When you take something the body makes you uncouple positive and negative feedback loops and extinguish both sides of the feed book loop. https://www.biorxiv.org/content/10.1101/2021.06.11.448038v1

 

^^^^^^the brain compensates for the shortage of signals (DC electric current and dopamine in neurons) by creating additional dopamine receptors. This sensitizes the system to decreased production of the neurotransmitter. This has a positive effect initially, but if the environment does not revert back to normality, a chronic stimulus stimulates apoptosis and cell death via a variety of mechanisms. As cell death progresses further, the correct signal from a normal environment may not be able to elicit the same response, and eventually, the coupled system extincts the response and may disappear. At this stage, the compensation becomes so overwhelming in the coupled feedback loop that even small variations in the level of dopamine trigger the stop signal – which can therefore cause the patient to develop the disease. This is why taking dopamine drugs long-term with no environmental change is very unwise.

Many biological systems spontaneously organize themselves if they are forced away from thermodynamic equilibrium. This is how Nature uses the chaos of environmental signals to build order. If the organism is not facing a natural environment a system based on Nature will always fall back toward an equilibrium bias and die off or succumb to disease. This can occur from a lack of sun and/or an overdose of manufactured light or radiation from other unknown origins

 

It’s been known for decades that mitochondria have an intimate relationship with the nucleus, where most of the genes for mitochondrial proteins reside. Yet it’s becoming apparent that mitochondria also have numerous interactions with other organelles.

Studies of networks of mitochondria are already yielding insights into some diseases. For instance, some scientists suspect that defective energy metabolism plays a role in Parkinson’s disease, but so far, no clear difference has been found between the neuronal mitochondria of patients and healthy people. But a research team led by Feng He of the Luxembourg Institute of Health recently directed a computer to crunch through 700 gigabytes’ worth of microscopy videos of gut neurons from Parkinson’s disease patients. The system identified nearly 20 features that mathematically characterized the mitochondrial networks in their cells in terms of the organelles’ density, proximity to one another, and interactions. The study, which examined only a small number of patients, found that the features could collectively differentiate patients from healthy people. To He, it seems that mitochondrial networks in Parkinson’s disease might be less efficient and that this inefficiency could contribute to the disease. By capturing layers of biology that more reductionist approaches tend to miss, such network studies could “reshape [our understanding] of different cell types in our body,” he said.

 

Disease-modifying treatment of Parkinson's disease by phytochemicals: targeting multiple pathogenic factors https://pubmed.ncbi.nlm.nih.gov/34654977/

 

Real science is creative, as much so as painting, sculpture, or writing. Beauty, variously defined, is the criterion for art, and likewise a good theory has the elegance, proportion, and simplicity that we find beautiful. Just as the skilled artist omits the extraneous and directs our attention to a unifying concept, so the scientist strives to find a relatively simple order underlying the apparent chaos of perception.

Did you know that the strength of electrical oscillations at 40 Hz intensifies electric coupling of networks in the human brain? It is true. So now the question you should be asking, what happens when the devices you use and abuse oscillate at a different resonant frequency for your brain? Is this how disease begins?

Could this be how sleep is disrupted in the cases of neurodegeneration? Almost all forms of AD and PD are associated with massive sleep issue. Did you know that stimulating a sleeping human brain with a weak electric field pulsing at low gamma frequencies can induce lucid dreams? Lucid dreams are markers of REM sleep when we are actively replacing our defected mitochondria throughout our colony so we can fight on the next day. People often forget that strong magnetic fields are associated with sleep and anesthesia in animal studies (Becker)

Since our civilization is irreversibly dependent on electronics, abolition of EMR is out of the question. However, as a first step toward averting disaster, we must halt the introduction of new sources of electromagnetic energy while we investigate the biohazards of those we already have with a completeness and honesty that have so far been in short supply. New sources must be allowed only after their risks have been evaluated on the basis of the knowledge acquired in such a moratorium. nnEMF stimulates neurodegeneration probability.
https://www.medicalnewstoday.com/articles/can-flickering-light-and-sound-treat-alzheimers

 

The first study demonstrates that the application of PBM is cable of altering the microbiome in people with parkinsons disease.

https://www.linkedin.com/feed/update/urn:li:activity:6884757119929864192/

 

Role of mitochondria DNA A10398G polymorphism on development of Parkinson's disease: A PRISMA-compliant meta-analysis http://dlvr.it/SJwdNq

 

Statins are mitochondrial toxins because of their effect on CoEnzQ10. There are many ways in which they increase coronary artery calcification. One way is depletion of Vitamin K2 from the gut, another is lack of sun to control calcium flows, and another is direct arterial melanopsin damage liberating Vitamin A to cause intimal damage and a loss of arterial NO.

Sufficient production of vital biochemicals such as Geranylgeraniol (GGPP) is required to maintain endotoxin tolerance in macrophages in our arteries once the damage occurs. Macrophages are the hallmarks of CVD/Atherosclerosis, contributing to plaque development, inflammation, and the promotion of thrombosis. Geranylgeraniol is downstream of Mevalonate in the cholesterol synthesis pathway, and GGPP synthesis is inhibited by Statins, as is CoQ10 and K2. Vitamin K2 is the cofactor for matrix Gla-protein activation, which PROTECTS arteries from calcification.


Statin use is independently associated with increased calcification in patients, & using an animal model of hypercholesterolemia, we present a molecular mechanism whereby statins promote the calcification of atherosclerotic plaque. https://www.ahajournals.org/doi/10.1161/ATVBAHA.119.313832

 

Why is a lack of sunlight a big problem for PD and HD-like diseases?

NO is altered in these diseases and this causes problems in the nigrostriatal pathways due to aberrant calcium flows in mitochondria. It also affects adenosine levels which control the entry into proper sleep cycles.

Did you know that many studies have also implicated the gaseous neuromodulator nitric oxide (NO) in striatal synaptic plasticity? Roles for NO in synaptic plasticity in the hippocampus, cerebellum, and other brain regions had been known since the early 1990s. Without NO plasticity of neurons in these tracts are LOST. Let that sink in. Remember that NO release is linked to UVA diurnal light in terrestrial sunlight.

Sun hits the retina at daybreak, and the photic stimulus begins to shut off the secretion of melatonin from the pineal gland in the brain. Morning sunlight contains mostly IR light at daybreak and as we approach noon, UV light frequencies soon appear on the skin and via the eyes and are transmitted through the visual axis and pituitary system. When morning sunlight hits your retina and receptors in skin cells throughout your body, the signal travels through the optic nerve to other regions of the brain, including the pituitary & pineal gland. The light cue prompts melatonin levels to fall in our plasma, while serotonin and cortisol levels spike within 30 minutes of waking. Adenosine levels are highest at darkness and this is why they stimulate sleep. Adenosine levels decrease steadily as you sleep, and are low when you awaken, increasing alertness. The adenosine-cortisol-serotonin effect is most effective closest to dawn, another reason to try to rise with the light of day!

Prolactin is created by the pituitary system in response to AM light and links to many other important metabolic functions in the brain. It also regulates behavior, the immune system, metabolism, reproductive systems, and many different bodily fluids like CSF. This means it is linked to the action of hydrogen bonds in water. The production of prolactin is controlled by two main hormones: dopamine and estrogen. Dopamine is lacking in PD. These hormones send a message to the pituitary gland primarily indicating whether to begin or cease the production of prolactin. Dopamine restrains the production of prolactin, while estrogen increases it. So artificial light has major poor influences on prolactin and dopamine production via the eyes.

Our brain wakes up with a morning surge of cortisol. That is what turns our brains on at 6 am while melatonin is dropping. All of this is controlled by ambient light. VIP (vasoactive intestinal peptide) helps do this in long light cycles on Earth. VIP is highest at 6 am, and lowest at 6 pm.

Parkinson’s disease is a progressive neurodegenerative disorder that is characterized by a loss of dopamine neurons in the substantia nigra that supply the dopaminergic innervation to the dorsal striatum. PD is effectively treated with levodopa (or L-DOPA), the biosynthetic pathway precursor molecule to DA. However, prolonged L-DOPA treatment results in side effects involving abnormal involuntary movements, or dyskinesia. Since the dorsal striatum is richly endowed with a dopaminergic innervation, and neuronal degeneration preferentially occurs in the substantia nigra as opposed to the ventral tegmental area in PD, cell loss dramatically affects the dorsal striatum. Given that corticostriatal eCB-LTD is D2 receptor-dependent, the profound implication is that this form of synaptic plasticity is lost as striatal DA content diminishes, possibly contributing to the cardinal PD clinical features of tremor, rigidity, and bradykinesia. the endogenous endocannabinoid (CB-LTD) is lost upon striatal DA depletion based on the new data we have on Parkinson's disease. This should alter how we use dopamine analogs which make the disease worse over time (Calabresi et al., 1992; Kreitzer and Malenka, 2007).



FIGURE 1. MECHANISMS OF CORTICOSTRIATAL LONG-TERM DEPRESSION (LTD). Four, one-second bouts of afferent (corticostriatal, CTX) stimulation at 100 Hz (high-frequency stimulation, HFS) synchronized with postsynaptic medium spiny neuron (MSN) depolarization (depol.) to 0 mV every ten seconds induce endocannabinoid (eCB)-mediated LTD (eCB-LTD). Induction of eCB-LTD involves metabotropic glutamate receptor (mGluR) activation as well as suppression of cholinergic tone that requires dopamine (DA) D2 receptor activation on tonically active cholinergic interneurons (TANs). Relief of cholinergic tone on M1 acetylcholine (ACh) receptors, coupled with postsynaptic depolarization, enhances activation of L-type voltage-gated calcium channels (VGCCs) resulting in calcium influx (Ca2+). This triggers eCB production and subsequent liberation of eCBs that signal retrogradely to activate presynaptic cannabinoid type 1 receptors (CB1), resulting in a persistent suppression of glutamate release. Adenosine A2A receptors also play a role in eCB-LTD, with current evidence indicating the location of action on both TANs and D2 receptor-expressing (indirect pathway) MSNs. A balance between A2A and D2 receptor activation may govern downstream effectors modulating eCB production, including PKA/cAMP and RGS4, which in turn regulate mGluR5-induced signaling. The role of A2A receptors on presynaptic terminals is presently unclear but links light to the story unfolding in research. Serotonin (5-HT) modulation of substantia nigra pars compacta DA cell firing and excitation of TANs likely influences this form of plasticity. Moreover, serotonergic activation of corticostriatal 5-HT1b receptors induces LTD that is mutually occlusive with eCB-LTD. Thus, a complex interplay of several neurotransmitter systems orchestrates the fine-tuning of the corticostriatal synapse. It appears terrestrial light frequencies may be the levers that cause all basal ganglia diseases

In PD, we see the progressive degeneration of striatal dopaminergic innervation, but the striatal serotonergic innervation is relatively spared in PD. When PD is treated with levodopa (or L-DOPA), the striatal serotonergic innervation is enriched. This leads to problems = L-DOPA induced dyskinesia.

The nigrostriatal dopaminergic system is implicated in action control and learning. A large body of work has focused on the contribution of this system to modulate the corticostriatal synapse, the predominant synapse type in the striatum of the basal ganglion. Signaling through the D2 dopamine receptor is necessary for endocannabinoid-mediated depression of corticostriatal glutamate release. This synapse is complicated in how it operates, but the wiring diagram of this cortical loop is being teased out by multiple labs. It is now clear the feedback loops on the controller levers of this synapse I am mentioning here are all under circadian control and linked to G-coupled receptors like dopamine, adenosine, and endocannabinoid systems. This is a big clue that light is at the root cause of all basal gangion diseases.

The discovery of the cannabinoid signaling system grew out of studies of the actions of cannabis-derived drugs that contain Δ9-Tetrahyrocannabinol (Δ 9-THC). The discovery of a Δ9-THC-activated G protein-coupled receptor (GPCR), termed the cannabinoid 1 or CB1 receptor (Matsuda et al., 1990), stimulated the search for endogenous ligands (endocannabinoids, eCBs) that could activate the receptor. Eventually, two lipid metabolites were found to have CB1 agonist action. Arachidonoyl ethanolamide (AEA or anandamide) is derived from phosphatidylethanolamide, with several potential synthesis pathways described in the literature (Devane et al., 1992; Di Marzo et al., 1994; Liu et al., 2008). The other major endocannabinoid, 2-arachidonoyl-glycerol (2-AG) is produced from membrane lipids via a two-stage reaction catalyzed by phospholipase C and diacylglycerol lipase (DAGL; Mechoulam et al., 1995).

The dorsal striatum is the entry nucleus for basal ganglia processing cortical information in humans. Cortical fibers innervate the striatum and synapse on striatal medium spiny neurons (MSNs), release glutamate and drive the activity of these GABAergic projection cells. As such, the corticostriatal synapse represents a crucial, initial step in the complex series of mechanisms underlying basal ganglia control of actions. They are dependent on dopamine controls. Indeed, an aberrant corticostriatal function is implicated in various basal ganglia disorders, including Parkinson’s disease (PD), Huntington’s disease, obsessive-compulsive disorder, and addiction.

Investigation over the past quarter century has revealed that glutamatergic signaling at the corticostriatal synapse is tightly modulated by a complex array of neurotransmitters and cognate receptors located on either presynaptic or postsynaptic elements. The eCBs have emerged as important modulators of these inputs. This doesn't mean that drugs will fix the synapse that is defective in PD/HD. It means that we are getting closer to understanding how aberrant light is behind these diseases. The finding that CB1 activation depresses corticostriatal glutamatergic synaptic transmission (Gerdeman and Lovinger, 2001; Huang et al., 2001), provides just another mechanism contributing to intrastriatal CB1 agonist injection-induced hypomotility and catalepsy (Gough and Olley, 1978). We have much more to learn but these updates are telling us how we are treating patients with these diseases must evolve as the new data evolves. So far it hasn't. That is a centralized healthcare problem.

 

If you have Parkinson's Disease you better listen to Uncle Jack about light.

Two things I carry with me daily: Death is certain, but life is not. Does blue light always buy us all a stairway to heaven? No one destroys our brain before it kills us. Sometimes you need to be reminded of this FACT. Today is your reminder.

We need the sun's version of blue poetry. It is the blue prose of modern lighting that lines our march to death. What powers our ability to slow time so we can live a few decades are buried in frequencies that resonate in hues of purple and red. Such is the disturbing comforts of life.

Physics isn't the most important thing in life, but love is. It's funny bio-physics is what underpins love, how ironic. The human heart is like a black hole--it's so dense that there's no room for light, but that doesn't mean it can't still suck others into its vortex. Life is strange; stranger than we can comprehend. We're all born strangers to ourselves and each other, and yet we are all connected in some small way that we're seldom formally introduced to unless we dig through the nature of the cosmos. The universe, it seems was made, to be full and brimming with lonesome places so life could fill in those spaces with love. Might life exist to freshen up the dry wells so many of us help create?