As we progress into the age of molecular medicine, unraveling the intricacies of the human immune system is an increasingly achievable goal. One can only marvel at the carefully regulated feedback pathways that, under a range of conditions, allow the immune system to maintain a natural state of homeostasis. What happens though when pathogens, medications, and supplements upset this delicate balance? Research that reveals how the immune system can be affected during an infant’s first weeks of life is shedding light on many of the factors driving the current epidemic of chronic disease.

The human immune system has two components – the innate immune system and the adaptive immune system. The innate immune system is the body’s first line of defense against invading pathogens. White blood cells of the innate immune system called phagocytes engulf and kill bacteria. The adaptive immune system is primarily made up of white blood cells called lymphocytes. Once lymphocytes encounter a pathogen, they create proteins called antibodies that allow the adaptive immune system to ‘remember’ the infectious agent and prevent it from causing disease at a later time.

While the innate immune system is functioning at birth, it takes several weeks for an infant to develop a working adaptive immune system. Little is known about what happens when a baby encounters pathogens during this early period of life. However, a recent study by 1996 Nobel Laureate Rolf Zinkernagel and team at the Institute of Experimental Immunology in Switzerland illustrates how pathogens may affect infants during the period before their adaptive immune systems are up and running.^[1]

Zinkernagel and team injected a virus called Cytomegalovirus (CMV) into the brains of a group of mice that were only a few days old. Their adaptive immune systems had not yet developed and consequently they were not producing lymphocytes. The researchers found that the innate immune systems of the mice were able to eliminate CMV from most of the tissues except for those of the central nervous system. As a result, the virus persisted in the brains of the mice. Later in life, when the same mice were challenged by infection with a similar virus, they developed a condition resembling a type of autoimmune disease and died. The team referred to this concept as viral “deja-vu.”

A second group of mice were not exposed to the CMV virus until they were fully grown and their adaptive immune systems had completely developed. When these mice were exposed to CMV later in life, they were able to successfully fight the virus and lived.

The results of this study reveal what may be one of the main reasons behind why some people seem much more susceptible to the L-form bacteria that cause chronic disease and acquire these pathogens at higher rates than much of the rest of the population. As Zinkernagel states, “In genetically susceptible individuals, early childhood infections seem to predispose them to [such disease as] multiple sclerosis or type 1 diabetes years even decades before clinical onset.”

According to a study just published in the New England Journal of Medicine, in some infants, the innate immune system may also not be able to clear bacteria from other tissues besides the brain during the first weeks of life. Researchers led by Dr. Hans Bisgaard at Copenhagen University Hospital in Germany found that newborns who harbor certain types of bacteria in their throats, including Streptococcus pneumoniae, a common cause of pneumonia, and Haemophilus influenzae, which causes upper respiratory infections, are at increased risk for developing recurrent wheeze or asthma early in life.^[2]

This finding “opens new perspectives for the understanding and prediction of recurrent wheeze and asthma in young children”, says Bisgard. The researchers assessed the development of recurrent wheeze and asthma in 321 newborns who had throat cultures taken at 1 month of age and who were then followed through 5 years of age.

Twenty-one percent of infants were colonized with S. pneumoniae, H. influenzae, another type of bacteria called M. catarrhalis, or a combination of these bugs and this finding more than doubled the risk of persistent wheeze, wheeze flare-up, and hospitalization for wheeze.

The prevalence of asthma at age 5 was significantly increased in the children who harbored these organisms as newborns compared with children who did not (33 percent versus 10 percent).

In a related editorial, Dr. Erika von Mutius, from University Children’s Hospital in Munich, Germany, comments that these findings may be interpreted to suggest that the presence and growth of bacteria in the throat in the first four weeks of life “indicates a defective innate immune response very early in life, which promotes the development of asthma.”^[3]

O’Connor and team at the Centers for Disease Control and Prevention agree, stating, “A person’s age at the time of infection—from intrauterine or perinatal (the time period surrounding birth), through childhood and adolescence, to adulthood and the elder years—may further influence the risk for chronic outcome. For example, perinatal herpes virus infection dramatically increases the risk of developing adult or pediatric chronic liver disease. Recurrent infections or perhaps serial infections with certain agents might also determine a person’s risk for chronic outcome.”

If certain human babies are infected at birth with L-form bacteria and other persistent pathogens, it is very possible that just like the CMV virus that persisted in the brains of Zinkernagel’s first group of mice, and the bacteria that remained in the throats of the infants in Bisgard’s study, these pathogens could persist in the human brain and other tissues. This could make the same infants more susceptible to the L-form bacteria they are exposed to later in life – in essence they would develop “bacterial deja-vu.”

This may explain why people react differently to insect bites. Only about 5% of people who are bitten by a tick and fall ill with Lyme disease go on to develop chronic Lyme disease – a condition where the body is simply unable to kill the bacteria responsible for causing the illness. The pathogens transform into the L-form and persist inside the tissues and the cells of the immune system.

Take, for example Matt Russell, who is currently using the MP to treat his chronic Lyme disease. Matt was born 5 weeks premature. He was breast-fed, but also given formula supplemented with vitamin D through a tube. Ten days later he ended up in the neonatal intensive care unit and tested positive for quite a few forms of bacteria. He stopped breathing on several occasions but was revived each time and put on a cocktail of antibiotics. He responded favorably to the antibiotics and his parents were later told that he had an E. coli urinary tract infection.

Twelve years later, after being bitten by an insect that also carried bacteria, Matt started to suffer from intense headaches and recurrent infections, including bladder infections. Gradually, he developed full-fledged Lyme disease. It is very likely that the pathogens he had acquired at birth had persisted in his tissues, and accompanied by the bacteria introduced by the insect bite, caused him to develop a serious chronic disease later in life.

“We have always wondered why, out of the 1600 boys in Matt’s school, he is the only one in recent memory who has missed a couple of years of schooling due to a chronic disease. We are sure he is not the only one to be bitten by an insect,” says Matt’s mother, Robin Russell.

When assessing Zinkernagel’s study, it must be noted the human adaptive immune system takes even longer to develop than the rat adaptive immune system. While it takes rats only days to fully acquire innate immunity, it takes humans several weeks. Certainly this model hints at why Th1 diseases often run in families. If parents, grandparents and relatives with high loads of L-form bacteria hold and care for babies during the first weeks of life, it appears that their pathogens can easily be transmitted to the child and persist in the child’s brain and other tissues. A recent study by Dave Relman and team at Stanford University, which found that infants pick up many of the species that make up their gut flora from family members within a few weeks of birth, further indicates that pathogens are easily transmitted from family to child during the initial periods of life.^[4]

“The really important thing to be drawn from [Rolf Zinkernagel's] work is the reminder that the infant is unprotected in the days and weeks following birth, until it starts producing antibodies. The innate immune system is all it has got although many think that antibody transfer from the mother may be present in the breast milk. I am not sure that would be much help, but I just don’t know. Nobody does,” says biomedical researcher Trevor Marshall PhD of Autoimmunity Research Foundation. Unfortunately, the idea of pathogen deja-vu and the presence L-form bacteria are not being considered by the vast majority of other researchers and doctors besides Marshall.

As discussed above, children with a weakened innate immune system will be even more vulnerable to acquiring pathogens early in life, since this branch of the immune system is supposed to kill bacteria before the adaptive response kicks in. Furthermore, the human adaptive and innate immune systems are intertwined, so that a lethargic innate immune system will affect a baby’s ability to develop a working adaptive immune system.

Sadly, children who are bottle fed with vitamin D fortified milk and born to mothers given pre-natal vitamins that contain vitamin D are at increased risk of developing compromised innate immune systems. New molecular modeling research has revealed that the precursor form of vitamin D – a steroid called 25-D – binds and inactivates the Vitamin D Receptor (VDR) – a fundamental receptor of the body that controls the activity of the innate immune system and the transcription of thousands of genes.^[5] As an infant ingests high levels of vitamin D, the activity of the VDR decreases and the child’s innate immune system becomes less active, making it more difficult for them to kill pathogens. As these infants grow, they are often fed vitamin D fortified baby food that can also negatively affect the activity of the VDR if it reaches high enough levels. Add to this the fact that the L-form bacteria they harbor also create substances that bind and block the VDR, adding to the level of immunosuppression.

In what has become a public health disaster of massive proportions, the vast majority of doctors and researchers are unaware of the molecular models which show that 25-D is immunosuppressive. They don’t realize that the primary effect of large doses of vitamin D when used in cancer and chronic disease reflects the ability of the steroid to slow the innate immune system and subsequently the cytokine release generated by dying L-form bacteria. They also fail to understand that the low level of 25-D observed in patients with chronic disease is not a cause but a RESULT of the disease process, and is due to the fact that L-form bacteria create substances that bind and block the VDR, thus interfering with the intricate feedback pathways that keep 25-D in the correct range.

It is essential that doctors stop thinking of “vitamin” D as a nutrient and recognize that it is a secosteroid, whose active form (1,25-D) functions as a powerful hormone. As Marshall states, “The epidemic of imbalance we are facing now, where the genomes of the microbiota which I call the “Th1 pathogens” [L-form bacteria] have started to gain dominance over the genome of their host, is due to mistakes made during the 20th century, particularly the decision to call ["vitamin" D] a vitamin. More about the effects of “vitamin” D on the immune system here.

In the same vein, many doctors advise pregnant women to supplement with higher than usual levels of vitamin D during pregnancy because the level of 25-D in pregnant women often drops. They fail to realize that the low 25-D observed in pregnant women is a natural part of the hormonal changes that occur during pregnancy. It has long been known that the level of the active vitamin D metabolite 1,25-D rises during pregnancy, meaning that levels of 25-D drop as the precursor form (25-D) is increasingly converted into its active form (1,25-D).^[6][7] There are also feedback pathways in place that naturally cause elevated 1,25-D to downregulate the production of 25-D.^[8] Yet, the vast majority of researchers fail to test the level of 1,25-D in their pregnant subjects and therefore misinterpret the low level of 25-D as an indicator of deficiency. Surely this explains why researchers at the University of Pittsburg found that “vitamin D deficiency” was still common in a group of pregnant women, 90% of whom were taking pre-natal vitamins containing vitamin D.^[9]

Based on this disastrous misunderstanding, the Canadian Pediatric Society has recently released a statement recommending that during pregnancy and while nursing their babies, women should consider taking 2,000 IU of vitamin D daily – an amount that is 10 times higher than the current Canadian recommendation for adults under 50. Meanwhile, in the United States, two government-sponsored studies are investigating the effects of giving 4,000 IU of “D” daily to pregnant women and 6,000 IU to nursing mothers. These high levels of vitamin D are meant to “stave off” the chronic diseases caused by what doctors misinterpret as vitamin D “deficiency.” In reality, not only do these ridiculously high levels of vitamin D suppress the innate immune systems of newborn children, they also greatly lower the innate immunity of the mother, allowing her to acquire substantially more pathogens which she will subsequently pass to her child.^[10]

Besides these excessive amounts of vitamin D, as they age, people are routinely given anti inflammatory drugs, ranging from over the counter anti-pyretics and anti-histamines, to prescription steroids, such as prednisone, in order to suppress what is regarded as pointless inflammatory responses by an immune system that is out of control (e.g autoimmune disease). Unaware that these immune responses are really attempts by the body to eliminate L-form and biofilm bacteria, they try to palliate the symptoms of patients by giving medications that slow the immune system. As the immune system slows down, these persistent pathogens gradually spread to new organs and tissues.

The end result of all of the above – the current epidemic of chronic disease. According to the report comparing U.S. and European health published online in the journal Health Affairs, the treatment of obesity and other chronic diseases adds between $100 billion and $150 billion to the annual health care tab in the United States. But who can deny that the greatest tragedy is the lives that are ruined by these massive and systemic misunderstandings surrounding chronic disease. For babies to begin a life in which they are destined to become chronically ill is one of the greatest tragedies imaginable.

Note: The disease process described above can be reversed with the Marshall Protocol: http://www.autoimmunityresearch.org/

REFERENCES

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2. Bisgaard, H., Hermansen, M. N., Buchvald, F., Loland, L., Halkjaer, L. B., Bønnelykke, K., et al. (2007). Childhood asthma after bacterial colonization of the airway in neonates. The New England journal of medicine, 357(15), 1487-95. [↩]
3. Bacteria in newborn airways may raise asthma risk. (2007). Reuters. [↩]
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6. Viganò, P., Lattuada, D., Mangioni, S., Ermellino, L., Vignali, M., Caporizzo, E., et al. (2006). Cycling and early pregnant endometrium as a site of regulated expression of the vitamin D system. Journal of molecular endocrinology, 36(3), 415-24. [↩]
7. Gray, T. K., Lowe, W., & Lester, G. E. (1981). Vitamin D and pregnancy: the maternal-fetal metabolism of vitamin D. Endocrine reviews, 2(3), 264-74. [↩]
8. Bell, N. H., Shaw, S., & Turner, R. T. (1984). Evidence that 1,25-dihydroxyvitamin D3 inhibits the hepatic production of 25-hydroxyvitamin D in man. The Journal of clinical investigation, 74(4), 1540-4. [↩]
9. Bodnar, L. M., Simhan, H. N., Powers, R. W., Frank, M. P., Cooperstein, E., Roberts, J. M., et al. (2007). High prevalence of vitamin D insufficiency in black and white pregnant women residing in the northern United States and their neonates. The Journal of nutrition, 137(2), 447-52. [↩]
10. Kirkey, S. (2007). Massive doses of vitamin D urged to protect babies. [↩]