The first episode of my Childhood Vaccine Safety is all about “Immunity” and
How the immune system works and how this affects the effectiveness and timing of vaccines.
The information is very surprising considering the vaccination schedule. I am sharing with you a very short description of what I learned. If you have any questions please don’t hesitate to contact me. If I don’t know the answer I will point you in the right direction. Medical Doctors, Naturopaths, Pediatricians and Midwives have gathered to present this Vaccine Safety webinar.
Immunity is very important to understand because the purpose of giving a vaccine is to spark an immune response
I learned about many different immune cells, more specifically, “T Helper Cells” and their role in the body.
T Cells spilt off into two main subtypes: TH1 & TH2
Infant is born with TH2 cells- combat allergies and parasites
Infant starts to develop TH1 cells around 6 months and older- combat bacteria & viruses and builds antibodies towards these
So naturally the body can make a transition to TH2 to TH1 around 6 months. However, what’s interesting is vaccines disrupt this natural process…
Aluminum in vaccines and other adjuvants stimulate TH2 cells.
Prolonged stimulation of TH2 cells can lead to an imbalance
inhibit the natural switch that is supposes to happen around 6 months
TH2 cell domination creates:
We do not want this, we want to allow the body to naturally switch over to TH1 cells because it deals with bacteria and viruses.
Vaccines that are used and given to children are bacteria and viruses.
You want the body to be able to create an immune response so therefore you need strong TH1 cells.
Why do we vaccinate our babies before their immune system is developed?
We need to wait until babies are at least 6 months, if not 1 year, to BEGIN vaccination, in order for their little bodies to create immunity. Otherwise, the vaccines are stimulating the wrong parts of the immune cells and can create problems early on.
The current schedule by CDC as of 2016, is to vaccinate infants 14 times before they are 6 months of age and up to 26 times in the first year of life.
Furthermore, a study (summary below) was presenting showing that TH1 cells are required in order to create an immune response. Without it, immunity to the bacteria (in this case, pertussis) doesn’t happen (in mice). The dominance of TH2 cells lowers the ability to create immunity to any vaccine:
Th1/Th2 cell dichotomy in acquired immunity to Bordetella pertussis: variables in the in vivo priming and in vitro cytokine detection techniques affect the classification of T– cell subsets as Th1, Th2 or Th0
,* , , & Infection and Immunity Laboratory, Department of Biology, St Patrick’s College, Maynooth, Co. Kildare, Ireland and The National Institute for Biological
Standards and Control, South Mimms, Potters Bar, Hertfordshire, UK
In studies of the mechanism of immunity to Bordetella pertussis in a murine respiratory infection model, we have previously demonstrated that natural infection of immunization with a whole cell vaccine induces a potent protective immune response, which is mediated by T-helper type-1 (Th1) cells. In contrast an acellular vaccine generates Th2 cells and is associated with delayed bacterial clearance following respiratory challenge. In the present study we have investigated the apparent Th1/Th2 cell dichotomy in acquired immunity and have examined the factors that affect their induction or detection. The cytokine profiles of B. pertussis-specific T cells in immune animals were determined using antigen- stimulated ex vivo spleen cells or CD4+ T-cell lines and clones established in the presence of interleukin-2 (IL-2) or IL-4. Antigen-specific T cells derived from mice immunized with the acellular vaccine were almost exclusively of the Th2 cell type. In contrast, T-cell lines and clones established following respiratory infection or immunization with the whole cell vaccine were predominantly of the Th1 type. However, a proportion of T cells from convalescent mice, especially when cultured in the presence of IL-4, secreted IL-4 and IL-5 with or without detectable IL-2 suggesting that Th0 or Th2 cells were also primed during natural infection in vivo. Furthermore,when mice were assessed 6 months after infection, spleen cells produced significant levels of IL-4 and IL-5, which were not evident at 6 weeks. The route of immunization and the genetic background of the mice were also found to influence the preferential priming of Th1 cells, and this was directly related to the level of protection against respiratory or intracerebral (i.c.) challenge. Our findings underline the critical role of CD4, Th1 cells in immunity to B. pertussis, but also demonstrate that a number of factors in the in vivo priming and in vitro restimulation can skew the apparent dominance of one Th cell type over another.
Transparency in the medical community is needed & I thank Dr. Taylor Bean, ND, for teaching this webinar on Immunity.