There is no doubt that we are caught up in an epidemic of childhood brain disease. There are hundreds of thousands of autistic children in the late 1990s where only a decade ago there were seemingly only a few thousand. And there are millions of milder cases, which carry a diagnosis of Attention Deficit Disorder, with or without hyperactivity, therefore ADD or ADHD for short. The ADD children often have delays in speech development and selective impairment of school learning and social behavior. In their areas of interest they are often very intelligent and accomplished; but as a group, ADD kids run into increasing trouble in their adolescent years as they struggle with school, conflict with family, experiment and get hung up on drugs, and run afoul of the law.

ADD is not a trivial condition and it almost certainly reflects damage to the process of brain development. In fact, research at Stanford University recently shed light on the process, literally, by demonstrating a lack of activity in the brain control centers, called the Corpus striatum, of children with ADD. This area failed to light up when visualized by PET scan. PET is an abbreviation for 'positron emission tomography,' and the injected glucose sugar tracer material gives off positrons that are recorded by a computer-linked scanner. ADD children failed to light up--until they were given Ritalin. This indicated that brain cells in that area, particularly the caudate nucleus, were underactive. The research gave visual evidence for the efficacy of this drug, which increases the action of the neurotransmitters, dopamine and serotonin. It is certain that additional research of this type will verify the benefits that parents report after the use of orthomolecular and herbal treatments, such as phosphatidylserine, Panax ginseng, deanol, caffeine, tyrosine, biopterin, vitamin B12, folic acid, hydroxy-tryptophan, piracetam, vinpocetine, and others.

The same can be said about autism, the more severe form of developmental brain injury, which is obvious by age 3 years old. Autistic children fail to develop speech and their social interaction and natural curiosity is replaced by repetitive behaviors, staring, posturing, head-banging and self-stimulating in ways that range from excess sleeping to frequent raging. As they improve they may become obsessed with specific objects, sounds, images, books, etc. and they can tolerate no interruption or change in their connection with it. Those that do develop speech may appear normal, but they often fail to develop comprehension and common-sense judgment. They seem to lack an intact sense of before-after, cause-effect--and right-wrong. And if these unfortunate children do improve to this higher level of recovery, there is the next challenge, context. This is the ability to predict the consequence of their own acts and be able to feel and believe them in advance. Those who fail at this stage are identified as Asperger's Syndrome, named for the researcher who described this phenomenon. There is no doubt that some of those who get in trouble with the law are actually victims of early life brain injury. This is especially prevalent in violent criminals who end up on 'death row.'

What can cause such injury? How can anything so severe as to cause autism or ADD and lead to criminal behavior in the unlucky ones, be so subtle as to defy detection? For example, many parents of autistic children have independently made the connection between vaccinations and autism. Of course this is not 100 percent; but it may be as high as 30 percent if my cases are any example and that is high! Are the parents wrong? In two cases that come to mind, the children had obvious distress, fever, and behavior change after diphtheria, tetanus, pertussis (DTP) vaccinations in their first year of life, were hampered by ADD thereafter, required tutoring to graduate high school, fell into drug usage, and died of heroin overdose before age 25 despite all the love and support their parents could provide.

Brain damage was not such a rare occurence after DTP vaccination before the acellular vaccine was introduced in 1986 and special legislation was enacted to create a fund to reimburse for vaccine injuries. Millions have been paid out to families of injured children. Some of the neurological injuries are immediate and obvious, with paralysis and loss of mental alertness within days or weeks. But there can also be subtle effect due to the immune-depleting effects of the vaccines, which makes some infants more vulnerable to otitis and other infections. As resistance falters, viral and other infections excite cytokine immune hormones, such as Il-2, Il-6, Il-10, IFN-alpha, which stimulate production of corticotropin releasing hormone (CRH), thus turning on the pituitary-adrenal axis.

There is another reason why pertussis vaccine is adverse for neural development. A glance at any neurotoxicology or biochemistry text shows pertussis vaccine as a reliable activator of nerve cell G proteins. In other words, pertussis strongly activates nerve cells. It also activates the immune cells. That is what vaccines are supposed to do. The hazard may be as simple as over-stimulation of nerve cells that are primed for the process of apoptosis. Such cells are found during periods of accelerated development and unfortunately these periods coincide with the schedule of vaccinations for infants: first week (hepatitis B), 2nd month (DTP and hemophilus), 18 months (MMR) and this increases the risk of excessive nerve cell death, from which there can be adaptation but not full recovery. New tracts may develop but new cells are unlikely to appear--or at best to a limited extent.

Aside from direct toxic effects, indirect brain inflammation and vascular damage by metabolic products of vaccine stress can also occur. Homocysteine is one of these. Many toxins can provoke release of free amino acids, including methionine, and thus induce increased homocysteine, a well known excitotoxin. Homocysteine can cause apoptosis and if high levels should occur during a time of accelerated development this might indeed cause harm. If the nerve activity is further accelerated by pertussis (or fluoride, which also stimulates G proteins) then the damage would be that much greater.


Auto-immune effects, can interfere with myelination and cause prolonged inflammation that magnifies damage. Thus an injury can become chronic and prevent recovery from otherwise minor episodes of brain inflammation and developmental dysregulation. This may be more common now that newborns are vaccinated for hepatitis B on their very first day of life!

This is all by way of conjecture about how pertussis vaccine in particular can alter neural development. Aside from direct toxic effects, indirect brain inflammation and vascular damage by metabolic products, such as homocysteine, can also occur. Any stress or toxin can provoke release of free amino acids, including methionine, and thus induce increased homocysteine. It may be as simple as that; however the necessary research in this area has yet to be done. The damage is known to occur; only the explanations lag behind.

Auto-immune inflammation can become chronic and prevent recovery from otherwise minor episodes of brain inflammation and developmental dysregulation. This may be more common now that newborns are vaccinated for hepatitis B on their very first day of life! Another possibility is that the brain remains a fetal organ for a considerable time after birth: it is not nearly complete in its development until at least three years. There are cycles of development of various parts of the brain: cerebellum in the first months; sensory organs soon after; and cerebral cortex last. The auditory cortex, site of language development, reaches a critical period between 12 and 30 months, just about the time scheduled for MMR vaccination and booster shots.

The MMR vaccinations in the second year are targeted against viral illness, specifically measles, mumps and rubella (MMR). The vaccines contain live but weakened virus and though it is less virulent than the 'wild' type viral infection, the vaccine virus can overload the immune and anti-inflammatory systems in vulnerable children, especially if they are depleted in nutrients, such as selenium, vitamin E, or glutathone. High levels of immune hormones can be induced by infection, and some of these, such as interferon-alpha and interluekin-6 and 10, can act as neurotoxins. Since neural systems development relies heavily on a process called apoptosis, pruning away neurons that are extraneous or in some way do not fit into the competitive process involved as axon growth cones seek their receptors, it is possible that during critical periods of accelerated development, a disruption of apoptosis could lead to excessive cell death and loss of neurons that would better have been preserved by a more efficient process. In other words, accidents can and certainly do occur.

For example, in a very important research, a team led by the great neurologic research toxicologist, John Olney, has determined that blockade of glutamate receptors, also called NMDA receptors, even for a few hours during late fetal and early neonatal life, causes widespread apoptosis and degeneration of neurons in laboratory rats[i]. The authors suggest that this might be relevant in case of drug-abusing mothers or pediatric anesthesia. Their rats were most sensitive to nerve cell death for the first week post-natal, which would correspond to a few months if the human biology runs a parallel course. The agents they used to block the NMDA receptor were gentle anesthetics in common use, such as ketamine and nitrous oxide. They also found the hallucinogen and street drug phencyclidine (PCP) to be equally dangerous to the fetus and newborn infant. And alcohol (ethanol) has similar dangerous properties. Luckily, they also found that it required at least 4 hours of exposure to these toxins before damage was observed.

Their research confirms that the stage of development governs neuronal vulnerability. Thus, the memory centers of the hippocampus were most vulnerable in the last week before birth and the cerebral cortex more vulnerable after birth. Another conclusion: "blockade of the NMDA receptors gives rise to different patterns of neuronal loss depending on the stage of development at which the interference occurs. Such a mechanism could contribute to a variety of neuropsychiatric disorders."

This work on NMDA receptor effects is a breakthrough in our understanding of developmental brain disease. At first I considered the possibility that homocysteine might fit into the puzzle; however on second thought I think not: the damaging chemicals are all NMDA blockers. Homocysteine is an NMDA stimulant. But it is certainly active in the same territory. On the other hand, there is another chemical agent that may well turn out to be the secret demon behind the epidemic of autism. This is 4-phenyl-cyclohexene (4-PC), a compound found in the glue backing that holds synthetic carpets together. It is also released from indoor latex paints, and all kinds of sealing compounds in common use in home repairs. It is a solvent, absorbs by inhalation and through the skin, and has a structure almost identical to 1-PC, which is the active metabolite of phencyclidine. Phencyclidine (PCP) is also a street drug known as 'angel dust' and it is known to cause fetal brain damage, sometimes presenting as cerebral palsy at birth. It is also one of the chemicals that was found to be most effective at causing apoptosis in brain cells of newborn rats.

4-PC was found in air samples from the US-EPA headquarters in Washington, DC, which had to be evacuated in 1988 due to contamination of the building by carpet fumes. The investigation that followed revealed that 4-PC was preset at 70 parts per billion, which was sufficient to cause irritation of the throat, lungs, eyes and nerve cells, even in adults and neurological symptoms have been quite prominent in many reports of "chemical sensitivity" from carpet fumes. Children are particularly susceptible, but no one has considered carpet and paint fumes to be much of a danger to newborn infants before. In fact, it is commonplace for expectant parents to carpet and paint the nursery as a happy welcome for their newborn child. However the new information on NMDA blockade and nerve cell death makes this a whole new ball-game. The paradox is that it was only a few years ago, 1991, when mercury was removed from indoor paint after a baby died under just such circumstances. It is very possible that this 4-PC and perhaps toluene, another newcomer to indoor paint since the departure of mercury, are sinister culprits in causing childhood brain disease.

Let us not depart entirely from the additional concern that vaccines are also part of the problem. It may be that an initial injury at a critical time, leaves a baby with less reserve with which to cope with additional injuries later. In one study, 17 autistic children were re-diagnosed from home videos and abnormal movements were observed in all of them, starting as early as 3 months. If vaccines are involved, this points to hepatitis, which is given on the first neonatal day, or DPT or hemophilus influenza, which are given at 2-3 months of age in most infants.

Nevertheless, the most common story told to me by parents of autistic children is that the children were developing speech at a normal pace until after the MMR vaccine vaccination between 15 and 24 months of age. I know one such case that lost all speech at age 18 months, then had a partial recovery and was able to start nursery school, and then lost all speech again after the booster MMR vaccine at age 4 years. It would seem that the MMR vaccine can both cause a new injury and/or aggravate an old one.


©2010 Richard A. Kunin, M.D.


[i] C Ikonomidou, F Bosch, M Miksa, J W Olney: Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain. 1999; Science, 283, 70-74.

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