Listening to Mr. Williams (lawyer for the parents) cross examine Dr. Brent the toxicologist (from May 19, Day 6) was difficult most because after 45 minutes of discussion of the toxicokinetics of ethyl-, vs. methyl, vs. inorganic-mercury all I could hear was “Blah, blah, don’t you agree that the Charleston monkey adult brain study showedgreaterinflammationoftheinorganic glutamaturgicneuron silvergrainsBurbacherinfant paper? Blah blah and further, isn’t it true thattheVahtergroup onlygave80milligramsperkilogramsperdayofmercuricchloride because the defensereferencemasterlist 436page8 indicatesthatSeychellesIslanders spoke at the IOM?”
Nevertheless, I forced myself to listen to portions of it again and again until I thought I understood what they were talking about exactly. There were several times, maybe 8 or 10 even where it seemed obvious to me that Dr. Brent had totally demolished the point that Mr. Williams was attempting to make and Mr. Williams continued on as if it was of no consequence. I kept getting this picture of King Arthur and the Black Knight from Monty Python and the Holy Grail after King Arthur has sliced off the Black Knight’s arm:
ARTHUR:
Now stand aside, worthy adversary.
BLACK KNIGHT:
‘Tis but a scratch.
ARTHUR:
A scratch? Your arm’s off!
BLACK KNIGHT:
No, it isn’t.
ARTHUR:
Well, what’s that, then?
BLACK KNIGHT:
I’ve had worse.
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The following is more of my rough transcribing of the audio. I have no idea what that word is that sounds like “AT-trib-ated.” If you know I’d be happy to correct my spelling of it. I believe this first paper he’s referring to is one of the Charleston or Vahter adult monkey studies where they gave very large doses of methyl mercury to the monkeys every day, orally. Click here to hear this segment of the cross examination of Dr. Brent.
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Mr. Williams: It’s says: “the microglia population is a responsive cell type. Once damage has been repaired following activation after injury microglia are known to return to a quiescent state. However, the number of attribated (sp?) microglia remained elevated … in the monkeys of the clearance group which were kept unexposed for 6 months following 12 months of methyl mercury exposure . This group had very low concentrations of methyl mercury, but retained elevated concentrations inorganic mercury at levels comparable to the 12 month exposure group and this suggests that inorganic mercury may be the proximate species of mercury responsible for microglial activation…” a situation similar to that proposed for the cortex study we already looked at. Now, do you agree that normally microglia have a protective role, they come in and clean up whatever’s there and then they return to their quiescent state?
Dr. Brent: To the extent that I understand microglia… which is limited, I would say, yes.
Williams: And if they stay activated then they can become toxic to neurons and astrocytes.
Dr. Brent: Once again, my, my understanding of microglia is more limited than other people who will be testifying later… my understanding is that microglial activations is not necessarily a bad thing and that … the effects here are not necessarily indicative of any neuropathology.
Once again, you know, we are talking about inorganic mercury effects at the concentrations they give here, and if the inorganic mercury is causing adverse effects at the concentrations, then it’s the seafood and the chicken that people are eating and not the vaccines because that’s where the far greater exposure comes from. And that doesn’t make any sense, because everyone is eating seafood and chicken, including children who are getting mercury via breast milk, and we don’t think of breast milk as a neurotoxin!
Williams: If we go down the column on the same page to about 4 sentences above… yeah about where you have it highlighted…
It says: “Further loss of astrocytes would be expected to have deleterious effects on the neuron population, for example through a excitotoxic mechanism. You were here when Dr Kinsbourne testified that that was his … understanding of the mechanism that could likely be at work here that you would have astrocytes no longer able to take up glutamate, so yyou’d have excess of glutamate and have neurons get over excited. Right?Dr. Brent: Once again your getting a little out of the mercury area, so my answer here is going to be quite limited, what I took away from Dr. Kinsbourne’s testimony was that he was hypothesizing it was excitotoxic mechanism, related to astrocyte effects. But here for example it says, “further loss of astrocytes,” in this study there wasn’t even that much loss of astroycytes! And certainly, uhm, well we talked about the exposure scenario, so I won’t bring that up again …
Williams: And although, you want to talk about the methyl mercury dose here, you recall that the authors of the infant monkey study made a point of saying that the levels of inorganic mercury in these adult monkeys was only 5 times higher on average than the levels they found in those infant monkey brains, right?
Dr. Brent: That’s right, and that’s very good evidence therefore, that the inorganic mercury is not acting as a neurotoxin, or else we are being poisoned every day, and we are having autism being formed every day, from breastmilk, from seafood, from chicken.
Williams: (Clears throat.)
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I don’t know if it’s immediately obvious to those who haven’t followed the discussion closely, but basically, Mr. Williams had pointed out that inorganic mercury is the “proximate” cause of damage to brain cells. Which is to say that, it doesn’t matter if the original source of the mercury was methyl-, ethyl- or inorganic mercury, because the mercury doesn’t hang around in the brain as either methyl- or ethyl-mercury. Those forms get changed into inorganic mercury, and it’s the inorganic mercury that hangs around. Inorganic mercury (referred to sometimes in the hearing as “Hg-plus-plus,” Hg++) is the same stuff whether or not it started out as methyl-, ethyl-, thimerosol, breast milk, or chicken. And the exposure to breast milk and chicken for the infant and toddler set is much higher than their exposure to thimerosal from vaccines, now or ever. Dr. Brent had said earlier in the cross examination that over the course of 6 months and infant gets “about 250 micrograms of methyl mercury.”
Besides that the PSC keeps bringing up these studies where macaques were given significantly higher doses, even massively higher doses, of mercury, either thimerosal or methyl-mercury, than babies ever got. The monkeys in the Vahter study were given 50 mcg per kilogram per day of methyl mercury, which Dr. Brent explained is the equivalent in a 70 kg person getting 3,500 mcg a day of methyl mercury. The average diet for that 70 kg person would expose him or her to 11,000 mcg a year. A year! So essentially, the monkeys got a level of mercury in 3 days what they’d get in a year if they had been eating a typical American diet. But some of the monkeys were fed like this for a year. That’s the “12 month exposure group” referred in what I transcribed (above).
And even though they had had that large continual dose of mercury for a year and many of their brain cells were pretty much impregnated with mercury, the monkeys were normal behaviorally. Even if you wouldn’t expect them to become autistic because they were exposed as adults, surely they’d show some outward sign of brain damage if that much mercury were extremely dangerous to brain function.
It was also interesting to me that Burbacher had used 3 or 4 times the amount of thimerosal to dose his infant monkeys as humans got. Had Burbacher used the equivalent amount of thimerosal in the human vaccine schedule the outcome would likely have been that the levels of mercury in the monkey’s brains would have been so low that it wouldn’t have been detectable. (Clears throat.)
There was also some fun discussion about how there’s no increased autism in the Faroe and Seychelle’s islands in spite of the fact that infants have high levels of mercury in their brains (from maternal diet). Mr. Williams stated that “fish is very good for brains” as if that was a point for his side.
Dr. Brent was the first of the respondents expert witnesses to testify in this portion of the Omnibus hearing. He also had testified in the Cedillo hearing. Some of the points about Kinsbourne’s hypothesis regarding astroglial activation, glutamate excess, and cell death were dismantled by Dr. Johnson, and by other experts who testified in the past weak. Dr. Deth’s hypothesis about autism being the result of oxidative stress was pretty much smithereened by two or three of the petitioners experts. I’m still catching up with listening to all of their testimony, but of extensive portions I’ve listened to so far, well, I think it’s looking really bad for dead parrot hypothesis.






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