© HundertwasserVase Tree Man, 1974
When we think about vaccine injuries such as autism and epilepsy, we generally consider a direct assault on the brain. But the reality may be far different where injury begins in the gut, leading to brain damage. This article will explore potential mechanisms of gut-brain injuries by vaccination.

As with Parts 1 and 2, we'll consider individual microbial predisposition as crucial to susceptibility to intestinal injury. The theory is that protective microbes such as Bifidobacteria are why some people appear to escape injury while others are not so fortunate.

Neurodegenerative diseases including multiple sclerosis (MS), Parkinson's and Alzheimer's are strongly associated with gut dysbiosis where these problems are now thought to begin in the gut. Diabetes and obesity are associated with brain inflammation. Gut-brain is known to be a two-way street, so diabetes and obesity are improved by reversing brain inflammation. In fact, 90% of fibers in the vagus nerve travel from gut to brain, not brain to gut, surprising and unsettling.

So, to consider vaccine injury as beginning in the gut isn't such a stretch of the imagination. This connection began the controversy about vaccines and autism proposed by Andrew Wakefield. But the message was lost over the years as people focused on Thimerosal and direct damage to the brain by mercury. Yet the MMR vaccine does not and never did contain mercury. There's something else going on where vaccines harness the body's immune system, beginning in the gut, making some individuals their own worst enemy.

Studies have attempted to thwart the idea that vaccine injury begins in the gut. This study refuting the relationship of MMR and inflammatory bowel disease (IBD) leading to autism found "only" 20% of subjects received MMR before the onset of gastrointestinal disturbances leading to autism. That's quite a large percentage! Such gastrointestinal complaints include constipation associated with low blood levels of serotonin. Given current technology, it would be important to know the microbial balance of these subjects to learn if they were absent or reduced in protective anti-inflammatory microbes such as Bifidobacteria.

Several studies were published before massive changes in technology allowed us to identify differences in microbial balance and new biomarkers of inflammation. They were written before it was common knowledge that human diversity includes microbial diversity. Nobody suspected individuals and races have different microbial makeup. Moreover, the fetal gastrointestinal tract was wrongly considered sterile, condoning vaccination within 12 hours of birth.

Intestinal injury caused by the rotavirus vaccine was recently added to the government compensation program for adverse events. This type of injury called intussusception is difficult to distinguish from necrotizing enterocolitis (NEC) which occurs most frequently in preterm infants known to have different microbial balance based on gestational age according to new research. Colonization begins in the womb where the sequence occurs as follows: first Bacilli flourish, then Gammaproteobacteria such as E. coli become abundant and, finally, Clostridia. Bifidobacteria then flourish with breastfeeding. Environmental factors such as c-section vs. vaginal birth and antibiotics do not affect this progression, though may slow it down. Knowing this, it should be alarming that current vaccine protocol for preterm infants is to treat as full term when weighing over 2.2 lbs. Perhaps preterm infants are at greater risk of autism because gut flora are predominantly Gammaproteobacteria at birth and this triggers an adverse immune response upon vaccination. Protective Bifidobacteria and potentially protective strains of Clostridia are not yet developed at birth.

Another illustration of the point that children are born with unique microbial footprint is a profound 2013 study of meconium from infants of diabetic and gestational diabetic mothers found enriched in Proteobacteria and Bacteroides. Bacteroides are known to train the immune system in Peyer's patches of the intestines, inducing high IgA production. Might this explain the Mayo Clinic conundrum where Somali immigrants react to rubella vaccination with twice the antibodies?

In most recent news regarding microbial predisposition, research linked gut bacteria passed generationally to susceptibility to gut injury. This is a new way of considering how traits are inherited through microbial DNA. Research detailed how vertical transmission of bacteria can make offspring more vulnerable to gut injury. Scientists used a chemical to test intestinal response, but what if this chemical were a vaccine? Such vaccine safety research is yet to be done, but scientists are using gnotobiotic pigs to successfully test probiotics used to guard against intestinal injury by rotavirus infection and improve vaccine response.

How can a gut injury lead to a brain injury?

Let's focus on serotonin imbalance related to glutamate excitotoxicity to answer this question. About 95% of the body's serotonin is produced in the gut, not the brain. Gastrointestinal symptoms such as constipation and diarrhea are associated with serotonin imbalances in blood. In constipation, serotonin is retained in mucosal cells of the intestine leading to low levels in blood. In diarrhea, serotonin is released and inflammatory. But it's low levels of serotonin in blood which may be most associated with glutamate toxicity and brain damage. This construct is applied to SIDS, SUDEP, epilepsy and vaccine injury.

Experiments regarding serotonin levels altered by vaccination include dramatic changes in sensitivity to the lethal effects of serotonin. Some vaccines may dramatically increase serotonin, while others such as BCG (tuberculosis vaccine) appear to lower serotonin to the extent of SSRI resistance leading to depression. Thimerosal (mercury) was found to cause exocytotic release of serotonin. Sertotonin levels may rise and then fall dramatically in vaccination.

To illustrate the order of events from gut-to-brain (vaccination to gut disturbance to serotonin imbalance to glutamate excitotoxicity), we'll use Sudden Infant Death Syndrome (SIDS) as example. SIDS is the leading cause of death among infants one month to one year old. SIDS is associated with serotonin deficiency in the brainstem:
  1. A child is born with high levels of Proteobacteria, low levels of Lactobacilli and reduced or absent Bifidobacteria along with pathogenic strains of Clostridia and high gram-negative Bacteroides, an inflammatory microbial predisposition. Vitamin B12 and folate act as cofactors in synthesis of serotonin, both regulated by flora.
  2. Vaccination begins within 12 hours of birth and continues following CDC protocol of 23 vaccinations in the first year of life leading to constipation and low blood levels of serotonin. Antibiotic abuse in newborns may also be a factor, i.e., shifting flora to raise clostridia which cross-feed hydrogen and CO2 to methanogenic archaea where methane causes constipation.
  3. It's stated boldly in many papers that serotonin doesn't cross blood-brain barrier (BBB) as if gut-derived serotonin doesn't enter the brain, yet papers show serotonin penetrates BBB. Serotonin may also cross BBB from the brain to circulating blood. Blood and brain serotonin levels are positively correlated. Alternatively, an infant with acute tryptophan depletion leads to serotonin deficiency in the brain where tryptophan level is dependent on gut microbiota and enhances immune response. Bifidobacteria are known to elevate tryptophan, precursor of serotonin, while reducing serotonin metabolites in the brain. Tryptophan depletion leading to low serotonin is also the result of hypoglycemia caused by vaccination. Blood sugar is regulated by flora where insulin removes competing amino acids allowing tryptophan into the brain.
  4. CO2 chemosensors in the brainstem activate the serotonergic system. Reduced brain serotonin affects CO2 chemosensitivity. Microbial overgrowth may also affect CO2 levels in blood as microbes utilize CO2 to manufacture metabolites such as acetate. Intracellular microbes may affect CO2 production in the Krebs cycle. Note: CO2 inhalation is a technique used to halt seizure.
  5. Serotonin, or lack of serotonin, then activates thalamocortical networks associated with glutamate receptors. Cytokines are induced by LPS (gram-negative bacterial toxins) and modulate serotonergic transmission in the brain.
  6. In SIDS, the face-down prone position means a child inhales CO2, activating the serotonergic system leading to glutamate excitotoxicity, dysregulating cardiac vagal neurons and parasympathetic activity to the heart.
Alternating constipation and diarrhea is a way of life for many. Serotonin levels may swing like pendulum. Blood levels of serotonin are high in diarrhea leading to Serotonin Syndrome. High blood levels of serotonin are known in autism where many people suffering are still in diapers as adults. Perhaps overgrown Proteobacteria are the culprit as they may be most responsible for production of tryptophan, precursor of serotonin. Constipation is also a widely known side effect of antipsychotic drugs, not yet commonly viewed as root cause of mental illness.

High serotonin in blood of autistic children may be a matter of hydrogen sulfide (raising serotonin in the brain) produced by the Proteobacteria known overgrown in autism, Desulfovibrio. Seizures may be caused by both high and low serotonin, a balancing act. Scientists also report serotonin levels in autism as high in blood, but low in brain. The point is levels may be in flux based on activity in the gut and serotonin, or lack of it, activates glutamate excitotoxicity.

Dietary glutamate is thought protective and doesn't cross BBB, enhancing digestion and absorption of nutrients in the small intestine packed with glutamate receptors. But gut dysbiosis is known to increase BBB permeability via LPS where a more porous BBB may allow circulatory glutamate into the brain. Recent research found maternal microbes regulate fetal BBB permeability as well as throughout life without consideration of imbalanced fetal intestinal flora causing leaky brain. Clostridial toxins induce excessive glutamate release in the hippocampus leading to seizure and neuronal damage.

Recent study found high levels of glutamate in autistic subjects and excitotoxicity associated with neuroinflammation. Glutamate is a product of intestinal flora, substrate for production of butyrate and acetate. Bifidobacteria and Lactobacillus convert glutamate to calming GABA and CO2 using the enzyme glutamate decarboxylase.

How does glutamate toxicity damage the brain?

Dr. Russell Blaylock provides an excellent overview of immunoexcitotoxicity in this video presentation. Neurodegeneration is a matter of mitochondrial damage by intracellular calcium. Factoring intracellular microbes is not yet part of science. Cells may release endogenous glutamatebased on microbial enzymatic (transaminases such as ALT) interference with the Krebs cycle. Deficiency of microbial enzymes such as glutamate dehydrogenase may also lead to mitochondrial damage as glutamate cannot be deaminated to remove excess nitrogen, so ammonia builds. Lactobacillus paracasei is a common lactobacillus used in yogurt and cheese manufacturing and found in breast milk, prized for glutamate dehydrogenase activity, reducing ammonia overload in such scenario. Bifidobacteria are also known to reduce ammonia levels.

Dr. Blaylock mentions formation of nitric oxide as part of immunoexcitotoxicity. Gut microbes produce nitric oxide. Nitric oxide inhibits glutamine synthetase which would otherwise clear glutamate.

Studies of excitotoxicity as cause of autism include cannabinoids as mechanism of success in calming the brain. The role of glutamate receptors in autism and the serotonin hypothesis, including use of SSRIs during pregnancy leading to increased risk of autism, awaits further study. Recent evidence reveals disturbed, excitatory glutamate metabolism in autism.

Why are boys 5x more likely to become autistic than girls?

We'll discuss two factors: serotonin and estrogen. Boys have naturally higher levels of tryptophan in blood, precursor to serotonin. This translates to 52% higher levels of serotonin synthesis in the male brain. Approximately 60% of SIDS victims are male despite or because of higher levels of brain serotonin. Are male infants more prone to hypoglycemia leading to tryptophan depletion due to gender differences in flora?

Differences in microbiota between male and female intestines control tryptophan metabolism affecting serotonin levels, influencing neurotransmission of the gut-brain. Papers also reveal significantly lower levels of GABA in men than women. Females adapt better than males because of differences in the GABAergic and glutamatergic systems.

Estrogen receptors in the female brain are anti-inflammatory. A recent dietary study illustrates how estrogen receptors of the female brain are protective in high fat diet. What is generally not yet factored are microbial fatty acids of gut origin and how they affect the brain. It's not a simple matter of diet as we aren't the only ones consuming what's placed in our mouths.

Uric acid

Retention of uric acid in cells affecting levels in blood serum is somewhat similar to retention of serotonin and has been subject of debate for over a century in fields of epilepsy and migraine, largely forgotten. In 1899, migraine was called a "uric acid headache." Today, migraine treatment options include probiotic therapy.

In epilepsy, uric acid is retained in cells leading to low levels in serum until seizure when it is released in high levels. At optimal levels, uric acid is a natural antioxidant found protective. Elevated levels are associated with risk of stroke. These cerebral microbleeds are also the subject of vaccine brain injury as described by Dr. Andrew Moulden. Uric acid is studied as damage-associated molecular pattern (DAMP) associated with severe adverse events after vaccination. Interestingly, lactic acid bacteria (LAB) lower serum uric acid. High levels of uric acid are associated with significantly low levels of serotonin.

In closing, the current one-size-fits-all approach to vaccination does not factor individual immune systems regulated by gut microbiota. In order to assess potential risk of vaccine injury, meconium and stool testing pre-vaccination to identify microbial balance is justified.

And if vaccine scientists are fortunate, new probiotic adjuvants in development will not only improve vaccine response, but also reduce risk of injury. Unfortunately, vaccine scientists are concerned only with improving vaccine effectiveness, not safety. Most importantly, the public should become aware of how gut flora dictate immune response in order to improve general health and immunity. This is the major difference between health, injury and survival with and without vaccination.

About the author

Keith Bell is a 25 year veteran of the recycling industry with interest in sanitation and health. During the 1980s, he was a UNICEF radio spokesperson in Chicago for the annual release of State of the World's Children Report. He's particularly interested in gut-brain connection including gut-origin of seizure, underdiagnosed in epilepsy.