Restoring Health by Systemically Treating the Cell Danger Response
Story at a Glance: â˘Cells have a variety of adaptive processes they undergo to handle stress. One of the most consequential ones is cells ceasing normal functioning via their mitochondria to enter a defensive mode (the Cell Danger Response) and then initiating a healing cycle to repair themselves. â˘In health, this cycle resolves itself, but in chronic illness, the CDR becomes stuck, creating weakened tissue, inflammation, fatigue, and a variety of systemic illnesses. â˘Extensive research has shown that autism results from a sustained CDR, and that when appropriate CDR blocking therapies are given, significant improvement can be observed in autistic children. â˘A sustained CDR underlies many chronic illnesses, and in turn, many effective natural therapies, work, in part, by alleviating the CDR, often by creating an environment which signals safety to the body. As such, understanding the CDR is necessary to understand a myriad of chronic illnesses. â˘This article will discuss the treatments that have been discovered to treat the CDR, detail how we use them in practice to ensure they benefit patients, and highlight many of the different types of illness (e.g., fatigue, hair loss, COVID spike protein injuries, autism, Alzheimerâs, the inability to exert oneself with age or injured tissues that refuse to heal) which respond to appropriate CDR treatments. Many diseases result from cells no longer functioning the way they should, in many cases appearing to âturn offâ or be âdead.â Through studying a large number of metabolites present, Robert Naviaux realized that much of this results from the mitochondria in the cell sensing danger, then diverting their cellâs resources from promoting the normal function of the cell to creating a low-functioning cell that is more capable of neutralizing microbial threats (e.g., viruses) and surviving otherwise lethal stressors. Once this âCell Danger Responseâ (CDR) is triggered (e.g., by a shock, loss of blood flow, infection, or significant injury), cells disconnect from the tissue and organism they belong to (hence no longer being able to serve their vital functions and in some cases also turning cancerous) and also signal cells in their vicinity to enter the CDR as well. Note: this disconnection causes cells to partially stop responding to a wide range of hormones (e.g., thyroid hormone or insulin) and signals from nerves (which can be quantified through abnormal changes in things controlled by the nervous system, such as the heart rate and its variability). Two ways thus emerge to look at the CDR. The first is that it is a remarkable adaptation that makes life possible by protecting and healing cells from each injury they encounter (which is why the leading CDR researcher Naviaux now refers to it as the healing cycle). The other is that it is the disastrous root cause of chronic illness worldwide (as a small number of cells being in the CDR can significantly impact the performance of a tissue, and in many cases, the quality of life for the organism they belong to). The critical distinction between these two is that in health, the CDR cycle can complete itself (thereby exiting the CDR), while in disease, something goes wrong, and it canât, trapping patients in an endless cycle of issues like mitochondrial âdysfunction.â As this is a pivotal concept to understand when working with chronic illnesses, I have tried to bring attention to it in this newsletter and previously wrote two articles describing many key aspects of the CDR which help set the stage for this article. In our modern world, we are exposed to a massive number of environmental stressors we never evolved to handle (e.g., numerous harmful chemicals which are each present in âsub-toxicâ amounts), and as a result, many patients eventually reach a tipping point from those collective stressors where the CDR flips to becoming chronically activated and creates symptoms arising from the specific tissue where the CDR is activated. This, in turn, describes precisely what transpires in many complex illnesses the medical profession struggles to address or even understand. Most recently, I and colleagues realized it was a key issue in many of the patients with spike protein injuries, as much of what I and my colleagues saw mirrored our experiences from working with other complex patients trapped in the CDR. Naviaux likewise reached a similar conclusion: Evidence is emerging that patients with long-COVID, also known as post-acute sequelae of SARS-CoV-2 infection (PASC), do not have a generalized defect in mitochondria. Instead of a generalized defect, long-COVID is associated with entry into a specifically altered state of [hypometabolic] mitochondria function. The evidence for this comes from [simultaneously measuring all of the metabolites that reflect the current metabolic function of the body]. In the case of [hypometabolic survival states like] chronic fatigue syndrome (ME/CFS), long-COVID, and related [metabolic states], bouts of physical and emotional stress can lead to setbacks called âcrashesâ and post-exertional malaise that result from a transient shift from Phase 3A to more glycolytic metabolism and inflammation in Phase 1C of the healing cycle caused by autonomic and neuroendocrine activation. Mitochondrial hyperfusion leads to hypersensitivity to ATP signaling, abnormalities in innate immunity, neutrophil and natural killer cell dysfunction, neurologic symptoms, latent DNA virus reactivation, endogenous retrovirus activation, misfolded protein aggregates, and a predisposition to apoptosis, ferroptosis, and other cell death pathways. Restoration of long-distance brain-body signal transduction at the end of Phase 3 of the Healing Cycle [reduces purinergic signaling]âŚand enables normal organ function to return, and marks the re-entry to Health Cycle. Once something triggers the CDR, the following phases should occur: â˘CDR1: An inflammatory phase where the cell seals itself off and eliminates microbial invaders. A sustained CDR1 creates chronic inflammatory disorders. â˘CDR2: A proliferative phase where missing cellular components and cells are replaced (e.g., via making new blood vessels, new cells, and recruiting stem cells). A sustained CDR2 can create chronic proliferative disorders like cancer. â˘CDR3: An anti-inflammatory, reintegration, and differentiation phase where the cell becomes able to resume its normal function and reconnect with the rest of the body. A sustained CDR3 can lead to various complex disorders (e.g., neurodevelopmental, affective, neuropsychiatric, or neurodegenerative). When CDR3 completes, the cells and tissues are frequently healthier than they were before initiating the CDRâa fundamental principle regenerative medicine utilizes to restore lost functionality. The healing cycle is initially sustained by the cells signaling danger to each other (and later the body), then is terminated by safety signals from the entire body (e.g., via the vagus nerve). This termination requires CDR3 to re-establish the cellâs communication with the body and for the individual to exist in a âsafeâ environment that produces safety signals for the body. Conversely, if the initial threat that triggered the CDR has not been eliminated, the body evolved not to send signals to terminate the CDR. This is a key reason why the long-lasting synthetic mRNA (which continually produces the toxic spike protein) is so problematic. Note: In addition to getting stuck along the progression of CDR1 â CDR2 â CDR3 â normal cell function, cells can also be shunted into the hypometabolic survival state mentioned above (e.g., this happens in chronic spike protein injuries, CFS, or chronic Lyme disease). Typically, for the first 3-6 months, the mitochondria that have switched to sustain the CDR can easily switch back to their normal function. If the CDR persists past this point (which frequently happens in these illnesses), the mitochondria become much more challenging to switchâŚ
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