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Why does blue light cause insulin resistance? Ans: Melanopsin.

Discussion in 'Educating Doctors' started by Jack Kruse, Aug 9, 2018.

  1. Jack Kruse

    Jack Kruse Administrator

    The realization of just how far behind nature I was in 2003 described in a simple math analogy of my life. Consider the plight of any clinician my age now trying to change within this paradigm and you'll see how hard it truly is. I graduated from college in 1986. In the 31 years since then the amount of biological information has increased 16 fold; during these 4 decades, my capacity to absorb new information has declined at an accelerating rate according to neuroscientists (if you believe them) and now is at least 50% less than when I was a medical student. If one defines ignorance as the ratio of what is available to be known to what is known, there seems no alternative to the conclusion that my ignorance is at least 25 times as extensive as it was when I got my bachelor’s degree. Although I am sure that my unfortunate condition comes as no surprise to my students and younger colleagues, I personally find it somewhat depressing looking at the math. My depression is tempered, however, by the fact that all biologists, young or old, developing or senescing, face the same melancholy situation because of an interlocking set of circumstances. But does this situation stop me from being optimistic now that I am inside my sixth decade? No.

    The result of any project is not an endpoint to your life unless you are actually going to die at the end of the project.

    The outcome of a project or life event opens up a new door, path, or change.

    And whether the project succeeds or fails by your standards doesn’t actually matter to the black swan. It still leads you to the next event in your life.

    And while it is true that each outcome leads somewhere different, you don’t actually know whether the success or failure door is the better one to go through.

    Each result in your life is just a fork in a path that is endlessly forking. Nature is a pattern of forced decision making pathways for living creatures. This is why life remains dynamic and evolution really exists. And it is impossible to predict where it is leading until you understand the steering currents present in the environment at that present moment.

    We need to begin to treat bad fortune with the same equanimity as you treat good fortune. Bad or good information is just that........information. Use it properly and you will still win when you understand how the steering currents of nature works on us.

    And go do something big. Focus. Work hard. Aim for an outcome, if you want. But know that it’s just a tool to use to motivate yourself, not something that will make or break your life. There will be plenty more projects and outcomes afterward for the black swan mitochondriac. this is why hard things become OUR way. Discomfort and bad outcomes are the wind in our sails that allow us to tack a different course in our journey to gain Optimal.
    drezy, Phosphene, Petrad and 2 others like this.
  2. Jack Kruse

    Jack Kruse Administrator

    Bart Wolbers posted an interesting blog: https://www.naturebuildshealth.com/blog/iron

    My answer:

    Iron's toxicity is mediated by sunlight and few people seem aware of it. the first steps of heme synthesis begin in the mitochondria in humans. Simcox JA, Mitchell TC, Gao Y, et al. Dietary iron controls circadian hepatic glucose metabolism through heme synthesis. In a series of elegant studies, they show that higher iron intake, and consequently higher hepatic iron, was associated with the change in the circadian rhythm of glucose and gluconeogenesis mediated by the repression of key gluconeogenic enzymes, PEPCK, and glucose-6-phosphatase (G6Pase).

    The effects of iron were mediated by increased oxidative stress, resulting in increased peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) transcripts and protein levels; induction of aminolevulinic acid synthase 1 (ALAS1), the first enzyme for heme synthesis; and an increase in total heme and heme B in the liver. The mechanism of the repressive effect of iron was shown to be the requirement of heme for nuclear receptor subfamily 1 group d member 1 (Rev-Erbα) to bind nuclear receptor corepressor 1 (NCOR) to form a repressor complex without any change in its protein levels, instead of increasing hepatic heme by administering aminolevulinic acid, thus bypassing ALAS1 or by feeding heme repressed gluconeogenesis. Here is more food for thought: an endogenous ligand of Rev-erb is heme (the iron-binding element in red blood cells). RBC's have a serious diurnal cycle. Heme is degraded into bilirubin. Elevated levels of bilirubin cause jaundice in kids born from parents who germlines are blue light toxic. The older treatment for jaundice was exposure to UV light but today's treatment of neonatal jaundice is now exposure to blue light in NICU's. This has been associated with pigmented skin and higher risks of skin and ocular melanomas as the kids get older because of the stimulatory effect of blue light on melanocytes. Blue light is a major regulator of circadian rhythms and Rev-erb is an executive-level player in this game. When heme is degraded carbon monoxide (CO) is made. CO prevents Clock/Bmal1 from binding to DNA. This binding Inhibits this process and throws off numerous other circadian rhythms in the liver. This is why blue light exposure is causative in most cases of diabetes. When you add in the melanopsin issue it is no surprise why diabetes is now explosive globally. In humans, there is reciprocal regulation of carbon monoxide and the circadian clock mechanism. (Klemz et al., 2016)

    Bart seems very worried that eating more iron means more diabetes. That science has also been done and it is not true. The study by Simcox et al. underscored an important feature of chronobiology. A change in dietary iron did not perturb the periodicity of the chronome and it only impacted the amplitude of expression. The periodicity of expression of transferrin receptor, ferritin, PGC-1α, ALAS1, PEPCK, or G6Pase did not change and peaked at zeitgeber time (ZT) 10 and is likely related to activity and food intake. The key is the LIGHT that food was eaten under. If you eat that TOMAHAWK steak at 10 PM under LED light then being a carnivore could be an issue, not because of the steak but because of the effect of light. Most human-carnivore prior to 1879 never had to worry about this because we have no artificial light. I'm glad Bart post this because I hope he slays this dragon of bullshit because it once again shows my thesis light always trumps food nutrients in chronobiology always exists. Food is not the primary driver in anything. It just appears this way when you are missing the key data as this post points out.

    The sequence of peak expression of ALAS1 at ZT10, followed by heme concentration at ZT12 and of heme oxygenase 1 (HO1) at ∼ZT18 ensures the tight regulation of the cellular concentration of heme at the mitochondrial level. People keep forgetting that heme is a mitochondrial process and blue light causes melanopsin dysfunction and destroys iron-based photoreceptors. High dietary iron was associated with higher peak expression of PGC-1α, ALAS1, HO1, and the total heme in the liver, but it never causes a problem unless the toxic light is present. The antioxidants (SOD1 and catalase) peaked at ZT6. These data point to the exquisite regulation of diurnal rhythm by central oscillators tied to LIGHT, not the diet.

    What has Uncle Jack always said in his Leptin Rx?

    SUNLIGHT and food in the morning are most wise and let endogenously produced CO from heme breakdown rhythmically tune the clock in the evening. This is why ALAN has to be absent!!!!! ALAN = artificial light at night.
    KalosKaiAgathos, JanSz and drezy like this.

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