sudden infant death syndrome Archives

SIDS and Vaccination

Published on December 4, 2023

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Posted on Child Health and Safety on January 13, 2015 was an announcement that vaccines had been proven to cause sudden death in children (SIDS). The announcement indicated that death in 67 cases was only explicable as caused by vaccines. Drug safety regulators were said to have had the information for over two years. In this post, I am going to contest vaccination as the sole cause and try to explain why I think it is a much more complex problem.

In 2001, I published a paper that hypothesized the requirement of three variables: Sudden infant death syndrome requires genetic predisposition, some form of stress and marginal malnutrition. I have just published another paper on the same subject: Thiamin and Magnesium Deficiencies: Keys to Disease.

What History Tells Us about SIDS

Back in the seventies, I was working at Cleveland Clinic in Cleveland Ohio in the Department of Pediatrics. At that time there was a great deal of professional interest in SIDS. In the course of my research, I had found a paper written in a prestigious medical journal in 1944 by a British Medical Officer of Health by the name of Lydia Fehily. Readers will remember that Hong Kong was then a British protectorate and Fehily was sent out from England in order to investigate a common form of sudden death in breast fed infants of Chinese mothers in the colony.

A little bit of history is important to the final solution. Before World War II, the Japanese had invaded China. The rice ration was cut to starvation levels, thus cutting down the calorie intake. Although the symptoms of starvation prevailed in the mothers and the infants, the sudden infant death had disappeared. After the Japanese were driven out, the pregnant mothers in Hong Kong had as much rice as they wished. The calorie intake had been restored, overwhelming the required concentration of vitamin B1 for adequate oxidation of the calories. The sudden death in the breast fed infants immediately reappeared.

Fehily had discovered that the reemergence of SIDS was due to infantile beriberi because the infants were fed by vitamin B1 deficient breast milk (Human milk intoxication due to B1 avitaminosis). Those affected were almost always regarded by their mothers as the healthiest appearing infants in the family prior to their death. These events were rare under two months and after six months of age. It occurred almost always at night, was often associated with a runny nose interpreted as a mild cold and was more common in winter months. The epidemiology of this is almost exactly like that of modern SIDS. Although the modern interpretation is related to the positioning of the infant in the crib, it is certainly not the whole story. I came across the report of a meeting of beriberi researchers held at that time. A statement in that report had said that:

“any sudden otherwise inexplicable infancy death is a guarantee of infantile beriberi. No other disease has a similar outcome”.

Predicting SIDS

During the early part of the seventies it was thought that SIDS could not be predicted, that there were no symptoms to provide a warning. Later on in the decade, it was shown that there was such a thing as “threatened SIDS” judged by a few non-specific symptoms. Coincidentally, an alarm system had been invented that an infant could wear in the crib. It indicated when breathing stopped for a given interval or when the heart slowed. If and when such a thing happened, it was very easy to resuscitate the infant by a simple slap on the buttock.

SIDS, Thiamine and Brain Development

I began to admit infants with this kind of history to the hospital and place them on an alarm system. Believe it or not, by giving thiamine by injection to these infants, the alarms ceased to be initiated. I found this to be very exciting and I continued my research. I even went to Australia to do sabbatical research with the late Dr. Read at the University of Sydney who had evidence of implication of thiamine metabolism in SIDS. I found that there were families where SIDS had been occurring in more than one related infant. There was no pattern that indicated a direct genetically determined outcome and I concluded that it was a genetic risk rather than a genetically determined disease.

The overall logical conclusion to this series of facts was as follows:

That genetic risk implied an unusually well developed brain that required a great deal of energy to function. The only means by which this could be acquired was through pristine nutrition for the mother during pregnancy.
That calories from simple carbohydrate with insufficient thiamine was extremely dangerous. (Note that rice rationing had stopped the infancy deaths in Hong Kong). The brain of an infant in the first six months of life grows at a tremendous rate and the oxidation of glucose to provide the required energy is crucial. Vitamin B1 is essential to that oxidation. This had been shown by Dr. Peters in Cambridge, England as early as 1936.
That some form of stress may or may not be necessary, depending on the state of biochemistry in the brain. The infant is already at risk at birth because of the nature of nutrition supplied by the mother during pregnancy. A state of marginal malnutrition in the infant is insufficient to meet the energy demands of adapting to the vaccination as a stress factor.

Readers of this website may or may not be aware of a series of posts on the relationship of post Gardasil postural orthostatic tachycardia syndrome (POTS) with thiamine deficiency. I believe that this post on SIDS bears comparison with the logical reasoning applied in that post. Also, Dr. Marrs has repeatedly pointed out the relationship between drugs and seemingly unrelated disease caused by them.

Does Thiamine Deficiency Underlie Post Vaccination SIDS?

The epidemiology (study of cause) of infantile beriberi (vitamin B1 deficiency) is sudden death. The commonest time for this is between three and four months and more commonly in male infants. Although this is almost the exact epidemiology of modern SIDS, this well researched truth is ignored. The classical vitamin deficiency diseases (beriberi, pellagra, scurvy) are considered to be of only historical interest because vitamin enrichment of foods has abolished them. This is simply not true. A high intake of sugar in the form of simple carbohydrate, empty calories is widespread in America and other Westernized countries, automatically overwhelming the insufficient concentration of vitamin B1, the equivalent of a choked engine in a car. “Soft” drinks are all too well advertised and encouraged in opposition to the consumption of “hard” alcohol that is regarded as more dangerous. Although the dangers of alcohol are well known, the danger of “soft” and “Diet” drinks, particularly during pregnancy, is almost totally unknown to consumers who erroneously believe they are preventing weight gain and contributing to personal health. The advertising is misleading.

Looking again at history, we also know that the very first symptoms of beriberi could occur in a group of patients when exposed to sunlight. We now know that ultra violet light is very stressful to the human body, demanding an adaptive “stress” response that is automatically initiated by the lower part of the brain, the limbic system and brainstem. The word “stress” must be used in its proper connotation. It must be defined as a mental or physical force to which we have to adapt. For an infant, stress would include weather changes, infection, trauma, vaccination, partial suffocation from being placed in the prone position, inhalation of chemicals in the crib mattress and other possible variables. This part of the brain is particularly sensitive to thiamine deficiency, diminishing the supply of energy required by the cells in order to perform this complicated adaptive process.

We live in a hostile environment to which we have to adapt automatically 24 hours a day by brain/body mechanisms initiated by the lower brain. Damaging the brainstem affects the nervous control of automatic breathing and control of heart rhythm. Thus, breathing or heart beat may cease in an infant during sleep when thiamine deficiency prevails. During the first six months of life brain growth is tremendously fast, requiring an enormous amount of energy. I am proposing that the infant with the highest, genetically determined brain energy requirement is more at risk. If this is true, the tragedy of SIDS may be removing the most superior future citizens. Obviously, the mother’s diet must provide a proper balance between the calories that provide the fuel and the capacity of the cell to burn the calories by means of the appropriate vitamins. Because we now know that sufficient thiamine or vitamin B1 is critical to prevent beriberi and I have published evidence for deficiency of this vitamin in threatened SIDS, it makes sense to consider the interplay of three variables in SIDS. The three variables are as follows:

Genetic risk, “e.g. a high brain energy requirement”
A non specific stress factor, “e.g. vaccination”
Marginal high carbohydrate calorie malnutrition

It also makes sense to consider the possibility that the stress of vaccinations is too great a risk for infants who are genetically and/or environmentally predisposed to oxidative damage in the brainstem.

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This article was published originally on Hormones Matter on January 21, 2015.

Sudden Infant Death Syndrome, Autism, and Maternal Thiamine Deficiency

by Derrick Lonsdale MD, FACN, CNS

Published on April 16, 2018

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SIDS, Autism, Maternal Thiamine Deficiency

I have addressed this problem before on this website. However, in the Wall Street Journal on Tuesday, March 27: an article appeared entitled “A Study of Sudden Infant Deaths Divides Doctors“. It goes on to say “The finding on sudden and unexpected infant deaths is surprising, says Joel Bass, of the pediatrics department at Newton Wellesley Hospital in Newton Mass”, the first author of the study, who said “that’s more than one newborn baby dying of SUID [sudden and unexpected infant death] a day”. Oddly enough, the article indicates that “among the possible causes, some researchers point to the promotion of certain hospital practices to encourage breast-feeding. But some doctors vehemently disagree with that theory”. Apparently, the theory alluded to the practice of encouraging skin-to-skin care between mother and infant during breast feeding. I had not read the article so I do not understand how this connection was made. What arrested my attention was the reference to breast-feeding, long encouraged by pediatricians as the best way to feed newborn infants. How could skin-to-skin contact be involved? However, an article was published in 2011 in which the author had carefully examined the nutrient content of breast milk in the United States (Shamberger, 2011). It reminded me of an extremely important article that was written in the 1940s.

Breast Milk Toxicity Syndrome

It may be remembered that Hong Kong at that time was a British protectorate. A medical officer of health was sent out from Britain to Hong Kong to investigate a relatively common occurrence of sudden death in breast-fed infants of Chinese mothers. This death commonly occurred between three and four months of age and happened in infants that, from their appearance, were considered to be the healthiest in the family. Fehily, the author, was able to show that the breast milk was deficient in vitamin B1 and it was well known by early researchers of beriberi that this form of infant death was virtually pathognomonic (indication of cause) of the infantile form of this disease. In fact it was well known by these early researchers that there was no other disease of infancy that behaved like this. Fehily herself was struck by the exact likeness to “cot death”, the term used in England for what we call Sudden Infant Death Syndrome in the United States today.

Autism Rates for Each State Connected to Maternal Nutrient Status

The paper published in 2011, referred to above, was in consideration of the cause of autism, not SIDS. The author had studied the rate of autism associated with nutrition. The paper stated that autism rates in the United States are increasing at a rate of 15% per year. The study abstract reported that the design of the study used nutritional epidemiology and an ecologic study design. In other words, he studied public health data and the nutrient content of breast milk. The objective was to try to link the possible cause of autism to nutrition by creating autism rates for the 50 states of America and comparing them with published measures of infant nutrition. These included the duration of exclusive breast-feeding and participation in the Women, Infants and Children (WIC) program. The results were impressive. The states with the highest WIC participation have significantly lower autism rates (P <0.02).

In contrast, there was a direct correlation with the increasing percentage of women exclusively breast-feeding from the years 2000 to 2004. Infants who were solely breast-fed had diets that contained less thiamine, riboflavin, and vitamin D than the minimal daily requirements. Although the author was studying the rates of autism and was not in the least interested in SIDS, his study supports the finding of vitamin deficiency in breast milk, in turn supporting the possible relationship between breast-feeding and SIDS. Of course, the modern medical model would find it objectionable to hypothesize a cause common to two diseases, although both autism and SIDS have a slight male dominance and are diseases that occur during rapid growth, particularly of the brain.

My Particular Interest in SIDS

Many years ago, because of clinical experience, I became interested in SIDS. At about that time, the idea of threatened SIDS had become an acceptable diagnosis, whereas previously it had been considered that the death was truly sudden and completely unpredictable. I can remember two parents who had brought their infant to see me. They had observed him in his crib when he had stopped breathing. When one of them picked him up he started breathing again. They took him to the nearest emergency room where he was pronounced completely fit and the situation was dismissed. The parents were so scared that one of them took turns to sit up all night to watch in case this thing should happen again.

This is exactly the clinical situation that I began to experience with other infants. A monitor had been invented that could be attached to an infant that would sound an alarm if either his heart slowed or his breathing stopped. It had become well-known that picking the infant up or giving him a little slap on the buttock would instantly return him to a normal state (SIDS is more common in male infants). To cut a long story short, my colleagues and I performed a lot of clinical research on these threatened SIDS babies. We had found that a machine known as brainstem auditory evoked potential (BAEP) gave abnormal readings . This strongly suggested that the mechanism was an electrochemical dysfunction in the brainstem. This is the part of the brain that connects with the spinal cord and it contains the controls for automatic breathing. Let me explain this a little.

Most of us are not aware that our essential breathing is controlled by centers in the brainstem when we are unconscious, as in sleep. The condition known as sleep apnea is a failure of this mechanism (apnea is a temporary cessation of breathing). It was during my library research that I discovered the 1944 paper by Fehily. It seemed only to be common sense to look at the possible association of thiamine deficiency as the underlying biochemical cause. We treated several infants with thiamine injections that seemed in every case to stop their episodes of apnea. I received a visit from a university researcher in Australia. His group had been studying SIDS and they had come to the same conclusion. I was so impressed by their work that I took sabbatical leave in Australia with Dr. Read who was the leader of the group. Abnormal brainstem responses in infants at risk of SIDS was reported at about the same time. The authors said that this suggested immature development of brainstem. A recent publication found an association between maternal alcohol consumption and SIDS. The relationship of thiamine deficiency in brain and alcohol consumption is well-known. It is not too difficult to imagine that the concentration of alcohol in the blood of the mother would have an exaggerated effect in the brain of the fetus, perhaps injecting a risk factor for the infant after birth.

Conclusion

Can a parent who has not experienced the sudden death of a precious infant at the age of 3 to 4 months even imagine the horror and the enormous stress imposed on such a parent? We now know that there are quite nonspecific symptoms that may appear in an infant who threatens SIDS. They are sometimes unusually irritable and a “runny nose” may be mistaken for a cold, but such symptoms may be so slight as to be ignored. I must emphasize that the lower part of the brain that organizes automatic body functions, including breathing, is peculiarly sensitive to thiamine deficiency. If the infant is breast-fed with thiamine deficient breast milk as the 2011 study suggests, studies that I have reported here would make sense. Even if only a few of the cases were due to this biochemical phenomenon, giving some thiamine on suspicion can do no harm.

A diet history from the mother might offer clues, particularly emphasizing whether there is ingestion of sugar in all its different forms. If I were a physician in charge of such a pregnancy, I would not hesitate to add thiamine supplementation, starting as early as three months of gestation, as advised in the book written by an American obstetrician/gynecologist by the name of John B Irwin, M.D. He had found that supplementary thiamine removed the complications of pregnancy such as toxemia and even prevented premature delivery. It might well provide a nutritional legacy for the infant. Of course, I am not suggesting that alcohol ingestion by the mother is THE cause of SIDS. However, I am suggesting that the present widespread use of unhealthy nutrition may well be at fault for both SIDS and autism. Genetic risk, coupled with some form of stress (e.g. mattress flame retardants, a cold virus) and vitamin deficiency breast-feeding, might be more or less important individually, or more than one of the three items collectively.