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Granpa John's Optimal Journal

Discussion in 'My Optimal Journal' started by John Schumacher, Jul 18, 2019.

  1. Adding to @Dan2 -> UVB rays are what you want for "vitamin" D production

    upload_2021-3-9_19-34-49.png

    UVB rays are available during your summertime. That is when the sun is greater than 50 degree or higher in the sky. Due to the physics and wavelength of UVB rays it will only penetrate the atmosphere when the sun is above an angle of about 50° from the horizon. When the sun is lower than 50°, the ozone layer reflects the UVB-rays but let through the longer UVA-rays

    upload_2021-3-9_19-37-30.png

    https://blog.insidetracker.com/vitamin-d-sun-exposure-optimize-levels

    Sunlight is a nutrient - https://thepointretreats.com/blog/c...-a-picture-book-of-the-points-latest-retreat/

    https://selfhack.com/blog/dr-alexander-wunsch-on-the-sun-circadian-rhythms-and-light-therapies/

    Dr. Alexander Wunsch - "A Controlled Trial to Determine the Efficacy of Red and Near-Infrared Light Treatment in Patient Satisfaction, Reduction of Fine Lines, Wrinkles, Skin Roughness, and Intradermal Collagen Density Increase" - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3926176/

    So how do you supplement that -> https://forum.jackkruse.com/index.php?posts/296168
     
    Last edited: Mar 11, 2021
  2. Billybats

    Billybats New Member

    Hey Dan and John,

    Both UVA/UVB rays come through. Yaaaay. I already have a farmers tan. Lol. The other thing is that I think my body thinks it's summer. I am wondering if I should eat like it's summer. If my back didn't hurt so much I could work a long time, meaning I am not tired but in pain. I went from a couch potato to physical work, so my body is still adjusting. I am going to the chiropractor and this Sunday a body massage. A word to all, keep moving.
     
    Freebird, Dan2 and John Schumacher like this.
  3. Billybats

    Billybats New Member

    Really? Interesting. I just read this. When I have time I will read this thread from the beginning.
     
  4. Just make sure you're eating plenty of seafood and sea vegetables.
     
  5. Dan2

    Dan2 New Member

    "The other thing is that I think my body thinks it's summer. I am wondering if I should eat like it's summer."

    If you can eat some of the food grown in the greenhouse, that'd be a perfect match.
     
    John Schumacher likes this.
  6. Billybats

    Billybats New Member

    Yes, very good idea and what John suggested along with sirtuin foods. I may be leaving the greenhouse job for a nanny job. The nanny job I can do a lot of outdoor activities with the children, a little bit less physical, using my creative abilities, have fun like a kid and more pay. Lolhahaaaaa I am a work in progress.
     
    John Schumacher likes this.
  7. Billybats

    Billybats New Member

    Hey John,

    This may be a dumb question. When I cut myself the bleeding is short and I almost healed by the next day. Would that mean a good redox.

    Thank you
    Susan
     
    John Schumacher likes this.
  8. You are clotting well. The quick healing is a good sign.
    Redox is a general concept Dr. @Jack Kruse has coined. There is currently no medical definition for it.
     
  9. Billybats

    Billybats New Member

    I thought so. Very cool. Thank you.

    Another thing I came across. Beta-glucan. They were talking about oatmeal and mentioned seaweed was a source. I had no clue. I found that very interesting. Now they say beta-glucan helps reduce cholesterol. Wouldn't that be a bad thing or it only reduces bad, if there really is a bad cholesterol. Cholesterol is confusing to me. It's fat, right? Now if beta-glucan reduces the bad, lolhahaaaaa how does it know it's taking the bad. Obviously there is something that attracts it in it’s make up.
     
  10. Freebird

    Freebird New Member

    Doesn't one get plenty of K2 with grass fed meats?
     
  11. JanSz

    JanSz Gold

    When in doubt check your K2 level.

    ..............
     
    John Schumacher likes this.
  12. Just ask @JanSz -> getting your values, witch tests, etc is valuable basic information; without it, your supplementing completely blind.

    What may help is a basic book "Cholesterol Clarity - What the HDL is wrong with my numbers?" by Dr Eric Westman MD

    Cholesterol is your basic building block for all your hormones. The question maybe what is the make up of your cholesterol?
     
  13. Billybats

    Billybats New Member

    Hey John,
    I was just wondering what cholesterol is and does. I am really not interested in my cholesterol levels. I was asking if cholesterol is a fat, I guess what kind of fat. Your did answer my question. I was wondering how beta-glucan can only reduce bad cholesterol and not good. What mechanism in beta-glucan attracts the cholesterol and whatever else to reduce it. Just really wanted to know the science behind it all.
     
  14. Cholesterol is a steroid hormone lipid-protein. It is the basic building block for all your hormones. https://www.ncbi.nlm.nih.gov/books/NBK513326/
    • Cholesterol is the most common steroid and is the precursor to vitamin D, testosterone, estrogen, progesterone, aldosterone, cortisol, etc.
    • Cholesterol is a component of the phospholipid bilayer and is vital in the construction healthy cellular structure and membrane function.
    • This steroid is found throughout the body including the brain facilitating the electrical activity neurons.
    • It is used by the body as communication messengers throughout all neurotransmitters.
    • Cholesterol is synthesised in large amounts to form the myelin that surrounds the axons.

      Cholesterol is transported to neurons in the form of Apo E complexes in discoidal HDL-like particles, for which seven main receptors have been identified in brain cells that take up cholesterol from these lipoproteins. Apo E is synthesised in the brain, and its transcription is regulated by 24-hydroxy-cholesterol concentrations.

      In the brain and central nervous system, cholesterol synthesis is regulated independently of that in peripheral tissues, mainly by forms of the liver X receptor (LXR).

      Cholesterol and oxysterols are involved in providing neuroprotective effects and lowering neuroinflammation, dysregulation of their concentrations has been noted in many neurodegenerative disorders.

      Most of the lipoproteins in cerebrospinal fluid differ from the nascent poorly-lipidated HDL secreted by astrocytes, suggesting that the latter are modified during maturation.

      Cholesterol esters are major constituents of the adrenal glands.

    • https://opentextbc.ca/biology/chapter/18-2-how-hormones-work/
    • http://www.allnaturaladvantage.com.au/home/wp-content/uploads/2014/11/Oxytocin-and-Cholesterol <- Your sex hormone
    upload_2021-4-14_19-15-15.png

    Cholesterol diffuses across the lipid bilayer of the plasma membrane of all cells and adhere to intracellular receptors within the cytoplasm, organelles and nucleus. It signals pathways for regulation of gene expression and synthesis of mRNA.
    upload_2021-5-12_18-35-45.png

    β-glucan is a polysaccharide found most abundantly in fungal cell walls of edible mushrooms. There are many studies have shown a beneficial effect of the β-glucans; however, the mechanism of action is unknown.

    Fungal β-Glucan in Health and Disease –
    From the very small interactions within human cells to gross human biological functions, cholesterol is vital in every step. Cholesterol is a component of the phospholipid bilayer and is vital in the construction healthy cellular structure and all membrane functions. So, what is it? -> Cholesterol is a steroid hormone lipid-protein. It is the basic building block for all our hormones. https://www.ncbi.nlm.nih.gov/books/NBK513326/

    When investigating any human biological function, what is important to understand is the mechanism of action. Since cholesterol is a fundamental biologically molecule for all steroid hormones, let’s take a look into how cholesterol is used for some of them.

    https://vdmeta.com -> real-time analysis in 84 studies -> Sunlight is an effective treatment for COVID-19.

    When UVB solar light penetrates our derma, the free cholesterol under the skin begins its first transformation to cholecalciferol. Cholecalciferol is shuttled from the lymph to the blood; however, it must be converted in the liver and kidneys into 25-hydroxyvitamin D. This does not always work so well. We know “vitamin” D is vital for immune function. However, so many people are “vitamin” D deficient. There are three main reasons. 1) Their free cholesterol is too low 2) They do not get proper UVB solar exposure 3) They have liver &/or kidney dysfunction. There are now thousands of articles on this subject. Here is one to start with: “Sunlight & Vitamin D” - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3897598/

    https://www.academia.edu/18487482/E...he_Mediator_Responsible?email_work_card=title
    “Vitamin” D is a human hormone - https://courses.lumenlearning.com/wm-biology2/chapter/vitamin-d-synthesis/#:~:text=In the presence of sunlight,the vitamin) in the kidneys.

    Toll-like receptors (TLR), NOD receptors stimulates the upregulation of CYP27B1, and further downstream intracrine effects on immune cells including antimicrobial peptide synthesis and increased cell activity. A rate-limiting step in this local synthesis may occur during vitamin D deficiency when there are low circulating levels of 25(OH)D. Indeed, immune cells may require a high level of 1,25(OH)2D3 for optimal functionality. Less well recognized is how polymorphisms in the vitamin D binding protein can influence its binding affinity with 25(OH)D3, the uptake of 25(OH)D3 by immune cells and the subsequent 1,25(OH)2D3 production. Vitamin D binding protein has its own immunoregulatory effects including activation of macrophages and stimulation of neutrophil and monocyte chemotaxis. Many immune cells respond to 1,25(OH)2D3 through the nuclear association of the VDR with the retinoid X receptor and numerous transcription factors. The expression of the VDR is up-regulated in T cells through activation of the T cell receptor, while for macrophages and other cells, cellular differentiation reduces VDR expression.

    Since cholesterol is the precursor for all endogenous human sex steroid biosynthesis, its deficiency may be obvious.

    http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/basics/steroidogenesis.html

    Let’s start with testosterone. Free cholesterol must be converted into pregnenolone and progesterone, which are sequentially converted to DHEA. DHEA must then be converted by the 5α-androstanedione pathway into the sex hormone testosterone. The metabolism of these biofluids is greatly influenced and hindered by cholesterol-lowering herbs (such as red yeast extract) or statins which destroy this pathway.

    Let’s step through this: Within our mitochondria’s inner membrane, a cytochrome enzyme called P450scc oxidoreductase (CYP11A1), cholesterol is converted into pregnenolone by the electron-donated redox in the ATP synthesis.

    The ATP electrons are transported to microsomal forms (i.e. cytochrome P450). It begins by the acceptance of electrons from NADPH. These negatively charged electrons (from NADPH) to the ferredoxin (Fedx) reductase (FeRed) which are used by P450 to convert cholesterol to pregnenolone. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3365799/

    So, what could go wrong with that? -> Cytochrome enzyme P450 deficiency. It turns out P450 is dependent on DHEA which facilitates the flow of electrons to P450. This translates to an inability of P450 to convert progesterone, resulting in hyponatremia, hyperkalemia, acidosis, hypertension, and high concentrations of cortisol.

    What is interesting is our mitochondria’s cytochrome enzyme P450 is also used in the process to convert 17α-hydroxypregnenolone to DHEA. This process also uses the NADPH pathway as described above. https://www.researchgate.net/public...released_intermediate_17a-hydroxypregnenolone

    And wonders of wonders DHEA conversion by the 5α-androstanedione pathway into the sex hormone testosterone is also metabolized within the cytochrome enzyme P450. https://sci-hub.se/10.1023/a:1007124417566

    Once the cholesterol molecule has been “rebirthed”, the now testosterone molecule is bathed in cholesterol, adding rich cholesterol receptors onto the testosterone molecule. If this process “fails” or is diminished, the testosterone molecule will not have the cholesterol’s protective mechanism and will fall subject to DHT degradation. https://academic.oup.com/jcem/article/84/9/3217/2864438, https://itestosterone.com/dht-hormone-benefits/ & why you shouldn’t block it.

    So, what is interesting is -> the conversion of NADPH to NADP+ within the ferredoxin reductase “process” is very important, because it is where we get the “energy” electron transport to step the biosynthesis of the cholesterol molecule. And what is this primary energy conversion? -> it comes from sunlight into biomass oxygenic photosynthesis. https://earth.callutheran.edu/Academic_Programs/Departments/BioDev/omm/jsmolnew/fnr_fd/fnr_fd.html But, but, wait a minute, photosynthesis is a plant “thing” right? We now know it’s a fundamental human thing too. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4125832/

    For a nice overview: “Functional Characterization of Cytochrome P450 17A1 (CYP17A1) Gene Variants for their Steroidogenic Enzymatic Activities”
    https://deepblue.lib.umich.edu/bitstream/handle/2027.42/120831/ccapper_1.pdf?sequence=1

    Let’s take a look into this NADPH to NAD+ mitochondria process. NADPH oxidases (Nox) enzymes comprise around 500 amino acids. These lipid proteins are activated by – drum roll please – cholesterol & arachidonic acid (AA). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4221629/ It is well known that Nox2 is not only expressed in macrophages and neutrophils, but also in somatic tissues like epithelial cells through the COX pathway. https://link.springer.com/article/10.1007/s10354-018-0640-4 We know NAD+ is the central role of energy transduction within the mitochondria.

    From the very small interactions within human cells to gross human biological functions, cholesterol is vital in every step. It is very anti-inflammatory. Nature uses it to “calm” the fire of inflammation in our body. It is often “the first responder at the scene of the crime”. Whether, it’s a cardiovascular issue, metabolic issue, digestive issue, brain or cognitive issue, muscle tissue injury, cholesterol is there in its various forms to mediate and facilitate healing.

    Ok, so cholesterol is needed. How did it get villainized? Over 160 years ago, a hypothesis arose that cholesterol was blamed as the primary reason for cardiovascular disease. It was affirmed, in 1856, by Rudolf Virchow who described atherosclerotic plaque as fundamentally comprised of the molecule cholesterol (C27H460). Then the home-run for this hypothesis was headed up by Dr. Ancel Keys with the “China Study” also known as the Seven Countries Study. Dr. Keys “cherry picked” the data and with a little “statistical license”, he “proved” cardiovascular disease was associated with cholesterol.

    In the 1950s, the pathway for cholesterol synthesis in the body had four stages: 1) condensation of three acetate units to form a six-carbon intermediate, mevalonate; (2) conversion of mevalonate to activated isoprene units; (3) polymerization of six 5-carbon isoprene units to form the 30-carbon linear squalene; (4) cyclization of squalene to form the steroid nucleus, with a further series of changes to produce cholesterol.

    In the 1960s, many drug companies pursued R&D money for identify molecules which could inhibit the synthesis of cholesterol from acetyl-coenzyme A (CoA). In 1979, Merck isolated a statin first called mevinolin (then lovastatin), which had a structure similar to compactin from the fungus Aspergillus terreus. Since then, statin drugs have become one of the largest profitable medical products.

    But let’s step back a moment in time to Dr. Ancel Keys and let’s look at one of his disciples - Dr. Ivan Frantz. He developed and conducted a study called the Minnesota Coronary Experiment. In this study, he controlled for “saturated fat” and “vegetable oil”. He recruited seven institutions (hospitals). Patients were separated into matched groups and given either the “saturated fat” diet or the “polyunsaturated fat” diet. The only food the patients got was delivered on trays by the hospital staff, and Frantz arranged the meals to look identical. The study was truly a randomized double-blind design. It went from 1968 to 1973. However, Frantz never published the results. It turns out that after Frantz’s death, the raw data was reviewed and published by Dr. Ransden in the British Medical Journal: “Available evidence from randomized controlled trials shows that replacement of saturated fat with linoleic acid effectively lowers serum cholesterol – but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease”.

    Every study since Keys’ monumental success has had rich pharmaceutical support and wonder of wonders they all say cholesterol is associated with cardiovascular disease.

    However, in recent years there has been a riff in the fabric…

    Serum total cholesterol and risk of cardiovascular and non-cardiovascular mortality in old age - https://bmcgeriatr.biomedcentral.com/articles/10.1186/s12877-017-0685-z
    o The mean age of the 3090 participants was 73.3 (standard deviation, 10.4) years and 63.7% were women. The competing risk regression models revealed that the reduced all-cause mortality was associated with high total cholesterol.

    Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4908872/ High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.

    The Highs and Lows of Cholesterol: A Paradox of Healthy Aging? - https://agsjournals.onlinelibrary.wiley.com/doi/full/10.1111/jgs.16302
    o It is well established that cholesterol for many body functions including nerve conduction, intracellular transport (eg, for the fat‐soluble vitamins A, D, E, and K), as a precursor for important molecules (eg, sex and steroid hormones), and as a part of all cell membranes.

    The triglyceride paradox in the mortality of coronary artery disease - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6343235/ This study found an inverse association between TG levels and mortality risk in CAD patients, which suggests that the “TG paradox” may exist in CAD patients. A total of 3061 patients with CAD were included in the study. The average age was 64.4 ± 10.7 years.

    Inflammation, not Cholesterol, Is a Cause of Cardiovascular Disease –
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986484/

    Ok, so there’s a riff in the fabric of cholesterol reporting. But that doesn’t change the hypothesis that cholesterol is associated with cardiovascular disease. -> Right?

    We know cholesterol is on the first line of defense against inflammation as it serves as an antioxidant within our cells as well as external of our cells. All antioxidants whether it is vitamin E or other antioxidant become damaged as they try to fix the inflammatory issue through the bio-chemical redox process. How many studies now show vitamin E has been associated with cancer? https://cancerpreventionresearch.aacrjournals.org/content/5/5/701 https://news.cancerconnect.com/head...y-be-harmful-in-head-and-neck-cancer-patients “Vitamin E supplements may raise lung cancer risk” -> https://www.medicinenet.com/script/main/art.asp?articlekey=87525

    Why is that? -> oxidative damage of the vitamin E lipid molecule.

    Name the study, antioxidants become damaged and must be shuttled out of the body just like ox-LDL. Does that make antioxidants bad? -> No

    Those publishing the riff in the fabric of cholesterol reporting are being very careful not to cut off their funding support from the pharmaceutical industry. They use words like: Paradox, “We currently don’t know the mechanism of action”, but they also putting in the important qualification: “We know cholesterol is associated with cardiovascular disease.”

    So, what’s a clinician to do with her CVD patients? -> Glycation

    It’s the low hanging fruit and it’s the easiest to work on.

    Although food is not the end-all, it can help. Specifically, a low carbohydrate vegetable diet with some cold-water fish, typically has a low inflammatory response for most people. Of course, a good food sensitivity iGg test will provide better specifics. A good set of antioxidants to help out the anti-inflammatory action of cholesterol including: Astaxanthin.

    Endothelial dysfunction can be assisted with both a Coronary Calcium score and an Ultrasound Bilateral Carotid Arteries analysis. If these are issues, Chelation and/or Pulsed Ultrasound therapies have proven to be successful. https://pubmed.ncbi.nlm.nih.gov/26578361/ However, when these oxidated molecules are broken loose, it is important to provide binders to collect, clean up and help transport them out of the body. These can include: charcoal and chlorella.

    Blood pressure is primarily managed by the renin-angiotensin-aldosterone system (RAAS) system. A Renin Activity and Aldosterone lab analysis will show where in the RASS system it maybe misfunctioning. https://www.aacc.org/science-and-re...aboratory-medicine/2020/aldosterone-and-renin

    Secondarily, high blood pressure can be managed by two endothelial mechanisms for vasodilation -> eNOS and prostaglandin-endoperoxide synthase (PTGS), which is an enzyme that is responsible for formation of prostandoids, such as prostacyclin from arachidonic acid.

    So, when is it time to lower cholesterol? According to recent journal studies -> the higher the cholesterol the better the outcome.
     
    Last edited: Sep 1, 2021
  15. On the subject of fatty acids - It turns out Higher fish intake seems good for you.

    The relationship of EPA with mortality was most pronounced at lower levels and then appeared to plateau at higher levels. https://www.nature.com/articles/s41467-021-22370-2#Tab3

    • The use of fish oil supplements was linked to a lower risk for death from any cause in a study from the UK including over 427,000 individuals.
    • ALA did not reduce CVD mortality
    The study found the higher circulating levels of LC n-3 PUFAs may beneficially affect diverse cellular systems that together could contribute to a reduced risk for death.

    The benefits of these LC n-3 PUFAs were hypotriglyceridemic, antihypertensive, and antiplatelet effects; as well as positive effects on adipocyte biology, endothelial function, and autonomic balance. All of these appear to be mediated by effects on membrane physiochemistry, gene expression, and the production of a myriad of bioactive oxylipins. These fatty acids have been reported to inhibit the mammalian (or mechanistic) target of rapamycin (mTOR) in animal studies showing benefits in cancer, metabolic syndrome, spinal cord injury, and depression. mTOR inhibition extends lifespan in many species and acts as an energy sensor to coordinate gene expression, ribosome biogenesis, and mitochondrial metabolism.

    https://pubmed.ncbi.nlm.nih.gov/26359712/
    https://pubmed.ncbi.nlm.nih.gov/25139562/
    https://pubmed.ncbi.nlm.nih.gov/19185299/
    https://pubmed.ncbi.nlm.nih.gov/32179408/
    https://pubmed.ncbi.nlm.nih.gov/29436695/
    https://pubmed.ncbi.nlm.nih.gov/28419244/

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7565554/
     
    Richard Watson likes this.
  16. Billybats

    Billybats New Member

    Thank yooooooou verrrryyy much. Very interesting to what you both wrote.
     
  17. Last edited: Jul 30, 2021
    ND Hauf likes this.

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