My machine has indicated high wbc, indicative of chronic infections, and systemic anemia quite often. There are two minerals to address anemia with. Iron or copper. Iron feeds pathogens, and copper kills pathogens. Copper also helps to resolve anemia. Will monitor my organs and tissues and see how the copper addition affects these ongoing issues.
https://nutritiondata.self.com/facts/beef-products/3468/2
It's always felt like my liver just isn't functioning like it should. The 3 biggest nutrients of the liver are copper, retinol, and B12. B12 stimulates dopamine loss so that's out. Preformed retinol seems to be toxic for us, which leaves natural beta carotene.
On 3/27/2022 at 6:33 PM, Thommy280495 said:@SaffronAideYou're just crazy. You have HPA Hyperactivity and want to fast for 30 days, which puts so much more stress on the body. Also proclaiming it to be the cure, when you're not even cured yourself is inappropriate.
HPA Axis is indeed linked to the sympathetic nervous system and could cause this 24/7 fight or flight mode. I already took lorazepam for some time and it makes you careless, but doesnt alleviate the symptoms.
I will ask my doctor to prescribe me mifepristone on Tuesday. It restores Glucocorticoidreceptordensity and repairs the negative feedback loop of the HPA axis.
Where the heck that you theorized that i have HPA Hyperactivity? Yes, Mifepristone is also a good choice, but we don't know eveyone's exact root cause. Ialso bought Mifepristone and will try if anything goes bad. Fasting can still heal the body and i don't think it would cause problems if not benefits to your HPA.
On 3/27/2022 at 8:55 AM, Pido said:Recently I was taking 3x600 mg ibuprofen a day, because I was in hallux rigidus surgery. I noticed that my skin wasless dry, but I was homebound and didn't care to take showers so it might have been that.
Why you are not trying my protocol list, that i gave on page 737, and wasting your life here? You may or may not recover but you will never know if you don't try those things man. Don't do that to your life. It took me years to eliminate certain protocols and experimentation to get here, you have a long way to go.
@SaffronAideAgain, I´m not going to waste my time arguing with you, when you cannot even read the study Ronnie shared.
For everyone who is interested, I've written the following summary of how HPA Hyperactivity occurs and about the Safety of Mifepristone. My doctors appointment got canceled due to Covid. I have a new appointment next week.
HPA Hyperactivity
Allopregnanolone (Allo) is important for the pregnant mother. Indeed, during pregnancy, an increase of Allo levels occurs in the maternal peripheral circulation, as well as in the maternal brain. In rats, the increased levels of this neuroactive steroid interfere with the hypothalamic-pituitary- adrenal (HPA) axis reducing, in particular during late pregnancy, the response to stress exposure of the mother.[1]A study showed that there is an apparent correlation between endogenous levels of brain allo and basal and stress-stimulated HPA axis activity.[2]
This could mean high Allo surpresses the HPA axis and low Allo, as reported in PFS, leads to HPA Hyperactivity. Definetely, HPA Hyperactivity is reported after the use of isotretinoin.[3],[4] Normally there is the negative feedback loop thorugh glucocorticoids at the Glucocorticoidreceptor (GR). However after taking Iso, the Glucocorticoid Dexamethsone does not surpress the plasma concentration of the glucocorticoid Corticosterone.[5] This means that the negative feedback loop is impaired. Histological examination and western examples affirmed this showing a significant decrease of GR-IR cells and GR density. The other pathway in which Isotretinoine increases HPA activity is an increase in the CRH-expression. This is through RARalpha activation, which could upregulate CRH mRNA expression via direct action on its promoter sequence.[6]
In general HPA Hyperactivity leads to more Glucocorticoids being produced.
The Glucocorticoids intervene with the secretion of GnRH. Glucocorticoids modulate the HPG axis by directly inhibiting the release of GnRH from the hypothalamus and the synthesis
and release of gonadotropins from the pituitary.[7] GnRH has the task to stimulate FSH and LH production. If it´s inhibited less FSH and LH will be produced.
Safety of Mifepristone
The mifepristone studies are relatively unique in that subjects received the medication for 7 days. Summary of seven clinical trials, five of them double blind (N ranging from 5 to 433), suggests that mifepristone has efficacy in reducing psychotic symptoms.Importantly, mifepristone™s effectiveness appears to be optimized when attaining a plasma level of ~1600ng/mL, which equates to roughly 1200 mg/day orally.
Patients with high mifepristone plasma levels also showed a reduction of depressive symptoms relative to placebo. Although mifepristone is associated with some gastrointestinal side effects and headache, very few patients discontinued due to side effects.
A metaanalysis said the following: Adverse Events (AE) from all five studies (n = 1460) were evaluated by dose group and by all doses combined.
Overall, the safety of mifepristone versus placebo was comparable, with a similar number of events noted in each group. The NNH (Number needed to harm) was calculated using the outcome of study dropouts due to AEs. For all studies combined, the NNH for mifepristone was incalculable because dropouts due to side effects were higher for placebo (1.6%) than for mifepristone (1.4%). In two studies, dropouts because of AEs were higher for mifepristone than placebo (1.0% vs. 0.9%, NNH = 1000 in study 1; 2.4% vs. 1.6%, NNH = 126 in study 3). Mifepristone appeared safe and well tolerated across all three dosage groups. The rates of treatment emergent adverse events were similar across placebo (62%), mifepristone total (67%), mifepristone HPL (69%), and mifepristone LPL (65%) groups. There was no statistically significant difference in rates of adverse events between mifepristone HPL and LPL groups.[8]
References
1. Central Opioid Inhibition of Neuroendocrine Stress Responses in Pregnancy in the Rat Is Induced by the Neurosteroid Allopregnanolone, https://www.research.ed.ac.uk/en/publications/central-opioid-inhibition-of-neuroendocrine-stress-responses-in-p
2. Allopregnanolone modulation of HPA axis function in the adult rat, https://pubmed.ncbi.nlm.nih.gov/24658404/
3. All-trans retinoic acid-induced hypothalamus“pituitary“adrenal hyperactivity involves glucocorticoid receptor dysregulation, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4030330/
4. Chronic all-trans retinoic acid administration induced hyperactivity of HPA axis and behavioral changes in young rats, https://pubmed.ncbi.nlm.nih.gov/20659790/
5. All-trans retinoic acid-induced hypothalamus“pituitary“adrenal hyperactivity involves glucocorticoid receptor dysregulation, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4030330/
6. Glucocorticoids and Reproduction: Traffic Control on the Road to Reproduction, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5438761/
7. Retinoic acid and depressive disorders: Evidence and possible neurobiological mechanisms, https://www.sciencedirect.com/science/article/abs/pii/S0149763420300014
8. Combined Analysis of Mifepristone for Psychotic Depression: Plasma Levels Associated with Clinical Response, https://www.biologicalpsychiatryjournal.com/article/S0006-3223(18)30035-0/fulltext
On 3/17/2022 at 9:37 PM, Thommy280495 said:Got bad news, all the special values from the Neurosteroid study cannot be determined in serum or liquor. I will do a regular blood test next week and determine LH and FSH bc it was lowish in people with the syndrome. I did some research and found the following:
Low Allo leads to HPA hyperactivity, which we have. HPA hyperactivity leads to too much glucocorticoids which inhibit the secretion of GnRH. GnRH has the task to stimulate LH and FSH production and if it's inhibited this causes low LH and FSH. The guy who took the mifepristone had low LH/FSH which went up a lot after taking mifepristone. My doctor will tell me about the risk profile of this drug, for now I read it has a good safety profile.
I want to try out a treatment soon.
Are you talking about zrt nuerotest? My LH ans FSH are are low. LH has even tested under range in the past. Mif seems like a potential consideration. My main symptoms are sexual (physical), pain, and brain fog. Libido is okay
https://pubmed.ncbi.nlm.nih.gov/23847298/
https://pubmed.ncbi.nlm.nih.gov/3203678/
I'd say fasting can be very beneficial for someone who is overweight, but is detrimental for anyone underweight. I'd supplement with key vitamins or minerals during the fast though. I'm doing copper and natural beta carotene before bed and will see how it goes.
2 hours ago, Thommy280495 said:@SaffronAideAgain, I´m not going to waste my time arguing with you, when you cannot even read the study Ronnie shared.
For everyone who is interested, I've written the following summary of how HPA Hyperactivity occurs and about the Safety of Mifepristone. My doctors appointment got canceled due to Covid. I have a new appointment next week.
HPA Hyperactivity
Allopregnanolone (Allo) is important for the pregnant mother. Indeed, during pregnancy, an increase of Allo levels occurs in the maternal peripheral circulation, as well as in the maternal brain. In rats, the increased levels of this neuroactive steroid interfere with the hypothalamic-pituitary- adrenal (HPA) axis reducing, in particular during late pregnancy, the response to stress exposure of the mother.[1]A study showed that there is an apparent correlation between endogenous levels of brain allo and basal and stress-stimulated HPA axis activity.[2]
This could mean high Allo surpresses the HPA axis and low Allo, as reported in PFS, leads to HPA Hyperactivity. Definetely, HPA Hyperactivity is reported after the use of isotretinoin.[3],[4] Normally there is the negative feedback loop thorugh glucocorticoids at the Glucocorticoidreceptor (GR). However after taking Iso, the Glucocorticoid Dexamethsone does not surpress the plasma concentration of the glucocorticoid Corticosterone.[5] This means that the negative feedback loop is impaired. Histological examination and western examples affirmed this showing a significant decrease of GR-IR cells and GR density. The other pathway in which Isotretinoine increases HPA activity is an increase in the CRH-expression. This is through RARalpha activation, which could upregulate CRH mRNA expression via direct action on its promoter sequence.[6]
In general HPA Hyperactivity leads to more Glucocorticoids being produced.
The Glucocorticoids intervene with the secretion of GnRH. Glucocorticoids modulate the HPG axis by directly inhibiting the release of GnRH from the hypothalamus and the synthesis
and release of gonadotropins from the pituitary.[7] GnRH has the task to stimulate FSH and LH production. If it´s inhibited less FSH and LH will be produced.
Safety of Mifepristone
The mifepristone studies are relatively unique in that subjects received the medication for 7 days. Summary of seven clinical trials, five of them double blind (N ranging from 5 to 433), suggests that mifepristone has efficacy in reducing psychotic symptoms.Importantly, mifepristone™s effectiveness appears to be optimized when attaining a plasma level of ~1600ng/mL, which equates to roughly 1200 mg/day orally.
Patients with high mifepristone plasma levels also showed a reduction of depressive symptoms relative to placebo. Although mifepristone is associated with some gastrointestinal side effects and headache, very few patients discontinued due to side effects.
A metaanalysis said the following: Adverse Events (AE) from all five studies (n = 1460) were evaluated by dose group and by all doses combined.
Overall, the safety of mifepristone versus placebo was comparable, with a similar number of events noted in each group. The NNH (Number needed to harm) was calculated using the outcome of study dropouts due to AEs. For all studies combined, the NNH for mifepristone was incalculable because dropouts due to side effects were higher for placebo (1.6%) than for mifepristone (1.4%). In two studies, dropouts because of AEs were higher for mifepristone than placebo (1.0% vs. 0.9%, NNH = 1000 in study 1; 2.4% vs. 1.6%, NNH = 126 in study 3). Mifepristone appeared safe and well tolerated across all three dosage groups. The rates of treatment emergent adverse events were similar across placebo (62%), mifepristone total (67%), mifepristone HPL (69%), and mifepristone LPL (65%) groups. There was no statistically significant difference in rates of adverse events between mifepristone HPL and LPL groups.[8]
References
1. Central Opioid Inhibition of Neuroendocrine Stress Responses in Pregnancy in the Rat Is Induced by the Neurosteroid Allopregnanolone, https://www.research.ed.ac.uk/en/publications/central-opioid-inhibition-of-neuroendocrine-stress-responses-in-p
2. Allopregnanolone modulation of HPA axis function in the adult rat, https://pubmed.ncbi.nlm.nih.gov/24658404/
3. All-trans retinoic acid-induced hypothalamus“pituitary“adrenal hyperactivity involves glucocorticoid receptor dysregulation, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4030330/
4. Chronic all-trans retinoic acid administration induced hyperactivity of HPA axis and behavioral changes in young rats, https://pubmed.ncbi.nlm.nih.gov/20659790/
5. All-trans retinoic acid-induced hypothalamus“pituitary“adrenal hyperactivity involves glucocorticoid receptor dysregulation, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4030330/
6. Glucocorticoids and Reproduction: Traffic Control on the Road to Reproduction, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5438761/
7. Retinoic acid and depressive disorders: Evidence and possible neurobiological mechanisms, https://www.sciencedirect.com/science/article/abs/pii/S0149763420300014
8. Combined Analysis of Mifepristone for Psychotic Depression: Plasma Levels Associated with Clinical Response, https://www.biologicalpsychiatryjournal.com/article/S0006-3223(18)30035-0/fulltext
I literally read this study years ago. Again, just because we took Accutane, doesn't mean we all have the same problem, you clearly don't even read my messages. Besides, what you mean by ''arguing'' we are literally on the same side, i even told that i bought Mifepristone as a B plan, calm down dude.
Thank you for sharing that Andy. Your testosterone is high due to accutane induced vitamin A deficiency. Vitamin A is needed to convert testosterone to dht via 5 alpha reductase. If we can clear accutane from your body and boost your true retinol levels, we can get the testosterone and estrogen numbers down and your dht number up.
Just started a 3 component program of defatted beef liver, natural beta carotene, and copper. These are basically all the components of whole beef or human liver, minus the retinol. I believe we must allow our body to make it's own retinol from natural beta carotene in order to recover. Will keep the board posted.
11 hours ago, Andy5 said:Are you talking about zrt nuerotest? My LH ans FSH are are low. LH has even tested under range in the past. Mif seems like a potential consideration. My main symptoms are sexual (physical), pain, and brain fog. Libido is okay
Yes, that's the test I meant. Thanks for sharing. I won't do it bc Allo turns up normal in the urine, I don't think its representative for what's going on in the CSF. LH and FSH are good biomarkers for what's going on with the HPA axis and can be heightened by mife.That's what happened to Ronnie who got cured by Mife.
@SaffronAideAll the animals in the studies had HPA Hyperactivity. You saying that accutane doing different things is not scientifically, when this is the underlying pathomechanism.
3 hours ago, Thomas76 said:Thank you for sharing that Andy. Your testosterone is high due to accutane induced vitamin A deficiency. Vitamin A is needed to convert testosterone to dht via 5 alpha reductase. If we can clear accutane from your body and boost your true retinol levels, we can get the testosterone and estrogen numbers down and your dht number up.
Just started a 3 component program of defatted beef liver, natural beta carotene, and copper. These are basically all the components of whole beef or human liver, minus the retinol. I believe we must allow our body to make it's own retinol from natural beta carotene in order to recover. Will keep the board posted.
Accutane as every medication has a half-life and is not in the body anymore.
Accutanes fat soluble metabolites get stuck in the cell nucleus, attached to retinoid x and retinoic acid receptors. It's the reason why none of us can tolerate cod liver oil or whole beef liver. Too much retinoic acid. This guy below, most of his solutions to the problem are off, but his core concept is correct.
This mornings liver scan showed improvement but calculary cholecystitis is still there. Adding back the wild yam, tudca, and also lecithin to address the gallstones. I agree with nature crazy guys lecithin and tudca recommendations. I dont agree with his other supplement recommendations.
As far as foods go, milk and gluten are your enemies. Mozzarella cheese, yogurt, whole grain rice, and oats are your friends.
The probiotics in yogurt and cheese deactivate the naturally occurring morphine in milk. Straight milk sends morphine to your brain, and destroys your health.
And you don't need a plate of cooked rice or oats. Quaker makes whole grain rice crisps, and there are plenty of brands of oat based granola bars.
15 hours ago, Thommy280495 said:Yes, that's the test I meant. Thanks for sharing. I won't do it bc Allo turns up normal in the urine, I don't think its representative for what's going on in the CSF. LH and FSH are good biomarkers for what's going on with the HPA axis and can be heightened by mife.That's what happened to Ronnie who got cured by Mife.
@SaffronAideAll the animals in the studies had HPA Hyperactivity. You saying that accutane doing different things is not scientifically, when this is the underlying pathomechanism.
Accutane as every medication has a half-life and is not in the body anymore.
I believe accutane impairs RXR receptor which means VDR, PPAR receptor, Thyroid receptor, and LXR receptor stop working because they are coupled with RXR.
Mif seems like it could work. Dexamethasone as well.
Have you considered the protocol below..
Joekool was on TRT and Anavar before going on HCG, but never mentioned that in his posts. From what I can gather this was the actual protocol. Anavar for two weeks to downregulate AR and hit the GR while also takingHCG + taurine + progesterone (ORAL MICRONIZED). Then come offAnavar and stay on others until fixed.
120-250IU HCG EOD
10G taurine ED
40-100mg Oral micronized prog ED
Well today's biofeedback scan revealed improved liver function, but with degenerative disk issues. Machine recommends chondroitin or glucosamine chondroitin, and so that was added to the protocol this morning. The question is, why the degenerative disk issues? And the answer is, because the body requires glucuronic acid to attach to accutane to flush it out of the body in the form of accutane glucuronide. Glucuronic acid is a derivative of glucose, and is found extensively in chondroitin. Like I said, nature crazy guy from the YouTube video, his core concept is correct, and he was right about the lecithin and Tudca. He was wrong about the other supplements.
Current Supplements includeTudca copperLecithinDefatted beef liverNatural beta caroteneGlucosamine chondroitin. Fingers crossed.
19 hours ago, Andy5 said:I believe accutane impairs RXR receptor which means VDR, PPAR receptor, Thyroid receptor, and LXR receptor stop working because they are coupled with RXR.
Mif seems like it could work. Dexamethasone as well.
Have you considered the protocol below..
Joekool was on TRT and Anavar before going on HCG, but never mentioned that in his posts. From what I can gather this was the actual protocol. Anavar for two weeks to downregulate AR and hit the GR while also takingHCG + taurine + progesterone (ORAL MICRONIZED). Then come offAnavar and stay on others until fixed.
10-40mg AnavarED(no more than two or three weeks then drop)
120-250IU HCG EOD
10G taurine ED
40-100mg Oral micronized prog EDstart all at once and just drop Var two or three weeks in
IfI remember correctly, Joekool had PFS, and people with pfs can recover with hcg. I don't think it can benefit PAS sufferers and @SaffronAidetried it and it didnt work.
44 minutes ago, Thommy280495 said:IfI remember correctly, Joekool had PFS, and people with pfs can recover with hcg. I don't think it can benefit PAS sufferers and @SaffronAidetried it and it didnt work.
I don't believe HCG alone works for either PFS or PAS. I've done HCG solo for 16 weeks straight. No cure.
There is one HCG cure i know, Vicecaz from Raypeatforum. But his recovery didn't last and he creashed back. He took solo HCG for few months i think.
But yeah, what i would do is, trying TRT on high doses for 3 months with HCG+ Progesterone maybe, to see if you have receptor issues or not.
But i think my issue must be gut related. I never reacted good to external androgenic treatments.
Im on my second day of waterfasting, 28 days to go 
Hi everyone! I've read the past 100 pages of the thread. I'm grateful for all of you who are doing the work in trying to figure this out. I'm going to throw my hat in the ring!
I'm a woman, so I know this is going to be very different from y'all...
My side effects are, in order of importance:
- Horrific problems with digestion - isotrentinoin induced celiac disease, SIBO, dysbiosis in my gut, no bile, etc. Luckily I've been tesed multiple times for Crohn's and other IBDs and that's never come up, maybe because I've cut gluten out since 2010.
- vaginal dsybiosis (and therefore painful sex)
- bladder problems (urgency, frequency), which seem to be dependent on my vaginal/gut issues
- Hashimoto's/hypothyroidism (I've been tested for other AI conditions and LUCKILY I am negative on all of those)
- histamine intolerance
- PCOS, but pretty sure this existed before
- dry skin
- slow wound healing
- rosacea
Here's my background --
I've taken the big 4 - antibiotics (proud of myself I haven't taken them since foot surgery in 2014), birth control (only 7 years, UGH), Accutane (1 full round, 1 failed round later...I'm an idiot), SSRIs (for ~6 months, wow NEVER AGAIN that taper was HORRIFIC), born a c-section, had lots of sinus infections as a child, mother took a lot of antibiotics and had a lot of sinus issues, mother craves sugar/alcohol, poor DAO genes
Here are my genetics:
MTHFR heterozygous, PCOS, poor DAO genes, poor VDR uptake, MAO-A issues,
Here's what's helping me --
- SAM-e immediately darkened my stools and lightened my mood because it helps with methylation and bile flow. I worked my way up to 400 mg 2x per day. Game changer for me.
- Bovine lactoferrn - helped with digestion
- nose surgery to help with deviated septum so I could sleep more thoroughly
- magnesium spray (helps me get into a deeper sleep)
- sunlight
I just got a GI Map and sent it off today, so I will post what I find. I do think that the gut theory is a big part of it. Whether I can heal my gut, I'm not sure, but I'm sure as hell going to try!
I need to apologize for putting so much stock into the naturecrazy YouTube video guy. He seems like an expert, and I was misled. I'm shifting away from that approach and trying some apigenin after it arrives tomorrow night.
Accutane syndrome has always felt like ptsd, with ibs-d and insomnia. My biofeedback machine has always listed chamomile as one of the top homeopathics. Homeopathy pellets is easily the weakest form of natural medicine. I never have and never will believe in it.
Whole herb chamomile is high in fodmaps, so it's no good for ibs due to the fodmap issue. But what if you could extract a certain component from chamomile that could singlehandedly address our issues? What if that component is apigenin? It seems to be a miracle worker for sleep and ibs issues based on the Amazon reviews I've read. First dose of apigenin should be tomorrow Friday night. Will see what happens.
Welcome aboard hh6, thank you for the input.
People people people. STOP! I cured my 12 year long term side effects of accutane! I did. I really did!
ready?...
i changed my diet. BOOM! What a concept!This is what I eat:
-all kindsofhigh water fruit
-simple salads (with clean avocado oil based dressings...Primal Kitchen makes great ones)
-meat! High quality meat! Organic pasture raised chicken, steak, ground beef, etc (salt free spices...Mr Dash makes a good one)
-only 3 supplements: digestive enzymes, probiotics, and collagen peptides
message me for more details. My life CHANGED 5-6 months ago when i made this change and I'd love to help others implement it!
L3, you were not suffering from accutane syndrome. You were suffering from a poor diet. We are suffering from accutane syndrome. I already eat grass fed beef on a regular basis. Pigging out on fruits and veggies makes our issues worse, not better. Wipes out our already low post accutane cholesterol levels. Collagen makes our liver issues worse, not better. Get lost.
A biofeedback scan of my prostate today indicated low retinol levels. I've gone back to whole beef liver, broccoli sprouts and tudca, washed down with organic kefir. Probiotics inhibit beta glucuronidase. Not even going to try the apigenin right now.
If the biofeedback machine indicates low vitamin A in my prostate, and my prostate has always been a major issue, then I will give this another try, minus the milk and with the kefir this time.
On 4/1/2022 at 6:32 AM, HopefulHuckleberry6 said:Hi everyone! I've read the past 100 pages of the thread. I'm grateful for all of you who are doing the work in trying to figure this out. I'm going to throw my hat in the ring!
I'm a woman, so I know this is going to be very different from y'all...
My side effects are, in order of importance:
- Horrific problems with digestion - isotrentinoin induced celiac disease, SIBO, dysbiosis in my gut, no bile, etc. Luckily I've been tesed multiple times for Crohn's and other IBDs and that's never come up, maybe because I've cut gluten out since 2010.
- vaginal dsybiosis (and therefore painful sex)
- bladder problems (urgency, frequency), which seem to be dependent on my vaginal/gut issues
- Hashimoto's/hypothyroidism (I've been tested for other AI conditions and LUCKILY I am negative on all of those)
- histamine intolerance
- PCOS, but pretty sure this existed before
- dry skin
- slow wound healing
- rosacea
Here's my background --
I've taken the big 4 - antibiotics (proud of myself I haven't taken them since foot surgery in 2014), birth control (only 7 years, UGH), Accutane (1 full round, 1 failed round later...I'm an idiot), SSRIs (for ~6 months, wow NEVER AGAIN that taper was HORRIFIC), born a c-section, had lots of sinus infections as a child, mother took a lot of antibiotics and had a lot of sinus issues, mother craves sugar/alcohol, poor DAO genes
Here are my genetics:
MTHFR heterozygous, PCOS, poor DAO genes, poor VDR uptake, MAO-A issues,
Here's what's helping me --
- SAM-e immediately darkened my stools and lightened my mood because it helps with methylation and bile flow. I worked my way up to 400 mg 2x per day. Game changer for me.
- Bovine lactoferrn - helped with digestion
- nose surgery to help with deviated septum so I could sleep more thoroughly
- magnesium spray (helps me get into a deeper sleep)
- sunlight
I just got a GI Map and sent it off today, so I will post what I find. I do think that the gut theory is a big part of it. Whether I can heal my gut, I'm not sure, but I'm sure as hell going to try!
You have to do a water fast. It will cure you, join our Telegram water fasting group, will send you through PM.
[Removed]
Guitarman's microbiome research still interests me. What if accutane impacted the microbiome in such a way that the body no longer absorbs beta carotene? What if apigenin could reverse this change in the microbiome? I think I'll stick with apigenin and chamomile only for a while as far as supplements go.