Dr. Jack Kruse

HOW THE EYE CONTROLS METABOLIC RATE

Added 2017-07-17 15:43:22 +0000 UTC

Mito-Hack number one to complete based upon this modern habit to break: "Scroll and bowl". See picture above to get a proper visual. The blue light of the phone directly effects the mitochondrial colony in your central retinal pathways and choroid that control all growth and metabolism pathways distally in the brain and the leptin receptor. Blue light increases blood glucose irrespective of the foods you eat and this raises your basal metabolic rate, increases your heart rate and BP, while lowering your heart rate variability, and shortens your lifespan as a result. Blue light lowers the amount of water a mitochondrion can make in this situation. When a lowered amount of water is created by a colony of mitochondria in you this means the tissue it occurs in has a lowered redox potential. A lowered redox potential is a lowered amount of charge. A lowered charge means the DC electric current in cells used to regenerate is much lower and makes disease much easier to manifest in tissues with suffering from the quantum deficit.

We're not designed to be strong or weak by nature. We're designed to provide exactly what the environmental situation calls for.......ultimately versatility. Versility is a function of unlimited possibilities that probability provides life and this is why life is based upon uncertainity. Nature's fabric is quantum and queer and counterintuitive at is core and confuse common sense. As a rule, man's logic excludes the versatility of life from its considerations and this is why man struggles to understand how nature really works.Proof: GAME CHANGER: THE EYE's CHOROID WAS THE TRAP DOOR to slow light down and make things with mass and structure. This causes the pituitary to enlarge to make the hormones in the gland. So a lack of all hormone tells you the quantum process is not optimized for some environmental reason.

I realized physics of light exposure controlled our biology at all levels. I told the world this in Vermont 2017 as the video below shows you in the cites. Within the talk are many more cites for you to read and learn about this science.

Much of what we believe about diet and exercise is based upon many false assumptions because we ignore the effects of light. If nutrition studies are done from season to season why don't we put animals in environments in labs that mimic those lighting environments to study the effects. Any person who observes mammals knows that mammalian appearanxces changes and reflects biochemistry changes in these animals that are entrained by light only. Many changes are also altered by temperature variations too. So it raises the point how can anyone infer anything about growth and metabolism if your experiments never controlling for variable changes that occur in seasons with respect to light and temperature? What if the light in the lab was not full spectrum sunlight, could that alone make a difference? Most researchers appear to be unaware that mammals normally do this seasonally as their environments change. As light changes, it affects the basal metabolic rate of circumpolar mammals via the solar spectrum and temperature variation. Those two environmental changes are capable of changing the coats of these mammals their their adipocytes below the skin to act differently than they do in summer months at these regions.

The reason this science is tough to get is because no one really understands the leptin-melanocortin pathways with respect to a varying light and temperature gradient. Neither are controlled for in biology or the nutrition studies so they are missing in all experiments. We see variations in all studies of plants and animals. Everyone knows you cannot naturally grow roses in Alaska. It hard to understand something when you do not realize its true quantized function.

All biologic scaling is non linear because the light we use to control metabolism is also non linear. The most non-linear part of the solar spectrum is UV light. It also turns out coupling rates in mitochondrion are also non linear because of the geometry of the cytochromes where the Fe-S couples are found. The only part of the visible spectrum that is capable of non linear optics is UV light (purple light) It turns our all biologic scaling reflects the underlying quantum principles in UV light. Not even the physicists seem to realize this link as the podcast linked in cite 3 shows below. My members of my website will find biologic scaling (Kleiber's law) an interesting discussion in reference to the discussion of the eye. Why? Mice have massive metabolic rates and elephants do not. Why? The reason is simple to grasp for a "mitochondriac". Metabolic rate is tied to the amount of coupling or uncoupled efficiency in a colony of mitochondria. This is measured as a function of heteroplasmy rate in those tissues. Mice are nocturnal uncoupled animals and elephants are tropical coupled mammals who eat nutrient poor foods under the powerful influence of UV light. Uncoupled animals need to eat more to make more heat. Coupled mammals need to eat less because they are tightly coupled and can use UV light to make ATP without any extra food. All mammals who are circumpolar/higher latitudes have large uncoupling efficiencies and these physicists missed these key links in their podcast discussion. Dr. Doug Wallace's work has point this out over 30 years now, but no one seems to make the connection. They also missed out why these facts also link to the size and shape of the scaling laws with the arterial tree in capillary beds in mammalian tissues where light is harvested from the sun. The funny part of this situation is one of the researchers clearly knew that uncoupled haplotypes can lower their metabolic rates using COLD and UV light. This is the basis of the Cold Thermogenesis-6 blog at my website. (www.jackkruse.com) UV-A and IR-A light from the sun is what causes by dermal pooling in the skin and the choroid to cause local nitric oxide (NO) release. Who are the scientists who proved this link first in biology with some key observations? Mayer, Lavoisier, and Dr. Doug Wallace. I covered this unique connection in my July 2017 webinar at my website.

The choroid, also known as the choroidea or choroid coat, is the vascular layer of the eye, containing connective tissue, and lying between the retina and the sclera. When this "coat" changes it affects the Tarkovsky effect of the retina below and above. This affects the Fe-S couples in the mitochondrion to alter spins and free radical signalling (July 2017 webinar). The human choroid is thickest at the far extreme rear of the eye (at 0.2 mm), while in the outlying areas it narrows to 0.1 mm. Choroidal thickness (CT) increases in childhood obesity. The thickeness occurs prior to the fat mass, why? Anything that loses energy gets bigger as a result. Think about you sprain ankle, your heart after heart failure, or a star that is dying. All get bigger as they lose energy. So this means as the eye is blocked from UV/IR light FOR ANY REASON, we should expect CT to happen followed by obesity and myopia, retinal tears and AMD as they person ages. Findings revealed that adiposity causes a significant increase in CT, and it may be related to ocular complications. When we use glasses, sunglasses or contacts we change the spectral density and energy density to the choroid of the eye. Melanopsin happens to be in the outside part of the retina that the choroid happens to bring blood flow too. This means that choroidal thickness is a sign of poor melanopsin regeneration and poor melatonin production in the eye. The choroid of the eye is primarily a vascular structure supplying the outer retina where the non visual photoreceptor, melanopsin resides. Melanopsin control all growth metabolism functions in the central retinal pathways that connect the retina to the SCN and to the leptin receptor. This is where obesity starts. You think Gary Taubes or any food guru understands this at this detailed level? The choroid has several unusual features: It contains large membrane-lined lacunae, which, at least in birds (high mito capacity like humans), function as part of the lymphatic drainage of the eye and which can change their volume dramatically, thereby changing the thickness of the choroid as much as four-fold over a few days (much less in primates). It contains non-vascular smooth muscle cells, especially behind the fovea, the contraction of which may thin the choroid, thereby opposing the thickening caused by expansion of the lacunae. It has intrinsic choroidal neurons, also mostly behind the central retina, which may control these muscles and may modulate choroidal blood-flow as well. These neurons receive sympathetic, parasympathetic and nitrergic innervation. This controls tone in the vagus nerve and paraventricular nucleus. This is where adrenal fatigue begins people! It begins in the eye and not the gland or in your gut.

The choroid has several other functions: Its vasculature is the major supply for the outer retina; impairment of the flow of oxygen from choroid to retina may cause Age-Related Macular Degeneration (AMD). The choroidal blood flow, which is as great as in any other organ in humans, may also cool and warm the retina which is important in how it operates with variable light frequencies from the sun as the diurnal variation in light occurs on a latitude altitude basis. In addition to its vascular functions, the choroid contains secretory cells, probably involved in modulation of vascularization and in growth of the sclera. Finally, the dramatic changes in choroidal thickness changes are capable of moving the retina forward and back, bringing the photoreceptors into the plane of focus (eye camera function), a function demonstrated by the thinning of the choroid that occurs when the focal plane is moved back by the wearing of negative lenses, and, conversely, by the thickening that occurs when positive lenses are worn by a person. This changes the Yarkovsky effect in the retina and this effect changes how protons precess in the mouth of cytochromes in mitochondria. Any time we alter the spin of electron and protons it changes the free radical signals that can occur in those tissues. This is how mammals use light to change their physics. Think about that when you put glasses and contacts on your eyes now. It is radically effected on the skin by clothing and sunscreens too.

In addition to focusing the eye, more slowly than accommodation and more quickly than emmetropization, the data now argue that the choroidal thickness changes also are correlated with changes in the growth of the sclera, and hence of the eye because of the amount of dopamine and melatonin are made by sunlight in the retina. Because transient increases in choroidal thickness are followed by a prolonged decrease in synthesis of extracellular matrix molecules and a slowing of ocular elongation, and attempts to decouple the choroidal and scleral changes have largely failed, it seems that the thickening of the choroid may be mechanistically linked to the scleral synthesis of macromolecules due to the variation in solar frequencies. Thus , the choroid maybe the key player and be the most important role with sunlight to give humans homeostatic control of eye growth, and melanopsin function and, consequently, in the etiology of myopia and hyperopia and circadian diseases that can ruin mitochondrial function in the RPE of the eye. As the picture below show small amounts of UV light getting through the lens into the choroid is critical in the eye.