“Mark Roe was a healthy baby–and then, for no apparent reason, he was dead. His parents had to know why. Their determination to find an answer is now helping doctors unravel the mystery of “crib deaths,” which take the lives of 25,000 infants a year.”

— Vivian Cadden, “Why Babies Die,” Redbook, 1963

In 1950s America, the typical suburban family had few worries. But in 1958, tragedy struck the Roe Family, an upper-middle-class family-of-four living in picturesque Greenwich, Connecticut when one morning in October, their healthy 6 month old son Mark did not wake up. Louise and her husband Jedd were stricken by his loss, but they soon perceived their son’s sudden death as part of the larger, growing mystery known as ‘crib death.’ In 1963, Louise Roe detailed Mark’s story to Redbook writer Vivian Cadden, bringing national attention to the issue. Frustrated by the lack of answers, the Roe’s transformed their heartbreak into a mission.

The Roe’s formed the Mark Addison Roe Foundation to support and fund research into the causes and prevention of sudden infant death. Eventually it would become the ‘National Foundation for Sudden Infant Death’ and by 1969, the term SIDS (Sudden Infant Death Syndrome) would be used to describe and track this mysterious cause of infant death that devastated families, but left few clues.

More than six decades have passed since Mark died, and several modifiable risk factors have been identified, such as maternal smoking and prone sleeping position, but SIDS continues to be the leading cause of death in infants over 1 month to under 1 year.

SIDS has a preference for premature and low birthweight infants, males, African American and American Indian infants, and as many as half of the infants who died had a recent cold. However, its distinct mechanism or mechanisms have evaded pathologists and researchers alike for decades, but ironically appears to have been perfectly preserved in Mark Addison Roe’s story. Had we only given Louise’s testimony more careful consideration.

On this website, I share many vaccine injury stories because reading a personal account is much more illuminating than a series of numbers. While studies are incredibly useful, they are often very narrow snapshots and omit seemingly irrelevant information that may turn out to be important. We never know what wasn’t controlled for, or the confounding variables that were missed. With a person’s detailed story, however, we naturally get so much more. For instance, Mark was vaccinated two weeks before his death and he also had a history of low hemoglobin. Whether one aligns with an unwavering belief system in vaccination or not, one must consider both recent vaccination and how it relates to hemoglobin to understand what SIDS is.

Vaccination need not precede every SIDS death for it to be a trigger in some, when low hemoglobin is the mediator between the various risk factors (prematurity, maternal smoking, recent infection, male) and the fatal outcome. Just like not every infant who succumbs to SIDS is an infant of a smoking mother, or placed in the prone sleep position, the missing piece of the puzzle has always been low hemoglobin.

What I need you to know

It’s likely that most of you won’t read this entire post and make it to the end. So what is the biggest takeaway here, and what can we do to prevent SIDS?

I need you to know what I didn’t know before researching Mark’s story:

I didn’t know what physiologic anemia of infancy was, or how this developmental stage that all infants go through perfectly overlaps with the peak of the highest SIDS risk, ie. 2-4 months, which has hitherto never been able to be explained.

SIDS has always been filled with paradoxes, but everything makes sense now when we factor in physiologic anemia and low hemoglobin.

You see, when infants are first born they have predominantly fetal hemoglobin (Hb F) which has a high affinity for oxygen which is vital in the womb, but problematic for a baby. So naturally, our bodies start producing adult hemoglobin (Hb A), which replaces fetal hemoglobin by 6 months of age. Due to the waning of Hb F and the switchover to Hb A, an infant’s overall hemoglobin concentration dips to its lowest point, known as the nadir, around 6 to 8 weeks and can last several months, depending on the infant’s unique characteristics (premature, etc). This is physiologic anemia of infancy.

This graph below aptly shows how the nadir of hemoglobin correlates with the peak risk in SIDS. I am well aware that correlation is not causation, however all the risk factors for SIDS and anemia are identical.

As a mother who has given birth to two infants, I was surprised that I never heard of physiologic anemia before. And I even brought my infants into the pediatrician often as a first time mom. Because ‘physiologic anemia’ is normally not a problem, parents are not told to look for potential warning signs of a problem: such as paleness, fussiness, irritability, poor feeding, lethargy, or bluish lips or nails during sleep, crying or after eating. But if your infant experiences any of these symptoms around 2 or 3 months this could be a sign of hypoxia due to low hemoglobin or anemia.

I also wonder about babies who experience colic, GERD, or purple crying—all these begin around this same age of low hemoglobin—could these be connected as well, or serve as warning signs?

This natural phenomenon of high hemoglobin / low hemoglobin explains both the relative absence of SIDS in the first month, and the SIDS peak at the nadir, as well as its stark decline after 6 months.

But then I started asking more questions. And the answers shocked me. Infants who die of SIDS have lower adult hemoglobin at birth. A study found a dose response relationship between the lower the adult hemoglobin at birth and a higher the SIDS risk.

A dose response relationship usually indicates a causal pathway.

Several studies also suggested SIDS infants have persistent fetal hemoglobin which would also cause hypoxia (due to its high oxygen affinity), and SIDS infants have elevated hypoxanthine levels in the vitreous humor which could indicate hypoxia before death.

Then I found that some infants have lower total hemoglobin than others, like male infants, African American infants, premature infants and infants born to anemic mothers–all incidentally risk factors for SIDS.

And maternal smoking, minor infections and inflammation also cause drops in an infant’s hemoglobin levels, again more SIDS risk factors.

Even laying down is associated with lower hemoglobin, compared to being up and moving around.

Then I was shocked to find a few studies examined hemoglobin levels post-vaccination and found a statistically significant decline (>1g/dL) in hemoglobin 9-14 days after one vaccine in 8% of the 1 year old infants studied. And the sample size was small.

And another study, one my Movsas identified a drop in serum iron after infants received the 2 month vaccines. This demonstrates iron sequestration, which we know occurs after infection and vaccination, and it too leads to low hemoglobin. With less iron, we have less hemoglobin.

So basically, this means that vaccinating an infant at the nadir of hemoglobin (which is the current CDC recommendation by the way), would cause a sudden and devastating drop in hemoglobin that would be life threatening for some, ie. premature, male, African American, smoking exposed, or something else we still haven’t yet discovered, etc.

Then I found more confirmation in a study looking at infants who presented to emergency departments with apparent life-threatening events (sometimes thought of as interrupted SIDS) and they had a statistically significant reduced hemoglobin concentration compared to healthy infant controls, suggesting anemia prompts some ALTE visits.

Maybe I’m guilty of convincing myself, but how is no one looking at anemia as the most logical cause of SIDS?  Anemia, or low hemoglobin, compromises the body’s ability to deliver oxygen to tissues, including brain, known as hypoxia. Infants who die of SIDS have long been said to suffer from repeated episodes of hypoxia prior to death.

How is it a public health recommendation to vaccinate all infants during their physiologic anemia, when vaccination significantly reduces hemoglobin in over 8% of infants?

And then as if rubbing salt in the wound, there are no routine tests done on infants to monitor their hemoglobin before and after vaccination, and if you are unlucky enough to have your infant die suddenly, a typical infant autopsy does not look for evidence of anemia, does not analyze total hemoglobin concentration or examine the bone marrow.

I’m dumbfounded how this is allowed to continue unabated.

This is Mark Addison Roe’s story.

October 8, 1958. The day Mark died was a typical October morning, like any other morning. Louise and her husband, Jedd, lived in a quiet suburb in Greenwich, Connecticut, with their two young sons, Teddy and Mark. After breakfast in their sun-filled kitchen, Jedd left to catch the train to New York City where he worked in the financial district as an investment house, and Louise lingered on her third cup of coffee.

Around 8 a.m., Louise went to the nursery to check on her two sleeping sons. Teddy, two years old, was awake and quietly playing with his stuffed animal in his crib. Louise helped him up, and walked over to six-month-old Mark’s crib, noticing he had wiggled himself completely under his blanket. As Louise touched the blanket, her hand froze. Immediately, she knew something was not right.

This fright is one only a mother who has experienced “crib death” would know. What happens next starts to blur. Louise feels numb and frozen in time. Can’t cry. Can’t scream. A flurry of questions floods her brain and she can no longer process what is happening. “Was it her fault?” “Did she miss something?” “What if she checked on him earlier?”

Louise called her pediatrician, Dr. Lee, and said “This is Louise Roe. I just looked at my baby and I think he’s dead. I think he’s smothered.” She called a neighbor next, and that was all. Louise couldn’t go back into the nursery, troubled by guilt, shock and fear.

The Greenwich Fire Department arrived quickly, and worked on Mark trying to revive him. Her house was filled with people she didn’t know. But her baby was gone.

“The mystery of “crib death,” as they are often called, is all the more baffling because it persists in an era when infant mortality has dropped so spectacularly. There has never been a time when babies were safer than they are today. The old scourges–diphtheria, whooping cough, pneumonia, polio–that so often caused death in the first year of life have been all but eliminated.”

Dr. Lee arrived shortly after and was also in shock of Mark Roe’s death, remarking, “a pediatrician almost never sees death these days.”

Louise answered questions mechanically, and assumed it was her fault. But what happened?

Mark was born in March of 1958 at a respectable six pounds three ounces, despite being about four weeks premature. Mark was described as an easy baby, and Louise felt more relaxed with him than her first, Teddy, who was seven weeks premature and weighed five pounds at birth.

The doctor had just seen Mark for a ‘well visit’

Dr. Lee’s notebook reveals he examined Mark on August 27, 1958 when he was five months old. He weighed 15 pounds, 8 ounces and the word “Normal” is written all over his chart. The only special note was a somewhat low hemoglobin, for which Mark was getting added iron.

Mark visited Dr. Lee again on September 24th, just two weeks before his death. At this visit, Mark had a “routine injection for diphtheria, tetanus and whooping cough, and his first polio shot.” The hemoglobin was fine.

The article mentions Mark was found face down, wholly covered by a blanket. And his mother assumed he suffocated, at first. Though being found face down, and dying from being face down are technically two different things.

For example, recent studies have found that people who die from SUDEP (sudden unexpected death in epilepsy) are more likely to be found in the prone and face down position, similar to SIDS. In a study where people died (from SUDEP) during video-EEG monitoring, 3 of the 11 turned prone during the fatal seizure. It’s unclear if death is caused by the prone – face down position, or if face down is how the body turns during a terminal crisis–or some combination of the two.

The doctor urged them to consider an autopsy, which was not routine for infants at this time.

The autopsy left unanswered questions

Baffled as to why such a healthy, normal appearing baby would die, Dr. Lee insisted the bereaved parents have an autopsy performed.

Never in his eight years of pediatric practice had he encountered a case of sudden, unexpected death. The doctor had no doubt that a healthy 6-month-old baby like Mark would have no issue extricating himself from a single blanket. No one believed “crib deaths” were actually due to suffocation.

At autopsy, the pathologist found some fluid in the lungs and believed that Mark had died from acute bronchial pneumonia, but the results were not conclusive. There was a leap from “some fluid in lungs” to “bronchial pneumonia.”

But things just didn’t add up, not for the Roe’s and not for the pathologist. While finding a cause of death—any cause of death—was a functional strategy to pivot parents away from self-blame toward something other, something that would eventually be said is “not preventable,” there is no denying that the term SIDS was created with the intention of solving it. Naturally the attention shifted toward the infants: what was wrong with them?

Search for a cause and cure

Jedd and Louise Roe were ‘well to do.’ He worked in finance in Manhattan. They lived in Connecticut and had a sailboat–they were not financially struggling parents. Married in September 1955, Jedd was a graduate of William College and Louise a graduate of Wellesley. They were happy, educated, and privileged.

The Roe’s weren’t the typical ‘crib death’ family at the time, as the demographic data showed crib deaths were more likely to be of low-socioeconomic classes, African American, parents were unmarried, unemployed, under the age of 19, with alcohol and or drug use, whose infants were more likely to be bottle fed, nicotine exposed, premature, low birth weight, etc.

Little Mark was a typical healthy baby, meeting all milestones, even though he was born four weeks early. He had not appeared unwell before his passing. He was just at the doctors.

Within six months of Mark’s passing, Jedd had heard of five other cases that seemed to be just like that of his son. A good friend in New York City had wheeled her baby around the block, and then reached down to settle him more comfortably in the carriage, and found him dead. Acquaintances in New Canaan, Connecticut, lost a three-month-old baby without warning. Now that Jedd was looking for it, he found more and more cases of crib death.

Obsessed with the need to find out what happened to Mark, and stricken with the desire to prevent deaths like his, Jedd Roe contacted doctor after doctor, trying to find out what was being done about these mysterious infant deaths.

Jedd was referred to the work of a Philadelphia pathologist Dr. Marie Valdes-Dapena, who had just published the 1960 paper “Sudden and Unexpected Death in Infants: The Scope of Our Ignorance,” aptly named clearly demonstrating how little was known (and being done) about these deaths.

In that paper, the pathologist writes:

“In the city of Philadelphia there are 100 of these deaths annually; there has been a slight increase in the number of such deaths occurring each year in this city and elsewhere…This phenomenon is worldwide and that the number of infants involved is sufficiently great to constitute what might be termed a real public health problem, apparently one of progressively increasing importance.”

The study compiled demographic information from parents and found most commonly infants who died of “crib death” were:

Not part of the Valdes-Dapena study, these risk factors would be discovered later:

Though many of the infants were found in the prone position, and often face down, not a single authority at the time believed smothering to be a sufficient explanation for the crib-death tragedies for several reasons.

For one, crib deaths also occurred in infants found on their back and side.

For two, if smothering was the true cause they thought, it didn’t make sense why younger infants were often spared from crib death, as they have less neck and head control and seem more likely to be the ones who would suffocate.

And why such a peculiar age distribution of two and four months–if SIDS were due to suffocation?

Parents made SIDS a mainstream issue

The 1950s ushered in a trend where parents were now mobilizing together, asking questions, and creating a support system after experiencing a tragic “crib death.” Prior to this, there was no support for parents who often blamed themselves for what was presumed to be mechanical suffocation deaths.

When the Roe’s lost Mark, that would change. While “crib deaths” occurred more frequently in lower socioeconomic families (whose voices were not typically heard), it did not discriminate. First the Roe’s, then the Dore’s and then the Goldbergs.

In 1961, Washington State Legislator Fred Dore and his wife Mary put their healthy 2.5 month old daughter Christine to sleep one night, only to become another victim of “crib death.” Christine was a little shy of 3 months old, and again, her family had financial resources and security that stood in opposition to the majority of crib deaths. The family was privileged, educated, and likely had health seeking behavior. Was Christine Dore also recently vaccinated?

In 1963, the Dore’s introduced legislation mandating that autopsies be performed on all children under three years who died suddenly and their deaths studied at the University of Washington. The Dore’s created their own foundation to help counsel bereaved parents to support research into the causes and prevention of crib death.

Saul and Sylvia Goldberg’s 2 month old daughter Suzanne Elysa died suddenly at their home in Baltimore in 1963. The couple soon learned how little was being spent on research and how limited the resources were for parents facing the same tragedy, and they formed the parent organization Guild for Infant Survival in 1964. Was Suzanne also recently vaccinated?

These clearly privileged, wealthy families would transform this taboo, guilt-ridden tragedy into a pressing public health issue worthy of mainstream attention, culminating in a 1972 Senate Hearing. There are many personal accounts and testimonials in this hearing, including parents who described their recently vaccinated children dying, but it must have fallen on deaf ears.

Vaccine and SIDS research shortcomings

Even though SIDS strikes at its highest rate during the ages when vaccines are given, the research community in the 1960s and 1970s avoided investigating vaccines and SIDS, besides a few studies in German investigating sudden death after smallpox vaccine.

Some articles including “Why Babies Die” and the one pictured below mention a groundbreaking study by Dr. Renate Dische and Dr. Milton Helpern being undertaken where they were going to investigate everything including “recent inoculations”–it appears that nothing was ever published.

I can’t find anything besides news articles mentioning this first-of-its-kind study.

There also was a similar undertaking in Los Angeles in the 1960s where medical examiner Theodore Curphey recorded similar epidemiological data, including recent vaccination history, and many of those papers are sealed for 50 years, not being unsealed until 2062. Curphey was also the medical examiner who autopsied Marilyn Monroe.

Clara Raven was another medical examiner based out of Detroit who investigated crib deaths and gathered demographical data in the late 1950s and 1960s, but also did not mention vaccination history, even though the peak of deaths were 2.5 months to 4 months of age. The majority of the crib deaths she saw were in the Black community, but this is also a community at higher risk of anemia.

I can see it must have been confusing to have some babies die after vaccination, and others die after exposures such as smoking, or a recent cold—it was hard to see how all these things can connect on the same pathway. And yet, they all connect through their ability to affect hemoglobin. Vaccination mimics infection, and both cause iron sequestration, inflammation and antibodies, which has an inverse association with hemoglobin concentration.

After the Tennessee SIDS Cluster which occurred in 1978 and 1979 attracted undeniable (and undesirable) national attention to the possibility that vaccines can cause sudden death in infants, a death that looks exactly like the phenomenon of SIDS, several authors sought out to investigate the relationship…finally.

Without much effort, these studies identified positive associations between vaccines and SIDS:

Baraff et al in 1983

Investigated DTP vaccine only and reported that out of 27 deaths that occurred within 28 days of immunization, 6 of the deaths occurred within one day, 17 occurred within 1 week, 6 in the 2nd week, 4 in the 3rd week, and none in the 4th week, suggesting a strong temporal relationship:

“The excess of deaths in the 24 hours and first week following immunization and the absence of deaths in the fourth week following immunization were all statistically significant.”

Walker et al in 1987

Reported that the SIDS mortality rate in the period 0-3 days following DTP vaccination was 7.3 times higher than 30 days after immunization. Because the infants were at different ages when they died, there is no logical reason why so many deaths would occur in the post-vaccination window if vaccines did not somehow contribute.

After this many authors sought out to debunk the findings of the case only series, and sought out case-control studies where healthy vaccinated infants would serve as controls to demonstrate the safety of vaccination relative to SIDS. A healthy control is not, however, a suitable control for an infant who died of an unexplainable cause. Case-control studies failed to “control” for important variables such as sleep environment and recent illness, making their findings non-significant anyway.

Flahault et al, 1988

In France the relation between SIDS and DTCP immunisation (sic) after a cluster of five cases of Sudden Infant Death Syndrome occurred in France among infants who had received within the previous 24 hours an injection of diphtheria, tetanus toxoid, pertussis, poliomyelitis vaccine. The author Flahault conducted a case control study including only infants over 3 months of age (which is terrific because other case controls include infants too young to be immunized to make look vaccines appear less related to SIDS). And guess what: there were no significant differences between the cases and controls in DTCP immunisation overall, which is important because usually it’s expected that SIDS cases are vaccinated less often due to being unwell or in families who are less likely to follow routine caregiving advice. [Many infants who subsequently die of SIDS are infants who had a mild cold, and in some cases, were not vaccinated timely due to the “cold” or other social factors]. So the fact that a study found that the SIDS infants were vaccinated the same as the controls means…vaccines cannot prevent SIDS.

What’s more, in specific intervals post vaccination, the SIDS infants were more likely to be vaccinated than the controls, which points to a positive association between vaccines and SIDS. For example, 5.9% of the SIDS cases were vaccinated 2 days before death, whereas only 4.2% of the controls were vaccinated 2 days before their interview, and 12.6% of SIDS cases were vaccinated 7 days before death, whereas 11% of controls were vaccinated 7 days before interview.

Overall, it appears as the majority of studies sought to find elevations in SIDS risk in narrow post-vaccination windows. It didn’t occur to anyone that vaccines could cause a death 2 or 3 weeks later, and the ‘control period’ should never have been a time period potentially filled with vaccine deaths. A control period should be at minimal 40 days after a vaccine, and not sooner.

So, how did vaccines contribute to Mark’s death?

Drilling into the details of Mark’s story, he had a somewhat low hemoglobin at his 5 month visit which was ‘corrected’ from iron supplementation by the time of his 6 month visit. And he died exactly 14 days after two vaccines, an injection of DPT and a polio shot.

While roughly half of SIDS infants had a mild viral infection in the days or weeks before death, many infants had a vaccine in the days or weeks prior to death, and no viral infection. It would be logical to assume then, that whatever causes SIDS, it’s a mechanism that is similarly associated with both vaccination and mild infection. What is affected by vaccination and infection? Hemoglobin concentration.

And Mark already had a history of low hemoglobin, suggesting a particular vulnerability that is not unique to Mark, but all infants who are a few months old, and especially premature infants like Mark: physiologic anemia.

Physiologic anemia of infancy

So here’s the theory. Around 6 weeks to 3 months after birth, every newborn enters a development phase called physiologic anemia of infancy, which is a normal decline in hemoglobin concentration that occurs around 6 to 9 weeks, which just happens to be the age where the CDC recommends an assortment of vaccines against 8 diseases and this time frame ALSO is the age of peak SIDS risk. This low hemoglobin can persist for months, however. And both infection and vaccination can cause a sudden drop in hemoglobin.

It has been said over and over that it’s ‘just a coincidence that SIDS peaks at 2 months of age when multiple vaccinations are given’—but that couldn’t be further from the truth. SIDS peaks at 2 months of age because of the compounding effects of vaccination and multiple vaccines. An infant who is unvaccinated may still have a baseline risk of SIDS at 2 months due to physiologic anemia alone, but we have no idea what that risk truly is, because vaccination of all infants including premature infants persists despite this obvious vulnerability.

When first born, an infant has high hemoglobin levels (characterized mostly as fetal hemoglobin) (>14 g/dL) which rapidly decline, reaching a nadir or lowest amount of approximately 10 to 11 g/dL at 6 to 9 weeks of age. During this time, an infant’s body is switching from fetal hemoglobin to adult hemoglobin, each of which have a different affinity for oxygen.

Preterm babies are at a higher risk of a more severe physiologic anemia. Their bodies are growing quickly, and they lose red blood cells faster than they can make new ones. This is because preterm babies’ red blood cells only last about 35 to 50 days, compared to 120 days in adult red blood cells. Their hemoglobin level can drop to around 8 to 10 g/dL.

Hemoglobin (means “blood” + “ball”) is a protein in red blood cells that binds with oxygen in the lungs to deliver oxygen to tissues and organs throughout the body, including brain cells. Each hemoglobin molecule contains four iron atoms which binds to oxygen atoms. When the hemoglobin detects carbon dioxide it exchanges oxygen and collects the carbon dioxide (a waste product), goes back to the lungs where carbon dioxide is released and exhaled, and starts this process all over again. 

This is how our bodies, tissues, and brain gets oxygen and how our body removes carbon dioxide.

Is SIDS due to unrecognized anemia?

Anemia (meaning “lack of blood” or reduced red blood cells) is a condition in which the body does not have enough healthy red blood cells or when the red blood cells do not function properly. As mentioned earlier, every infant has a physiologic anemia at around 2 months of age. Anemia may be diagnosed when a 2 month old infant’s hemoglobin is less than 9.5 g/dL (95 g/L). 

So naturally, the question is, what evidence is there to draw an association between SIDS and anemia?

For one, the risk factors for infant anemia are identical to the risk factors for SIDS:

• premature
• low birth weight
• exposed to smoking
• maternal anemia
• low socioeconomic
• African American
• male excess
• history of gastrointestinal disorders or malabsorption disorders  
• history of respiratory infection
• introduction of cow’s milk before 1 year (for many years cow’s milk allergy was investigated as a cause of SIDS)

 

The calcium in cow’s milk inhibits absorption of iron, increasing an infant’s risk of anemia.

 

Secondly, vaccines, infections and inflammation each independently reduce hemoglobin concentration, which would push an infant who is at the nadir of physiologic anemia into a sudden, pathologic anemia.

This is why SIDS researchers have looked at overreactive immune system in relation to SIDS; they just didn’t realize that when the body produces large amounts of white blood cells (leukocytosis) in response to vaccination, that this inflammatory response leads to iron sequestration, which significantly reduces hemoglobin levels, causing or worsening preexisting physiologic anemia, which means less oxygen in the blood can get to the brain, causing periods of hypoxia and hypoxemia.

Sleeping in the prone, or supine position, also is associated with a decrease in hemoglobin concentration, and sleeping prone is associated with lower cerebral oxygenation, which is why the same baby can appear alert, albeit listless and tired, cranky or fussy while awake, but then once asleep, drifts into a low oxygen state that he or she cannot recover from.

Little Mark had a history of low hemoglobin, and died exactly two weeks after two vaccines. Had he not received those vaccines at that time, he may still be here today. While vaccines are certainly not the only thing that can cause leukocytosis, iron sequestration or reduced hemoglobin concentrations, it is the primary thing happening at 2 months, 4 months and 6 months, and between 12 and 15 months, and the clear and logical explanation for the clusters of deaths at these intervals is vaccination.

Breastfeeding may protect against SIDS by providing passive immunity, reducing the risk of infections, providing a more bioavailable form of iron, thus resulting in less iron sequestration and a milder infection. Breastfeeding has been shown to blunt immune responses to certain vaccines in infants, suggesting it’s a strong form of immunity.

 

Research and evidence

The 1961 paper “The changes in serum proteins and blood volume during immunization” documented the effects of rabbits injected with a pneumococcal vaccine, and compared them to control rabbits. The authors observed an increase in serum gamma globulin concentration (caused by increase in antibody protein) and a proportional drop in hemoglobin concentration.

“In rabbits hyperimmunized with pneumococcal vaccine high concentrations of gamma globulin are produced….The red cell volume was the same in immunized and in normal rabbits and consequently hemoglobin concentration fell with increasing gamma globulin.”

Remarkably, the more gamma globulin (containing high levels of antibodies) produced by the rabbit, the bigger drop in hemoglobin, suggesting an inverse relationship between antibody production and hemoglobin.

This suggests that the more antibodies produced, the lower the hemoglobin drops.

Similarly, a more recent paper published in 1999 found elevated white blood cells (known as leukocytosis) in 51.7% of SIDS cases. We can infer that elevated white blood cells are correlated with reduced hemoglobin because inflammation due to infection or vaccination causes iron sequestration. Also, C-reactive protein was elevated in 25% of the SIDS group.

A transient leukocytosis, or a high white blood cell (WBC) count, is common after vaccination, and was documented in 50% of healthy infants who received several vaccines.

The 1989 study titled “Anemia of a mild viral infection: the measles vaccine as a model” sought to define hematologic changes during a mild viral infection, but they used a live measles vaccine. Thus, a total of 93 infants were immunized and studied prospectively at different intervals post vaccination, ie. days 0, 4, 9, 14, 21, and 30 days.

Hemoglobin concentration decreased significantly by days 9 and 14. (Mark died 14 days post-vaccination and had a history of low hemoglobin.)

“Hemoglobin concentration decreased significantly by days 9 and 14. The decrease was >1.0 g/dL in 8.6% and >0.6 in 24.3% of the infants. Of the nonanemic infants, 22% became anemic. Serum iron and percentage saturation of transferrin decreased, whereas serum ferritin increased significantly.These results suggest that a mild viral infection in infants induces a significant decrease in hemoglobin that may persist for 14 to 30 days and may be difficult to distinguish from iron deficiency.”

The infants in the paper were healthy, well nourished 12-month-old infants with no history of febrile illness in the previous 15 days. This was the effect of one single injection.

In 1993 the same authors as the previous paper showed that hemoglobin drops after a single vaccination against measles or measles-mumps-rubella vaccine in healthy infants.

Authors observed:

“A significant haemoglobin drop was seen on days 9 and 14 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. All these but protoporphyrin recovered by day 30.”

Iron sequestration

In 2013, Tammy Movsas investigated serum levels of essential elements and aluminum pre and post vaccination in “Effect of Routine Vaccination on Aluminum and Essential Element Levels in Preterm Infants”, she reported a significant decline in serum iron levels:

“We observed a significant decline of serum levels of iron, manganese, zinc, and selenium and a significant increase in copper level (a marker of inflammation) on the day after vaccination. These same EE have been described as declining after inflammation from trauma or burns.”

Iron witholding or iron sequestration is a protective mechanism of the innate immune system in which the body limits the availability of iron to pathogens by storing iron in macrophages, or certain organs.

The Movsas study reported a significant decline in serum iron in the 24 hours post-vaccination. The paper only reports one pre-vaccine hemoglobin level for the 2 month old infants: 10.7 g/dL. It is unknown how much their hemoglobin dropped postvaccination. But based on Olivares, 1987, over 8% of infants experience a drop in hemoglobin >1.0 g/dL from one single vaccine given at 12 months. Could there be a small subset who experience a more significant drop in hemoglobin the limited study didn’t capture? What about younger infants, and more vaccines, as is the current protocol?

Several papers have reported significant drops in serum iron after injections of lipopolysaccharide, infusions with interleukin-6 and experimental infections.

This is a natural response to infection and supplementation with iron during infection can be deleterious. For example, in Sub-Saharan Africa, iron supplementation to infants and young children increased susceptibility to infection and mortality from malaria, possibly because iron enhanced growth of the infection. This may be the reason why the body sequesters iron during infection.

Infection and anemia

From the 1989 study Changing characteristics of childhood anemia:

“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.”

 

SIDS and anemia

A 1976 study by Naeye, et al titled Sudden Infant Death Syndrome: A Prospective Study gathered various demographic information from families who lost an infant to SIDS. Maternal anemia was more common in mothers of SIDS victims. Vaccination of infants was not mentioned, but vaccination of mothers was:

Two hundred sixty-nine different drugs and immunizing agents were used by one or more SIDS and matched control mothers during pregnancy. Utilization rates for these agents were less in SIDS cases than in the controls, with several exceptions. The exceptions were as follows, expressed as rates for SIDS and control mothers, respectively: polyvalent influenza vaccine, 3.2% and 2.7%; smallpox vaccine, 1.6% and 0%; phenobarbital, 7.2% and 0%; iron dextran, 9.6% and 3.2%; hydrochlorothiazide, 15.2% and 9.9%.

Iron dextran is to treat iron deficiency. Many more of the SIDS infants required oxygen at birth and their mothers had a lower hemoglobin than control infants, and were more likely to smoke, which also reduces hemoglobin.

A 1992 study looked at hemoglobin levels in infants reporting to the emergency room presenting with apparent life-threatening events (ALTE) sometimes called brief resolved unexplained event (BRUE). It is unknown if ALTE or BRUE events are interrupted SIDS. Curiously, low hemoglobin is associated with ALTE or BRUE.

“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. For 41 infants (25 male, 16 female; 38 Caucasian, three Asian) a venous red blood cell count was available. Their median age at the time of the apparent life-threatening event was 2.0 (0.6-6.7) months. The Hb levels in these 41 infants were plotted against normal data from the literature. 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.”

Infants who died of SIDS have excessive brain iron accumulation, whereas control infants have none. A 2011 paper revealed that 12 (33%) of 26 SIUD/SIDS victims had nonheme iron deposits in the brainstem and cerebellum, compared to none of the control group.

“The iron deposits were scattered along the interstitium or, more frequently, concentrated in the neuronal cytoplasma. In these cases, the modified Bielschowsky’s method confirmed that the cells with iron accumulations were neuronal cells.”

A highly significant correlation was evident between maternal smoking and alterations of brain iron homeostasis.

Several studies found that infants who died of SIDS had elevated fetal hemoglobin, (not adult hemoglobin) compared to controls, suggesting a compromised delivery of oxygen to sensitive tissue sites. In healthy infants, adult hemoglobin typically completely replaces fetal hemoglobin by 6 months of age.

This 1997 confirmed a similar finding:

During the period of postnatal development most associated with SIDS cases (2 to 6 months after birth), fetal hemoglobin levels were found to be significantly elevated in postmortem whole blood samples from SIDS infants compared with gestational age-matched control infants dying of causes other than SIDS.

This 2001 paper found that elevated fetal hemoglobin is related to common risk factors of SIDS, such as prematurity and smoking.

An elevated newborn HbF fraction, defined as 77% or greater, was significantly associated with maternal smoking, maternal anemia, intrauterine growth restriction, and pregnancy complications associated with reduced placental blood flow.

A 2004 study investigated adult hemoglobin levels at birth in infants who died of SIDS, and found that the infants with the lowest adult hemoglobin at birth corresponded with the highest rate of SIDS.

Study authors conclude:

These findings suggest that infants with low levels of adult hemoglobin in the first hours after birth are at elevated risk of SIDS. Delayed maturation in production of adult hemoglobin may play a role in the etiology of some SIDS cases.

There’s actually a dose response relationship between adult hemoglobin level at birth and SIDS:

A 2007 paper by Krous et al tried to refute that SIDS infants have elevated %HbF compared to controls, however the study compared post conceptional ages between SIDS cases (n=77) and controls (n=30) rather than post natal age (the youngest control was 3 days old whereas the youngest SIDS infant was 19 days). We know SIDS is a post-natal event that occurs for both premature and full term infants at 2-4 months peak. The paper wrote:

“%HbF values for both groups are plotted against PCA (as opposed to post-natal age) since the normal post-natal decline in HbF levels is developmentally programmed from conception rather than birth. After adjusting for PCA (postconceptional age), %HbF levels for SIDS cases and controls did not differ significantly.”

Which to me is another way of saying, before adjusting for PCA there was a difference. Also, birth does influence HbF levels. Once born, an infant’s HbF levels begin to drop due to their lungs receiving higher amounts of oxygen. Birth triggers the body to begin producing HbA. Curiously, the controls in this study were much more likely to be exposed to smoking than the SIDS cases, which could on its own have a relationship to persistent fetal hemoglobin. Controls were on average younger, and the youngest being 3 days. The paper did find that Black infants and preterm infants both had higher mean Hb F, which are, of course, SIDS risk factors.

A 1999 paper investigated erythropoietin blood levels in sudden infant death. Erythropoietin (EPO) is the main red cell growth factor and its release into the blood is stimulated by anemia, and also various kinds of hypoxia. The EPO was elevated in the 0-2 month age group compared to controls, but not in other age groups. The paper’s control infants (explained deaths) were due to a cardiorespiratory distress, so these controls may not have been the best choice, as that is a condition that induces dramatic EPO stimulation. But it’s interesting to note that SIDS and cardiorespiratory distress induces similar amounts of EPO.

Authors mistakenly dismissed an anemia hypothesis because the fetal hemoglobin appeared in normal range, however, total hemoglobin concentration is more predictive of detection of anemia, which they didn’t test.

Authors conclude:

In conclusion, the increased EPO level that was observed in SIDS cases, associated with the increased values of stress hormones, suggests a heavy hypoxic premortem stress. Whether this hypoxic stress was chronic or repeated during the weeks preceding the death or on the contrary deep and long lasting but unique and limited to the agonic phase still remains to be established.

A 2001 case-control study reveals of the 31 infants who died within 2 weeks of immunization, 2 infants had blue fingernails or toenails, and 6 infants were less alert than normal. Blue fingernails or toenails is cyanosis and a sign the infant’s blood does not have enough oxygen. This is just what was reported or seen, it’s unknown how many actually had reduced hemoglobin or anemia because it’s not a laboratory value that is gathered postmortem.

This 1999 paper revealed that infants who die of SIDS suffer repetitive insults of hypoxemia prior to death.

Our results indicate the occurrence of an acute insult at least several hours before death, an insult from which the infants had apparently recuperated. This suggests that SIDS victims suffered repeated apoptosis resulting in significant neuronal damage and, thus, functional loss in key brain regions. 

These repeated episodes of hypoxemia could be the result of an anemic hypoxia, the effects of low hemoglobin or reduced red blood cells.

Many parents report their infants had blue lips or blue fingernails prior to death. I’ve had a mother just recently tell me she was anemic during pregnancy and her baby was very pale, despite being African American. She knew something was wrong but no doctors listened to her. Sadly, he died suddenly.

I am not the only one who suspects SIDS is related to the nadir of physiologic anemia, but I am the only one who is showing how vaccines are related, and this is the most likely explanation for SIDS, whether the infant was vaccinated or not.

From SIDS–Sudden infant and early childhood death:

“It is important to note that levels of total hemoglobin cannot be accurately determined after death, and therefore the relationship between low total hemoglobin, anemia, and SIDS death cannot be quantitated. However, the fact that the peak incidence of SIDS co-incides with the nadir in the physiologic anemia of infancy is possibly suggestive of such a relationship.”

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Vaccination causes significant drop in hemoglobin:

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.

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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.

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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.

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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%).

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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.

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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

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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.

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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.

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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.

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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.

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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.

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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.

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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.”

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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].”

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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.”