August 8, 2021
The spike protein invades the hypothalamus. This may explain the accelerated aging being observed. The underlying cellular mechanism for the hypothalamus-mediated aging progression comprises dysregulation of nutrient sensing, altered intercellular communication, stem cell exhaustion, loss of proteostasis, and epigenetic alterations.
Spike protein invasion of the hypothalamus also explains the aberrant inflammation both PRO and ANTI inflammation through regulating the expression of glucocorticoids. This also explains why the use of steroids is so controversial. It depends on which side of the coin the body is on.
Are they PRO inflammatory, or ANTI?
In addition, this also explains the telomere shortening, which I believe is almost certainly occuring. To our knowledge, Telomere dysfunction has not been described in either endogenous hypercortisolism (Cushing's syndrome) or acromegaly where excessive amounts of GH and consequently IGF-1 are produced. This review focuses on the possible relationships between telomere dysfunction and the hypothalamic–pituitary–adrenal (HPA) axis and GH-IGF-1 system.
I believe each exposure to the Spike Protein further damages, extends existing damage to the hypothalamus. The spike protein must not be adminstered and therapeutics against it must be developed and employed.
Telomeres and endocrine dysfunction of the adrenal and GH/IGF-1 axes
One Hormone, Two Actions: Anti- and Pro-Inflammatory Effects of Glucocorticoids
Role of hypothalamus in aging and its underlying cellular mechanisms