Dr. Jack Kruse

CPC #64: SCHIZOPHRENIA'S/FTD BROKEN CLOCKS

Added 2022-08-08 16:17:38 +0000 UTC

Is Schizophrenia a circadian disease that I expect to have a higher incidence & prevalence in a 4G-5G blue-lit world? Yes, that is my belief. Blue light/nnEMF alters the periodicity of clocks in the brain. The periodicity of our clocks determines the shape of our lives. Time sculpts life, not energy. What happens in your colony of mitochondria every AM writes a story in your eyes and eventually your frontal lobes where this disease begins.

People forget schizophrenia tends to happen in young men and this is because their brains do not myelinate as fast as women do until 28 years old. This makes them more susceptible to charge changes in their eyes and frontal lobes as the picture above shows. Young people tend to get schizophrenia due to clock disruption while older people who have such bad clock disruption that it leads to apoptosis of neurons in the damaged area of the brain get frontotemporal displasia. I believe these diseases are linked via the amount of trauma and destruction to the brain over time.

Frontotemporal dementia, especially the behavioral variant (bvFTD), is difficult to recognize in its early stages because it is often confused with schizophrenia. Thus, the similarities are obvious: in sufferers of both groups, personality as well as behavioral changes occur.

The SCN optical clock is activated by the sun and the absence of light at night. Meck was the first to postulate that the rate at which signals traverse this loop offers the brain a timekeeping mechanism to control the chronobiology of hormones, protein turnover, neurotransmitter release, and metabolism pathways. Before Meck's work on timing, no one thought to link these functions to the SCN. This implies that even minor brain injuries could lead to SCN dysfunction. The SCN operates as an optical lattice clock who's proteins gears and their associated chemical bonds seem to pulse and resonate (periodicity) with electromagnetic frequencies. The pulse rate and resonance are key features of how the clock handles time sensation and circadian control of timing in cells connected to it. The clock was built by evolution to operate with terrestrial sunlight frequencies but it also appears to be affected by other parts of the electromagnetic spectrum when they are present. Trauma also affects its physiologic abilities. It appears the SCN is the distal target for information processing of light between the retina and basal ganglia and neocortex of man. This makes it very critical in mental illness and diseases associated with altered light environments. It also means it is very critical in pituitary dysfunction and hormone release. Dopamine controls pituitary hormone release with prolactin.

Melatonin and dopamine control all the photoreceptors in humans that allow for proper communication. Melatonin controls mitochondrial DNA change programs and dopamine controls how we decipher and sense time between the inside and the outside world we inhabit. Creating melatonin & dopamine in the eye is the most critical physical change at a surface for humans because of how it controls our sense of time via photoreceptor regeneration. Melatonin controls all regeneration of the photoreceptors in man except the Muller cells in the eye. Both of these chemical molecules are made by sunlight as it collides with aromatic amino acids in our eye to slow light down. That is how they link to one another.

There was ample opportunity for DNA modification in life for the first 2.5 billion years of life on Earth. Yet, there is no evidence of significant change in life forms during that time span in the fossil record. It was not until about 600 million years ago when the oxygen tension rose to a point where air-breathing life forms became thermodynamically possible and favored, that a significant change can be abruptly seen in the fossil record. In other words, DHA creation and use in the central retinal pathways were critical to allowing our DNA to change. Today, the light flowing through our eyes has changed and now diseases like schizophrenia can manifest.

The SCN optical clock activated by the sun and the absence of light at night. Meck was the first to postulate that the rate at which signals traverse this loop offers the brain a timekeeping mechanism to control chronobiology of hormones, protein turnover, neurotransmitter release, and metabolism pathways. Before Meck, no one thought to link these functions to the SCN. This implies that even minor brain injuries could lead to SCN dysfunction. The SCN operates as an optical lattice clock who's proteins gears and their associated chemical bonds seem to pulse and resonate with electromagnetic frequencies. This is called periodicity.

Clocks become more accurate the more periodicity they have. Mitochondria regulate circadian rhythmicity through NAD+ production, SIRT1 & SIRT3 activation & mitochondrial dynamics. Those things make molecular clocks more accurate. SIRT1 and SIRT3 activity in HDACs is dependent on NAD+ recycling in cells. NAD+ recycling is highly dependent on tryptophan being used accurately as a time crystal at cytochrome 1. SIRT1 and SIRT3 counteract CLOCK (gene product); NAD+ synthesis is highly dependent on proper circadian rhythmicity set by the light and dark cycles of the sun.

The pulse rate and resonance are key features of how the clock handles time sensation and circadian control of timing in cells connected to it. The clock was built by evolution to operate with terrestrial sunlight frequencies but it also appears to be affected by other parts of the electromagnetic spectrum when they are present.

DHA's main effect on cells was done by evolution to improve a cell's ability to tell time. How? DHA improved the periodicity of the SCN. This is why today in humans the central retinal pathways have more DHA in their cell membranes than any neurologic tract in our species. The periodicity of our clocks determines the phenotype in our brain circuits. In this way, time sculpts life, not energy. What happens in our colony of mitochondria every AM writes a story in our circuitry that goes awry in schizophrenia.

Trauma also affects our physiologic abilities because it lowers the periodicity of clocks. It appears the SCN is the distal target for information processing of light between the retina and basal ganglia and neocortex of man. This makes it very critical in mental illness and diseases associated with altered light environments. It also means it is very critical in pituitary dysfunction and hormone release from any cause.

We know now that increased dopamine increases the rate of the basal ganglia loop cycling. This forges connections between disparate parts of the brain to create a larger web of interconnections. Melatonin and cortisol are critical in trimming those connections at night to optimize function. This suggests that the more dopamine we make, the faster our internal clock would seem to run to us. People with schizophrenia tend to have more dopamine released rapidly over short time scales. This leads to the disease phenotype.

As a result, our perceptions would be associated with a slower perception of external time. This is what the "time dilation experience" of childhood appears to be.

This occurs with increases in body temperature and yokes perfectly to UV light's ability to make dopamine in the eye/skin during the daytime. Darkness lowers levels of dopamine levels and a slower rate of neural circuit frequency would correspond to a slower internal clock and a perceived acceleration of external time. This is likely why low dopamine states" are associated with time contraction and disease states and are linked to circadian de-coupling events. One must also realize that dopamine levels also control pituitary hormone release. This is why hormone abnormalities are often found in trauma victims and mental illness patients.

Today the 4G-5G RF/microwaved blue-lit world is the major de-coupler of human physiology of the SCN. The association of dopamine and melatonin function is a non-linear relationship because both molecules are created and linked to specific light frequencies diurnally that vary and this makes the relationship not so clear-cut for those who do not understand the non-linear aspects of photonics or optics well.

The under- or over-activity of the dopamine system is linked with impairment inaccurate time estimation, sometimes making it seem slower, sometimes faster. There is no obvious or linear correlation between perceived speed of time and the amount of dopamine present as one might suspect, but I believe there is a fractal relationship of dopamine levels to protein dynamics due to a lack of UV and IR light perception in the retina, because of Meck's work. Why do I say this?

Schizophrenics have an altered sense of time that begins in the SCN but is amplified in the midbrain dopamine regulation centers of the basal ganglia and reward processing tracts of the orbital frontal gyri which are known to be disrupted in schizophrenia. They also have altered fragmented thoughts because of this inability to time reality properly. This is one reason why nnEMF affects attention and awareness because light can alter charge variation in aromatic amino acids and this ACUTELY can raise and lower dopamine/melatonin levels seemingly altering reality as it unfolds. We see this in TBI victims as well. Unfortunately, that is the world a schizophrenic observes 24/7 when their illness takes hold. Focus and attention come easier when one’s CNS is not being pulled down multiple pathways by contravening evoked potentials from man-made electromagnetic waves. This is why we often too EEG/ERP on our TBI victims.

Paying attention, establishes traction between your internal frequencies and the external world, synchronizing with it, and using it to help calibrate your internal pace of timing.

Deficits in time perception in Schizophrenic patients is helpful for the quantum clinician in understanding how sunlight builds time management in the brain.

Deficits in time perception have been observed in a range of disorders, and there is typically a trend to misjudge durations in most of them because of the uncoupling of the circadian mechanism:

•Manic patients tend to overestimate the duration

•Depressive patients tend to underestimate the duration

However, schizophrenic patients show poor estimation without a trend. Results are not systematic (Vogeley and Kupke, 2007)

Schizophrenic patients were asked to answer two kinds of discrimination questions:

•Do two stimuli have the same duration?

•Are they short or long?

They performed worse than controls but without a systematic bias toward over or underestimating. (Elvevag, 2003)

Dopamine transmission plays a massive role in schizophrenia. Goldsmith et al (1997) found an increased number of dopamine receptors in post-mortem and PET scan studies of schizophrenics.

Interestingly, an increase in dopaminergic transmission increases the speed of one’s ‘internal clock’, whilst inhibition slows it down. (Rammsayer, 1993)

As schizophrenia is characterized by a disruption of dopamine and melatonin communication in the brain, the unsystematic nature of impairment is not surprising. It demonstrates that in healthy individuals, integration across the brain is key for temporal perception. We can use cortisol assays in Schizophrenia the same way we can use them in TBI victims when we treat them using light hygiene protocols.

Do not think that the use of exogenous melatonin is free of risk. It is the biggest mistake modern centralized medicine makes today.

SUMMARY

More and more evidence indicates that the circadian clock and mitochondrial functioning are related. Most available evidence shows how the circadian clock controls the abundance and morphology of mitochondria by regulating biogenesis, fission/fusion and mitophagy. Additionally, several studies suggest that mitochondrial functioning also is regulated by the circadian clock as Knock Out gene/protein studies show altered mitochondrial respiration and ROS metabolism, although in these studies, it is difficult to separate effects on substrate availability and mitochondrial function itself. Conversely, direct evidence for mitochondrial regulation of feedback to the circadian clockwork remains limited in centralized research done by Big Pharma dollars. I think this being done by design to keep the focus on drug development instead of solar phototherapy.

For a better understanding of how mitochondrial morphology and functioning change throughout the day, more experiments on diurnal animals are needed in sunlight. Performing imaging and respiration assays throughout the day in different tissues seems to be essential in order to get a clearer picture whether morphology and respiration oscillate throughout the day, whether this is tissue dependent and whether this is related to the molecular clock, substrate availability or a combination of both. Furthermore, data on other regulators such as hormone signaling and the autonomic nervous system, both outputs of the central clock, are scarce, and need to be done. Light frequencies humans use now clearly exert influences on mitochondrial functioning. One first candidate hormone to investigate is melatonin & dopamine since both control photoreceptor regeneration that is linked to SCN function. Tryptophan and tyrosine biology are key gears in clock mediated disease.