Aluminum - causal factor in jab related autism - but how does that relate to histamine excess as a cause?

The aluminum leads to the excess of histamine which over activates brain support cells called microglia. Moderating histamine levels can moderate negative mental and physical symptoms.

I wrote a comment on a post by JB Handley about the apparent cause of autism being aluminum and an excess of the cytokine IL-6, and I am saving it here.

International scientists have found autism's cause. What will Americans do?

My comment was to one made by Dr. Exley on JB Handley’s post.

Chris Exley is an aluminum researcher who has taken a lot of mainstream flack for his work.

• Brave AI makes mistakes but tends to reflect what is readily available and it had no problem showing that microglia are regulated by histamine. A microglia can also be a source of histamine when stimulated by LPS, a bacterial endotoxin, that also seems to be part of the CoV injections. Geoff Pain PhD is the person to follow for more information about endotoxin risk in modern jabs.

• One of Geoff’s posts (Substack) about additives in the Monkeypox ACAM2000 jabs - it also has 2% human albumin, and that makes no sense - why would anyone want to become ‘vaccinated’ against their own/other people’s albumin? Autoimmune disease to albumin is what I seem to have been suffering from since ~ 2016.

Monkeypox Jab ACAM2000 contains Endotoxin scavenger Polymyxin B

• Autism, and Alzheimer’s dementia seem to be related to each other, and both seem related to an ongoing overactivation of Mast Cells and an excess of histamine as a result.

• Niacin and pomegranate peel can help by reducing Mast Cell degranulation. (my Pom paper draft discusses this, post) Pomegranate peel has metal chelating phytonutrients and inhibits inflammatory proteins like TNF alpha or IL-6.

Evaluating the Potential Role of Pomegranate Peel in Aluminum-Induced Oxidative Stress and Histopathological Alterations in Brain of Female Rats. (Moneim, 2012)

“PPME protected brain through decreasing the aluminum accumulation and stimulating antioxidant activities and anti-apoptotic proteins namely Bcl-2. Therefore, these results indicated that pomegranate peel methanolic extract could inhibit aluminum-induced oxidative stress and histopathological alternations in brain of female rats, and these effects may be related to anti-apoptotic and antioxidants activities.” (Moneim, 2012)

- Evaluating the Potential Role of Pomegranate Peel in Aluminum-Induced Oxidative Stress and Histopathological Alterations in Brain of Female Rats.

Brain Coral, under the ocean. Photo by Daniel Öberg on Unsplash

Addition, a reader shared that Chris Exley wrote a Substack about JB Handley's article - saying it is past time for the US to admit aluminum has a causal role in autism. *Thanks for the comment Solo!

Aluminium and Autism Again

Thanks Dr. Exley, and JB Handley, this is a great summary of great work - as an independent researcher with Alzheimer's in my genetic risk and in my mother - an important word is missing from this lengthy article - histamine. How is the toxic aluminum leading to overactive microglia in the brain? What makes microglia activated? . . . and this directly relates to JB Handley's question of What to do about this? A very restricted low histamine food diet can make major enormous differences in daily function.

My mother calls me Jenny often enough now that it didn't surprise me, but it did surprise the Hospice worker. Seriously 'a miracle' - of changed diet. And Pomegranate juice/peel is also protective - reduces IL-6. "What to do about it," is my main focus as I prefer health to illness, whether mental or physical. My mother's brother died of Alz. and her other brother has it, and her function has gotten better under my dietary care, though she is still in end stages. The extreme paranoia/running away behavior is gone unless I screw up and give a wrong food.

Brave AI on the question of "role of histamine in activation of brain microglia"

https://search.brave.com/search?q=role+of+histamine+in+activation+of+brain+microglia&source=desktop&summary=1&summary_og=9c116e54e86f4255856735

It gave me: Histamine Activates Brain Microglia

Histamine, a neurotransmitter and peripheral inflammatory mediator, plays a significant role in modulating brain microglial activity. Microglia, the resident immune cells of the central nervous system, are activated in response to various stimuli, including histamine.

Histamine Receptors in Microglia

Histamine binds to four G-protein coupled receptors (H1R, H2R, H3R, and H4R) in the brain. Microglial cells express histamine receptors, particularly H1R and H4R, which are involved in regulating their function.

Activation of Microglia by Histamine

Histamine can activate microglia through both autocrine and paracrine signaling pathways. In response to lipopolysaccharide (LPS) stimulation, microglia produce histamine, which then binds to H3R, inhibiting chemotaxis, phagocytosis, and cytokine secretion. This suggests that histamine can regulate microglial function by modulating their migratory behavior, phagocytic activity, and inflammatory mediator release.

In Vivo Evidence

Studies have demonstrated that histamine modulates microglial migration and cytokine release in vivo. For example, histamine has been shown to impair midbrain dopaminergic development in vivo by activating histamine type 1 receptors (H1R).

Clinical Relevance

The role of histamine in microglial activation has implications for neurodegenerative diseases, such as Parkinson’s disease (PD), where neuroinflammation is a hallmark feature. Unraveling the cellular and molecular mechanisms triggered by histamine in neurodegenerative conditions, including PD, is crucial for understanding the pathophysiological relevance of histamine concentrations used in these studies.

Conclusion

In summary, histamine plays a modulatory role in brain microglia activation, regulating their migratory behavior, phagocytic activity, and inflammatory mediator release through autocrine and paracrine signaling pathways. Further research is needed to elucidate the specific mechanisms by which histamine influences microglial function and its implications for neurodegenerative diseases.

Follow up .... (click through for the Follow-up questions generated by the AI)

1. Histamine induces microglia activation and dopaminergic neuronal toxicity via H1 receptor activation https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-016-0600-0

2. Histamine: a new immunomodulatory player in the neuron-glia crosstalk, https://www.frontiersin.org/journals/cellular-neuroscience/articles/10.3389/fncel.2014.00120/full

3. Histamine modulates microglia function, https://jneuroinflammation.biomedcentral.com/articles/10.1186/1742-2094-9-90

4. Histamine H3 receptor in primary mouse microglia inhibits chemotaxis, phagocytosis, and cytokine secretion, https://pubmed.ncbi.nlm.nih.gov/25754956/

Disclaimer: This information is being provided for educational purposes within the guidelines of Fair Use and is not intended to provide individual health care guidance.

Reference List

(Moneim, 2012) Abdel Moneim, A.E. Evaluating the Potential Role of Pomegranate Peel in Aluminum-Induced Oxidative Stress and Histopathological Alterations in Brain of Female Rats. Biol Trace Elem Res 150, 328–336 (2012). https://doi.org/10.1007/s12011-012-9498-2 https://link.springer.com/article/10.1007/s12011-012-9498-2