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Guru, where is this from?the preferred ratio is 10 IU D3 : 2 mg+ MK-4.
I don't remember.Guru, where is this from?
I didn't know what to reply:
- Is Vitamin D Supplementation Even Neccessary
1-1.5 mg K2 MK-4 orally for each 30-35 ng/mL of 25(OH)D. Unsure how that translates into topical amounts. Also need to ensure sufficient vitamin A (RDA), magnesium, and calcium (at least 1:1 ratio with phosphorus; 0.75:1 if 25(OH)D is near/at 100 ng/mL).Can anyone comment on how much vitamin k one might need to balance out approx 3-4 drops of Calcirol daily? I tend to eat a lot of grass fed butter, so I’m not sure how that factors in, but I also use a few drops of estroban about 2 times weekly. I have noticed what I perceive to be adrenaline symptoms lately and lack of ability to sleep 7 hours the last week.
Jorge, you know what goes well with the Rolex? No, another one would be weird, especially on the same arm. A Montblanc.
- Mechanisms of Neuroprotective Action of Vitamin D3
"Although affinity of [] receptors to calcidiol is ~700 times less than to calcitriol, calcidiol concentrations in blood are much (700-1000 fold) higher than those of calcitriol [1]."
"Traditionally, vitamin D3 was considered as a hormone-regulator of Ca2+ and phosphate homeostasis [1, 3, 18]. However, results of recent studies provide convincing evidence on the role of vitamin D3 in other biochemical processes in various tissues including the nervous system [2, 3]. Physiological concentrations of calcitriol in brain are around 10 pM; this vitamin can cross the blood–brain barrier and bind to nuclear vitamin D3 receptors in the brain [19, 20]. Nuclear vitamin D3 receptors have been found in brain neurons, glial cells, spinal cord, and the peripheral nervous system [20-24]. Membrane vitamin D3 receptors have also been identified in the brain [25], which also contains enzymes of biosynthesis and metabolism of active forms of vitamin D3 (figure) [6, 26]. So, vitamin D3 can be considered as para- and autocrine hormone neurosteroid playing an important role in the nervous system [3, 4, 23, 27, 28]."
"The neuroprotective effect of vitamin D3 is associated with reduction of Ca2+ level in the brain [3, 27, 29]. High level of this ion increases manifestations of neurotoxicity [8], which is attenuated by administration of calcitriol [27, 29]. Vitamin D3-induced decrease in brain Ca2+ may involve two distinct mechanisms. Calcitriol stimulates expression of Ca2+ binding proteins—parvalbumin and calbindins D9k and D28k [11, 14, 22, 30, 31]; it also inhibits expression of L-type Ca2+ channels in hippocampus [11, 14]. Both effects protect neurons against toxic damage by reducing cell calcium [11, 22, 30]."
"The second mechanism of the neuroprotective action of vitamin D3 is related to inhibition of brain γ-glutamyl transpeptidase, the key enzyme of glutathione metabolism [3, 19]. Increasing antioxidant defense by increasing brain glutathione, 1-100 pM calcitriol decreased hydrogen peroxide and exerted a neuroprotective effect during brain damage caused by iron and zinc ions [32, 33]. Neuroprotective effect of calcitriol was also demonstrated using experimental brain ischemia, administration of glutamate, 6-hydroxydopamine, and other neurotoxic agents [8, 27, 29, 34]."
"The interaction of vitamin D3 with reactive oxygen and nitrogen species is also important for neuroprotection. Nanomolar concentrations of calcitriol (0.1-100 nM) protected neurons against direct effects of superoxide and hydrogen peroxide [29, 33, 35]. However, reactive oxygen and nitrogen species modulate effects of vitamin D3: they inhibit association of nuclear vitamin D3 receptors with DNA; singlet oxygen, superoxide, and peroxynitrite cause irreversible inhibition, whereas the effect of peroxide is partially reversible [36]. In contrast to these reactive species, nitric oxide causes reversible inhibition of receptor association with DNA. This suggests that nitric oxide (NO) might act as a natural modulator of genome effects of vitamin D3 in the brain [36]. Calcitriol can reduce NO level by inhibiting expression of inducible nitric oxide synthase in the spinal cord and brain [3, 19]. Thus, one of the important mechanisms of neuroprotective action of vitamin D3 involves inhibition of production of an oxidant (NO) molecule in the brain [3]."
"The neuroprotective role of vitamin D3 is also associated with neutrophin induction [32]. In brain neurons and glial and Schwann cells, calcitriol stimulates expression of nerve growth factor, NT3 neurotrophin, glial neurotrophic factor, and also neurotrophin receptor p75NTR [4, 21, 22, 28, 34, 37, 38]. Calcitriol stimulates neuritogenesis and its deficit results in decreased expression of p75NTR and the neurotrophins [18, 27]. Neurotrophin induction underlies the neuroprotective effect of vitamin D3 in brain ischemia [13] and the general anti-neurodegenerative properties of this vitamin [3]. For example, D3 prevents death of dopaminergic neurons in experimental models of Parkinson’s disease in animals [7, 29, 34]. The development of Alzheimer’s disease is characterized by significant reduction in nuclear vitamin D3 receptors [31]. Administration of vitamin D3 (accompanied by induction of nerve growth factor) decreases the progression of Alzheimer’s disease [12, 29]. Chronic administration of vitamin D3 to rats decreases degenerative processes in hippocampus during aging [20]. This suggests the importance of antineurodegenerative activity of vitamin D3 for manifestation of its neuroprotective effect."
"Results of recent studies provide convincing evidence for involvement of vitamin D3 in immunological processes protecting the nervous system [16, 39, 40]. In the central nervous system, calcitriol plays the role of an immunosuppressor. It acts as inducer of anti-inflammatory cytokine interleukin-4 and transforming growth factor; calcitriol also decreases expression of proinflammatory cytokines interleukin-6, tumor necrosis factor, and macrophage colony stimulating factor [19, 41-43]. Calcitriol decreases expression of proteins of major histocompatibility complex class II and cofactor CD4, which play important roles in autoimmune processes in the nervous system [3, 39]. In a model of experimental allergic encephalomyelitis (in mice or rats), calcitriol inhibited autoimmune damage of nervous system, whereas deficit of this vitamin increased the autoimmune damage [19, 39]."
What it already does when you supplement the parent substance, but less controlled for skipping regulatory steps, although it can still be degraded. Killcidiol is also active (as implied in the first sentence quoted above) and stays in the body for longer, a sharp elevation in killcitriol will be cleared fast and signal decomposition of killcidiol. It would be amalgam to poisonoic acids supplementation.@Amazoniac what do you expect activated d3 aka calcitriol supplementation to do in healthy subjects
What it already does when you supplement the parent substance, but less controlled for skipping regulatory steps, although it can still be degraded. Killcidiol is also active (as implied in the first sentence quoted above) and stays in the body for longer, a sharp elevation in killcitriol will be cleared fast and signal decomposition of killcidiol. It would be amalgam to poisonoic acids supplementation.
- Calcirol - Liquid Vitamin D3
You can find decent amounts of killcidiol in foods, making it possible to appear to nature if you want. In spite of eventually being converted, killciol seems better for being mostly inert and because it supports Rolex, Montblanc and a bulgarian's finesse. There are discussions on this topic:
- Is calcifediol better than cholecalciferol for vitamin D supplementation?
I guess that the system of control is not adapted to these odd inputs, it can make the situation worse. It will be cleared fast and call for more to maintain a desired concentration, but the previous excess signalled the degradation of the original metabolite; you can end up low on both toxins. But depleting toxins can't be a bad thing, it's a dream therapy.what do you think of calcification risks? also are you saying theres negative feedback?
this is synthetic calcitriol im talking about, bypassing the mostly biologically inert to detrimental d3 oral supp conversion pathway
I guess that the system of control is not adapted to these odd inputs, it can make the situation worse. It will be cleared fast and call for more to maintain a desired concentration, but the previous excess signalled the degradation of the original metabolite; you can end up low on both toxins. But depleting toxins can't be a bad thing, it's a dream therapy.
The risk of unwanted calcification should increase, but the same protective factors apply to it as well. Example:
- Magnesium Modifies the Impact of Calcitriol Treatment on Vascular Calcification in Experimental Chronic Kidney Disease
It's one of the justifications to develop analogs of killcitriol that can exert some of its functions while being less impacting on killcium, another toxin whenever supplemented since leads to instant killcification of soft tissues followed by premature death; extremely toxic!!1thanks for that - and good tip on mag
I guess i just want to give the VDR receptors a good hit and oral cholecalciferol aint gonna do that.
calcifediol might be a better option being up the chain like you suggested