Ulcerative Colitis / IBD

[Mey]

I think we have a pretty good idea. Likely a compromised system from poor microbiome + too many cells in G2/S phase (acute stress response) of replication while exposure to environmental/solar radiation or some kind of toxin that dysregulates mitochondria. Then we get too much ROS, too much mito fission. This sets off a cascade of problems afterwards (including inflammation) because it dysregulates systemic metabolism, microbiome more so, and mineral/protein balance. I would 100% expect there to be variation between individuals regarding what second-order effects are seen, so debating those second order effects seems kind of like intellectual masturbation IMO.

The problem starts at the cellular level and works it's way up to more systemic levels. This is why things like radiation exposure (whether ambient or direct) can cause UC - but when they know it's caused by radiation they just call it radiation colitis, but there is no difference between the two conditions. ROS/fission is the first response. What happens afterwards, although interesting, is much less relevant for finding a treatment.

Just my two cents.

But yes, if this is just an intellectual activity in trying to discover all of the systems that are dysregulated when there is excess ROS/mito fission, then by all means carry on. I just don't want other people getting the idea that this is discussing a true treatment. The treatment is fasting. The more we discuss it the more it becomes clear to me. The refeed is all about raising HCl first before introducing protein - but this has been in practice in many fasting clinics for a long time.

I fast 30 days intermittently (16/8) every year but after 3 years I am not cured yet.

 

[mattyb]

I fast 30 days intermittently (16/8) every year but after 3 years I am not cured yet.

IF does not do much. It could help mitigate problems, but it won't fix UC. To fix UC, or most inflammatory conditions, you need to do a long fast (not IF, water or breuss), long enough for cells to clean up excess fractured mitochondria and chelate excess metals from autophagotic processes. Depends on the severity of the issue, could be as long as ~40 days.

IF will do a few things, it will put pressure back on cortisol to get it start producing again, might help with some very minor amounts of fission, but beyond that not much. ADF could be effective if practiced for a very long time (like a year), but it still won't do much compared to a full fast.

 

[Nighteyes]

MgCl, KCl, and NaCl are fine. I always prefer food for myself though.

You can try out other dietary sources, most vegetables are high in chloride. Rye bread is high in chloride. You can always try greens with no oxalates - most lettuces are low in oxalates and have decent amounts of chloride. Greek salad is my favorite type of salad: cucumber, tomatoes, purple onion, red/green peppers, olive oil, salt, goat cheese, and oregano - and olives if you like them, but I hate olives.

Steaming or boiling vegetables and greens will reduce the oxalate content significantly as well, by as much as 75%. Most of my veggie intake, especially in winter, is through cooked veggies. My grandma, who is a very healthy 87 and on the path to crossing 100, never eats raw vegetables (or drinks milk, or eats cheese) and swears by it.

Thanks matty - funny you should mention rye bread! It is the season for rye bread here in the north and I crave it for sure so I wont hold back then. I try and vary the salads to rotate the different type of leafs. Some definitely are worse at creating the coated feeling in my mouth from the oxalates. I have also cut back on the breuss juices I make as I think it contributes with a lot of oxalates as well. Increasing dairy (cheese and yoghurt) is a tool for binding oxalates too I suppose. And occational charcoal.

 

[Helen]

@HerrFisch

https://www.ncbi.nlm.nih.gov/pubmed/13129463

https://link.springer.com/article/10.1007/BF02706326?no-access=true

 

[Helen]

http://www.ebi.ac.uk/pdbe/widgets/QuipStories/insulin/insulin.pdf

Insulin has histidine so, I guess one can observe levels of histidine by insulin levels, hemoglobin levels, and cortisol levels.

 

[Helen]

http://ajcn.nutrition.org/content/87/6/1860.full

 

[Helen]

@HerrFisch

If you have high histidine , lets say , then may be zinc with beta alanine to form carnosine and lower it?

 

[Helen]

It is so weird I found so many posts of people with different diseases , starting from MS to alzheimers to IBD, ME, CFS And most of them had low histidine levels in serum. They tested it . Now we have to figure out , is this an actual imbalance or this is a compensation for another imbalance.

I know low levels of folate can cause histidine waste. Could this be a problem? I

 

[Canari]

It is so weird I found so many posts of people with different diseases , starting from MS to alzheimers to IBD, ME, CFS And most of them had low histidine levels in serum. They tested it . Now we have to figure out , is this an actual imbalance or this is a compensation for another imbalance.

In body work we also find imbalances that are compensations, and when you fix the compensation, then you have the boomerang coming back in the face! Seem to be equivalent to withdrawal symptoms.

Then I know sb who made a body method that fixes asthma, by removing the fantom signals on the vagus nerve, and then of course it could also cure eczema, as people go from one to the other often.... then it also showed that it worked for pso AND ALLERGIES. And he was figuring out that it could also help MS... (no scam for asthma and eczema, I know cured people)

 

[HerrFisch]

It is so weird I found so many posts of people with different diseases , starting from MS to alzheimers to IBD, ME, CFS And most of them had low histidine levels in serum. They tested it . Now we have to figure out , is this an actual imbalance or this is a compensation for another imbalance.

yes, that article I posted before said that too. As decreased histidine levels predict risk of relapse in UC.
Thats why I would say that its low levels of histidine in UC/ my case.

I think that the gut microbiome/ gut barrier has something to do with it too.

 

[Helen]

http://www.encognitive.com/files/Ur...tion in Patients with Classical Allergy_1.pdf

@HerrFisch

 

[HerrFisch]

I just can't help but think to myself that low histidine is a problem that will mostly fix itself when the underlying cause of the disease in question is fixed

I also think that if you would somehow solve the problem of mito fission, low histidine will fix itself. Maybe just by less need for histamine. Without inflammation you dont need as much. (Fasting)

But otherwise UC is a disease where you are stuck in inflammation for some time, the possibility to get depleted is pretty high.
And with little Acetate, Butyrate and Propionate, and therefore bad intestinal epithelial barrier, I'm sure your needs for histamine will hold on. If there is pathogens on that barrier, the immune system reacts. And that immune reaction consists of histamine.

And as some Antihistamines can make things better and some make things worse (different receptors), I think Histamine is just one effect of Inflammation.

But if the gut barrier is built back up, and the body is not reacting as fast with inflammation (&histamine), maybe ROS is not a problem anymore.
I mean, there are so many ways to cope with excessive ROS which are all pretty much low. And some of them need histidine, which gets depleted with high demands on histamine.

But with no barrier, the immune system needs to react as quickly as possible. And it does so with Histamine to increase permeability for white blood cells & fight pathogens.

I think that the immune system is reacting too fast on ROS because theintestinal epithelial barrier is bad.
Maybe with intact barrier, all ROS scavengers would work and inflammation would not start as fast as effect of high ROS?

And @mattyb , I know you think fasting will help UC in every way. But I think its important to focus on healing too. ROS will be back at some time after the fast.

 

[mattyb]

And @mattyb , I know you think fasting will help UC in every way. But I think its important to focus on healing too. ROS will be back at some time after the fast.

I can absolutely agree with this. This is why I think doing the refeed in a proper manner is so important. It is not just about the fast, it never has been. If you fast and just go back to eating like shit and not taking care of yourself your risk of relapse will be way higher. It's a sustained approach that must be maintained until things are 100% healed.

 

[HerrFisch]

When a UC person fasts, ROS will go down, inflammation will go down, and pressure will be taken off HDC. CRH may put a bit of pressure back on HDC while fasting, but it won't be even close to the stimulation they were getting from ROS/inflammation. UC is much more an issue of localized tissue damage and inflammation upregulating HDC.

Why do we focus so much on getting ROS down with fasting? Its for sure one way to get rid of it (temporarily) I think we need to understand the reason for that ROS / high fission.
To some extent, ROS is normal.

Its like Blood pressure.
Its not about to lower it in general. Its about to know why its not regulating anymore. Always high is not good. As is always low.


Epithelial barrier function in UC is damaged.
Once ROS increases, ROS can go near that barrier.
Immune system reacts (too) quickly on that "pathogen" because of that reduced "safety space" (barrier).
With H2o2, that barrier cant get repaired. -> http://www.physiology.org/doi/full/10.1152/ajplung.00177.2003
H2o2 working like a desinfectant reduces SCFA producers and beneficial bacteria.
If Acetate, Propionate and Butyrate as HDAC inhibitor is missing, fission is high. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2036.2007.03562.x/full
So no resistance against ROS. Always full immune system reaction (+histamine). And no stop to fission because of no SCFA.
-> More ROS

I think with a good barrier, and therefore without the immune system reaction, SOD CAT Glutathione could all work to get rid of ROS. (With help of histidine )
So mito fission would lower itself after that. And there would be no need for TCells and Histamine and all that crap. It would be regulative.

But with that missing barrier, which acts like a open wound, even the smallest increase in metabolism produces enough ROS, which will go as "detected pathogen" on that barrier.
And if you have high ROS and ongoing inflammation, all histidine will be used for Histamine (h2o2-> increased HDC).
Thats why you wont get into a flare that easy when you are in remission for some years.
But if you get flare after flare, your histidine will depleted and all antioxidant defensive mechanisms are low.

Basically Butyrate is the barrier against ROS and the brake for mitochondrial fisson which causes ROS.



Inhibition of butyrate oxidation in experimental animals resulted in mucosal inflammation similar to ulcerative colitis.
I think we should focus more on SCFA in the gut. Butyrate is regulating mitochondrial fission and fusion in the gut.
https://www.intechopen.com/books/au...short-chain-fatty-acids-in-colon-cancer-cells

Potential beneficial efects of butyrate in intestinal and extraintestinal diseases
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3070119/

Butyrate is doing everything we want. And if we want to lower ROS and fission local in the gut. -> its butyrate thats missing local in the gut thats doing that.

Inuline which increases Butyrate, but only really slow, stopped my UC flare in 2 days. And it stopped ~8 months flare from @wuf in only a few days too.
I think we should not leave that behind.

Again what Butyrate does:

-preservation of gut barrier functions
-protection against pathogens by producing bacteriocins
-resistance to oxidative stress (ROS)
-inhibition of nuclear factor κB
-regulating IL-1b, TNF-α, IL-2, IL-6, IL-8, IL-12
-produce vitamins, antioxidants, polyphenols, and conjugated linoleic acids

 

[mattyb]

Why do we focus so much on getting ROS down with fasting? Its for sure one way to get rid of it (temporarily) I think we need to understand the reason for that ROS / high fission.
To some extent, ROS is normal.

Its like Blood pressure.
Its not about to lower it in general. Its about to know why its not regulating anymore. Always high is not good. As is always low.


Epithelial barrier function in UC is damaged.
Once ROS increases, ROS can go near that barrier.
Immune system reacts (too) quickly on that "pathogen" because of that reduced "safety space" (barrier).
With H2o2, that barrier cant get repaired. -> http://www.physiology.org/doi/full/10.1152/ajplung.00177.2003
H2o2 working like a desinfectant reduces SCFA producers and beneficial bacteria.
If Acetate, Propionate and Butyrate as HDAC inhibitor is missing, fission is high. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2036.2007.03562.x/full
So no resistance against ROS. Always full immune system reaction (+histamine). And no stop to fission because of no SCFA.
-> More ROS

I think with a good barrier, and therefore without the immune system reaction, SOD CAT Glutathione could all work to get rid of ROS. (With help of histidine )
So mito fission would lower itself after that. And there would be no need for TCells and Histamine and all that crap. It would be regulative.

But with that missing barrier, which acts like a open wound, even the smallest increase in metabolism produces enough ROS, which will go as "detected pathogen" on that barrier.
And if you have high ROS and ongoing inflammation, all histidine will be used for Histamine (h2o2-> increased HDC).
Thats why you wont get into a flare that easy when you are in remission for some years.
But if you get flare after flare, your histidine will depleted and all antioxidant defensive mechanisms are low.

Basically Butyrate is the barrier against ROS and the brake for mitochondrial fisson which causes ROS.



Inhibition of butyrate oxidation in experimental animals resulted in mucosal inflammation similar to ulcerative colitis.
I think we should focus more on SCFA in the gut. Butyrate is regulating mitochondrial fission and fusion in the gut.
https://www.intechopen.com/books/au...short-chain-fatty-acids-in-colon-cancer-cells

Potential beneficial efects of butyrate in intestinal and extraintestinal diseases
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3070119/

Butyrate is doing everything we want. And if we want to lower ROS and fission local in the gut. -> its butyrate thats missing local in the gut thats doing that.

Inuline which increases Butyrate, but only really slow, stopped my UC flare in 2 days. And it stopped ~8 months flare from @wuf in only a few days too.
I think we should not leave that behind.

Again what Butyrate does:

-preservation of gut barrier functions
-protection against pathogens by producing bacteriocins
-resistance to oxidative stress (ROS)
-inhibition of nuclear factor κB
-regulating IL-1b, TNF-α, IL-2, IL-6, IL-8, IL-12
-produce vitamins, antioxidants, polyphenols, and conjugated linoleic acids

The reason for the excess ROS is because that is the first stage in the inflammatory cascade. For example, if you are exposed to solar or non-natural irradiation, it directly creates hydroxyl radicals out of water. What actually happens afterwards though, is that peak superoxide production during the next 72 hours decreases because the mitochondria have been damaged from hydroxyl radicals and this localizes DRP-1 and fragmentation begins in order to upregulate metabolism, then you get a sharp and sustained increase in ROS once fission is going. We don't want to stop our body from making ROS - not at all, part of the reason fission is occurring is because a key ROS from metabolism wasn't there for a short period of time. Nothing will ever stop that, ROS are essential to biological function. We just want to lower the relative amount for an extended period of time to give the tissues some time to heal and become more robust. And then we want to enhance our bodies ability to neutralize early stage ROS so things don't get out of hand in the during the next exposure. Everyone gets exposed to solar irradiation, but not everyone develops an auto-immune condition for it. That's because the tissues need to be robust, and that's where things like butyrate, gut barriers, and gut bacteria come into play.

We fast not just to lower ROS, but mainly to upregulate mitochondrial fusion to it's maximum. Yes, butyrate will regulate fusion, but it will not lead to a full reversal because the environmental pressure to engage in protein recycling isn't that strong. We want to use the natural process of autophagy to clean things up, because it's more powerful than any exogenous stimulant. It's the difference between giving a person who just ate an appetite stimulant to get them to eat more, or just starving a person for a while and putting food in front of their face. The latter option will always work better. At least that is my suspicion. I wholeheartedly encourage you to experiment with things like inulin to get butyrate up if you think that is a good strategy though. It is better to try something than do nothing IMO, especially if the intervention is low risk and not that difficult.

I think butyrate is 100% necessary for healthy gut function, but we establish good bacteria that make butyrate for us during the refeeding phase. That's when the person truly recovers and becomes robust to any future flare ups. I also think consuming dietary sources of butyrate on top of that is very beneficial. Finding a good high quality grass fed butter and cooking with that frequently is a really good idea, it's a regular part of my diet. I also use a good grassfed milk for some recipes (even though I don't drink much milk these days).

 

[Canari]

establish good bacteria that make butyrate for us during the refeeding phase.

What's about AIP?
AIP
autoimmune wellness

 

[mattyb]

What's about AIP?
AIP
autoimmune wellness

It takes a similar approach to the refeed I've outlined. You start with really basic foods and easily digestible foods and then slowly work your way back up to a more diverse diet.

 

[Helen]

http://encognitive.com/files/Histidine-GLA-Zinc Complex to Block Pain & Inflammation in Treatment-resistant Sydromes_0.pdf

 

[HerrFisch]

Re: Mitochondrial problems.

I though I would write down ALL my Labs here. To have everything at one place.

Blue=too low
Red= too high

oxidized LDL 527 ng/ml (range<133) (in APRIL)
oxidized LDL 175 ( in SEPTEMBER)
DAO 16,3 U/ml (range >10)

Blood:
Sodium 1965 mg/l (range 1900-2000)
Potassium 2097 mg/l (range 1750-1850)
Calcium 57,3 (range 59-61)
Magnesium 40,3 (range 34-36)
Copper 0,82 (range 1,1-1,2)
Iron 559 (range440-480)
Zinc 7,3 (range 7,3-7,7)
Selenium 136 (range 100-140)

Blood levels adapted:
Sodium 2158 mg/l (range 1900-2000)
Potassium 1879 (range 1750-1850)
Calcium 62,9 (range 59-61)
Magnesium 38,2 (range 34-36)
Copper 0,84 (range 1,1 -1,2)
Iron 487 (range 440-480)
Zinc 6,5 (range 7,3-7,7)
Selenium 122 (range 100-140)

Dont really know what the difference is between blood levels and blood levels adapted. They do really differ.

Hematocrit 0,48 l/l (range 0,39-0,52)
Lipidperoxidation 35 umol/l (range<200)
(Lipidperoxidation in September 20 umol/l)

Lactate in April 934 umol/l (range <1528)
Lactate in September 1860
Pyruvate in April 272 (range 58-136)
Pyruvate in September 152

CoQ10 APRIL & SEPT 0,48 (range 0,88-1,43)
Cholesterol 142 (range <200)

Biotin >600 (range >200)
Vitamin C 11,7 (range 4,5-24,5 but opitmal 14-25)
Vitamin B6 140 (range 4,1-43,7) I took some p5p back then.
B12 in April 597 (range 200-1000)
B12 in Sep 665
Vitamin D3 25 OH: 148 (range 62-170)
Folic acid 760 (range 480-1210)

CRP 0,31 mg/l (<0,5)
Homocysteine 8,3 umol/l (range <12)
Lipoprotein a <7 (range <75)
malondialdehyde APRIL 3,4 (range 1,2-2,8)
Malondialdehyde SEPT 2,3

intestinal bacteria:
ok : echeria coli, coli biovare, proteus species, klebsiella species, pseudomonas species, enterobacter species, serratia species, hafnia species

too low:
Enterococcus species <1,0 x10^4 (range10^6-10^7)
bifidobacterium species 10^7 (range 10^9-10^11)
Lactobacillus 10^5 (range10^5-10^7)
Bacteroides species 10^9 (range10^9-10^11)

Candida species normal
Cadida albicans normal
Geotrichum candidum normal

fecal ph 6,5 (range 5,8- 6,5)

pancreatic elastase in stool 313 (range>200)
bile acid in stool negative

Calprotectin 44,98 (range <50)
Alpha 1Antitrypsin 51 (range<27,5)
Zonulin 29 (range<55)

Histamine in stool 3504 (range<600)

m2-PK 3,1 (range <4)

Fructose ok
Sorbitol ok

Cortisol
7 AM 4,3 (range 3-9)
1 PM 1,17 (range 0,6 -2,4)
PM 1,91 (range 0,2- 0,8)

New neutransmitter after 5HTP

Serotonin 108 (range 140-230)
Adrenaline 2,59 (range 4-10)
Norephineprin 15,22 (range 32- 55)
Dopamine 79 (range 150 -280)
Kreatinin 494 (range 400-2780)

Estradiol 31 pg/ml (range 11-43)
Progesterone 19 ng/dl (range 5-14)
Testosterone free 12 pg/ml (range 7-36)
Prolactin 18 (4-15)
DHEA-S 259 (range 210-490)

FEB 17
TSH: 4,13

SEPTEMBER 17
T3 4,3 (2-4,4)
T4 1,6 (0,9-1,7)
TSH 2,9

If I go back to my blood work, Im still not too sure why my progesterone and prolactin is that high.

About that high lactate again, @mattyb do you think it was that high for all the time I have UC now?

@gbolduev whats weird is, that on this labs I actually have too high blood-iron levels

 

[mattyb]

I don't trust any of those blood tests because they don't make sense. Their electrolyte reference ranges are way off.

You need to go to a different lab, I don't know what the hell is going on with the lab you went to.

Also you were doing things like keto around these blood tests. You need fresh tests from when you haven't been screwing around with things that much.