Other than infection the two main modes of cell death are apoptosis
(programmed) or necrosis (uncontrolled traumatic). Since a metamorphic Die-
off is certainly not an infection and does not appear to create inflammation
in the tissues, it is apparent that the catabolic breakdown during a Die-off is
orchestrated by apoptosis. With the cells being recycled through phagocyctosis by
the macrophages and turned into building blocks for the regenerating body. As I
have said elsewhere the main phase of this “self digesting” event is three days in
which bed rest is imperative. Since the HPA axis reduces immunity to conserve
energy for fight-or-flight, Die-offs occur months after the hyperaroused peak, after
the intense activity of the HPA axis has dropped off somewhat. As soon as there
is adequate energy for immune activation made available a Die-off will occur. The
intervening period reflects the intensity of the hyperaroused nervous system. That
is if the hyperactivation is extreme the Die-off might come 6 months after the
influx-peak, or 3 months after a less intense arousal. For example for a full-on
awakening following the normal annual cycle the peak HPA activation occurs in
July and the corresponding Die-off occurs in November.
It appears that the key player in switching into this Die-off mode is the
mitochondria of our cells. In fact we must look to mitochondria as being the
chief orchestrators of the entire kundalini alchemy. Mitochondria play a central
role in apoptosis by amplifying and mediating extrinsic apoptotic pathways, and
in the integration and propagation of death signals originating from inside the cell
such as DNA damage, oxidative stress, starvation. Apoptosis is most often induced
through the disruption of the mitochondrial inner transmembrane potential
and through a sudden increase in the permeability of the inner mitochondrial
membrane. This causes an influx of water by osmosis into the mitochondria with
the eventual rupture of the outer mitochondrial membrane, resulting in the release
of pro-apoptotic proteins from the mitochondrial intermembrane space into the
cytoplasm. Proteins released start a apoptotic cascade, ATP synthesis is stopped
and free radical generation exceeds the cells antioxidant capacities leading to the
oxidation of lipids, proteins, and nucleic acids.
The apoptosis signaling pathways in viable cells are kept in an inactive state and
are only turned on in response to a death stimulus. It is thought that all cells of a
multicellular animal might be intrinsically programmed to self-destruct and would
die instantaneously unless cell death is continuously repressed by survival signals
from growth factors, antioxidants, hormones, nutrients. These anti-apoptotic
regulatory molecules keep in check the activation of pro-apoptotic factors. During
a Die-off however the pro-apoptotic factors become dominant and an exquisite
cascade of cell death and self-digestion is set in motion.
Free radicals are generated in the mitochondrial electron transport system.
Mitochondria are the source of 80% or more of the oxyradicals generated in the
neuron. Reactive oxygen species were shown to cause neuronal degeneration by
activation of ionotropic glutamate receptors. Ca2+ deregulation causes excessive
activation of glutamate ionotropic receptors, disrupting the mitochondrial electron
transport system. Mitochondrial glutathione peroxidase (GSH) depletion