1. Registering for the Forum

    We require a human profile pic upon registration on this forum.

    After registration is submitted, you will receive a confirmation email, which should contain a link to confirm your intent to register for the forum. At this point, you will not yet be registered on the forum.

    Our Support staff will manually approve your account within 24 hours, and you will get a notification. This is to prevent the many spam account signups which we receive on a daily basis.

    If you have any problems completing this registration, please email support@jackkruse.com and we will assist you.

Atherosclerosis and the Tensegrity 7 blog.

Discussion in 'Educating Doctors' started by Jack Kruse, Jul 18, 2015.

  1. Jack Kruse

    Jack Kruse Administrator

    If you want real change you have to go for wisdom that is uncommon to modern humans, why? Society has become so synthetic and artificial that the truth now offends people.

    Fake blue light causes your mitochondria ECT to slow because the respiratory proteins enlarge to slow electron tunneling. The blue light has another quantum effect on the battery in cells, it lowers melatonin levels. This lowering of melatonin can occur two ways, two much blue light at night or not enough UV-A or IR-A during the day and when melatonin drops so does tissue sulfation.........…..when ECT slows our cells up regulate carbohydrate metabolism by way of AMPK pathways. Why do we do this? Because carbohydrates are loaded with serotonin and serotonin is one of the aromatic amino acids that make melatonin. This is why nnEMF causes the up-regualtion. Nature is telegraphing to us that any EMF other than the sun destroys melatonin and the quantum battery in cells. We just ignor all this. All this occurs from the change in frequency of light on our surface like the eye and skin. The brain can not tell sunlight from blue light when it is present at night because of melanopsin.......and ancestral health is unaware of this key link. You no longer can afford to be.

    Hemoglobin’s peak light absorption peaks at 280 mm 420nm 540nm and 580nm and has sharp cutoff at 600 nm since green and yellow wavelengths of krypton ion lasers peak at 531 mm and 568 mm respectively they almost perfectly match the absorption peaks of hemoglobin so these laser colors are used for coagulation of blood and blood vessels. These peaks ideally match the spectral absorptions of the aorta where atherosclerosis predominates.

    So what has Seneff et al. missed in her writings about sulfation? The absorption spectra of the skin, aortic wall and cornea show us some interesting connections when we look at them all plotted together. In the visible range of light (sunlight). The absorption spectra of the skin is 20-30 times that of the cornea. The absorption spectra of the aortic wall exhibits VERY SIMILAR peaks as hemoglobin. This data has been published for years. No one seems to link it. Parrish and Anderson from 1983, Keijzer et al. in 1989 and Eichler and Seiler in 1991 have all shown this..........Seneff wants to suggest it is all about eating more foods with sulfur but what good is that when your skin and eye are constantly getting overwhelmed with blue light frequencies..........look again how the absorption spectra is in the cornea with respect to the skin........Blue light destroys the signaling optically. Food can give you sulfur but you need the proper light signal to make use of it to build a quantum rechargeable battery!

    Seneff believes and has argued that an underlying deficiency in Cholesterol-Sulfate, is due principally to insufficient dietary sulfur. I do not buy this at all!!!!! I think the largest components is a lack of the appropriate IR and UV signals from the sun in the AM that is the most critical component. Many papers have shown that inadequate sun exposure to the skin leads, over longer timescales, to severe depletion of cholesterol and sulfate in many tissues. This loss is ADVANCED by blue light signaling. This is the world we live in today. This is why I see heart attacks in young people and carotid artery occlusions in 20-and 30 year old commonly today. This sulfur deficiency in cholesterol, chondroitin, and heparin becomes life-threatening with age in tissues and the blood plasma to eventually lead to an atherosclerotic plaque and a lack of blood flow and the development of pseudohypoxia that cause a loss of triplet superoxide production. I think this is why blood clots occur too. Heparin needs sulfation on platelets to work. Moreover, blood viscosity increases with blue light too because RBC's and platelets clump as the redox potential and EZ in blood drops as sunlight is absent from our skin. This fast forwards the disease further and the tissues ages faster and the patient dies sooner. It is a well-choreographed program for renewal of cholesterol that is sulfated. Seneff missed the point completely on superoxide. Singlet SO is a bad player but triplet superoxide is the ideal player cells need to run the sulfation program in our tissues to work with IR and UV light. UV-A and IR-A light are needed to make melatonin and melatonin sulfates things in tissues and sulfur can act like a "quibit" in tissues. This sets up the conditions of existence for quick solar recharging in nature (sun and magnetosphere). The Russian data on the correlation of oxygen availability, UV light, and triplet state SO is crystal clear to those who go deeper than just food. Seneff in her own paper says the following, "Unfortunately, there is necessarily collateral damage from superoxide exposure". That alone tells me she does not understand light. She thinks it is a food story. Sorry..........it is not, in my opinion, for atherosclerosis a food story. Triplet state superoxide is required to oxidize the LDL and to catalyze the reaction that produces sulfate from homocysteine thiolactone.

    After absorption of light photons, the photosensitizer is first transferred to an excited singlet state by the quantized energy in the photon. Then 3 possible decay channels are possible. This is why quantum physics works on probabilities and not absolutes. The 3 cases are non radiative, radiative singlet state decay to the ground state, and intersystem crossing to an excited triplet state. The last one, may also promote a reaction leading to the singlet ground state by either non radiative decay or by radiative triplet decay. The radiative decays are called fluorescence and phosphorescence, respectively. Life time for fluorescence are on the order of nanosecond time scales where phosphorescence may last up to milliseconds or even seconds. According to Foote (1968), two alternative reaction mechanisms exist for the decay of the excited triplet state which are called Type 1 or 2 reactions. They are characterized by either the generation of free radicals (Type 1) reactions, or the transfer of excitation energy to oxygen molecules directly in a Type 2 reaction.

    During Type 1 reactions the triplet state next interacts with a target molecule or protein, other than oxygen. Stop and think about mitochondria now at cytochrome 1 and what should happen seasonally for mitophagy. Type 1 reactions result in the release of free neutral or ionized radicals. We use these to signal. Further reaction with triplet oxygne may also lead to the formation of hydrogen dioxide or superoxide. Where have you heard that before?
    In Type 2 reactions, the triplet state of the photosensitizer directly interacts with molecular triplet oxygen (3O2) which is then transferred to an excited singlet state of (1O2). During this reaction the electronic spins are flipped of the electrons in oxygen.

    Both reactions are designed to occur simultaneously but when the environment around a mitochondria is altered by pseudohypoxia the Respiratory Quotient can be altered dramatically. The RQ and metabolic rate are synonymns. The reason for this is because all electrons in ECT are designed to move to oxygen for reduction. Their flow is 100% dependent upon the electron density, size of the respiratory chain proteins, and the amount of oxygen present at the end of the respiratory chain. This makes pseudohypoxia within the mitochondria a very powerful environmental variable because it controls the pull of electrons in ECT. Pull in ECT is measured in voltage. So pseudohypoxia means that voltages in mitochodria are falling and that means the magnetic field developed in mitochondria have diminished.

    Excited singlet oxygen is very reactive and toxic. It leads to cellular oxidation, mitochondrial swelling and necrosis. Weishaupt in 1968 identified singlet oxygen as the TOXIC agent in photoactivation of tumor cells.

    Carotenoids promote the toxic singlet oxygen to triplet oxygen which is harmless................Does the skin and retina have carotenoids? Yep.

    Now.......did you know blue light increases singlet oxygen and decreases triplet? No bueno

    Did you know that diabetics, who all get atherosclerosis have no measurable superoxide?

    See why now SO and blue light and sulfur and a bad quantum battery are all linked to atherosclerosis?

    With pseudohypoxia and blue light exposure you make singlet oxygen over triplet superoxide...........that is the reason why diabetes and most anterior eye diseases are blue light over exposures. This is why we see alterations in Vitamin A in the brain. We are using carotenoids up in tissues chronically exposed in blue light diseases.........and once it is used up there are severe downstream effects..............singlet oxygen predominates in a microwaved blue lit world and you never see triplet superoxide again until you get rid of this bad mitochondria.

    Time for you and everyone else to understand details matter in quantum biology.
  2. Jack Kruse

    Jack Kruse Administrator

    Since type 1 and 2 reaction occur simultaneously, quantum mechanics dictates the path of least resistance. Which probability or mechanism is chosen depends solely on the concentration of oxygen and available triplet oxygen and the appropriate target molecules................
    Retina is also loaded with xanthophylls especially in the macula.
    The skin is also loaded with carotenoids.

    Seneff mention atherosclerosis is linked to inflammation but she never fully develops it. Why? Cause she is stuck on food........and not light.

    The pigments that make apples red and carrots orange—called carotenoids—are an integral part of the body’s immune system and help us fight against aging and other kinds of damage. Clinicians like me place emphasis on seasonal eating of fruits and vegetables, seafood and animal fats because, like other animals, our bodies can’t make these carotenoids and we have to get them from food sources that grow in certain seasons.

    We store carotenoids especially in our skin. The outer most layer of skin specifically where LIGHT interacts with them—the stratum corneum—is especially good at absorbing carotenoids. Guess what signal nitric oxide in its dual role in the skin? Endothelial nitric oxide synthase (eNOS) is the key with sun exposure. Why? eNOS catalyzes sulfate production in erythrocytes, endothelial cells, platelets and keratinocytes in the skin using carotenoids interaction with the sun's light. In this way, eNOS is a dual-purpose enzyme, that uses UV light as the key metric to either producing sulfate when it is membrane–bound and producing nitric oxide when it is free in the cytoplasm. Why is Aluminum such a bad player in biology? Aluminum reflects UV light more than any other atom on the periodic table........so you can't make the proper amount of eNOS that the sun's light signals for.

    The surface chemistry of skin drives the results of the tissues below.............this is where arteries live. This is where atherosclerosis begins.
  3. Jack Kruse

    Jack Kruse Administrator

    Why do you need to understand quantum light signaling in your skin, eye, gut in detail? A general feature of most biomolecules is their complex optical band structure between 400-600 nm. Since neither macromolecules or water strongly absorb in the near IR spectrum, what we see, if we observe carefully, is that life, cells and tissues all developed a therapeutic window between roughly 600 nm and 1200 nm of the spectrum of light. This is why near infrared light penetrates most biologic tissues fully. Note, it is light that is the key to cellular construction and why DNA codes for what it does that allows these optical interactions to occur properly. Food is a secondary aspect in this quantized evolutionary design. In this optical spectral range mentioned above, radiation penetrates biologic tissues at a lower loss of energy, therefore enabling the treatment of deeper tissues to the surface tissues. This is how light is used to make Vitamin D3 and how we use sunlight in RBC's, the water fraction of plasma, the cholesterol in that plasma, and the arteries that channel this magnetohydrodynamic fluid all over our body. When the tissue optics are off every signaling cascade distal to it becomes altered to manifest in some disease state. The uniqueness of the absorption spectrum of tissues is unique and it contains the Rosetta stone of how biology really works in my opinion. I view the absorption spectra of tissues with respect to light as the fingerprint of optimal signaling. This is why hemoglobin and artery walls look almost identical..........when they differ you can bet your ass you have atherosclerosis at some level. When you have inhomogeneity in tissues for any reason.........this tells you light and atoms relationship to time is off and time is altered and can be macroscopically measure in telomere lengths and ubiquitin marking levels. As I mentioned in the June 2015 webinar..........Time is a function of the interaction of light and atoms at surfaces.

    Now you can see how atherosclerosis manifests at its most fundamental levels.
    Last edited: Jul 18, 2015
    Joe Gavin likes this.
  4. Jack Kruse

    Jack Kruse Administrator

    Now back the skin surface..........most people would think it is nuts to blame the the skin as a cause of atherosclerosis..........but consider this:

    Ross Whitehead, Ph.D. candidate at the University of Saint Andrews in Scotland and lead author of new research published in PLoS ONE on the affect of diet on appearance, and his colleagues wanted to know just how small a shift in diet is required to see that healthy carotenoid glow. They followed 35 college students for six weeks, keeping tabs on their diet as well as measuring the color of their skin. What they failed to do is control for the light their skin saw..........but the results they posted were about the color of their skin: Most of you now know color is tied to frequency of light interaction........and this is how foods and sunlight work in unison and why skin color and atherosclerosis maybe linked. If you have yellow and red skin you are more healthy? Why? Yellow is a complementary color of blue light and red light increases RBC's mass and it increases arterial health because both hemoglobin and arterial walls absorb light best in these frequencies..........How is that for homology!

    They subjects who, on their own, chose to eat more animal fats or seasonal fruits and vegetables showed increased carotenoid pigmentation on the surface of the skin where light interacts to control the optical signaling of eNOS. So wellness is tied to yellower and redder skin and not a pale skin like your dermatologists will pound into your brain. What color does your skin get with UV light exposure? Sunburns are pink to red are they not? Still think the sun is bad?
    Joe Gavin likes this.
  5. Jack Kruse

    Jack Kruse Administrator

    One final point.......why has Terry Wahl's advocated veggies and plants for her template for MS? This is why. MS patients have altered carotenoid production in the skin and this is why Vitamin D3 is low across the board in all MS patients. They also have serious eye diseases linked for the same reason. She misses this boat too. Most people think carotenoids are a fruit veggie story.........NOT TRUE. They are deeply tied to seafood and animal fats because of the heavy link to PUFA's. I will remind you all that DHA is a PUFA.

    Therefore anyone who tell's you a healthy skin is about eating fruits and vegetables, in isolation is dead wrong. Carotenoids travel through and are stored in our bodies with the help of these most critical fats. A 2005 study found that pairing carotenoid-rich foods, like shrimp with avocados or avocado oil, which are also high in unsaturated fats, improved absorption into the surface skin and deeper tissues..........so light can do its thing.
    jenaf, Joe Gavin and thisbirdhaswings like this.
  6. Jack Kruse

    Jack Kruse Administrator

    This entire thread points out why clinicians like myself who use pulse oximeters have found this iron clad result in patients:
    Increased blood glyco-hemoglobin A1c levels lead to overestimation of arterial oxygen saturation by pulse oximetry in patients with type 2 diabetes. All diabetics are pseudohypoxic and we seem to not understand why?

    Chronic blue light exposure is the reason because of the spectral pattern of hemoglobin.
  7. Jack Kruse

    Jack Kruse Administrator

    So what do good surgeons and anesthesia personal do when they are taking care of a patient with severe T2D or high blood sugars? They don't rely on a hemoglobin O2 sat and suggest getting an arterial blood gas analysis instead because it will be far more accurate for type 2 diabetic patients with poor glycemic control during the treatment of hypoxemia.

    A high HbA1c is a very direct optical sign of severe pseudohypoxia at the skin level and developing at the deep intracellular level around the mitochondrial respiratory proteins.

    Glycation increases hemoglobin-oxygen affinity and reduces oxygen delivery to tissues effectively. So this menas if you use an optical signal like a pulse oximeter alone to check blood saturation the reading is faulty because while O2 is high in the blood it cannot be released to tissues because of the glycation. This means glycated Hb is less paramagnetic than normal un-glycosylated Hb.
    Last edited: Jul 18, 2015
  8. Jack Kruse

    Jack Kruse Administrator

    Glycosylated Hb is produced via a non-enzymatic reaction between the free aldehyde group of glucose or other sugars and the unprotonated form of free amino groups of hemoglobin. Today in medicine we know definitively that chronic hyperglycemia accelerates the accumulation of advanced glycation end products (AGE) in the skin collagen, which produces a specific autofluorescence feature. What we don't realize is how this pattern manifests in many diseases. The skin of diabetics is thicker because thick skin is an adaptation to strong light signals in foods. Carbohydrates grow in stronger light seasons and as such it thickens the skin to protect the skin from summer time high UV wavelengths. In diabetics who get thick skin from altered blue lit environments, foods, or technology screens, the thickened skin emits light by absorbing specific wavelengths light and this can interfere with the accuracy of pulse oximetry. Humans should have thicker skin in equatorial or summer time environments and thinner skin at colder polar regions where UV light is sparse by natures design. So if you are a modern human who lives at the pole eating carbs all day and watching Netflix and using your tech gear you can affectively develop T2D and thick sick. If this persists you can eventually develop atherosclerosis via the mechanisms in this thread. T2D is a toxic blue light disease........the carbs are just additive to the fire that blue light causes on our surface tissues.
  9. 1. Wow - so arteriosclerosis is similar to Alzheimer’s and prion diseases as it’s root cause is an altered light spectrum and protein mis-folding is that right? I love the homology. Very cool how you tie it all together!
    2. I’ve learned over the 4+ years not to dismiss any of your ideas. It seems that as the blog goes on, and more context becomes apparent and my mind has more time to grapple with a concept, the ideas that I didn’t completely make sense blossom.
  10. n........Blue light destroys the signaling optically. Food can give you sulfur but you need the proper light signal to make use of it!

    Seneff believes and has argued that an underlying deficiency in Ch-S, is due principally to insufficient dietary sulfur. I do not buy this. I think the largest components is a lack of the appropriate IR and UV signals from the sun in the AM that is the most critical component. Many papers have shown that inadequate sun exposure to the skin leads, over longer timescales, to severe depletion of cholesterol and sulfate in many tissues. This loss is ADVANCED ...

    You are right, she totally misses the light connection.
    How weird, as she herself is talking about sun light being responsible for the sulfatation of cholesterol in skin, and sulfated Vit d not being the same as Vit D pills- (hence the tensegrity 7 connection) in the video Billy posted:

  11. Jack Kruse

    Jack Kruse Administrator

    Mitch I told you all these principles are going to explain things that modern science is perplexed about because when you know fundamentally how things work.........then the science begins to make sense of our observations.
  12. Krapule

    Krapule New Member

    Falsely elevated SaO2 in diabetics... Again learning new stuff! Going to test this in the next few days
  13. Jack Kruse

    Jack Kruse Administrator

  14. Krapule

    Krapule New Member

    It is known, that in patients with diabetes mellitus (DM) the glycated haemoglobin (HbA1c) concentration is increased in comparison with healthy subjects (Marschner and Rietbrock, 1994). In HbA1c oxygen affinity is increased and this causes impaired oxygen release to tissues (Iino et al, 1997
    is this what you're referring to?
  15. Lahelada

    Lahelada New Member

    Rosacea is also in that mix somewhere,is it not.A permanently brewing "sunburn" if you will. ( ?)
  16. Jack Kruse

    Jack Kruse Administrator

    yep.........many things are. But we got to get past the basic biophysics to explode the quantum biology of disease management. I just did that for atherosclerosis here.
  17. I was pleased to see my Hba1c (hope I got that right the letters I mean) was 5.7 when I tested last December. I am 'officially' a T2D. Over the years it hovered around 7.0 or higher. This is a few years in following Dr K's protocols. And following them a bit un-evenly - now as best as I can I try to put it 'all' together and I seem to feel a kind of increase in well being like I am firing on all or at least most cylinders. Anyway it was gratifying to see that number not that it is so great. But I hope when/if I test again it will be tending towards 5.0
  18. Jack Kruse

    Jack Kruse Administrator

    good sign Pat.........real good.
  19. JanSz

    JanSz Gold

    Glycosylated Hemoglobin (Hemoglobin A1c)=5.7
    what is your fasting insulin?

  20. JanSz, I havn't done any other tests. To be honest I don't even check my fasting blood sugar.............I am missing a 'part' for the meter etc. But I really should do that, in fact thanks JanSz this will spur me to at least do that................

Share This Page