Fasting ups estrogen & cortisol, decimates vitamin D, may cause diabetes

haidut

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A really interesting study, which will likely generate more than a few hateful emails for my Inbox :): Anyways, as the study demonstrates, fasting achieves these negative effects due to the elevated fatty acids working through PPAR activator PGC-1α, to activate both the estrogen receptor (ER) and glucocorticoid receptor (GR). So, aside from the important findings on vitamin D, IMO the bigger takeaway from the study is that fasting ALWAYS increases both estrogen and cortisol signalling, as fasting always increases PGC-1α. In terms of vitamin D inhibition, the situation is just as bad. The activation of ER and GR not only inhibited vitamin D synthesis but also increased its degradation. More specifically, a 12-hour fast decreased vitamin D synthesis by ~50% while a 24-hour fast completely blocked vitamin D synthesis! Imagine what happens during the multi-day fasting regiment so many high-profile doctors and Internet gurus recommend these days...
Considering the study discusses all of these changes in the context of diabetes, I think it is reasonable to state that fasting may mimic diabetes (and probably cause it, when practiced long term) and that diabetes is an endocrine condition driven by high estrogen/cortisol and low vitamin D. While most doctors will certainly not deny that diabetes I is an endocrine disease, they universally balk at acknowledging the same for diabetes II, and most certainly balk at the idea that estrogen/cortisol may be the direct causes of both diabetes types. The good news is that vitamin D is known to be a GR antagonist while also inhibiting ER activation and aromatase. This may be one of the reasons vitamin D supplementation has been shown to be therapeutic in diabetes II and, if the study findings below are correct, it may also be helpful in diabetes I. Actually, the buck does not stop with diabetes. Excess estrogen/cortisol are now known to be involved in virtually all chronic diseases, which may make vitamin D one of the universally protective factors on par with aspirin, progesterone, and thyroid.

Fasting-Induced Transcription Factors Repress Vitamin D Bioactivation, a Mechanism for Vitamin D Deficiency in Diabetes
"...We next investigated the mechanisms of CYP2R1 repression and hypothesized that nutrition-responsive coactivator PGC-1α would be involved in this process since PGC-1α plays a central role in the fasting response and in uncontrolled diabetes (34). PGC-1α overexpression in mouse primary hepatocytes with PGC-1α-Ad downregulated CYP2R1 strongly and dose dependently, resulting in only an 11% expression at MOI 1 compared with GFP-Ad control (Fig. 2A). To explore the mechanism in more detail, we transduced mutant PGC-1α into hepatocytes (Supplementary Fig. 2A). Gaillard et al. (35) described PGC-1α mutants selective for nuclear receptor interactions; PGC-1α-L2L3M mutant is unable to bind any nuclear receptors, whereas PGC-1α-2x9 mutant interacts selectively with nuclear receptors ERRα or HNF-4α. Interestingly, PGC-1α-2x9 downregulated CYP2R1 expression almost similarly to the WT (Fig. 2B), whereas the L2L3M mutation abolished the CYP2R1 repression and even resulted in weak induction (Fig. 2B). These results indicate that an interaction with a nuclear receptor, most probably ERRα, is indispensable for PGC-1α–mediated CYP2R1 suppression. Supporting this hypothesis, several ERRα target genes (35) were upregulated by the WT and the PGC-1α-2x9 mutant (Supplementary Fig. 2BD). Moreover, the majority of the PGC-1α-2x9 mutant–induced genes are dependent on ERRα (35)."

"...Furthermore, we confirmed the role of ERRα by using ERRα inverse agonist XCT790. Indeed, 2 μmol/L XCT790 prevented CYP2R1 repression by PGC-1α (Fig. 2D) without any effect on PGC-1α or ERRα expression (Supplementary Fig. 2G and H). Analysis of public Encyclopedia of DNA Elements data indicates that PGC-1α and ERRα bind to two common regions within the human CYP2R1 gene in HepG2 cells (31) (Supplementary Fig. 2M). We performed a bioinformatics promoter analysis of the mouse Cyp2r1 gene with MatInspector software and identified a potential ERRα binding site in the proximal promoter. When −1.2 kb Cyp2r1-5′-luciferase-reporter construct was transfected into human hepatoma HepG2 cells and the cells were infected with PGC-1α-Ad, luciferase activity was repressed; however, mutation of the ERRα binding site at position −1,117 to −1,122 bp (relative to the TSS) abolished the PGC-1α response (Fig. 2E). Interestingly, ERRα-Ad did not have an effect on the luciferase activity, indicating a crucial need for PGC-1α (Fig. 2E). Altogether, these data indicate that ERRα plays a novel, indispensable role in PGC-1α–mediated downregulation of CYP2R1 expression in mouse hepatocytes."

"...GR activated by cortisol is another key pathway controlling the fasting response in the liver and is also activated in diabetes (38). To investigate the role of GR in the regulation of CYP2R1, we treated mice with a GR agonist, dexamethasone, for 6 h. The treatment decreased liver CYP2R1 mRNA levels by 49% along with changes in the expression of several known GR target genes, including ANGPTL8, NR1D1, and TAT (38,39), and increased PGC-1α levels 3.3-fold (Fig. 3A), suggesting involvement of GR in the regulation of CYP2R1 in vivo. GR is also a known interaction partner for PGC-1α (34). The CYP2R1 protein was decreased 26% by 6-h dexamethasone treatment (Fig. 3B). Furthermore, analysis of the published microarray data (accession number GSE24256) (40) supports the effect of dexamethasone on CYP2R1 expression in mouse liver (Supplementary Fig. 3A)."

"...We now show that the CYP2R1 enzyme may be repressed also functionally at the level of gene regulation. Twelve-hour fasting suppressed liver microsomal vitamin D 25-hydroxylation ∼50%, and after 24-h fasting, we were unable to detect any 25-OH-D formation. Thus, the first vitamin D bioactivation step is under the strict control of nutritional state. Although the acute food deprivation resulted in a strong effect on vitamin D 25-hydroxylase activity, this was not reflected in the plasma 25-OH-D concentration, presumably because of the long half-life of 25-OH-D (47). Therefore, it seems unlikely that short-term fasting would have a significant effect on vitamin D functions at the systemic level. This raises the question of the physiological purpose of the CYP2R1 repression during fasting. A likely explanation is that fasting launches physiological adjustment as precaution for possible longer-term food shortage. This may potentially be related to the role of vitamin D in energy homeostasis (1) and could have been evolutionarily beneficial during periods of starvation. Alternatively, 25-OH-D could have some unknown local function in liver. Furthermore, we observed induction of CYP24A1 in the kidney during fasting. This is a mechanism that limits the level of 1α,25-(OH)2-D and consequently activation of VDR (10). The CYP24A1 induction and the CYP2R1 repression are expected to suppress vitamin D signaling in a synergistic manner."

"...PGC-1α is one of the major molecular factors regulating gluconeogenesis and other metabolic pathways activated in the diabetic liver (34,50). We now show that PGC-1α, ERRα dependently, also represses vitamin D bioactivation and, thus, establishes regulation of vitamin D metabolism as a novel metabolic function under the control of PGC-1α. Furthermore, the CYP24A1 induction by fasting in the kidney was demonstrated to be under the control of PGC-1α-ERRα. Thus, the PGC-1α-ERRα pathway appears to play a major role in the crosstalk between energy homeostasis and vitamin D metabolism. Interestingly, a recent study showed that Cyp2r1-deficiency in zebrafish affected lipid metabolism through vitamin D–regulated function of PGC-1α (51). PGC-1α and vitamin D metabolism could thus form a regulatory loop."

"...Although, the PGC-1α-ERRα pathway was found to be an effective regulator of CYP2R1, the PGC-1α KO did not prevent CYP2R1 suppression during fasting. This indicates that additional molecular mechanisms play a role in the regulation of CYP2R1 during fasting. Activation of GR was found to be a second mechanism capable for CYP2R1 suppression. Indeed, cortisol levels are increased during fasting as well as in diabetes (38). By using pharmacological inhibition of GR, we could partially prevent fasting-mediated repression of CYP2R1, suggesting that GR is involved in CYP2R1 repression by fasting. However, we cannot exclude the possibility that additional regulatory mechanisms mediate CYP2R1 repression by fasting. From the point of view of drug therapy, the observed repression of CYP2R1 by pharmacological glucocorticoid treatment may explain the observed association between glucocorticoid use and vitamin D deficiency (52)."

"...In summary, our results reveal a novel crosstalk between energy homeostasis and the vitamin D pathway, suggesting a physiological need for suppression of vitamin D signaling during nutrient deprivation (Fig. 6). This may be related to the role of vitamin D in energy metabolism (1,3). Altogether, our study provides a mechanism that may explain the lower vitamin D levels in patients with diabetes..."
 

dukesbobby777

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276
Makes sense. Being without food and not knowing where your next meal is coming from, the stress hormone system needs to put you on full alert to find/hunt for food opportunities.

There’s a lot of fasting gurus out there. Many of them ‘appear’ to be doing ok health wise at the moment. I guess I’m really intrigued to see how they age as the years pass.
 

haidut

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Makes sense. Being without food and not knowing where your next meal is coming from, the stress hormone system needs to put you on full alert to find/hunt for food opportunities.

There’s a lot of fasting gurus out there. Many of them ‘appear’ to be doing ok health wise at the moment. I guess I’m really intrigued to see how they age as the years pass.

Even intermittent fasting (IF) is showing bad results in human trials, so let's see how long before the blogosphere catches up.
 

Queen foodie

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Oct 28, 2019
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Even intermittent fasting (IF) is showing bad results in human trials, so let's see how long before the blogosphere catches up.
This is interesting! I've been doing intermittent fasting everyday since 2013. I also have high estrogen and cortisol but I've blamed it on my daily drinking of wine or even my menopause! I am 53 years old and I've used t3, and progesterone to mitigate the cortisol and estrogen quite effectively. My body seems to be in a good place.
 

LeeLemonoil

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Sep 24, 2016
Messages
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Vitamin D is an immunomodulator acts homeostaticaly. Calorie restriction and IM have proven and logical benefits that mediate estrogen and GC signaling. As long as these is on the good and beneficial side of homeostasis, Vitamin D isn’t needed much, hence the reduction here.

Everything can be overdone, so IF and CR have their limits and homeostasic spectrum when it will become detrimental.
Then Vitamin D decimation will reinforce the bad sides.

But it also indicates that Vitamin D isn’t an allround do-gooder in any context. There are situations where GC-R antagonism is bad, where inhibiting aromatase isn’t good and so on. Everything has its balance, every second anew
 

Ras

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Joined
Sep 12, 2015
Messages
515
A really interesting study, which will likely generate more than a few hateful emails for my Inbox :): Anyways, as the study demonstrates, fasting achieves these negative effects due to the elevated fatty acids working through PPAR activator PGC-1α, to activate both the estrogen receptor (ER) and glucocorticoid receptor (GR). So, aside from the important findings on vitamin D, IMO the bigger takeaway from the study is that fasting ALWAYS increases both estrogen and cortisol signalling, as fasting always increases PGC-1α. In terms of vitamin D inhibition, the situation is just as bad. The activation of ER and GR not only inhibited vitamin D synthesis but also increased its degradation. More specifically, a 12-hour fast decreased vitamin D synthesis by ~50% while a 24-hour fast completely blocked vitamin D synthesis! Imagine what happens during the multi-day fasting regiment so many high-profile doctors and Internet gurus recommend these days...
Considering the study discusses all of these changes in the context of diabetes, I think it is reasonable to state that fasting may mimic diabetes (and probably cause it, when practiced long term) and that diabetes is an endocrine condition driven by high estrogen/cortisol and low vitamin D. While most doctors will certainly not deny that diabetes I is an endocrine disease, they universally balk at acknowledging the same for diabetes II, and most certainly balk at the idea that estrogen/cortisol may be the direct causes of both diabetes types. The good news is that vitamin D is known to be a GR antagonist while also inhibiting ER activation and aromatase. This may be one of the reasons vitamin D supplementation has been shown to be therapeutic in diabetes II and, if the study findings below are correct, it may also be helpful in diabetes I. Actually, the buck does not stop with diabetes. Excess estrogen/cortisol are now known to be involved in virtually all chronic diseases, which may make vitamin D one of the universally protective factors on par with aspirin, progesterone, and thyroid.

Fasting-Induced Transcription Factors Repress Vitamin D Bioactivation, a Mechanism for Vitamin D Deficiency in Diabetes
"...We next investigated the mechanisms of CYP2R1 repression and hypothesized that nutrition-responsive coactivator PGC-1α would be involved in this process since PGC-1α plays a central role in the fasting response and in uncontrolled diabetes (34). PGC-1α overexpression in mouse primary hepatocytes with PGC-1α-Ad downregulated CYP2R1 strongly and dose dependently, resulting in only an 11% expression at MOI 1 compared with GFP-Ad control (Fig. 2A). To explore the mechanism in more detail, we transduced mutant PGC-1α into hepatocytes (Supplementary Fig. 2A). Gaillard et al. (35) described PGC-1α mutants selective for nuclear receptor interactions; PGC-1α-L2L3M mutant is unable to bind any nuclear receptors, whereas PGC-1α-2x9 mutant interacts selectively with nuclear receptors ERRα or HNF-4α. Interestingly, PGC-1α-2x9 downregulated CYP2R1 expression almost similarly to the WT (Fig. 2B), whereas the L2L3M mutation abolished the CYP2R1 repression and even resulted in weak induction (Fig. 2B). These results indicate that an interaction with a nuclear receptor, most probably ERRα, is indispensable for PGC-1α–mediated CYP2R1 suppression. Supporting this hypothesis, several ERRα target genes (35) were upregulated by the WT and the PGC-1α-2x9 mutant (Supplementary Fig. 2BD). Moreover, the majority of the PGC-1α-2x9 mutant–induced genes are dependent on ERRα (35)."

"...Furthermore, we confirmed the role of ERRα by using ERRα inverse agonist XCT790. Indeed, 2 μmol/L XCT790 prevented CYP2R1 repression by PGC-1α (Fig. 2D) without any effect on PGC-1α or ERRα expression (Supplementary Fig. 2G and H). Analysis of public Encyclopedia of DNA Elements data indicates that PGC-1α and ERRα bind to two common regions within the human CYP2R1 gene in HepG2 cells (31) (Supplementary Fig. 2M). We performed a bioinformatics promoter analysis of the mouse Cyp2r1 gene with MatInspector software and identified a potential ERRα binding site in the proximal promoter. When −1.2 kb Cyp2r1-5′-luciferase-reporter construct was transfected into human hepatoma HepG2 cells and the cells were infected with PGC-1α-Ad, luciferase activity was repressed; however, mutation of the ERRα binding site at position −1,117 to −1,122 bp (relative to the TSS) abolished the PGC-1α response (Fig. 2E). Interestingly, ERRα-Ad did not have an effect on the luciferase activity, indicating a crucial need for PGC-1α (Fig. 2E). Altogether, these data indicate that ERRα plays a novel, indispensable role in PGC-1α–mediated downregulation of CYP2R1 expression in mouse hepatocytes."

"...GR activated by cortisol is another key pathway controlling the fasting response in the liver and is also activated in diabetes (38). To investigate the role of GR in the regulation of CYP2R1, we treated mice with a GR agonist, dexamethasone, for 6 h. The treatment decreased liver CYP2R1 mRNA levels by 49% along with changes in the expression of several known GR target genes, including ANGPTL8, NR1D1, and TAT (38,39), and increased PGC-1α levels 3.3-fold (Fig. 3A), suggesting involvement of GR in the regulation of CYP2R1 in vivo. GR is also a known interaction partner for PGC-1α (34). The CYP2R1 protein was decreased 26% by 6-h dexamethasone treatment (Fig. 3B). Furthermore, analysis of the published microarray data (accession number GSE24256) (40) supports the effect of dexamethasone on CYP2R1 expression in mouse liver (Supplementary Fig. 3A)."

"...We now show that the CYP2R1 enzyme may be repressed also functionally at the level of gene regulation. Twelve-hour fasting suppressed liver microsomal vitamin D 25-hydroxylation ∼50%, and after 24-h fasting, we were unable to detect any 25-OH-D formation. Thus, the first vitamin D bioactivation step is under the strict control of nutritional state. Although the acute food deprivation resulted in a strong effect on vitamin D 25-hydroxylase activity, this was not reflected in the plasma 25-OH-D concentration, presumably because of the long half-life of 25-OH-D (47). Therefore, it seems unlikely that short-term fasting would have a significant effect on vitamin D functions at the systemic level. This raises the question of the physiological purpose of the CYP2R1 repression during fasting. A likely explanation is that fasting launches physiological adjustment as precaution for possible longer-term food shortage. This may potentially be related to the role of vitamin D in energy homeostasis (1) and could have been evolutionarily beneficial during periods of starvation. Alternatively, 25-OH-D could have some unknown local function in liver. Furthermore, we observed induction of CYP24A1 in the kidney during fasting. This is a mechanism that limits the level of 1α,25-(OH)2-D and consequently activation of VDR (10). The CYP24A1 induction and the CYP2R1 repression are expected to suppress vitamin D signaling in a synergistic manner."

"...PGC-1α is one of the major molecular factors regulating gluconeogenesis and other metabolic pathways activated in the diabetic liver (34,50). We now show that PGC-1α, ERRα dependently, also represses vitamin D bioactivation and, thus, establishes regulation of vitamin D metabolism as a novel metabolic function under the control of PGC-1α. Furthermore, the CYP24A1 induction by fasting in the kidney was demonstrated to be under the control of PGC-1α-ERRα. Thus, the PGC-1α-ERRα pathway appears to play a major role in the crosstalk between energy homeostasis and vitamin D metabolism. Interestingly, a recent study showed that Cyp2r1-deficiency in zebrafish affected lipid metabolism through vitamin D–regulated function of PGC-1α (51). PGC-1α and vitamin D metabolism could thus form a regulatory loop."

"...Although, the PGC-1α-ERRα pathway was found to be an effective regulator of CYP2R1, the PGC-1α KO did not prevent CYP2R1 suppression during fasting. This indicates that additional molecular mechanisms play a role in the regulation of CYP2R1 during fasting. Activation of GR was found to be a second mechanism capable for CYP2R1 suppression. Indeed, cortisol levels are increased during fasting as well as in diabetes (38). By using pharmacological inhibition of GR, we could partially prevent fasting-mediated repression of CYP2R1, suggesting that GR is involved in CYP2R1 repression by fasting. However, we cannot exclude the possibility that additional regulatory mechanisms mediate CYP2R1 repression by fasting. From the point of view of drug therapy, the observed repression of CYP2R1 by pharmacological glucocorticoid treatment may explain the observed association between glucocorticoid use and vitamin D deficiency (52)."

"...In summary, our results reveal a novel crosstalk between energy homeostasis and the vitamin D pathway, suggesting a physiological need for suppression of vitamin D signaling during nutrient deprivation (Fig. 6). This may be related to the role of vitamin D in energy metabolism (1,3). Altogether, our study provides a mechanism that may explain the lower vitamin D levels in patients with diabetes..."
Study results that disagree with the results of practice don't matter. With few exceptions, the reality experienced and espoused by thousands from many centuries is that fasting is healthful and curative. Countless Scientific™ studies done on rodents have testified data that never realized in actual practice with mankind, because no matter what the evolutionist's genetic dogma preaches, men are not murine. The most-high arbiter of truth is the man experimenting with himself.
 

GelatinGoblin

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Apr 15, 2020
Messages
813
Vitamin D is an immunomodulator acts homeostaticaly. Calorie restriction and IM have proven and logical benefits that mediate estrogen and GC signaling. As long as these is on the good and beneficial side of homeostasis, Vitamin D isn’t needed much, hence the reduction here.

Everything can be overdone, so IF and CR have their limits and homeostasic spectrum when it will become detrimental.
Then Vitamin D decimation will reinforce the bad sides.

But it also indicates that Vitamin D isn’t an allround do-gooder in any context. There are situations where GC-R antagonism is bad, where inhibiting aromatase isn’t good and so on. Everything has its balance, every second anew

Interesting
 

TheBeard

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May 16, 2018
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Study results that disagree with the results of practice don't matter. With few exceptions, the reality experienced and espoused by thousands from many centuries is that fasting is healthful and curative. Countless Scientific™ studies done on rodents have testified data that never realized in actual practice with mankind, because no matter what the evolutionist's genetic dogma preaches, men are not murine. The most-high arbiter of truth is the man experimenting with himself.

Amen
 

schultz

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Jul 29, 2014
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Study results that disagree with the results of practice don't matter. With few exceptions, the reality experienced and espoused by thousands from many centuries is that fasting is healthful and curative. Countless Scientific™ studies done on rodents have testified data that never realized in actual practice with mankind, because no matter what the evolutionist's genetic dogma preaches, men are not murine. The most-high arbiter of truth is the man experimenting with himself.

These studies will never be done in humans.

We have all heard of calorie restriction and fasting being helpful for certain people, but it's good to try and figure out why. If we figure out that it's because, as an example, it lowers endotoxin or some such thing then we can come up with a dietary approach that allows for an increase of calories while limiting the effects of endotoxin.

It is equally important to figure out the shortcomings of fasting and calorie restriction, whether they be the effects on cortisol or mitochondrial respiration.

Applying this knowledge may allow us to get whatever benefits there might be from fasting or calorie restriction but without the negative side effects that are associated with them.

I should also mention that it is important to try and understand why something makes us feel good. Stress hormones can make you feel good, but they cause long term damage.
 

GelatinGoblin

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These studies will never be done in humans.

We have all heard of calorie restriction and fasting being helpful for certain people, but it's good to try and figure out why. If we figure out that it's because, as an example, it lowers endotoxin or some such thing then we can come up with a dietary approach that allows for an increase of calories while limiting the effects of endotoxin.

It is equally important to figure out the shortcomings of fasting and calorie restriction, whether they be the effects on cortisol or mitochondrial respiration.

Applying this knowledge may allow us to get whatever benefits there might be from fasting or calorie restriction but without the negative side effects that are associated with them.

I should also mention that it is important to try and understand why something makes us feel good. Stress hormones can make you feel good, but they cause long term damage.
Exactly :darts: :thumbup:
 

Broken man

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The only thing that is controversial here is that fasting works through the same mechanism as methylene blue does....
 

Aegon24

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I took a lot of vitamin d 6 months ago and it made my semen liquid with a disgusting greenish color.
One girl told me sarcastically, if I didn't have 80 years to squirt something like that.

I started fasting three weeks ago. and it became all white and thick like it used to be.
 

TheBeard

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I took a lot of vitamin d 6 months ago and it made my semen liquid with a disgusting greenish color.
One girl told me sarcastically, if I didn't have 80 years to squirt something like that.

I started fasting three weeks ago. and it became all white and thick like it used to be.

You've been fasting for 3 weeks on just water?
 

Aegon24

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You've been fasting for 3 weeks on just water?
I fast only 20 hours a day on average, without water.
Even that is effective, to detoxify the body.

But I will try to do more than that when I have time.
 

GelatinGoblin

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I fast only 20 hours a day on average, without water.
Even that is effective, to detoxify the body.

But I will try to do more than that when I have time.
Why not just use antibiotic or coconut oil with insoluble fiber, or lowering Methionine intake and upping Gelatin intake? I heard the good effects of fasting are from lowering Endotoxin and the lowered total Methionine intake.
 

Risingfire

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Joined
May 10, 2016
Messages
485
I took a lot of vitamin d 6 months ago and it made my semen liquid with a disgusting greenish color.
One girl told me sarcastically, if I didn't have 80 years to squirt something like that.

I started fasting three weeks ago. and it became all white and thick like it used to be.
Green? And you didn't think to go to the doctor?
 
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