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Discussion in 'Optimal Labs' started by Jenny S, Mar 17, 2020.

  1. Sue-UK

    Sue-UK New Member

    @John Schumacher

    Thanks for the mention of osteocalcin, its had me thinking ...:confused::D

    I've recently watched a programme about fat, and the research on the Hadza tribe shows that women and men eat about 1900 and 2500 calories a day respectively, (which they considered comparable to basal metabolic rate in the west). They don't seem to need to eat more, which the programme, in terms of the conventional CICO model, found surprising because it didn't account for the daily activity including walking an average of 5 miles a day for women and 9 miles a day for men. (It also showed the hunters using a poisoned arrow to shoot prey, before trailing them til the prey dropped, i.e. they didn't seem to do much of things like sprinting).

    What interested me from @Jenny S 's bone scan is how easily the bone in her foot broke. I had a bad fall on Tuesday from slipping on decking whilst carrying plates .. Went down with a helluva smack, with my left knee and foot taking the full brunt before letting go of the plates and my hands hitting the deck too (I have a massive bruise on my left foot and still using a crutch to support the weight of my left leg while my knee heals ...). A painful way of finding out my bones are stronger than I thought ..... luckily I didn't hit my head. :)

    The Hadza absence of many of the diseases like osteoporosis may be partly down to the distance they cover in a day, as well as the sun, and eating enough to maintain their mass. My being overweight may offer some protection to my bones, but I changed a habit at the start of lockdown. Instead of just sunbathing, at the start of lockdown I took to doing barefoot walking around the polytunnels and veg garden part of the field, doing 25 laps .... 25 laps is around 2 miles a day in sunshine or under cloudy or rainy skies. So nearly 5 months of that, plus it being weight bearing exercise because I'm carrying the excess pounds :oops: may be why I've not broken any bones ...(that and fat producing estrogen, another osteoporosis research focus, but excess estrogen is a different problem .....). I've kept it at a plod round to reduce lactate and ROS production, and to make it a multitasking operation ... (walking, getting sun, fresh air, meditative state etc). Change of shape, but no weight loss - perhaps by stimulating osteocalcin, I now have heavier bones ..... :rofl:

    Now going through this ....

    New Insights into the Biology of Osteocalcin
    John Schumacher likes this.
  2. @Sue-UK - I don't know your age, but from the maturity of your writing, I will guess that menopause maybe in your rear view mirror.
    With that said, I believe that "we" know very little about this "better" time of a woman's life.
    She's done with spending all her hormonal energy on reproduction.
    So what's an optimal hormone panel for ladies who have a potential 40 more years?
    We know grounding, IR-A into our bones, into our head (brains), through our chest, into every organ -> is vital for health. UV stimulates and up regulates every known hormone. Nutrients rich in bio-available minerals, and DHEA rich proteins are basic building blocks.
    What are the specific protocols for protecting and building healthy rich mylene sheath over our nervous system?
    I think skinny may not be "the better way", although it helps our emotional vanity.
  3. Sue-UK

    Sue-UK New Member

    I was reading that a third of all hip fractures are seen in elderly men, but many aren't treated or diagnosed because osteoporosis is seen as largely a post menopausal female disease. (I was interested in that as DH is 64, I'm 63 in a couple of months).

    Even for tribes like the hadza, despite the sun, UV, IR, grounding and the lack of blue light at night etc, being too skinny is a risk. It may be that they just don't survive long enough to get the chronic diseases or cancer. Or it could be that the sun and the amount of walking they do are are factors in protection against chronic things like osteoporosis, but not the acute diseases related to semi starvation or malnutrition.

    I've got Matthew Walker's book, Why we Sleep. One of the things I came away with was about the Hazda. If they survive high rates of infant mortality and make it through adolescence, a common cause of death is infection, and intestinal infection is common.

    "For example, the Hazda will face days where they obtain 1400 calories or less, and routinely eat 300 to 600 fewer daily calories than those of us in modern Western cultures. A large portion of their year is therefore spent in a state of lower-level starvation, one that can trigger well-characterised biological pathways that reduce sleep time, even though sleep need remains higher than that obtained if food were abundant."

    I get the odd low dopamine state of "emotional vanity" but on the whole its gone. For chronic "successful" dieters, that paragraph could just as easily be written as

    Humans can face days where they obtain 1400 calories or less, and routinely eat 300 to 600 fewer daily calories because of the modern Western culture's desire for thinness. Although self imposed, a large portion of their year is therefore spent in a state of lower-level starvation, one that can trigger well-characterised biological pathways that reduce sleep time, even though sleep need remains higher than that obtained if food were abundant.

    I'm less troubled by emotional vanity when I'm a "successful" sleeper. :D
    John Schumacher likes this.
  4. Sue-UK

    Sue-UK New Member

    John Schumacher likes this.
  5. Cracking the code of neuronal apoptosis and survival - https://www.nature.com/articles/cddis2015309

    Neuronal apoptosis - A regulator of gene expression, retinoid X receptor (RXR), can boost scavenging cells in their mission to clear the brain of dead cells - https://www.technologynetworks.com/...retinoid-x-receptor-on-stroke-recovery-330399

    BsmI (rs1544410) and FokI (rs2228570) vitamin D receptor polymorphisms, smoking, and body mass index as risk factors of cutaneous malignant melanoma in northeast Italy - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5570607/

    One SNP named VDR taq affects about 27 percent of the global population. Approximately 26 percent of the world’s population has inherited another similar mutation called VDR bsm.

    VDR bsm SNP alterations have Fitzpatrick type 1 skin. The validity and practicality of sun-reactive skin types I through V.
    A qualitative exploration of parental perceptions regarding children’s sun exposure, sun protection,and sunburn. - https://psyarxiv.com/f8brk/download

    GLI1 genotypes do not predict basal cell carcinoma risk: a case control study - https://molecular-cancer.biomedcentral.com/articles/10.1186/1476-4598-8-113 - These results suggest that different GLI1 genotypes alone or in combination with past sun exposure patterns as assessed in this study do not affect basal cell carcinoma risk.

    Most people who have these SNP alterations have Fitzpatrick type 1 skin. This version of skin obviates the need for the SNP alterations. This situation of SNP inactivation with white skin increases mitochondrial energy production when the skin is placed in the sun. The VDR gene provides instructions for making a protein called vitamin D receptor (VDR), which allows the body to respond to vitamin D. This vitamin can be acquired from foods in the diet or made in the body with help from sunlight exposure. Vitamin D is involved in maintaining the proper balance of several minerals in the body, including calcium and phosphate, which are essential for the normal formation of bones and teeth. One of vitamin D's major roles is to control the absorption of calcium and phosphate from the intestines into the bloodstream. Vitamin D is also involved in several processes unrelated to bone and tooth formation.

    The VDR protein attaches (binds) to the active form of vitamin D, known as calcitriol. This interaction allows VDR to partner with another protein called retinoid X receptor (RXR). The resulting complex then binds to particular regions of DNA, known as vitamin D response elements, and regulates the activity of vitamin D-responsive genes. By turning these genes on or off, the complex helps control calcium and phosphate absorption and other processes.

    Although the mechanism is not completely understood, the VDR protein is also involved in hair growth. Studies suggest that this process does not require calcitriol binding.

    My interest (here) is in cognitive function.
    Last edited: Aug 24, 2020
  6. How are you measuring your sleep success?
  7. Sue-UK

    Sue-UK New Member

    The link between neuronal survival and strong bones could be aluminium, and/or silicon. Bone is a storage area for aluminium, but as our bones are constantly being remodelled, there would be a continuous release of aluminium during the demolition phase, which, if the rebuilding phase was slowed, (which would put some safely back in storage) could lead to increased blood levels, at a level higher than the main aluminium detox pathways (urine and sweat) could handle. I've wondered if the storage of aluminium in the bones of the skull would have an adverse effect in terms of things like ROS in a high UV environment, or on hair growth or early greying. But theoretically I could see how we could be exposed to aluminium decades ago, and it still going in and out of bone. Lose the ability to rebuild bone .....:eek:

    With aging, the silicon content of skin drops and that might link to the older we are, the longer we have to stay in the sun to get enough vitamin D. Vitamin D also facilitates aluminium elimination by the kidneys. But if the available silica is "used up" in detoxing aluminium, and its not replaced, then the elimination routes are stalled. It might only take a damaged BBB (nnemf, 5G, head trauma, or something else) for catastrophic consequences in the brain, either from current exposure or from lack of bone rebuilding increasing blood levels. Also aluminium taken in via the olfactory bulb bypasses the BBB anyway .... There's implications to AD, Parkinsons, MS, epilepsy .... I did an 8 month hack last year using silica rich mineral water to reduce body burden of aluminium, I still drink a litre a day as a preventative. As aluminium interferes with osteoblast function and number and leads to lower BMD and weaker bones, that may have been a factor in my not breaking a bone when I fell. :cool:
    John Schumacher likes this.
  8. Sue-UK

    Sue-UK New Member

    Because of our extremes of day length (roughly 16 hours mid summer to 8 hours midwinter), its getting 7.5 hours in summer and 9 hours in winter. Going through the night without needing to get up for a pee, or waking up because of an adrenaline or cortisol spike. Then with roughly 90 minute sleep cycles, 5 would be a minimum, the extra sleep cycle in midwinter is welcome. :) Dreaming, particularly when waking from a dream that seems more detailed, it seems less about what I'm remembering but more that I'm noticing more whilst I'm dreaming, which I then remember IYKWIM.

    Waking feeling rested, and optimistic. At the moment its also the daily physical improvement in my leg .... 5 laps walking round my garden circuit yesterday, slowly without the crutch. 6 this morning and aiming to get a few more in this afternoon. :cool:
    John Schumacher likes this.
  9. Sue-UK

    Sue-UK New Member

    Another possible link goes back to Becker and the perineural system, and the extracellular matrix (ECM). The book Energy Medicine, the scientific basis by James L Oschman talks about the ECM being produced by "generative cells" such as osteoblasts, and also neuroblasts, myoblasts and fibroblasts etc.

    "In terms of evolution and phylogeny, the perineural system is ancient. This system is responsible for overall regulation of the classical nervous system, and for regulating wound healing and injury repair."

    (about Becker) " He has presented evidence that the perineural system actually regulates the operation of the neurons and not the reverse."

    Aluminium toxicosis: a review of toxic actions and effects.

    "Subchronic exposure to Al was associated with reduced population of neural stem cells and hampered cell proliferation and neuroblast differentiation in the brain of mice (Nam et al., 2014, 2016)."

    Then from Silica Water the secret of Healthy Blue Zone Longevity in the aluminium age by Dennis N Crouse PhD, aluminium impairs the body's ability to use stored fatty acids as an energy source by lowering L carnitine levels in the blood. So apart from any effects on obesity, and the ability to exercise etc, I see that as having the potential to disrupt sleep (and therefore cognitive function ....)

    Aside from aluminium, the book also says that silicon increases with age in the kidney, brain, liver, spleen and lung, (which may be protective of those organs from accumulating aluminium?), but silicon decreases with age in the plasma, aorta and other arterial vessels. The impact of less silicon is development of general stiffening and hardening of the aorta and arterial vessels, resulting in higher blood pressure and a greater incidence of fatal coronary heart disease and stroke.

    Big rabbit hole....:eek::D
    John Schumacher likes this.
  10. Sue-UK

    Sue-UK New Member

    I was looking for the circadian rhythm of parathyroid hormone and found this

    (source https://www.semanticscholar.org/pap...rman/a8ec862df6d59642a6ad8f58c4cc1d7882c71a9f )

    Then from
    The Internal Circadian Clock Increases Hunger and Appetite in the Evening Independent of Food Intake and Other Behaviors

    came this chart


    Then from previously reading (about gastrointestinal physiology in relation to sleep), that basal acid secretion in the waking state is minimal in the absence of meal stimulation, but there is an endogenous circadian rhythm of unstimulated basal acid secretion, generally peaking between 10 pm and 2 am.

    So the question is: as most calcium is lost from bone during the night, would a calcium rich snack or drink at around 8 p.m., in line with the circadian rhythm of hunger, blunt the 2 a.m. circadian peak of parathyroid hormone, and be bone protective? :confused:
    John Schumacher likes this.
  11. Sue-UK

    Sue-UK New Member

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  12. Question: Since Osteocalcin and Osteopontin are by-products of osteoblasts, is it possible that there is missing piece in their understanding of Collagen and non-collagenous proteins molecular crosstalk in the pathophysiology of osteoporosis?

    Specifically, I noticed in reading these articles -> I wondered why do the authors feel a higher level of Osteocalcin & Osteopontin increased osteoporosis in postmenopausal women?

    We know bone density function involves the crosstalk between collagen type I and noncollagenous proteins (Transforming Growth Factor-β, Insulin-like Growth Factor-1, Decorin, Osteonectin, Osteopontin, Bone Sialoprotein and Osteocalcin), vitamin D3, K2, the "health" of our cholesterol (that is - it's not oxidized), the "quantum yield" derived from our sun's IR-A stimulation, and kinesthetic flex upon the bones.

    https://www.sciencedirect.com/topics/engineering/noncollagenous-protein see: Cartilage and Bone Regeneration - table 16.4 Extracellular Matrix Proteins in Bone
    Last edited: Aug 30, 2020
  13. Sue-UK

    Sue-UK New Member

    The shift in the sex hormones, particularly if a woman was thin (as fat cells produce estrogen), plus if osteocalcin is released as part of the stress response, the whole bone physiology might be chronically tipped into break down mode. That might have survival value if for example during a famine, because apart from calcium etc, the stored deuterium in bone could be released which could protect against infection. It is one of the reasons I don't buy into deuterium depleting as a lifestyle choice - not enough deuterium may just mean different diseases to when we have too much (or "enough", but its in the wrong place).

    Although its not about a biological process https://www.isowater.com/semiconductor-applications-of-deuterium/ has me wondering about its application in bone …. Its back to silicon again …. then add in phosphate as a potential doping agent (and the problems of excess serum phosphate …)….:eek: My rabbit holes have rabbit holes …. :D
    John Schumacher likes this.
  14. I agree with you on the "deuterium thing".
    Here's my post: https://forum.jackkruse.com/index.php?threads/granpa-johns-optimal-journal.23952/page-3#post-290958
    Sue-UK likes this.
  15. Sue-UK

    Sue-UK New Member

    (From Herrera's book The Human Photosynthesis) "Possibly ATP is just a metabolic intermediate, for instance as phosphate regulator..... "

    Serum Phosphate Is Associated With Fracture Risk: The Rotterdam Study and MrOS
  16. Yes - the article stated, “The findings of our study also suggest that the current upper limit of serum P may be too high”
    It is well known – high dietary intake of phosphorus is damaging. https://www.kidney.org/atoz/content/phosphorus
  17. Sue-UK

    Sue-UK New Member

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  18. Thank you for sharing

    So who likes to fast one day out of the week, or three days once a month, or restricting oneself to one moderate meal per day?
    Autophagy is all the rage right now - books, seminars, "health" coaches, NDs, Functional Medical practitioners - are all jumping surf boards for this "health wave".
    Because... there is good science for it.
    However, I believe it maybe worthwhile to take into consideration the client's current state & history, articulating 1) acute or 2) chronic:

    1) What stage in life (age) for example: Is she in childbearing phase? How is her cycle - length, regularity, per & post "symptoms"?
    • From these data points, we may begin to generalize an "autophagy plan", which includes carbohydrate cycling, protein cycling - these are dependent on her estrogen & progesterone monthly hormone cycling.
    2) How functional is her support group - depending on her children's ages, what is their "health", etc.?

    3) Does she have a disease pathology (acute or chronic); each specific diagnosis have protocols for remediation

    Autophagy can be employed; however a specific understanding of "where" the client is along the path to health, is vital.

    What is your current autophagy practice?
    Last edited: Sep 4, 2020
  19. Sue-UK

    Sue-UK New Member

    In the Ray Peat article on Osteoporosis, it says

    "The outstanding physical-chemical property of bone is that it is a reservoir-buffer of carbon dioxide, able to bind huge amounts of gas into its structure."

    Which implies that with osteoporosis, the reservoir-buffer is reduced (osteoclast = bone loss = reduced mass overnight? Does the release of CO2 from bone help initiate overnight breathing, as its the rise in CO2, not the drop in oxygen that initiates breathing? )

    https://derangedphysiology.com/main...Chapter 115/carbon-dioxide-storage-human-body
    Carbon dioxide storage in the human body

    Although this is about TBI, in the context of sleep, CO2 and protection of cognitive function, there may be some dots ….

  20. Sue-UK

    Sue-UK New Member

    I think there's diseases of starvation, or perceived starvation. "Autophagy" is too broad a term, just adding in the elements of mitochondrial fission and fusion and mitochondrial biogenesis makes it a whole different ballgame..... and potential risk. Fasting for one day a week, or 3 days a month or OMAD is out for me with my context, and would be out if I had osteoporosis. Its too zoo animal for me - on the days I was not eating, I would be reducing overall mass by breathing out CO2. That's OK if I could guarantee that came from burning my fat stores, but otherwise it could be a very risky ….

    I also don't think I could replenish bone mass without regular feeding. At the moment I'm doing the (Alzheimer's doc) Dr Dale Bredesen autophagy idea of 12/3 - 12 hours overnight fast, and no eating 3 hours before bed (that's a minimum, I'm generally doing more than that naturally). I'd extend that as per his protocol if I knew I had the APOE4 gene. Although insulin resistance is a red flag for AD, low insulin can also be a causal factor in AD.

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