers as part of the environmental component, save the polygenic theorists who cling to a single unproven model for which there is a lack of evidence.

The say that autism is not an infectious disease, like leprosy, is also somewhat misleading. The environmental component in autism has many pathogens linked to autism, including prenatal rubella infection:

http://neurodiversity.com/library_chess_1971.pdf

BTW among the similarities between the published genetic data found leprosy and autism I would also add that in leprosy there is also an unexplained high male to female ratio (3:1).

http://www.scielosp.org/scielo.php?pid=S0042-96862001000400007&script=sci_arttext

This is incorrect.

It has been a little over a month since many folks barely knew what a mitochondrion was, and are now asserting prevalence and etiology?

Dr. Poling has had his moment on the soapbox and now Drs. Shoffner and DiMauro have spoken back about jumping to conclusions. The question that I have is, if and when the scientists come through with the research, and if it should not show relation to current asserted causation, would we listen?

As far as David Kirby’s assertions of percentages, the relevance comes in relation to the percentages in the general population, and I believe even in that case only shows differences between groups, but not necessarily causation either without direct evidence.

The US government rightly identified mitochondria as being linked in some way to autism.

David Kirby and everyone do not doubt this.

Mercury does not just magically destroy and take out brain cells clinically and cleanly leaving the patient autistic.

Mercury is a mimic along with many other metals and chemicals which has a swathing action inside our bodies.

Mercury is catalytic, enzymatic, call it what you will.

One of its known actions is on the red blood cell formation which resides in the mitochondria.

Damage to mitochondria is the price we pay for exposure to mercury whether from vaccines or elsewhere.

Destruction of mitochondria by mercury does not of itself destroy our brain cells.

But in a collateral damage action while some of the mercury is destroying mitochondria, why shouldn’t the rest of the worlds most toxic non radioactive element attack and destroy brain cells?

So far the work on environmental triggers of autism is extremely poor. It has been a process of elimination chased primarily by people with agendas.

RAJ, I’ve seen you reference the leprosy-resistance before, but I still don’t see what parallel you are trying to make. Most genes are inherited as alleles from both parents, and resistance/susceptibility/tolerance factors to some things can be heritable. So what’s the point? Autism is not an infectious disease, unlike leprosy.

another question is: to what extent is mitochondria disorder/dysfunction/disease seen as a cause, or a contributing cause, for other disorders?

That also applies to the polygenic hypothesis you also wrote about. Leprosy susceptability is also polygenic but the cause is exposure to to the bacteria, myobacterium laprae.

In fact, the genetic data published over many decades mirrors the genetic data published in autism research. High concordance rates in MZ twins ( 60-85%) and a rapid fallof in concordance rates in fraternal twins ( 5-20%) , similar sibling risk ratios and high heritability estimates of 80%.

http://www.nature.com/ng/journal/v27/n4/full/ng0401_439.html