Beginning in the 1940s, researchers out of Columbia University discovered that they could experimentally induce elliptical seizures in rhesus monkeys by injecting alumina cream into different regions of their brain. The seizures were not induced instantaneously, rather the seizures began anywhere from 1 ¼ to 12 months post injection. Only 1.8-2.2 mg of aluminum was necessary to induce seizures–an amount of aluminum that is equivalent to what is injected into the body of a 2 month old infant at a ‘well-baby’ visit.

Unlike those experiments, vaccinations are not injected into the brain but rather into the muscle or tissue of the thigh or arm. But does this really make a difference? Just as an apparent dry plot of land has a network of underground rivers and streams that accumulate and distribute any pesticide sprayed on the soil above, so too the human body is interconnected, and has systemic circulation that transports both necessary and harmful substances in its never-ending attempt to preserve homeostasis.

The reason aluminum is regarded as a successful adjuvant is in part due to this low biodegradability and bio-persistance in immune cells; however, this may also be its ultimate downfall, from sensitization to allergens, asthma, autism, epilepsy, Alzheimer’s disease, and more. The benefits may not outweigh the risks once we honestly calculate all the collateral damage.

The Problem of Aluminum

Aluminum is added to vaccines as an adjuvant precisely because it’s toxic and thus it creates a more robust immune response. For the longest time, the science community didn’t understand how or why it worked, just that it resulted in an immune response. The type of aluminum that is used as an adjuvant is most commonly in particulate forms such as Aluminum Hydroxide, and contrary to other forms of aluminum, this has been shown to accumulate in the body. Experiments with animals found that a single injection of aluminum adjuvant accumulated in all major organs, including the brain in as short as 28 days at which point the animals were sacrificed (so it’s impossible to know how much accumulates after 28 days). That same small experiment showed that only 5.6% of the Aluminum Hydroxide was excreted in urine by 28 days.

Most young children are given dozens of injections today and we expect them to live well into their 80s or 90s–shouldn’t we pause and question whether this intentional bioaccumulation in the young, neurologically sensitive, developing body is safe? And if there are some groups more sensitive to these toxic effects than others?

You would think, or hope, that our blood-brain barrier would keep out all offending substances from entering our brain. But there are situations and times, such as during infection, fever or stress (and many other times), when these unwelcome additives can enter and even accumulate in our brain in larger amounts. Once there, anything is possible.

Convulsions Before Death

A recent study has shed light on a potential clue behind sleep-related deaths in children that remain unexplained after a thorough autopsy, similar to SIDS but for children over one year. The paper documents home video recordings of seven toddlers who died shortly after what appears to be seizure or convulsive activity. While the paper cannot determine the cause of the seizures, and isn’t able to draw any solid conclusions, it’s worth noting that only one of the seven children had a medical history of febrile seizure. Were the convulsions the result of a death process that had already begun? Or were the seizures responsible for the subsequent death, or in response to infection, or trauma, or some other inflammatory cause? We don’t know and we can’t be certain.

Near death, seizures are more common, and yet they aren’t necessarily the cause. Was there something else going on in their body that facilitated a brain injury via cytokine mediated neuro-inflammation, of which seizures are a symptom?

If we know that vaccine based aluminum remains in the body, may accumulate in the brain, and has the potential to cause neuro-inflammation including seizures, what is the relationship between vaccines and these sudden deaths?

Could infection and or vaccination (after all, isn’t vaccination modeled after infection?) induce an overreactive immune response, ie. pro-inflammatory cytokines and inflammation which goes uncontrolled perhaps due to a dysregulated cholinergic anti-inflammatory pathway or altered a7 nicotinic acetylcholine receptors?

About the ‘cases’

Funded by the SUDC Foundation, the paper examined a series of 7 consecutively enrolled “cases” with home video recordings of the child’s last sleep period, analyzed by 8 physicians. In all 7 videos, the physicians believe that what they are seeing is evidence of seizures or convulsive activity prior to death. Only one of the toddlers had a history of seizure.

About the 7 cases:

4 boys, 3 girls

Age range: 13–27 months

Three cases had no significant medical history; four had “common” pediatric conditions (according to the paper):

• preterm birth with recent otitis media
• chronic otitis media and bilateral myringotomies (ear tubes)
• egg allergy
• febrile seizures

The child with febrile seizures had first-degree relatives with febrile and afebrile seizures. All children had normal developmental milestones including independent ambulation.

Those four “common” pediatric conditions are actually not that common. I read them as evidence of vaccine injury. If you know, you know.

Four had disorders during the past 72 hours of life, 3 did not:

• cold symptoms
• cough and fever
• cough, diaper rash
• teething

All children were discovered prone with face down into bedding, except for one’s face to the side significant for airway obstruction at autopsy. Sudden Unexpected Death in Epilepsy (SUDEP) is strongly linked with prone position.

In all 5 continuously recorded videos, a convulsive event was identified shortly before death. All convulsive events were 8–50 seconds. The 2 motion-triggered videos had time gaps: one had indeterminant movement and the other had abnormal movements suggesting a convulsive event.

Of the 5 continuous videos, all had convulsions and 4 were alive postconvulsion for at least 2.5 minutes, some longer.

• Case 1: experienced a ∼8-second convulsive seizure. Subsequent agonal type breathing lasted ∼5 minutes.
• Case 2: was a 90-second continuous video. The child was prone with face down and had a ∼30-second convulsive seizure with side-to-side truncal movements and abnormal “whimpering” vocalization followed by cessation of motion or sound.
• Case 3: experienced a ∼40-second convulsive seizure caused the face to turn more prone into the pillow near the child’s face. Labored breathing followed, decreasing in frequency and depth over 25 minutes until there was no movement or sound.
• Case 4: A ∼50-second convulsive seizure primarily involved trunk and lower extremities followed by rhythmic lower extremity clonic activity alone before ∼5-minute postconvulsion.
• Case 5: included ∼11-second video segments triggered by a sound or movement, presumably the child’s. Across 6 segments over 105 minutes of the final sleep period, the child was in prone with face prone or to the side. No abnormal movement or sound were identified.
• Case 6: included ∼10-second video segments triggered by sound or movement, presumably the child’s. Across 4 segments over a 100-minute sleep period, the child appeared congested with face movement into his pillow. It was unclear if the movement was voluntary. The second segment recorded 1 deep inspiration. The third segment recorded an abnormal vocalization (sneeze-like sound), while the child extended his trunk rapidly from the child’s pose position to sitting, then returned quickly to prone face down into pillow position. Clinicians considered this suggestive of a seizure, possibly hypermotor or convulsive, but determination was limited by discontinuous recording.
• Case 7: The child was prone with face prone initially followed by a ∼25-second paroxysmal motor event primarily involving the trunk, appearing to be a hypermotor seizure. This followed with rhythmic hip motions and simultaneous irregular deep and shallow breathing motions until no further movement or sound ∼5-minute postictal.

Autopsy Findings

Formal neuropathologic examination of the brain was performed on 6 of 7 cases, 3 of which had hippocampal dentate gyrus changes previously reported in SUDC (cases 1, 2, and 4). None of these cases had a reported history of febrile seizures, whereas 1 case with a reported history of febrile seizure had hippocampi that were microscopically within normal limits.

I wonder if these changes are similar to what was seen in this experiment on rats fed aluminum chloride:

The present study investigate the effect of increasing doses of AlCl3 at different periods on body and brain weight, plasma and brain AlCl3 concentration. Histopathological analysis indicate that exposure rats to AlCl3 causes morphological alterations in dentate gyrus. In fact, AlCl3 had a destructive effect on subgranular layer and granular layer aspect in adult rat. The impairment induced by aluminum was accompanied primarily by the prolonged accumulation of aluminum in the rat brain.

Study doesn’t mention vaccine history

This particular study does not mention the child’s vaccine histories or give more details about each case. One of the study authors, Laura Gould, lost her own 15 month old daughter in 1997, and subsequently established the SUDC Registry and Research Collaborative. She was also the president of the SUDC Foundation.

I am aware that parents of children who died from SUDC are discouraged from discussing vaccines, and it’s true that grieving parents have been kicked out of the support group for bringing up the possibility that vaccination played a role in their child’s death. This is a dangerous form of bias which undoubtedly affects results of papers investigating the causes of SUDC.

How many of these children received vaccines?

A 2019 paper Potential Role of Febrile Seizures and Other Risk Factors Associated With Sudden Deaths in Children (also with Laura Gould Crandall as a co-author) includes relevant vaccine histories of the cases and controls in a supplementary section. For this paper, the controls are children who died of Sudden Explained Deaths in Childhood (SEDC).

Vaccination ‘up to date’ at death:

• SEDC Deaths: 78%
• SUDC: 81.1%

Last vaccination: < 2 weeks prior to death:

• SEDC: 9.2%
• SUDC: 13.3%

A child who died of SUDC was 44% more likely to have had a recent vaccine than a child who died from SEDC, which could be partially an effect of healthy vaccinee effect. If 13 percent of SUDC deaths occur within 2 weeks of a vaccine, compared to only 9% of explained deaths, what percent of living control children had a vaccine in the previous two weeks? If surviving, healthy children are much less likely to be recently vaccinated, we have a clear issue.

As it stands, 1 in 7 sudden unexplained child deaths were recently vaccinated (less than 2 weeks) prior to their death. And some parents I speak with who were included in that study do believe the vaccine killed their child and they are currently bringing the case to the Vaccine Injury Compensation Program.

A 2007 paper Sudden Death in Toddlers Associated with Developmental Abnormalities of the Hippocampus: A Report of Five Cases (also with Laura Crandall as a co-author) documents some brain abnormalities in five toddlers who died during sleep, all five had been vaccinated at some point prior to death, anywhere from 38 days to 317 days before death. Two of the five had a history of at least one febrile seizure; the other three had no history of seizure.

We suggest the possibility that the 5 toddlers reported here suffered SUDEP. Although they did not have histories of nonfebrile seizures, the striking hippocampal asymmetry and microdysgenetic foci raise the possibility that their deaths were seizure related, because these pathologic features have been observed in epilepsy patients.

Research on seizures and vaccination risk

Whether vaccines cause seizures appears to be a difficult area of study. The research is often biased by having only vaccinated subjects. For example, the reference population is also vaccinated, or a self case control method is used comparing windows of time to another window of time in the same vaccinated subject. Other studies compare rates of seizure post vaccination to “background rates” where vaccine history was not mentioned. It’s impossible to know what the true “background rate” for something is if the people in the background have had the same exposure one is attempting to study.

Regardless, every study finds increases in seizure risk in specific windows of time.

Examples:

A 2001 paper analyzing seizure risk after DTP vaccine and MMR vaccine found an elevated risk on the day of vaccination for DTP (adjusted relative risk, 5.70; 95 percent confidence interval, 1.98 to 16.42) and 8 to 14 days after vaccination with MMR vaccine (relative risk, 2.83; 95 percent confidence interval, 1.44 to 5.55).

Caveats: Data from Vaccine Safety Datalink so everyone was vaccinated. The reference group were children who did not have a vaccine in the previous 30 days, but were assigned more weight. For example:

“A child with seizures who had been vaccinated at Kaiser Permanente of Northern California would be assigned a weight of 1.0, but a child with seizures who had not been vaccinated would be assigned a weight of 5.0, since the random sample consisted of 20 percent of the population.”

Also, the background rates of febrile seizures are an interesting problem, because how do we assess “background rates” if the majority of children are or were vaccinated at some point? One of the papers relied on for background rates doesn’t mention vaccine history, and 7% and 31% of those with a febrile and non febrile seizure had a severe congenital anomaly; the 2001 paper does not mention congenital anomalies at all.

Are they comparing healthy children who develop a seizure post vaccination to a background rate / control child with a congenital anomaly?

This 2012 Danish study examined the risk of febrile seizure within 8 days of (DTaP-IPV-Hib) compared to other time periods. An increased risk of febrile seizure was found for the first 2 vaccinations given at 3 and 5 months.

Caveats: No one in the study was completely unvaccinated (zero vaccines) or if they were, they were combined with vaccinated subjects so we weren’t able to assess them separately.

Vaccination was treated as a time-dependent variable. Children entered the reference cohort at the beginning of follow-up and moved to the exposed cohort on the day of vaccination. Thus, both unvaccinated children and vaccinated children contributed person-years at risk to the reference cohort.

In the 2014 Pediatrics publication with lead author Frank DeStefano of the CDC, the paper examined the association between timing of vaccination and first seizure using Vaccine Safety Datalink data from 2004 to 2008.

When the MMR vaccine was administered according to ACIP recommendations at 12 to 15 months of age (361–488 days), it was associated with an increased risk of seizures in the 7 to 10 days after vaccination: IRR 2.65, 95% CI 1.99–3.55; and even higher after MMRV: IRR 6.53, 95% CI 3.15– 13.53. The toddlers who got the MMR vaccine between 16 to 18 months had an IRR of 5.09 (95% CI 2.05–12.66); and was most pronounced at 19 to 21 months of age, with an IRR of 8.75 (95% CI 2.35– 32.58). Varicella vaccine was associated with an increased risk for seizures 7 to 10 days postvaccination. When administered at 12 to 15 months, the IRR was 2.75 (95% CI 2.05–3.70); the IRR increased to 3.64 when administered at 16 to 23 months of age.

Caveats: Everyone in the Vaccine Safety Datalink is vaccinated. They used a self controlled case design. For the 2 month vaccines, they used a 0-2 day risk window. So if a seizure occurred on day 3 it would serve as the control for the 0-2 day window. For the MMR and MMRV vaccines, they used a risk window of 7-10 days after vaccination, and they excluded the 1-14 days before vaccine to reduce the potential of “healthy vaccinee effect” meaning a child who gets a vaccine is usually healthier than a child that must skip or delay a vaccine. The control period was a 14 risk window after vaccination risk window (so day 11-25 for mmr or day 3-17 for DTaP etc.) and also a 14 day window before the healthy vaccinee effect period.

So the risk windows are literally 3 or 4 days long, and yet the control period were two sets of 14 days, for a total of 28 days. And if the seizure didn’t happen those days, then that is considered the control. And yet, this is completely arbitrary, how could we say that a seizure that happens on day 2 is related to the vaccine, but the seizure on day 4 post-vaccination is unrelated? This is pseudoscience. This tells us nothing about whether vaccines increase one’s risk of seizure or epilepsy.

The authors mentioned they chose the risk windows based on evidence, and yet this case report documents a 2 year old boy whose tonic clonic seizures began on day 14 post measles vaccine; an adverse event that is categorically denied by the previous paper. His event would be in the “control period.”

Most of these studies rely on very short post vaccination windows. This is like splitting hairs. If something happens on a Wednesday, and not Tuesday–does it matter? The injection is inside the body. The aluminum based adjuvant persists in immune cells and can travel to distal regions as part of the signaling and recruitment of immune cells to repair damage. Perhaps these aluminum loaded cells are waiting for a fever, an injury or a trauma; and when we least expect it–like a trojan horse–cause harm.

Final Thoughts

Movsas showed that 24 hours after pediatric vaccination the injected aluminum was neither in the urine nor the blood. So where was it?

Could injected aluminum pose a risk to a child at a later date? Does it even matter when a child was vaccinated, as the aluminum adjuvant has not been demonstrated to significantly leave the body; we know there is a body burden we have to deal with. And the aluminum adjuvant may skew the immune system toward Th2 and influence how the body reacts to future exposures, ie. trained immunity.

As English chemist Christopher Exley has pointed out, the particulate aluminum is engulfed by macrophages, and is transferred to new immune cells indefinitely and then trafficked into the brain during times of stress or infection. At that point, it causes inflammation, possibly a seizure, or other brain abnormalities, or worse, death.

These [macrophage] cells are able to accumulate significant quantities of aluminium adjuvant without incurring immediate toxicity. This means that these migratory cells remain viable for days and perhaps longer during which time they can carry their cargo of toxic aluminium throughout the body. This transport of aluminium from a vaccine injection site to elsewhere in the body may be what we imaged in our research on aluminium in brain tissue in autism.

Aluminium adjuvant in macrophages and other cells slowly dissolves to release burgeoning amounts of Al3+ and hence eventually kills the cell. This aluminium is then released into the tissue surrounding the dying cell where it may also bring about toxicity. This may be a mechanism whereby potentially toxic amounts of aluminium can be accumulated in, for example an infant’s brain tissue, in a relatively short period of time. A mechanism of aluminium-induced encephalopathy (accelerated cell death) similar to what is acknowledged to occur in dialysis encephalopathy.

If you are unfamiliar with the risks of vaccines, and did not know they were connected to asthma, food allergies, seizures, autism and more, please utilize this website and its resources to get yourself educated. Start with these posts:

Start Here

Do Vaccines Cause Asthma?

What is the Blood-Brain Barrier?

Detox Success Story: Baby Is Seizure Free After Aluminum Detox

Vaccines and the Premature Infant