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Discussion in 'Educating Doctors' started by Jack Kruse, Aug 9, 2019.

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  1. Jack Kruse

    Jack Kruse Administrator


    SVT is a broad term for a number of tachyarrhythmias that originate above the ventricular electrical conduction system (Purkinje fibers). In ACLS codes we use adenosine via IV push to rid the heart of this detrimental rhythm when the patient is not symptomatic.

    IS THERE NOW EVIDENCE THAT INTENSE RED LIGHT can do THE same thing using the PER circadian gene? Does this imply that red light is a drug equivalent?

    YES, it does.

    Is there more to this circadian story you need to know? YES.

    You know my answer and you should know what Dr. Tina Kuru says about this...........

    In this paper below in an effort to find out why red intense light can do this, researchers developed a photonic strategy using optogenetics to protect the heart using intense light to target and manipulate the function of the PER2 gene which is expressed in a circadian pattern in the part of the brain that controls circadian rhythms. (Sounds like something Dr. Kruse would suggest no?)

    You do know that sunlight is made of 42% intense IR-A light huh?

    By amplifying this gene, the researchers using JUST LIGHT PHOTONS, found that it protected cardiovascular tissues against LOW OXYGEN conditions like myocardial ischemia, caused by reduced oxygen flow to the heart. Dr. Kruse called low oxygen situations pseudohypoxia. These are all associated with low NAD+ levels in cytochrome 1 and leptin resistance with low delta psi on the inner mitochondrial membrane.

    They also discovered that the light increased cardiac ADENOSINE, a chemical that plays a role in blood flow regulation. Hey didn't Dr. Kruse just do a massive post on ADENOSINE last week on this very page?

    Hey, isn't leptin resistance a synonym for melanopsin dysfunction? Yes, it is. Tell me again how that works Dr. Kruse?

    Dr. Kruse Response: Blue light and nnEMF liberate Vitamin A from our cells and cell membranes to raise its presence in the blood plasma and this lowers plasma levels of Vitamin C and Vitamin D. When Vitamin is liberated by non terrestrial light or trauma, it becomes an aldehyde that destroys the small molecule modulators of the mammalian circadian mechanism. PER1 and PER2 are gears in that eye clock mechanism. Once the molecular clock in the eye and peripheral clocks goes awry the implications for many neolithic diseases spiral out of control. What are some of the Vitamin A proteins involved in this downward spiral? They are called retinoic acid receptor-related orphan nuclear receptors or RORs for short. The RORs have several isoforms too called RORα-γ. These proteins are also under the transcriptional control of CLOCK/BMAL1 heterodimers. CLOCK and BMAL1 are positive regulators of circadian gene expression, and PER and CRY are the NEGATIVE FEEDBACK LOOP regulators that operate under day and night cycles. These are the positive and negative feedback arms of the circadian mechanism. They must be coupled properly to terrestrial light to operate well and control all growth and metabolism, protein synthesis and hormone production and release. It also controls receptor biology. It controls EVERYTHING. If they are not properly coupled to the light and dark cycles the eventual results are the extinction of both sides of the feedback loop. That is how all human disease begins. It is circadian biology that couples all the molecular clock genes in humans and the SCN of the eye drives the program and the major timekeeper.

    Remember this lesson from last week on my FB page on 7/31/2019:

    Classic Paroxysmal SVT has a narrow QRS complex & has a very regular rhythm. ... A rapid heart rate will significantly reduce the time which the ventricles have to fill.
    The heart fills during diastole, and diastole is normally 2/3 the cardiac cycle. A rapid heart rate will significantly reduce the time which the ventricles have to fill. The reduced filling time results in a smaller amount of blood ejected from the heart during systole. The end result is a drop in cardiac output & hypotension.
    With the drop in cardiac output, a patient may experience the following symptoms. These symptoms occur more frequently with a heart rate >150 beats per minute as the ECG strip shows below:
    Shortness of air (S)
    Palpitation feeling in the chest (S)
    Ongoing chest pain (U)
    Dizziness (S)
    Rapid breathing (S)
    Loss of consciousness (U)
    Numbness of body parts (S)
    The pathway of choice for SVT in the tachycardia algorithm is based on whether the patient is stable or unstable clinically.
    The symptoms listed above that would indicate the patient is unstable are noted with the letter (U) in a code situation. This can present outside a code situation when someone has a very low redox state because of a very poor environment linked to blue light and nnEMF toxicity. This mimics adrenal fatigue and brainstem pathology, sleep disorders, and eating disorders. Stable but serious symptoms are indicated with the letter (S) above.
    Insert any 3G-5G city or environment = an acute or chronic adenosine problem. What fucks up sleep ultimately? Problems with adenosine at the brain stem level. This is why ACLS uses adenosine to treat acute mitochondrial failure in the heart that results in SVT cardiac rhythms........guess what drug is used for cardiac tachycardias in ACLS?

    How do you like me now............?

    Do you still think tech is safe and has no side effects for the heart of your blood vessels? How about your eye clock or the molecular clocks in your skin. These are all places where melanopsin and leptin are.

    Adenosine building up occurs normally during the day as we live and is one thing that drives us to feel sleepy during the night. Then while you sleep, the adenosine is cleared out, leaving you refreshed and ready to go in the morning… for most people. Today, most people have a version of EHS that affects adenosine at the brainstem level. This mimics adrenal problems and causes wild symptoms doctors cannot explain.
    Who else can get these problems sans a technology addiction?

    if you follow your genetics from 23 and me...
    There is a genetic variant in the adenosine deaminase (ADA) gene that decreases the clearance rate of adenosine. People who carry the variant may get more slow-wave, deep sleep at night, but they also may need to sleep a little longer o feel refreshed the next morning.
    Check your genetic data for rs73598374 (23andMe v4, v5; AncestryDNA):
    C/C: normal clearance of adenosine
    C/T: reduced clearance of adenosine, more deep sleep but may feel sleepy when waking up
    T/T: reduce clearance of adenosine, more deep sleep but may feel sleepy when waking up.

    How do you like me now?

    Intense RED LiGHT via PBM/LLLT like I use at Kruse Longevity Center is cardioprotective. Shocking huh?

    It shocks only those who are not on the path of becoming a Black Swan.

  2. Jack Kruse

    Jack Kruse Administrator

    This is why being a ignorant of mitochondrial biology and its controling arms is useless. Having a colony of unfixed engines, ketosis is like using premium gas on an old jalopy.
    NAD+ is made from the arimatic amino tryptophan the same one melatonin is made from. Do you think this is coincidence or is Nature telling us something deep about the sun and the photon traps in these type of aromatic amino acids? You know that melatonin controls both autophagy and apoptosis huh, and NAD+ control the redox potential in your colony of mitochondria? You feeling me yet? SIRT1 regulates the activity of BMAL1 and CLOCK, two circadian transcription factors, which target NAMPT, an enzyme that synthesizes NAD. And in a curious feed-forward mechanism, CLOCK and BMAL1 enhance SIRT1 expression… genetic deletion of any of these players induces insulin resistance.
    Sunlight is a calcium channel blocker that alters the firing rate of voltage-gated channels on cells. This alters the free radical signal in mitochondria. This is done in a few ways with sunlight. UVA light = NO release = lowers BP and the blue light in sun balanced by red light also stimulates melanopsin relaxation of the arterioles in our skin as another collateral effect. This one reason why just going outside in the sun and clean air reduces depression and anxiety because sunlight slows breathing and improves oxygenation.
    Breathing indoors requires us to use suboptimal air which is not moving or mixing with the wind or interacting with the sun so its charge is lower. This poor oxygen level = pseudohypoxia = NAD+ drops = you age faster = More PVN firing = less vagal tone = you get sick quicker indoors. SIRT 1 lowers with INDOOR living.
    Why is this a big deal?
    NAD+ is one of the more immediate players in cytochrome 1 that is a huge driver of circadian biology in humans. It is the coenzyme called nicotinamide adenine dinucleotide (NAD+). It participates in a variety of redox reactions in the matrix that help generate DDW. Solar exposure and fasting work with light frequencies to slow ECT flow and this can increase the intracellular NAD/NADH ratio if the light environment is dominated by sunlight. It won't do this with artificial light. It lowers NAD+. This is what sets off a cascade of circadian events that can destroy tissues because they involve epigenetics and the regulation of growth and metabolism of man. LIGHT DOES THIS. NOT FOOD OR FUELS. The che nuclear cycles of metabolism are desgined to run well indefinitely as long as the quantum thermodynamics givens in the environment are maintained and water is made at cytochrome C oxidase (CCO). This is why ubiquitination is designed to be quiescent and so is the nuclear genome. The mitochondrial signals are what turn on and off the epigenetic software and this is entirely controlled by light. We can use any food stuff to replenish what we need in the process of living when the environment falls in range of natures givens. Today that has changed.
    SUN + fasting -> NAD+ -> SIRT1 -> BMAL1/CLOCK -> NAMPT -> NAD+
    NAD+ major effect is to activate the sirtuins as the reaction above shows. This is a family of deacetylase enzymes. When you understand what UV and IR light are doing to a matrix, you can see why fasting could potentially be seen as a circadian reset biohack. It won't work in fake light when ALAN is present.
    SIRT1 also activates PGC1a in liver (Rehan et al., 2014), which enhances fatty acid oxidation, at a time when HUMANS require it during sleep in the absence of ALL light at night.
    This is why you better be careful who packs your parachute.
    NDC74, Inger, Bob Stirling and 2 others like this.
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