“Vincent Schambach was born 8/29/2023 and passed in his sleep 11/15/2023, 13 days after his 2 month old vaccinations.

He was a strong, healthy, happy and super loved boy up until the week of his vaccinations. Immediately following his 2 month old shots, Vincent developed a 100 degree fever along with a cough that sounded like he was choking and gagging that would also turn his face bright red.

The doctors advised us to just keep giving him Tylenol and make sure he keeps drinking and having wet diapers which he did. The symptoms lasted for 4 days.

A week later, baby Vincent was found unresponsive in the morning along with frothy blood tinged bubbly liquid coming out of his nose. Just when we thought the worst was over, he died and we have been devastated ever since.

The signs can be so subtle to the point you don’t realize something is seriously wrong and a baby has no voice to tell us. We received the autopsy report 6 months later with a diagnosis of cerebral and pulmonary edema along with spinal cord and liver congestion.

The Dtap vaccine which Vincent received during his 2 month visit is known for a side effect of encephalitis (cerebral edema) which we are now trying to fight in court.

Thoughts, prayers and justice for our sweet Vincent “

Shared from his mother, Lauren Seeger.

Vaccines can cause SIDS, or sudden infant death

Parents are not informed that vaccines are capable of causing death, because doctors don’t want to discourage vaccination. They think the benefits outweigh the risks, but I don’t think many pediatricians know the actual risks of vaccination. For one: vaccines can cause SIDS.

Everyone knows that SIDS peaks at 2-4 months of age, but no one would be able to tell you why. At two months of age and sometimes as early as six weeks old, infants receive numerous vaccines. Why so many vaccines are given to very young infants, I don’t know. In 1933, they vaccinated newborns soon after birth against whooping cough, also called pertussis, and when several of the infants died within hours, they decided to at least delay the pertussis vaccine to a few months old. Today, some countries such as Japan and Sweden don’t recommend most vaccinations until after 3 months of age (and also give fewer vaccines), and also have a lower SIDS rate. The CDC pediatric vaccine schedule has added more and more doses over the years, but one thing has stayed the same: very young infants are getting a lot of vaccines during vulnerable periods of development.

When an infant is around two months of age, they enter a phase known as physiologic anemia. This is characterized as the lowest concentration, or nadir, of hemoglobin, because his or her body is transitioning from fetal hemoglobin to adult hemoglobin. For example, in healthy term infants, hemoglobin levels are high (>14 g/dL) at birth and then rapidly decline, reaching a nadir of approximately 10 to 11 g/dL at six to nine weeks of age. This is a normal physiological process but some things can further reduce hemoglobin, and one of those things is vaccination.

You may be wondering what hemoglobin is and why am I connecting this with SIDS. Hemoglobin is basically our oxygen delivery system. Hemoglobin (Hb) is the most important protein contained in our red blood cells that binds to oxygen in the lungs and delivers oxygen throughout our body to all our tissues and cells, including our brain. When red blood cells detect carbon dioxide in the body, hemoglobin swaps the oxygen for the waste product carbon dioxide, travels back to the lungs where the waste is exhaled and oxygen is attached again. This cycle continues unabated unless something happens to hemoglobin or red blood cells. Hemoglobin is critical to our survival.

It was discovered that infants who are born with the lowest concentration of adult hemoglobin have the highest rate of SIDS. Male infants, who have a higher rate of SIDS, have lower concentrations of hemoglobin than girl infants of the same age. In fact, the “risk factors” for SIDS are identical to the “risk factors” for infant anemia. Both are more common in infants who are premature, male, African American, maternal smoking, formula feeding, low socioeconomic, maternal anemia, and have a history of a recent viral infection. For infant anemia, cow’s milk is a risk factor as calcium inhibits iron absorption. This may explain why SIDS apparently increased in the 1950s as fewer women breastfed opting for cow’s milk formulas, and when many vaccines were introduced for pediatric use.

Infections are a well known cause of low hemoglobin and anemia. From the 1989 study Changing characteristics of childhood anemia, infants who had a recent illness were much more likely to have low hemoglobin:

“Among the 278 infants reported to have been “entirely well” during the previous months, only 8% had a hemoglobin level <11.5 gm/dl, close to the normal 10th percentile for this age. In contrast, 20% of the 189 other infants who were reported to have had an illness within 1 month had a hemoglobin level <11.5 gm/dl.”

I’m surprised pediatricians aren’t aware of the publicly available information that vaccines can also cause lower hemoglobin. It’s truly shocking that the CDC recommends so many vaccines to be given to an infant during ‘physiologic anemia’, knowing that vaccination reduces hemoglobin.

A study performed in Chile examined how a viral illness affected hemoglobin levels in infants by using a single injection of measles vaccine. At days 9-14 post vaccination all the infants in the study experienced a significant drop in their hemoglobin. In 8% of infants the drop was >1 g/dL and their hemoglobin did not recover until 30 days after the vaccine. This was the effect from one single vaccine presumably given to older infants outside the nadir of physiologic anemia; what would the effect be of several vaccines being administered at the same visit? What about several vaccines given to an infant during the nadir of hemoglobin, aka physiologic anemia?

In Vincent’s case, he was two months old, the peak age for physiologic anemia, and was found unresponsive 13 days after vaccination–the window of significantly reduced hemoglobin. Could this be an explanation for why SIDS infants have repeated episodes of hypoxemia prior to death? Hypoxemia is low oxygen in the blood.

Infection, vaccination and inflammation (which vaccines also cause) lead the body to sequester iron, which is a natural part of the immune defense. Movsas showed significant declines in serum iron one day post-vaccination in preterm infants. Less iron means less hemoglobin, as iron is necessary to form hemoglobin. That author did not report the post-vaccination hemoglobin values.

Several studies found that white blood cells and antibody production are inversely correlated with hemoglobin, suggesting that when the body is producing large amounts of antibodies, the concentration of hemoglobin drops in a proportionate way. For example, administration of immune globulin is known to cause hemolytic anemia as a side effect, a condition where red blood cells are destroyed faster than they can be replaced.

Another study detailed the serum of immunized rabbits and found that the rabbits that produced more antibodies had a bigger drop in hemoglobin.

In the case report “Sudden twin infant death on the same day: a case report and review of the literature” by Huang, et al, a pair of 10-week-old male twins died 14 days after an oral polio vaccine and a DPT vaccine. The infants had been fed cow’s milk since birth, both parents were non-smokers. Toxicological analysis revealed twin A had 8% and twin B had 10.6% carboxyhemoglobin (COhb) in their blood. Authors found no pathway from the vaccines to death, and did not even mention anemia.

The authors concluded:

“Therefore, the pathophysiologic cause of death was presumably hyperthermia.”

So, overheating as a result of a coal stove in the twin’s bedroom. And then quickly followed with this sentence:

“Most studies have shown that vaccinations are not associated with an increased risk of SIDS.”

But why that night? Why exactly two weeks after vaccination? Because of anemia. More specifically, a vaccine induced anemia.

Elevated carboxyhemoglobin concentrations could be indicative of hemolytic disease (the destruction of red blood cells faster than they can be replaced) which is also called hemolytic anemia (HA). These twins were regarded to have died of Simultaneous SIDS, were recently vaccinated, given cow’s milk, and all these details point to a post-vaccination anemia or post-vaccination hemolysis as the cause of their death. Many things can be true at once. The infants could have had many overlapping risk factors that point to anemia, but what caused the hemoglobin to drop that night of all nights, was vaccination.

How many other SIDS deaths are actually the result of a vaccine induced anemia during an infant’s physiologic anemia?

Why don’t autopsy protocols for infants who die of SIDS or SUIDS look for anemia? Or the effects of vaccination in general?

Final Thoughts

I am not the first to suggest that at least some SIDS deaths are related to physiologic anemia, but no one is willing to make a connection to vaccines. In the 2009 paper “A Unifying Theory for SIDS” authors regarded anemia as a risk factor for SIDS. They admitted a gap in knowledge related to detecting hemoglobin levels postmortem:

“accurate hemoglobin [Hb] levels cannot be determined after death [18]” due to rapid Hb breakdown resulting in the mottled and reddened areas known as livor mortis.”

A 1992 paper they referenced “Reduced haemoglobin levels in infants presenting with apparent life-threatening events–a retrospective investigation” found that 82% of infants who experienced an apparent life threatening event (ALTE) now called brief resolved unexplained event (BRUE) had hemoglobin levels below the mean.

“Anaemia has been shown to be associated with an increased apnoeic pause frequency and with cyanotic breath-holding spells. In this study, the relationship between anaemia and apparent life-threatening events was retrospectively investigated in 72 term infants referred for assessment and home monitoring following an apparent life-threatening event. 

Significantly more infants than expected had Hb levels below the mean (p less than 0.001, binomial test). Anaemia may have played a role in the pathophysiology leading to life-threatening events in some of the infants investigated in this study.”

Why is everyone in the research community afraid to blame vaccines, if vaccines are to blame? Shouldn’t science be honest?

Vaccinations represent the biggest, most dramatic immune activation event of an infant’s early life, much more than minor colds. If hemoglobin drops in proportion to antibody production, then some infants may produce antibodies in excess. Vaccinations cause tissue trauma and injury, and stimulates both cellular and humoral immune responses which can be prolonged as aluminum adjuvants are not quickly excreted by the body. An infant who receives the two month vaccines means several injections in each thigh, plus an oral vaccine–this is a physical onslaught of insults eliciting immune responses in several areas of the body at once. That is quite different than catching a cold the old fashioned way, ie. through the respiratory tract. However, vaccinating an infant who has a cold would no doubt cause more problems, as many of the vaccine injury stories I share the infants are often vaccinated while sick.

This cumulative effect of vaccination during subclinical infection is similar to how poliomyelitis is more likely to follow recent injection, than not.

This mechanism may not be the only way vaccinations cause SIDS or death. For example, a 2019 study “Sudden Infant Death After Vaccination: Survey of Forensic Autopsy Files” looked more carefully at deaths that occurred within just a few days of vaccination, and in at least three of the deaths that occurred within three days, evidence of hemophagocytic lymphohistiocytosis was found, which is an excessive immune overreaction.

There could be several mechanisms at play, and some of them could overlap, such as cytokine storm, seizure, cholinergic crisis, and still others we have not discovered. But for infants who die during their physiologic anemia post-vaccination, if there ever was such a thing as a smoking gun–this is it. I have no doubt in my mind that baby Vincent died from the vaccines during a critical period of development. His body shows evidence of encephalitis–anemic hypoxia can cause encephalitis.

Breastfeeding

On a positive note, breastfeeding has been shown to be protective against SIDS and some reasons may because breastmilk provides passive immunity, which reduces the risk and severity of infections, protects against inflammation, modulates an infant’s immune response, and can even interfere with some vaccines, such as the ‘live’ oral vaccines–suggesting it’s an effective form of immunity. Breastmilk also contains a much more bioavailable iron, compared to iron fortified formula.

While rarely an unvaccinated infant can die of SIDS, my hunch is many more infants are dying due to the extreme immune response generated by vaccination (which generates antibodies even if not to the targeted antigen) in an infant whose immune system has a bias toward being anti-inflammatory.

Can hemoglobin be detected after death?

Some of the papers I found suggests hemoglobin cannot be tested postmortem, but there may be some other methods that give us clues to hemoglobin postmortem.

• Carboxyhemoglobin (which was the lab result reported in the twin’s case report above)

  During medicolegal autopsies, the AVOXimeter® 4000 is often used as a point-of-care test to measure blood carboxyhemoglobin concentration. A carboxyhemoglobin test is used to diagnose carbon monoxide poisoning. Carbon monoxide binds to hemoglobin — a protein in red blood cells that transports oxygen. Too much carbon monoxide in your blood prevents your body from getting enough oxygen. 
• Glycated hemoglobin

  Measuring glycated hemoglobin (HbA1c) concentrations in autopsy material can help identify glycemic disorders that occurred before death. 

Evidence that vaccines cause hemoglobin to drop:

1.“Anemia of a mild viral infection: the measles vaccine as a model” https://pubmed.ncbi.nlm.nih.gov/2797979/

To define the hematologic changes during a mild viral infection, 93 infants were immunized with live attenuated measles virus and studied prospectively at 0, 4, 9, 14, 21, and 30 days. Hemoglobin concentration decreased significantly by days 9 and 14. The decrease was greater than 1.0 g/dL in 8.6% and greater than 0.6 in 24.3% of the infants. Of the nonanemic infants, 22% became anemic.

2.“[Changes in the hemogram and in the laboratory parameters indicative of iron metabolism in mild viral infections]” https://pubmed.ncbi.nlm.nih.gov/8211547/

Vaccination caused significant drop in hemoglobin days 9-14 post vaccination which did not recover until 30 days post vaccination. This descent was > 10 g/L in 8.2% of the cases, and > or = 6 g/L in 19.6%. Serum iron and transferrin saturation decreased significantly, whereas mean corpuscular volume, free erythrocyte protoporphyrin and serum ferritin were significantly increased.

3.“Post-immunization leucocytosis and its implications for the management of febrile infants” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5937853/

Half of febrile infants had elevated white blood cell counts (leukocytosis) post-vaccination and met criteria for sepsis workup due to recent vaccination. Hemoglobin levels dropped >1 g/dL within one day of vaccination.

Vaccination causes significant drop of serum iron (iron is necessary to form hemoglobin):

1.“Effect of Routine Vaccination on Aluminum and Essential Element Levels in Preterm Infants” https://jamanetwork.com/journals/jamapediatrics/fullarticle/1712578

Significant declines were noted postvaccination in serum iron (58.1%), manganese (25.9%), selenium (9.5%), and zinc (36.4%) levels, as was a significant increase in serum copper level (8.0%).

Males and premature infants more likely to have low hemoglobin, anemia:

1. “Seasonal and gender differences in hemoglobin value in infants at 5-7 months of age” https://pubmed.ncbi.nlm.nih.gov/20196391/

Boys have significantly lower levels of hemoglobin than female infants of same age. Prevalence of anemia was 41% among healthy infants ages 5-7 months. Anemia more common in premature infants.

Acute infection is associated with anemia:

1. “Anemia Associated with Acute Infection in Children” https://www.ima.org.il/MedicineIMAJ/viewarticle.aspx?year=2012&month=08&page=484

2. “Iron, anemia, and infection” https://pubmed.ncbi.nlm.nih.gov/9197131/

Infection or inflammation generate anemia and profound changes in iron metabolism mediated by cytokines.

Antibodies are inversely correlated with hemoglobin:

1.“Hemolytic anemia associated with intravenous immunoglobulin” https://pubmed.ncbi.nlm.nih.gov/9270670/

Immunoglobulin administration is associated with hemolytic anemia.

SIDS and reduced brain oxygen / anemia:

1. “Preterm infants experience a nadir in cerebral oxygenation during sleep three months after hospital discharge” https://pubmed.ncbi.nlm.nih.gov/38376100/

Nadir in cerebral tissue oxygenation in preterm infants at 3 months of age.

2. “Elevated Fetal Hemoglobin Levels in Sudden Infant Death  Syndrome” https://www.nejm.org/doi/pdf/10.1056/NEJM198704303161804

Infants who die of SIDS may have delay in the maturation of hematopoiesis. Infants transition from fetal hemoglobin to adult hemoglobin by 6 months of age. SIDS infants had higher fetal hemoglobin than non-SIDS controls.

3. “Adult Hemoglobin Levels at Birth and Risk of Sudden Infant Death Syndrome” https://jamanetwork.com/journals/jamapediatrics/fullarticle/485683

Infants who die of SIDS have lower levels of adult hemoglobin at birth. Infants with the lowest levels of adult hemoglobin at birth had the highest rate of SIDS.

4. “Extramedullary haematopoiesis in liver of sudden infant death cases” https://pubmed.ncbi.nlm.nih.gov/17008039/

Extramedullary haematopoiesis is a frequent finding in SIDS cases, and this may be a consequence of anaemia associated with intrauterine hypoxia, or infections.

5. “An Acute Respiratory Infection of a Physiologically Anemic Infant is a More Likely Cause of SIDS than Neurological Prematurity.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4993813/

“For example, physiological anemia is a natural phenomenon that occurs when fetal hemoglobin (HbF) disappears faster than it is replaced by adult hemoglobin (HbA). Hemoglobin (Hb) is not measured at autopsy because of hemostatic gravitational settling of red blood cells leading to lividity and also because it is a natural phenomenon that is compensated for by infants increasing heart rate to maintain oxygen throughput to the brain. …We note the high Hb at birth can explain the absence of SIDS in the first days of life when most other causes of infant death from neurological immaturity have their highest rates.”

6. “A Unifying Theory for SIDS” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2798085/#B18

“If physiological anemia is considered as a Hb deficit from a fixed level of 13.5 g/dL, that could, combined with apnea, cause transient hypoxia and inability to meet neuronal oxygen demand in the brainstem of SIDS susceptible infants [18].”

7. “Reduced haemoglobin levels in infants presenting with apparent life-threatening events–a retrospective investigation” https://pubmed.ncbi.nlm.nih.gov/1606392/

“Thirty-four infants had Hb levels below the mean, whilst six infants had values above the corresponding normal mean; the one remaining infant had a Hb value identical to the normal mean. Significantly more infants than expected had Hb levels below the mean (p less than 0.001, binomial test). Anaemia may have played a role in the pathophysiology leading to life-threatening events in some of the infants investigated in this study.”