Way To Go Einstein

A recent comment made by Joseph, over on the Autism - Natural Variation blog, reminded me of some of the unusual aspects of Albert Einstein's life and also his brain structure.

There are many good Einstein biographies on the web but most agree Einstein didn't speak until he was three and wasn't fluent in his native language until the age of nine.

One biography says he did not speak till three years old. In Einstein: The Life And Times author says, "Nothing in Einstein's early history suggests dormant genius. Quite the contrary. The one feature of his childhood about which there appears no doubt is the lateness with which he learned to speak. Even at the age of nine he was not fluent, while reminiscences of his youth stress hesitancies and the fact that he would reply to questions only after consideration and reflection. His parents feared that he might be subnormal."
He was not a good student, withdrawn: "was withdrawn from the world even as a boy -- a pupil for whom teachers held out only poor prospects."
When his father "asked his son's headmaster what profession his son should adopt, the answer was simply: 'It doesn't matter; he'll never make a success of anything.'"
"As remembered by Einstein in later years, this backwardness had its compensations, since it indirectly helped guide him towards the field he was to make his own. 'I sometimes ask myself,' he once said, 'how did it come that I was the one to develop the theory of relativity. The reason, I think, is that a normal adult never stops to think about problems of space and time. These are thing which he has thought of as a child. But my intellectual development was retarded, as a result of which I began to wonder about space and time only when I had already grown up."

Would Einstein meet the requirements to be labeled autistic and receive services if he was born today? It seems likely.

Albert Einstein was born with a misshapen head and abnormally large body to Hermann Einstein and Pauline Koch in Ulm, an old city on the Danube, lying in the foothills of the Swabian Alps. In 1880, his father moved to Munich to start an electronics business. He learned to talk so late that his parents feared that he was mentally retarded, not until he was three, and was not fluent until he was nine. For awhile, he was considered subnormal because of his slow development, and his teachers were continually saying that he would never amount to anything

It's also worth noting that one of his two son's may have been diagnosed as schizophrenic and he may have had a daughter born with Down Syndrome.

The couple had two sons, Hans Albert, and Edward. One died in a mental institution, the other became an engineering professor. New evidence has surfaced that Mileva gave birth to a baby girl, 1/27/1902, before their marriage. The daughter was named Lieserl and soon mysteriously vanished. The knowledge of this daughter did not come forward until 30 years after Einstein's death. There is some speculation as to the daughter being retarded or having Down Syndrome.

We all know the remarkable story of Einstein's life and his many achievements but the story of Einstein's brain after his death is equally fascinating and ultimately provided a few intriguing clues into the nature of his superior intelligence.

As the story goes, the pathologist who performed the autopsy of Albert Einstein brought home a souvenir; Einstein's brain.


The recent book Driving Mr. Albert tells the true story of pathologist Thomas Harvey, who
performed the autopsy of Albert Einstein in 1955. After finishing his task, Harvey irreverently
took Einstein's brain home, where he kept it floating in a plastic container for the next 40 years. From time to time Harvey doled out small brain slices to scientists and pseudoscientists around the world who probed the tissue for clues to Einstein's genius. But when Harvey reached his 80s, he placed what was left of the brain in the trunk of his Buick Skylark and embarked on a road trip across the country to return it to Einstein's granddaughter.

A scientist lucky enough to examine samples of Einstein's brain was interested in certain types of brain cell known as Glia:

One of the respected scientists who examined sections of the prized brain was Marian C.
Diamond of the University of California at Berkeley. She found nothing unusual about the numberor size of its neurons (nerve cells). But in the association cortex, responsible for high-levelcognition, she did discover a surprisingly large number of nonneuronal cells known as glia--amuch greater concentration than that found in the average Albert's head.

If Albert Einstein had an unusually high ratio of glial to neural cells it's possible that it had nothing to do with his intelligence or eccentricities but it is captivating to think that his brain was different at the cellular level and it may have involved neuroglia.

Last year a group of Researchers at Johns Hopkins detected changes in neuroglial cell populations in post mortem brain tissue samples from autistic subjects. The full study is available here:

Neuroglial activation and neuroinflammation in the brain of patients with autism

Vargas, et al, found evidence of CNS neuroglial activation, that is activation of the brain's resident immune cells, Neuroglia (microglial and astroglial cells). They did not report an increase in the number or density of microglia but rather they were in an alternate state of activation as opposed to a resting or ramified state.

Another group, led by Dr. Payam Rezaie, also reported alterations in neuroglial cells and varying degrees of astrocyte and microglial activation but no clear signs of an inflammatory process.

[...]Glial cell activation (restricted primarily to astrocytes) was noted within frontal cortical white matter (WM) in all cases of autism. The degree of astrocyte activation varied between cases from moderate to extensive and severe, with concomitant degeneration of astrocytic processes and reactive-gemistocytic astrocyte morphologies evident in latter cases. Sub-pial astrocytosis was present to varying degrees in all autism cases. In contrast, only very mild and typically focal microglial activation could be detected, strictly confined to the WM.

So there is some disagreement as to the nature and significance of neuroglial cell populations and activation within the brains of some autistic individuals. Fortunately, post mortem brain tissue from autistic victims is scarce.

Shortly after the Hopkins study was published, thimerosal proponents were quick to point out that mercury is able to trigger microglial activation and is therefore consistent with the new findings. True, of course, mercury at high enough concentrations can trigger mircroglial activation. One of the functions of microglial cells is to engulf and remove toxic and foreign substances away from neural cells. In high concentrations mercury in the brain is primarily located within microglial cells and bound to glutathione. exposure to certain toxins, including mercury, triggers expansion and proliferation of the brain's resident immune cells because they are in charge of responding to and removing agents that can harm neural cells. In other words, they are doing their jobs.

Let's assume that Einstein had more glial cells than the average Joe. Wouldn't that afford greater protection against toxins including mercury?

We don't know if an abundance of glial cells was responsible or even related to Einstein's genius but it apparently didn't cause him to be less intelligent or mentally disabled in ways we might expect from mercury toxicity. If glial cell expansion and activation is supposed to be an effect of thimerosal exposure how does that explain Einstein's brain?

Thomas Burbacher, best known for a recent study Comparison of Blood and Brain Mercury Levels in Infant Monkeys Exposed to Methylmercury or Vaccines Containing Thimerosal , is familiar with the effects of mercury exposure on neuroglial cells:

Changes in the number of astrocytes and microglia in the thalamus of the monkey Macaca fascicularis following long-term subclinical methylmercury exposure.

[...]Neurons, oligodendrocytes, endothelia, and pericytes did not show a significant change in cell number for any exposure group. Astrocyte cell number exhibited a significant decline for both the 6 month and clearance exposure groups. The microglia, in contrast, showed a significant increase in the 18 month and clearance exposure groups.

So mercury exposure caused astrocyte populations to decline and microglia to increase. Is that in any way consistent with cell morphology reported in autism? Probably not but that study was done with methylmercury at neurotoxic levels and Burbacher's more recent work tells us that the toxicokinetics of methylmercury are very different from thimerosal.

The initial and terminal half-life of Hg in blood after thimerosal exposure was 2.1 and 8.6 days, respectively, which are significantly shorter than the elimination half-life of Hg after MeHg exposure at 21.5 days

So mercury from thimerosal in vaccines is cleared faster than methylmercury by oral route.

Brain concentrations of total Hg were significantly lower by approximately 3-fold for the thimerosal-exposed monkeys when compared with the MeHg infants, whereas the average brain-to-blood concentration ratio was slightly higher for the thimerosal-exposed monkeys

So significantly less mercury from thimerosal was found in the brains of the monkeys as compared to methylmercury exposure.

Here's the part that is held up as a mechanism whereby thimerosal may be more toxic to brain cells:

A higher percentage of the total Hg in the brain was in the form of inorganic Hg for the thimerosal-exposed monkeys

The theory has morphed again to accommodate newer findings. Just ask your lawyer:

[...] Burbacher and colleagues found ethylmercury's fast breakdown leaves higher levels of so-called ″inorganic″ mercury in the brain. Inorganic mercury lingers in the brain for a year or more, potentially altering certain cells. A previous study has shown such damaged cells are also found in childrenwith autism.

Now the theory is that inorganic mercury is more toxic to brain cells because it sticks around longer. Methylmercury is far more toxic to brain cells but that point is ignored in favor of damage over time. How much time? Isn't the whole idea based on parent assertions of immediate and apparent regressions into autism following immunization with thimerosal containing vaccines? Additionally, what evidence of neural cell death do we have?

Burbacher used very sensitive equipment to detect very minute quantities of mercury in samples of primate brain tissue. As far as I know, he did not look for changes in neural or glial cell populations or morphology but saw fit to include this somewhat misleading sentence:


Stereologic and autometallographic studies on the brains of these adult monkeys
indicated that the persistence of inorganic Hg in the brain was associated with a
significant increase in the number of microglia in the brain, while the number of
astrocytes declined.

Except for one thing. These adult monkeys referenced here are not the same monkeys from the present study.

Reading on:

Notably, these effects were observed 6 months after exposure to
methymercury ended, when inorganic Hg concentrations were at their highest levels, or
in animals solely exposed to inorganic Hg (Charleston et al. 1994, 1995, 1996). The
effects in the adult macaques were associated with brain inorganic Hg levels
approximately 5 times higher than those observed in the present group of infant
macaques. The longer-term effects (greater than 6 months) of inorganic Hg in the brain
have not been examined

Interesting, no doubt, but misleading when discussed in the context of a study where none of these parameters apply and immediately followed by:


It is important to note that a recent publication has demonstrated “an active neuroinflammatory process” in brains of autistic patients, including a marked activation of microglia (Vargas et al. 2005).

Why is it important to note this if “an active neuroinflammatory process” wasn't observed in the current study animals? It wasn't assessed in the methylmercury group, not in the group where "Brain concentrations of total Hg were significantly lower by ~3-fold," and not in the control group.

Of course it is still possible that some of the mercury exposed monkeys developed “an active neuroinflammatory process” but it wasn't reported by this group in this study.

It should be interesting to see the results of this project http://www.safeminds.org/research/

Thimerosal Neurotoxicity, Thomas Burbacher, PhD, University of WashingtonThe specific aim of this research project is to determine the extent of changes in the absolute number of neurons, astrocytes and microglia within six specific regions of the central nervous system of the nonhuman primate (NHP) Macaca fascicularis following a known low-level thimerosal (ethylmercury) exposure.

Even if the changes in brain cell population don't resemble changes found in autistic brains, any significant changes in the brains of primates following thimerosal exposure at simulated vaccine levels will be a strong case against the safety of thimerosal in vaccines. Let's hope the study is well designed and will use vaccine levels of thimerosal.

Back to Einstein's brain.

Other than the microcellular peculiarities, what about structural differences?

Was Einstein's Brain Different?
When Einstein died in 1955, pathologist Thomas Harvey quickly preserved the brain and made samples and sections. He reported that he could see nothing unusual. The variations were within the range of normal human variations. There the matter rested until 1999. Inspecting samples that Harvey had carefully preserved, Sandra F. Witelson and colleagues discovered that Einstein's brain lacked a particular small wrinkle (the parietal operculum) that most people have. Perhaps in compensation, other regions on each side were a bit enlarged—the inferior parietal lobes. These regions are known to have something to do with visual imagery and mathematical thinking. Thus Einstein was apparently better equipped than most people for a certain type of thinking.

His Brain Measured Up
[...]But the elegant study on Einstein, published in the medical journal The Lancet by Sandra F. Witelson, Debra L. Kigar and Thomas Harvey, is consistent with the themes of modern cognitive neuroscience. Every aspect of thought and emotion is rooted in brain structure and function, including many psychological disorders and, presumably, genius. The study confirms that the brain is a modular system comprising multiple intelligences, most nonverbal. Contrary to widespread belief, we do not think exclusively in language.
Indeed, Einstein said he reasoned by combining mental images of a ''visual and muscular type.'' Only after he could reproduce a crucial episode of mental play at will did he ''laboriously'' seek words and symbols to convey the insight to others.

Hmmm. So Einstein was a visual thinker and didn't use language centers of his brain to come up with his ideas and theories.


The difference between the inferior parietal lobules of Einstein and of us mortals is not subtle. Our lobules are deeply cleaved by a branch of the Sylvian fissure, the horizontal Grand Canyon of each cerebral hemisphere. Einstein's fissure veered sharply upward, skirting the lobule and leaving it undivided.
Also, the inferior parietal lobule is ordinarily smaller in the left hemisphere, perhaps because it is crowded by adjacent areas involved in language. Einstein's left lobule was as large as his right, and both were larger than normal. But his brain as a whole was no heavier than average for a man of his age and height.

Too bad Einstein's parents didn't have access to doctors, therapists and drugs to help the poor boy cope with his differences. History might have been very different had they tried to 'fix' him.