Hirnschäden

**************************************************************************************************************************************
OLD Update from Nov 2015 (this is now old news, because of the Crepeaux 2017 paper. Read that instead, at link above).

A new study of Al adjuvant injections in mice has revealed even more complexity to the issue of Al adjuvant transport. As expected, it showed that Al adjuvant transport depends on MCP-1; mice that produce more MCP-1 (due to genetics) suffer greater transport of AANs into the brain.

Surprisingly, it also showed:
1) Transport depends on injection location. Subcutaneous injection (i.e. under the skin) is necessary for brain transport, at least for the dosages used. Intramuscular injection does not produce brain transport. This may be due to the presence of more-mobile white blood cells (dendritic cells) in the skin compared to muscle.
2) Transport depends inversely on dosage. A dosage of 200mcg/kg resulted in brain transport (and behavioral changes) and dosage of 400mcg/kg did not result in brain transport (and showed no behavioral changes). This may be due to macrophage mobility being impaired by high dosage. For example, higher local inflammation at the injection site may cause reduced macrophage mobility.

There may also be an interaction between injection location and dosage. The dosage range that causes transport may be different for different tissues.

These phenomena may explain why the prior Al adjuvant injection experiments by the Shaw Laboratory (using 100, 300 and 550mcg/kg in divided doses) showed such strong adverse effects. Though aluminum adjuvant is harmful, in human infants the incidence of harmful effects is likely lower than what was observed in the prior mouse experiments. This has been a criticism made by vaccine advocates. Specifically, vaccine advocates have asserted that the Shaw Laboratory results were implausibly severe and therefore must be wrong. This new study may explain why adverse effects in human infants are less frequent than what was observed by the Shaw Laboratory.

The authors state:

Although this study does show that the adverse effects of Al adjuvant are less frequent than observed by the earlier experiments, it is confirmation of the Shaw laboratory results. This study is further evidence that Al adjuvant can cause brain damage at dosages human infants receive from vaccines.

Clearly, there is much more to learn about the dangers of Al adjuvant. The risk of Al adjuvant depends on genetics, on dosage in a complicated way, and on which tissue receives the injection.

Persistence
Another key finding from this study is the extreme biopersistence of Al adjuvant particles. The particles were observed in distant organs and tissues up to 270 days after injection, including in the brain, spleen and lymph nodes. This is confirmation of prior experiments that also found high persistence. Al adjuvant nanoparticles dissolve very slowly and travel extensively around the body.

The authors state:

“The present study confirms that alum is extremely biopersistent [29, 37] and that alum biopersistence can be observed in both the injected muscle and distant organs, including dLNs and spleen. Regarding the strong immunostimulatory effects of alum and the unrequired depot formation for its adjuvant activity [36], long-term biopersistence of alum in lymphoid organs is clearly undesirable, and may cast doubts on the exact level of long-term safety of alum-adjuvanted vaccines [37].”
dLNs = draining lymph nodes
alum = aluminum adjuvant

Full Paper (Crepeaux et al): Highly delayed systemic translocation of aluminum-based adjuvant in CD1 mice following intramuscular injections

Further reading: see this review paper by Dr Romain Gherardi (a co-author of the Khan et al paper): Biopersistence and brain translocation of aluminum adjuvants of vaccines

___________________________________________________________

NOTES:

AANs: Aluminum adjuvant nanoparticles. Used in most vaccines.
BBB: Blood brain barrier. Protects brain from aluminum in normal conditions.
MF: Macrophage (same thing as monocyte). A type of white blood cell. Can travel through the BBB.
CNS: Central nervous system (brain + spinal cord).
CCL2/MCP-1: Macrophage chemoattractant protein. Immune system signaling substance that attracts MFs. Causes MFs to transport aluminum into the brain and around the body.

* Under physiologic conditions, some dissolved aluminum will not be in the Al3+ form, but rather AlOH4-. For the sake of this discussion, this is irrelevant, so we will use Al3+, even though this is not really correct. But AlOH4- arguably contains Al3+ in the center.

Monocytes and macrophages are basically the same thing. From nature.com: “Macrophages (and their precursors, monocytes) are the ‘big eaters’ of the immune system. These cells reside in every tissue of the body, albeit in different guises — such as microglia (brain), Kupffer cells (liver) and osteoclasts (bone) — where they engulf apoptotic cells and pathogens and produce immune effector molecules. Upon tissue damage or infection, monocytes are rapidly recruited to the tissue, where they differentiate into tissue macrophages. Macrophages are remarkably plastic and can change their functional phenotype depending on the environmental cues they receive. Through their ability to clear pathogens and instruct other immune cells, these cells have a central role in protecting the host but also contribute to the pathogenesis of inflammatory and degenerative diseases.”

Papers in this post: