The case of Hannah Poling has been the most discussed topic in the autism world in the last few months. Hannah is a 9 year old girl who was just awarded a settlement by the United States Department of Health and Human Services related to a vaccination she received. Shortly after she received a vaccination for 5 diseases at 19 months, she quickly developed various health problems along with the symptoms of autism. She had been developing normally, according to her parents, but in the months after the shots, she developed a fever and litany of other symptoms including diarrhea, appetite loss and intermittent screaming. A pediatric neurologist examining her later noted that she had lost some of the speech she had previously acquired, was no longer making eye contact, and was no longer sleeping through the night.[1]

After her symptoms of autism developed, it was discovered that she suffered from an abnormality of the mitochondria of her cells. Her attorneys argued to the US agency that the vaccines interacted with this genetic abnormality in a way that caused her autism symptoms and prevailed – she was awarded a settlement. This decision has been highly controversial. Some believe it is a sham judgment that has nothing to do with science. Others see it as a vindication and acknowledgement by government that the vast conspiracy to suppress the knowledge that vaccines cause autism is cracking.

As you can read on my ‘Vaccines and Autism’ page on this website, I personally believe that the evidence supporting the fact that vaccines have essentially nothing to do with autism is overwhelming. I have developed an alternative theory presented on this site as to what causes autism. As a further test of my theory, I applied its logic to the question of what caused Hannah’s autism if it wasn’t the vaccines. And, I think I have come up with a pretty persuasive argument, one that is better than any other that I have run across.

My Analysis of the Causation of Hannah Poling’s Autism

Hannah’s health issues center around a genetic mutation in her mitochondrial DNA that results in abnormalities in how the mitochondria of her cells process proteins. This impacts how her cells produce energy from glucose in her blood stream. Because mitochondria are vital to producing energy in the body’s cells, many organ systems can be affected by their dysfunction. The most common symptoms of mitochondrial disorders include muscle weakness, epilepsy, diabetes, liver failure and - as in Hannah’s case - encephalopathy or regressive brain disease. Psychiatric symptoms are also quite common in these patients.[2]

In the last few years, it has become apparent that mitochondrial disorders can be associated with autism. One recent study showed mitochondrial abnormalities in 5 of 69 autistic individuals enrolled in the study. The question is how are these two conditions tied together? My belief is that lactic acidosis is the key.

Lactic acidosis is a condition that results, among other causes, when mitochondria generate energy from glucose in the absence of oxygen. Most people have heard about lactic acid as a residue of intense exercise. It is produced, for instance, in leg muscles in sports like cycling when the legs don’t spin fast enough when pushing on the pedals. Straining to push the pedals results in lactic acid build up because the lack of spinning of the pedals causes inadequate blood flow to feed oxygen to the mitochondria in the muscle cells that generate the needed energy. Lactic acidosis in mitochondrial disorders involves lactic acid build up in the blood stream, turning the blood more acid than normal, as a result of mitochondrial conversion of glucose into energy and waste products without an inadequate introduction of oxygen into the combustion.

Lactic acidosis is almost always present in mitochondrial disorders.[3] The mitochondrial abnormality causes the mitochondria to function less efficiently than normal (if they didn’t function at all, the person would be dead), resulting in less than perfect energy creation, and the build up of lactic acid. Lactic acidosis is known as a condition that can result in autism.

Science doesn’t understand how lactic acidosis causes autism. However, there are several clues that I have identified. Most importantly, lactic acidosis is associated with abnormal EEGs and seizures[4], indicating that lactic acidosis somehow causes abnormal electrical function in the nervous system. Also, several types of mitochondrial disorders are closely associated with both high levels of both lactic acid and seizures / muscle spasm.[5] [6] Hannah Poling, as a sufferer of a mitochondrial disorder, showed high levels of lactic acid in her blood and the presence of seizures after she became symptomatic.

The question is what ties all of this together – the mitochondrial disorders, lactic acidosis, seizures and abnormal brain waves, and autism. I believe the answer is glutamate, the primary excitatory neurotransmitter in the brain that you will learn all about if you read my theory in detail. Glutamate is the chemical which causes the nervous system to be excitatory and propagate the electrical signals that cause us to function – it is our electrical motor.

One thing we know about glutamate is that it is involved in cell death that occurs resulting from oxygen deprivation – this works in part through its interactions with lactic acid. Studies have shown that during the initial minutes of cerebral ischemia (oxygen deprivation in the brain), lactic acid accumulates because of anaerobic glucose metabolism and acidifies brain pH to 6.0-6.7. Glutamate is also released during ischemia and induces excitotoxicity (the death of brain cells due to too high levels of excitation triggered by glutamate). One study investigated exactly how this works. The researchers determined that at pH 6.7, neuronal loss due to excitotoxicity was similar whether or not lactic acid was present. However, at pH 6.4 (lower acidity), neuronal loss was significantly greater in the presence of lactic acid suggesting that lactic acid potentiates the acidosis toxicity[7]. The researchers determined that glutamate reuptake (the absorption of glutamate at the synapse after glutamate has been present for an adequate time) was inhibited by acidic pH, and the amount of inhibition was significantly greater in the presence of lactic acid specifically.[8]

Other researchers delved into the exact mechanism of how glutamate reuptake is inhibited by lactic acid. What they found is that lactic acid causes the swelling of astrocyte cells, cells that support the function of neurons generally and in particular are largely in charge of the process of glutamate reuptake at synapses. And, glial cell (astrocyte in this case) swelling has been shown to inhibit glutamate uptake. The researchers showed that astrocyte cultures treated with lactic acid showed an inhibition of glutamate uptake by 65%.[9]

So, let me translate. What is happening is that the mitochondrial disorder results in inefficient conversion of glucose into energy and the resulting build up of lactic acid. The lactic acid distributes through the brain in the blood stream and preferentially seeks out astrocytes, where it causes the astrocytes to swell. This causes the astrocytes’ ability to cause the reuptake of glutamate to suffer by up to two thirds, resulting in synapses that are bathed in too much glutamate, the main excitatory neurotransmitter. In accordance with the theory set forth elsewhere on the site, this excess glutamate is responsible for altering the balance in the brain between excitation and inhibition, a crucial balance to neural function. This excessive excitation results in a host of problems including seizures (electrical spasming resulting from too much excitation) and abnormal epileptiform EEGs (brain waves that are similar to those with epilepsy). This elevated level of excitation also results in the symptoms of autism, as described in painstaking thoroughness in my theory in detail.

I think this is what caused Hannah Poling’s autism – a mitochondrial disorder that altered electrical balance in her brain. The vaccines were not the cause of the autism. It is possible that they did in fact trigger the onset of the autism at that point in time. However, it is highly likely that the autistic behaviors would have surfaced anyway in response to some future stressor, since they resulted ultimately from the mitochondrial defect which is part of her genetic makeup. The role on vaccines as a potential temporal trigger for autistic symptoms is discussed in detail on my ‘Vaccines and Autism’ page.