raypeatclips
Member
- Joined
- Jul 8, 2016
- Messages
- 2,555
You sure all of this was related? I've woken up from many naps with headaches.
-
By using this site you agree to the terms, rules, and privacy policy.
-
Charlie's Restoration Giveaway #2 (Entire Home EMF Mitigation & Protection Along With Personal Protection) - Click Here To Enter
-
Dear Carnivore Dieters, A Muscle Meat Only Diet is Extremely Healing Because it is a Low "vitamin A" Diet. This is Why it Works so Well...
Rest the rest of this post by clicking here
-
The Forum is transitioning to a subscription-based membership model - Click Here To Read
Click Here if you want to upgrade your account
If you were able to post but cannot do so now, send an email to admin at raypeatforum dot com and include your username and we will fix that right up for you.
Calcirol - Liquid Vitamin D3
- Thread starter haidut
- Start date
You sure all of this was related? I've woken up from many naps with headaches.
goodandevil
Member
- Joined
- May 27, 2015
- Messages
- 978
A 10,000iu/drop formula would be most welcomed, for transdermal application. Health natura's is prohibitevly expensive.
managing
Member
- Joined
- Jun 19, 2014
- Messages
- 2,262
The headache is speculative. But why would it send me into a deep sleep for 2 hrs in the middle of the day?
I had similar reaction when I first time supplemented D, last November. I took 8000 IUs orally, felt that things are going on in my brain and got really sleepy. This reaction went away with later applications.
OP
PTH in the bottom 25% of the range, calcitriol in range, D3 around 50, calcium and phosphorus in range with calcium preferably in the upper 75% and phos
It would depend on the results of these tests in combination as they all affect each other. There is no optimal number for each of them, there is optimal relation. Ideally D3 should not be in a deficiency state, but even that could be OK if say calcitriol is close to upper limit or above it.
OP
Vitamin D lowers cortisol, and this usually leads to sleepiness.
managing
Member
- Joined
- Jun 19, 2014
- Messages
- 2,262
Haha. Seems like everything good lowers cortisol and puts me to sleep (B3 also). It seems as if I am running on cortisol instead of sugar . . .
Mito
Member
- Joined
- Dec 10, 2016
- Messages
- 2,554
....and phos? (phosphorus in the.....)?
OP
Phosphorus and calcium are typically inversely correlated, so if calcium is in the upper 75% then phosphorus would typically be in the bottom 25%.
Amazoniac
Member
Zeus, what are these SFA esters after all? I want to let you know that the guy that copies your products is taking notes.
managing
Member
- Joined
- Jun 19, 2014
- Messages
- 2,262
so what is the conclusion on ADK proportions and which ones can be taken alone and which must be taken together. Starting to seriously supplement D (calcirol) and want to keep everything in balance.
Amazoniac
Member
Not just the kidneys, other cells are capable of doing the activatings as vvcll:
Extrarenal Expression of the 25-Hydroxyvitamin D-1-Hydroxylase (!)
"so far in humans quantitative expression of the functional gene product to a level that contributes to the circulating concentrations of 1,25(OH)2D and acts in an endocrine mode occurs only in disease-activated, tissue macrophages and the placenta. In the former situation production of the vitamin D hormone may be so prolific that the endocrine actions of 1,25(OH)2D at the level of the skeleton are sufficient to promote accelerated bone resorption with a pathological increase in the circulating calcium concentration. The placenta, on the other hand, is capable of providing far less hormone to the circulating pool [13]. Along with the maternal kidney, the placenta is capable of contributing to a rise in the serum level of 1,25(OH)2D during pregnancy; the elevated serum 1,25(OH)2D concentration of pregnancy does not lead to a pathological increase of bone resorption [13]."
"we propose that the more phylogenetically ancient function of 1,25(OH)2D is that of an inflammatory mediator meant to regulate the innate immune response and direct the adaptive immune response to invading microbes. Orthologs of the specific intracellular receptor for 1,25(OH)2D, the vitamin D receptor (VDR), can be found in single cell organisms (e.g., yeast), and both the VDR and its specific ligand 1,25(OH)2D are found in the lamprey eel, an ancient vertebrate lacking a calcified skeleton and teeth [15]; this is evidence that interaction of the VDR with its cognate ligand 1,25(OH)2D plays a role distinct from provision of calcium and phosphate for skeletal mineralization. In its role as a functioning cytokine (see Table 1), 1,25(OH)2D is made locally by inflammatory cells, specifically the macrophage and the dendritic cell [16], to act locally on other immune cells that express the VDR upon activation (Figure 1)."
-
"a woman with chronic renal failure and barely detectable serum 1,25(OH)2D [] increased [her levels] significantly during pregnancy [38]."
"it has been suggested that 1,25(OH)2D made by the placenta is not meant to function as a hormone, but as an immunomodulatory cytokine to i) prevent rejection of the fetus, ii) prevent a graft-(fetus)-versus-host (mother) reaction and iii) promote the orchestrated innate and adaptive immune response to prevent microbial invasion of the fetal-placental unit during pregnancy [40]."
"In conclusion and in concert with current evidence suggesting that placental production of 1,25(OH)2D is not needed for development of the fetal skeleton or the maintenance of maternal skeleton [13], an immunomodulatory role for placental 1,25(OH)2D production seems highly likely [64]."
-
"Barbour et al [18] described an anephric patient with sarcoidosis, hypercalcemia, and a high serum concentration of an active vitamin D metabolite that was detected as 1,25(OH)2D. Subsequent structural studies showed that the hypercalcemia-causing metabolite was 1,25(OH)2D [74], and that the extrarenal source of 1,25(OH)2D was the macrophage [19], the cells that make up a significant portion in the prototypical inflammatory granulomatous lesions characteristic of the disease. More recent work has revealed that macrophage synthesis of 1,25(OH)2D is the consequence of expression of a single gene, the CYP27B1 [75]. As shown in Table 2, clinical evidence for the extrarenal overexpression of the CYP27B1 gene can also be observed in a number of other granuloma-forming diseases, including be lymphomas and other malignancies; for example, immunohistochemical analysis of the human B-cell lymphomas associated with hypercalcemia and raised circulating levels of 1,25(OH)2D in the host suggests that the tumor itself is not a source of the steroid hormone. Rather macrophages adjacent to the tumor are likely to be the major site of 1,25(OH)2D synthesis [76]. Similar observations have been made for other hypercalcemia-causing tumors such as dysgerminomas [41]."
"Like its counterpart in the kidney, the extrarenal CYP27B1 functions as a mitochondrial, mixed function oxidase with cytochrome P450 activity [77]. Using reconstituted mitochondrial extracts it has been shown that electron transfer to the cytochrome P450 and subsequent insertion of an oxygen atom in the substrate 25OHD requires the following: flavoprotein; ferredoxin reductase; an electron source, and molecular oxygen [77]."
"Both renal and extrarenal 1-hydroxylase activities are inhibited by napthoquinones, molecules which compete with reductase for donated electrons and by the imidazoles which compete with the enzyme for receipt of O2 [79]. While the substrate-specificity and enzyme kinetics for the CYP27B1 appears to be the same for both kidney cells and macrophages [78], as just noted the regulation of 1,25(OH)2D synthesis at these sites appears to be very different. For example, as previously noted in Table 1 the macrophage CYP27B1 is not induced by PTH, but it is very sensitive to stimulation by immunoactivators such as lipopolysaccharide [78] and Th1 cytokines, particularly interferon-γ (IFN-γ; [80]). The molecular mechanism underpinning the expression of the CYP27B1 in the human macrophage has recently been elucidated employing ex vivo models of tuberculosis, another prototypical human granuloma-forming disease (see below)."
"microbial killing was more efficiently achieved with the pro-hormone 25OHD than with 1,25(OH)2D at similar extracellular concentrations, indicating that the robustness of the human innate response to microbial challenge is dependent upon the serum 25OHD status of the host"
"Although the existence of extrarenal production of 1,25(OH)2D by the human placenta and disease-activated macrophages has been recognized for many years now, the potential for this vitamin D metabolite to function normally in the host as something other than a calcium-regulating hormone is becoming more likely. The importance of 1,25(OH)2D as a normal functioning, locally-produced, locally-active immunomodulatory molecule in humans in vivo at the fetal-maternal interface in the placenta and/or at other sites of microbial/cancer cell invasion has been stymied by our inability to measure changes in the local concentration of 1,25(OH)2D at sites of immunoactivity in vivo. While there are examples of step-up gradients in the concentration of 1,25(OH)2D between the serum and loculated inflammatory sites, like the pleural fluid of patients with active tuberculosis [104, 105], the potential for 1,25(OH)2D to balance the innate and adaptive immune response to foreign agents (e.g., fetus, mycobacteria, etc., see Figure 2) at a micro-scale in vivo remains real but unproven. Breakthroughs in the field await: 1] prospective clinical trial evidence that provision of 25OHD substrate to vitamin D-deficient individuals will i) improve maternal-fetal outcomes and/or ii) limit disease or protect against microbial infection in exposed individuals (e.g., close family contacts of patients with active tuberculosis); and 2] development of a means for detecting changes in the level and bioactivity of 1,25(OH)2D in the local intra- and extracellular inflammatory microenvironment of the host."
Extrarenal Expression of the 25-Hydroxyvitamin D-1-Hydroxylase (!)
"so far in humans quantitative expression of the functional gene product to a level that contributes to the circulating concentrations of 1,25(OH)2D and acts in an endocrine mode occurs only in disease-activated, tissue macrophages and the placenta. In the former situation production of the vitamin D hormone may be so prolific that the endocrine actions of 1,25(OH)2D at the level of the skeleton are sufficient to promote accelerated bone resorption with a pathological increase in the circulating calcium concentration. The placenta, on the other hand, is capable of providing far less hormone to the circulating pool [13]. Along with the maternal kidney, the placenta is capable of contributing to a rise in the serum level of 1,25(OH)2D during pregnancy; the elevated serum 1,25(OH)2D concentration of pregnancy does not lead to a pathological increase of bone resorption [13]."
"we propose that the more phylogenetically ancient function of 1,25(OH)2D is that of an inflammatory mediator meant to regulate the innate immune response and direct the adaptive immune response to invading microbes. Orthologs of the specific intracellular receptor for 1,25(OH)2D, the vitamin D receptor (VDR), can be found in single cell organisms (e.g., yeast), and both the VDR and its specific ligand 1,25(OH)2D are found in the lamprey eel, an ancient vertebrate lacking a calcified skeleton and teeth [15]; this is evidence that interaction of the VDR with its cognate ligand 1,25(OH)2D plays a role distinct from provision of calcium and phosphate for skeletal mineralization. In its role as a functioning cytokine (see Table 1), 1,25(OH)2D is made locally by inflammatory cells, specifically the macrophage and the dendritic cell [16], to act locally on other immune cells that express the VDR upon activation (Figure 1)."
-
"a woman with chronic renal failure and barely detectable serum 1,25(OH)2D [] increased [her levels] significantly during pregnancy [38]."
"it has been suggested that 1,25(OH)2D made by the placenta is not meant to function as a hormone, but as an immunomodulatory cytokine to i) prevent rejection of the fetus, ii) prevent a graft-(fetus)-versus-host (mother) reaction and iii) promote the orchestrated innate and adaptive immune response to prevent microbial invasion of the fetal-placental unit during pregnancy [40]."
"In conclusion and in concert with current evidence suggesting that placental production of 1,25(OH)2D is not needed for development of the fetal skeleton or the maintenance of maternal skeleton [13], an immunomodulatory role for placental 1,25(OH)2D production seems highly likely [64]."
-
"Barbour et al [18] described an anephric patient with sarcoidosis, hypercalcemia, and a high serum concentration of an active vitamin D metabolite that was detected as 1,25(OH)2D. Subsequent structural studies showed that the hypercalcemia-causing metabolite was 1,25(OH)2D [74], and that the extrarenal source of 1,25(OH)2D was the macrophage [19], the cells that make up a significant portion in the prototypical inflammatory granulomatous lesions characteristic of the disease. More recent work has revealed that macrophage synthesis of 1,25(OH)2D is the consequence of expression of a single gene, the CYP27B1 [75]. As shown in Table 2, clinical evidence for the extrarenal overexpression of the CYP27B1 gene can also be observed in a number of other granuloma-forming diseases, including be lymphomas and other malignancies; for example, immunohistochemical analysis of the human B-cell lymphomas associated with hypercalcemia and raised circulating levels of 1,25(OH)2D in the host suggests that the tumor itself is not a source of the steroid hormone. Rather macrophages adjacent to the tumor are likely to be the major site of 1,25(OH)2D synthesis [76]. Similar observations have been made for other hypercalcemia-causing tumors such as dysgerminomas [41]."
"Like its counterpart in the kidney, the extrarenal CYP27B1 functions as a mitochondrial, mixed function oxidase with cytochrome P450 activity [77]. Using reconstituted mitochondrial extracts it has been shown that electron transfer to the cytochrome P450 and subsequent insertion of an oxygen atom in the substrate 25OHD requires the following: flavoprotein; ferredoxin reductase; an electron source, and molecular oxygen [77]."
"Both renal and extrarenal 1-hydroxylase activities are inhibited by napthoquinones, molecules which compete with reductase for donated electrons and by the imidazoles which compete with the enzyme for receipt of O2 [79]. While the substrate-specificity and enzyme kinetics for the CYP27B1 appears to be the same for both kidney cells and macrophages [78], as just noted the regulation of 1,25(OH)2D synthesis at these sites appears to be very different. For example, as previously noted in Table 1 the macrophage CYP27B1 is not induced by PTH, but it is very sensitive to stimulation by immunoactivators such as lipopolysaccharide [78] and Th1 cytokines, particularly interferon-γ (IFN-γ; [80]). The molecular mechanism underpinning the expression of the CYP27B1 in the human macrophage has recently been elucidated employing ex vivo models of tuberculosis, another prototypical human granuloma-forming disease (see below)."
"microbial killing was more efficiently achieved with the pro-hormone 25OHD than with 1,25(OH)2D at similar extracellular concentrations, indicating that the robustness of the human innate response to microbial challenge is dependent upon the serum 25OHD status of the host"
"Although the existence of extrarenal production of 1,25(OH)2D by the human placenta and disease-activated macrophages has been recognized for many years now, the potential for this vitamin D metabolite to function normally in the host as something other than a calcium-regulating hormone is becoming more likely. The importance of 1,25(OH)2D as a normal functioning, locally-produced, locally-active immunomodulatory molecule in humans in vivo at the fetal-maternal interface in the placenta and/or at other sites of microbial/cancer cell invasion has been stymied by our inability to measure changes in the local concentration of 1,25(OH)2D at sites of immunoactivity in vivo. While there are examples of step-up gradients in the concentration of 1,25(OH)2D between the serum and loculated inflammatory sites, like the pleural fluid of patients with active tuberculosis [104, 105], the potential for 1,25(OH)2D to balance the innate and adaptive immune response to foreign agents (e.g., fetus, mycobacteria, etc., see Figure 2) at a micro-scale in vivo remains real but unproven. Breakthroughs in the field await: 1] prospective clinical trial evidence that provision of 25OHD substrate to vitamin D-deficient individuals will i) improve maternal-fetal outcomes and/or ii) limit disease or protect against microbial infection in exposed individuals (e.g., close family contacts of patients with active tuberculosis); and 2] development of a means for detecting changes in the level and bioactivity of 1,25(OH)2D in the local intra- and extracellular inflammatory microenvironment of the host."
What else lowers cortisol?
Amazoniac
Member
https://onlinelibrary.wiley.com/doi/full/10.1359/jbmr.080420
"Pancreatic β cells express VDR, 1'last seen: Today at 9:37 AM'‐hydroxylase, and calcium‐binding proteins and respond to 1,25(OH)2D in vitro with increased insulin secretion."
"Pancreatic β cells express VDR, 1'last seen: Today at 9:37 AM'‐hydroxylase, and calcium‐binding proteins and respond to 1,25(OH)2D in vitro with increased insulin secretion."
I've been taking 5-6 drops of EstroBan lately (with just a little progesterone) and it's effect on my mood is nice.
Except I've noticed that I'm getting an acidy stomach and a little reflux. And mild diarrhea.
I searched Google and the site and the only thing I found was that the calcium from D3 combines with stomach acid and bile. Connection?
Anybody else have similar symptoms?
At first I thought this was a potato allergy. That has the same symptoms but I stopped the potatoes and the symptoms continued.
Except I've noticed that I'm getting an acidy stomach and a little reflux. And mild diarrhea.
I searched Google and the site and the only thing I found was that the calcium from D3 combines with stomach acid and bile. Connection?
Anybody else have similar symptoms?
At first I thought this was a potato allergy. That has the same symptoms but I stopped the potatoes and the symptoms continued.
OP
I would think that high calcium would cause constipation, not diarrhea. Not sure what is going on, maybe it increases acid production.
OP
Well, it is known that calcium has pyrogenic effect. And if vitamin D potentiates calcium effects then I can see it making people sweat.
managing
Member
- Joined
- Jun 19, 2014
- Messages
- 2,262
Maybe spread it out and/or take smaller dose. One drop before each meal totally eliminates cortisol response for me. IOW, its a net "cooler" not hotter for me.
Obi-wan
Member
- Joined
- Mar 16, 2017
- Messages
- 1,120
Vitamin D toxicity is rare.[24] It is caused by supplementing with high doses of vitamin D rather than sunlight. The threshold for vitamin D toxicity has not been established; however, according to some research, the tolerable upper intake level (UL) is 4,000 IU/day for ages 9–71[143] (100 µg/day), while other research concludes that, in healthy adults, sustained intake of more than 1250 μg/day (50,000 IU) can produce overt toxicity after several months and can increase serum 25-hydroxyvitamin D levels to 150 ng/ml and greater.
Exposure to sunlight for extended periods of time does not normally cause vitamin D toxicity. The concentrations of vitamin D precursors produced in the skin reach an equilibrium, and any further vitamin D produced is degraded.[145] -Wikipedia
Since Calcirol is a transdermal application I wonder if the body treats it like the sun...otherwise the drops should be limited...1 drop =1000iu
Exposure to sunlight for extended periods of time does not normally cause vitamin D toxicity. The concentrations of vitamin D precursors produced in the skin reach an equilibrium, and any further vitamin D produced is degraded.[145] -Wikipedia
Since Calcirol is a transdermal application I wonder if the body treats it like the sun...otherwise the drops should be limited...1 drop =1000iu
EMF Mitigation - Flush Niacin - Big 5 Minerals
Similar threads
