Gardasil and Vitamin Deficiency?

By Derrick Lonsdale, MD

In July 2013, I received an e-mail from the mother of an adolescent girl who had received Gardasil vaccination some four years previously.  Her many symptoms that had mystified her doctors were eventually diagnosed as Postural orthostatic tachycardia syndrome (POTS), published recently as a complication after the administration of this vaccination^[1].  The mother had conducted her own research and had come to the unlikely conclusion that her daughter suffered from beriberi.

A better name for this condition would be thiamin deficiency disease since the name beriberi was originally derived from its common occurrence in eastern countries where rice has been the staple diet for centuries.  Outbreaks of the disease were often associated with increased affluence when the peasants could afford to have the rice milled to remove the husks, yielding white rice that looked better when it was served.  The vitamins are in the husks, so this is a historical example of high calorie carbohydrate malnutrition, sometimes known as empty calories.

The question that this mother asked me was, “Does this make any sense and if so can it be proved?”

The idea of a vaccination actually causing a vitamin deficiency disease like this appears, at first sight, to be completely absurd. I reported to her that there was a very accurate blood test available to prove thiamin deficiency and this requires some explanation.

Erythrocyte (red blood cell) transketolase

All of our body and brain cells are chemical micro-factories.  Each cell must create energy in order to perform its specialized function. This energy is provided by “engines” (mitochondria) within each cell.

Using this energy to build complex molecules in the body (e.g. a hormone) is performed in a series of “steps” (chemical reactions), each of which requires an enzyme.  The enzymes, complex proteins, act as catalysts that enable a series of chemical reactions to take place as simpler chemical compounds are gradually made more and more complex.

Each enzyme, however, cannot work efficiently without one or more cofactors, naturally occurring vitamins, most of which, like thiamin, have to be obtained from diet.

Red blood cells, aside from their ability to transport oxygen from the lungs to the tissues, have another vital function involving a series of chemical changes, in which the enzyme transketolase is required.  Cofactors for this enzyme are thiamin (vitamin B1) and magnesium.  Without them, the enzyme is partially crippled.

By taking a blood sample and measuring the speed at which the chemical product of the transketolase enzyme is synthesized, we can ascertain its baseline efficiency.  If, by adding thiamin, this activity accelerates, we know that that is what the enzyme required in order to reach its maximum efficiency. The acceleration can be measured as the percentage increase over the speed of the first reaction before thiamin is added.

Although the so-called gold standard advised by the Mayo Clinic for ascertaining deficiency of thiamin is by measuring its level in the blood, this level may be completely normal in the presence of deficiency.  This is because thiamin is required inside the cell in order to maintain its vital functions.

Measuring the concentration of thiamin in blood when it is outside the cells that require it bears no relationship with its presence or biologic function inside the cell. The same thing applies to measurement of magnesium deficiency.

The enzyme transketolase is also present in brain where it has a vital function. Reduction of its activity from deficiency of thiamin or magnesium causes brain dysfunction, particularly in the lower part of the brain, the limbic system and brainstem that are known to be highly sensitive to these deficiencies.

Because thiamin is so vital to the enzymes involved in energy metabolism involving consumption of oxygen in the brain, thiamin and mild to moderate oxygen deficiency both produce exactly the same changes as recognized by a pathologist using a microscope.

POTS, beriberi and dysfunction of the autonomic nervous system

The courageous mother of this young lady followed through with the transketolase test. It was strongly positive for thiamine deficiency, providing scientific proof that her hunch was right.

Two other girls and a boy, all of whom were known to this mother and who were suffering from post-Gardasil POTS, also had the transketolase test done.  All showed thiamin deficiency.

Another girl, also known to the mother, had P OTS.  Although she had not received the vaccine, her transketolase test showed thiamin deficiency.

Let me explain this source of confusion.  We have two nervous systems.  One is called the voluntary system by which we can act according to will and controlled by the thinking brain.  The other one is called the autonomic nervous system (ANS), controlled by the limbic system and brainstem, the evolutionally more primitive part of the brain.  This computes a given mental or physical environmental situation (stress) by means of our senses and enables us to adapt automatically to what might be called the “stress factors” that we meet on a daily    basis. For example, we sweat when it is hot and shiver when it is cold, both activated as an adaptive response to the “stress” of environmental temperature.

When the function of the autonomic nervous system becomes abnormal it is known as dysautonomia (dys, meaning abnormal; autonomia referring to the ANS).  Because this part of the brain is automatic and acting on a 24 hour basis, its energy requirement is very great and it is highly sensitive to loss of efficiency in oxidative metabolism.

Thiamin plays a part in other enzymes besides transketolase and they all have a role in the fundamental basis of energy metabolism. The union of oxygen with glucose (cellular fuel) is catalyzed by thiamin in oxidation (burning) to provide energy used for function.  It is therefore not surprising that thiamin deficiency severely affects the limbic system and brainstem.

Beriberi in its early stages is exactly like POTS arising from other causes, both being forms of dysautonomia.  By depicting thiamin deficiency, one specific cause of POTS is isolated.

The potential role of stress

It took many years to discover that thiamin deficiency was the cause of beriberi and we can use the history of this discovery to illustrate what might be termed the stress factor.

In the 19^th century, factories were built in blocks, separated by corridors.  In the summer months workers would take their lunch in the corridors.  Initially they would be in the shade but when they were exposed to the sun as it began to shine into the corridor, some of the workers would get their first symptoms of beriberi.  It was because of the symptoms being initiated in a group of people at the same time that led to the long held and inaccurate conclusion that it was an infectious disease.

We now know that the ultraviolet component of sunlight imposes a significant stress on the human body and is the reason that we tan to provide a natural form of protection.  Any form of stress imposes a biological burden, requiring energy to meet the adaptive response.  There are in fact several, genetically determined diseases of metabolism that are intermittent in nature.

The affected person may be relatively normal until a stress factor such as a mild infection, an injury or even an inoculation is imposed.  The clinical expression of the disease then becomes manifest.

The stress factor, completely innocuous to a healthy energy metabolism, can initiate symptoms in a person where that energy metabolism is at risk.  The workers that succumbed to their first symptoms of beriberi under these conditions had a degree of thiamin deficiency that was as yet without symptoms or they were trivial, perhaps ascribed to other causes.

Conclusion and hypothesis

Three girls and one boy, all who have suffered the long-term effects of post-Gardasil P OTS, have been shown to be thiamin deficient by means of a transketolase study.

Without going into details, the family history of the boy suggests that genetics may play a part.  Another girl with P OTS had the same test and was thiamin deficient, but had not received the Gardasil vaccine.

All four of the vaccinated individuals were considered to be unusually bright students, athletes, or both, before they received the vaccine.

Thiamine deficiency results in an energy deficit and has been shown to damage mitochondria.  The brain has a high oxygen demand and it would be expected that its use would be proportional to the degree of intelligence.  Hence the intelligent student might be expected to be more at risk from high calorie marginal malnutrition.

I suggest that HPV vaccination acts as a non-specific stress factor, in a marginal state of energy metabolism, although there is another peculiar caveat to the Gardasil vaccine.  It is a yeast based vaccine in its synthesis.  The type of yeast used contains thiaminase II (another enzyme exists called thiaminase I), an enzyme that breaks the thiamin molecule down, making it biologically inert. 

Thiaminase disease has been described in Japan in conjunction with dietary thiamin deficiency.  The ingestion of sugar in its many different forms in the modern world, particularly in children and adolescents, overloads the capacity of thiamin to process it.  This results in a calorie to vitamin ratio that is abnormal and could be referred to as relative vitamin deficiency.

The HPV vaccination “stress factor” might be the “last straw” in those with a genetically, or dietary determined risk.