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Some ideas re Chris Armstrong's presentation at Stanford

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
Ah, but what does a healthy person's digestive system look like? Its hard to know as most people's digestive systems have been artificially altered through ingestion of processed foods, pesticides, antibiotics, genetically modified foods, and high carbohydrate nutrient poor foods.

One can go through the entire system, step by step, looking at the integrity of structure for each digestivecotgsn, proper biochemical production and microbiome composition. There are interventions to improve structural integrity, improve biochemistry and manipulate microbiome composition.

Digestive enzymes are one such intervention.

One can't regain health without good attention to optimizing digestive function, but this alone will not cure most of us. It may be a component of a cure, but there are another systems gone awry that need to be righted.
 

bertiedog

Senior Member
Messages
1,738
Location
South East England, UK
Probiotics would probably be best if they were precursor foods, rather than bacteria. For bacteria it seems acidophilus is a poor choice for us, and bifidus might be better.

This is definitely the case with me. Just one day of taking a probiotic with Lactobacillus Acidophilus brought back SIBO whereas taking Bifido bacteria in the form of Activia every day has really settled the SIBO and made my gut/stool function much improved. This is since the beginning of September.

I am also trying individual probiotic strains, 2 weeks of each one. Have just finished L Fermentum M3 and now on L Rhamnous but not sure yet whether they are good for me or not. The other one that really suits me is the soil based probiotic Prescript Assist.

Pam
 

bertiedog

Senior Member
Messages
1,738
Location
South East England, UK
What I suspect is that if digestion is compromised then many tiny meals might be much better than larger ones as they are less likely to overwhelm digestion. However this would also mean that the digestive system was on all the time.

Just to say this also suits me, I can only eat small meals so do need a top up of something like peanuts/cashews/pumpkin seeds/sunflower seeds about 2 - 3 hours after a main meal. Eating this way has kept me slim I am pleased to say but carbohydrates don't suit me especially gluten which I completely avoid. I do well with fat, vegetables, small amounts of meat and fish plus regular amounts of nuts/seeds.

Pam
 

Richard7

Senior Member
Messages
772
Location
Australia
I have been looking at a lot of commercial enzyme formulations and there is one (Klaire Labs Sibb Zyme) that is described as brush border support and should emulate it.

I have ordered it and when it arrives (in a few weeks as I could not find an Australian reseller) I will use it along side my Creon, ox bile, betaine HCL and pepsin.

There seem to be a lot of formulations that contain the same enzymes but also contain cellulases and hemicellulases and other enzymes that break down fibre which I do not want to do. My aim after all is to try to emulate a healthy digestive system.
 

Ben H

OMF Volunteer Correspondent
Messages
1,131
Location
U.K.
Hi.

This may take a bit to explain. But it relates to Chris Armstrong's presentation at Stanford. The one in which he explained that pwme/cfs seem to be locked into a vicious cycle.

The steps are:
1) we do not have enough ATP so we switch on AMP kinase;
2) which puts our cells into an energy efficient mode that favours the use of lipids and proteins for energy;
3) which means that they no longer have those lipids and proteins available for making enzymes and bile;
4)which means that fats and proteins are not properly digested in the small intestine and pass through to the colon;
5) where they change the balance of our gut bacteria leading to an increase in production of Short Chain Fatty Acids;
6)which in turn trigger AMPK, reinforcing the cycle.

And we do in a sense seem to have a kit to deal with this.
1) Betaine HCL plus pepsin allow us to emulate the acid and pepsin production and release of normal people breaking proteins into peptides.
2) Creon or another source of animal derived pancreatic enzymes can then break these proteins into small oligopeptides
3) ox bile to break fat down into manageable globules and lipases (in the Creon) to break them down into monoglycerides and free fatty acids.

(The creon also works on carbohydrates too but Armstrong was focussed on proteins and lipids, so I have too.)

I think that there is a problem though. We can kind of approximate a working stomach and pancreas and gall bladder but we are not replicating the brush border enzymes that activate some of the pancreatic enzymes and turn the oligopeptides into the amino acids, dipeptides and tripeptides that we can absorb.

(For lipids I think that the Creon and ox bile should be enough to do the job.)

I got to thinking about this because I was playing around with Oral Rehydration Solutions to try to reduce the severity of my PoTS.

In reading the ORS research I found that there are the usual sodium, potassium, glucose and citrate or bicarbonate solutions and others that use cooked cereal flours in the place of glucose. It seems like the cereal had an advantage when trying to rehydrate people with diarrhoeal infections that did not damage the gut, but were a disadvantage for those with infections that had damaged the gut.

The trick to ORS is glucose sodium symporters. These transport equal numbers of sodium ions and glucose molecules into the cells and create the osmotic pressure that brings the water across from the small intestine into the body. The cereal solutions uses brush border enzymes to break the carbohydrates into the glucose needed to make the trick work without increasing the osmolarity of the solution.

When I tried the cereal solutions on myself I found that they were indistinguishable from ORS minus glucose. Which is to say that they were of little use. I conclude from that rather unprofessional n=1 experiment (2 litres solution on 2 days) that they did not work for me, But had to read and think for a few weeks before it occurred to me that this might be because my brush border enzymes are not being produced, or not being produced in sufficient quantities.

The normal ORS really helps with the PoTS but I have issues with having too much glucose - it makes me feel ill, makes it hard to sleep, it feels a bit like being drunk.

So it occurred to me that it should be possible to use the same principle as ORS with sodium dependent amino transporters. So I tried it with whey protein and like the cereal based ORS it had no effect. (Even when I took it with Betaine hcl, Pepsin and Creon).

Which lead me to read about brush border enzymes and here.

My hope with the Betaine HCL + pepsin + oxbile +Creon combination was to digest and absorb the nutrients my body needs and to provide the right substrates to grow the right bacteria and get rid of the dysbiosis that is characteristic of ME/CFS.

I think Chris Armstrong's presentation underlines the importance of sorting out this dysbosis.

And the current kit has improved things, but if I am right it cannot get someone all the way.

What I am wondering is if people who have a better handle on the biology and biochemistry are aware of exogenous sources of enzymes that can fill the role of brush border enzymes.

Or if taking amino acids (glutamine and luecine perhaps) or something of the sort might be able to get those cells on the brush border to down regulate AMPK or at least get the lipids and aminos needed for making the brush border enzymes.

Or if I am just very very wrong, and have misunderstood something important.

In reading up on the above I have chiefly relied on this site for info on digestion.
http://www.vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/index.html

Keep at it @Richard7 . I've been looking at this theory recently too! I really enjoyed Chris's talk (and his work in general).


B
 

pattismith

Senior Member
Messages
3,931
I understand that AMPK inhibits mTOR, but I didn't understand how AMPK is activated in ME...

AMP which is an AMPK activator is low in ME, so do we know what is the pathway?


upload_2017-11-7_23-44-21.gif

( https://molecular-cancer.biomedcentral.com/articles/10.1186/s12943-017-0648-1 )

edit: I don't understand either why rapamune (an mTOR inhibitor) helps :bang-head:
 
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anni66

mum to ME daughter
Messages
563
Location
scotland
Low ATP activates AMPK. From testing both cellular and mitochondrial ATP levels are low for my daughter which explains the level of compromised function she has
 

Murph

:)
Messages
1,799
Low ATP activates AMPK. From testing both cellular and mitochondrial ATP levels are low for my daughter which explains the level of compromised function she has

AMPK cares about the ratio of ATP to ADP and AMP. If ADP or AMP is higher than ATP, it will turn on.

Naviaux measured outside the cell and found far higher ATP than AMP. That would suggest no AMPK activation.

But. AMPK is inside the cell. And if the abundant AMPK otuside the cell has come from inside the cell (this is precisely what naviaux's purinergic signalling theory is), there could be an ATP shortfall inside, leading to AMPK activation.

--
Lots of things in me/cfs seem to be activating ampk in the background. Also, A lot of PEM triggers seem to be things that activate ampk. Exercise, for one.

One idea I'm toying with is that ampk has been so perpetually hyper-activated that it is no longer really receptive to the activation signal, and when it is supposed to kick in it doesn't. Whatever positive processes it is supposed to produce don't happen and we feel terrible. (Precisely what is downstream of ampk seems to be glossed over in all the papers- I'm not sure we know all that well how it works).
 
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rodgergrummidge

Senior Member
Messages
124
I understand that AMPK inhibits mTOR, but I didn't understand how AMPK is activated in ME...

AMP which is an AMPK activator is low in ME, so do we know what is the pathway?

@pattismith @Richard7 @Ben H ATP is a universal energy source for essentially all our cells. ATP is 'burnt' to produce energy and the spent fuel is ADP and AMP.
Several metabolic studies in CFS patients have shown that they have defects in their ability to generate energy in the form of ATP. In such situations their ATP/AMP ratios are low. Cells have internal rheostats that constantly monitor ATP/AMP ratios and if they fall to low levels, cells respond to the energy crisis by activating a number of pathways to restore the deficit. One of the key enzymes that is activated by a low ATP/AMP ratio is AMPK which regulates an 'energy crisis program' in order to restore ATP levels. Unfortunately, because some CFS patients have mitochondrial defects in ATP production, ATP/AMP ratios can be chronically (or intermittently) low leading to the chronic (or intermittent ) activation of AMPK. Activated AMPK promotes 'energy sparing' by reducing non-essential anabolic pathways that may include restocking glycogen energy reserves, building new tissues, repairing damaged tissues and performing important tissue maintenance. The reduced levels of all these processes is thought to contribute to the reduced capacity of CFS patients to exercise as well as their prolonged recovery (PEM) after exercise.

edit: I don't understand either why rapamune (an mTOR inhibitor) helps

Several people have mentioned that rapamycin (or rapamune) can help in CFS and have mentioned several cases in Dallas (I think?). However, no-one seems to know the origin of the story, where the treatments were performed, how many patients, or any other details. Based on these stories, several people were going to try rapamycin. It would not be something I would try. In fact is 'on-target' activities of immunosuppression could actually make CFS worse or cause longer-term immune problems.

Rodger
 

anni66

mum to ME daughter
Messages
563
Location
scotland
AMPK cares about the ratio of ATP to ADP and AMP. If ADP or AMP is higher than ATP, it will turn on.

Naviaux measured outside the cell and found far higher ATP than AMP. That would suggest no AMPK activation.

But. AMPK is inside the cell. And if the abundant AMPK otuside the cell has come from inside the cell (this is precisely what naviaux's purinergic signalling theory is), there could be an ATP shortfall inside, leading to AMPK activation.

--
Lots of things in me/cfs seem to be activating ampk in the background. Also, A lot of PEM triggers seem to be things that activate ampk. Exercise, for one.

One idea I'm toying with is that ampk has been so perpetually hyper-activated that it is no longer really receptive to the activation signal, and when it is supposed to kick in it doesn't. Whatever positive processes it is supposed to produce don't happen and we feel terrible. (Precisely what is downstream of ampk seems to be glossed over in all the papers- I'm not sure we know all that well how it works).
Thanks@murph. I' m not at all scientific but learning. Ox phos is also inefficient and ADP to ATP conversion crap - so energy mechanism is pretty screwed...
 

Richard7

Senior Member
Messages
772
Location
Australia
Well I have had some feedback from the enzyme companies,

Creon's proteases are inactive zymogens. So the amylase and lipases will work but the proteases will not unless they are activated by an appropriate protease.

In a healthy gut some trypsinogen (a zymogen) is converted into trypsin by a brush border protease and the trypsin then converts the rest of the trypsinogen and other zymogens into active proteases.

It seems wrong to me that they can even list HUT values on proteases that are not active, or that are part of preparations that are not self activating.

The SIBB Zymes on Klaire Labs site they say
A variety of genetic and acquired factors can disrupt the small intestine brush border, which may result in low activity of brush border enzymes. SIBB-Zymes™ supplies a blend of enzymes normally found in the small intestinal brush border that are critical for the final steps of carbohydrate and protein digestion. Disaccharide enzymes (lactase, maltase, and sucrase) are supplied together with glucoamylase to assist optimal cleaving of sugars and carbohydrates that if left undigested may affect absorption and microbial fermentation, contributing to a shift in the balance of yeast and bacteria.
http://www.klaire.com/prod/proddetail.asp?id=K-SIB

But when I emailled them to ask if the enzymes were capable of activating Zymogens the answer I got was
... the purpose of the DPPIV in the formula is to cleave the proline rich peptide/proline bonds. It is not intended to act as an enzyme activator.

Now I had not asked what the purpose of the DPPIV was, but "Will any of the proteases in Sibb-Zymes cleave the zymogen trypsinogen turning it into the active protease trypsin?" So it is a weird answer/nonanswer but it seems that the SIBB Zymes will not activate zymogens.

I know that there are plant enzymes that are trypsin like (the first ones were found in lettuce in the 60s) but will have to look around for a source.

Its a shame though. If I had tonnes of money I guess I would just get a compounding pharmacy to make something up. Actually SIBB Zymes is pretty expensive, it might be best to talk to a compounding pharmacy ....

I certainly wish I had had the foresight to email the company before ordering their product. I only emailled them as an afterthought, a "i" I was dotting or "t" I was crossing for the purpose of this thread.
 
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RustyJ

Contaminated Cell Line 'RustyJ'
Messages
1,200
Location
Mackay, Aust
I get the complexity and multidimensionality, @Learner1 getting the gut right is not just about digestion and fermentation but peristalsis and other autonomic systems that I cannot get at.

(Well save that I know that it is worse if my diet does not have enough choline, or if my PoTS is too severe.)

But I do think that if we follow Armstrong's logic the obvious thing to do is to fashion a "crutch" that emulates a healthy person's digestion so that we might provide the right substrates to our gut and create the right environment for a beneficial microbiome.

I think from looking around online that this may be possible using appropriate digestive enzymes. I have not yet seen a promising formulation as most of them seem to be designed to also break down fibre which I do not want to do.

I am not sure this is possible, or rather I think it likely that it is not entirely possible but hope that I will be able to get close enough.

I see this as a crutch that will get me on my feet and make life with ME/CFS easier to endure, not a cure to ME/CFS - though that would be nice too.

Have you made any progress on this issue. I recently underwent a colon biopsy which identified inability to breakdown disaccharides (sucrose/maltose/lactose). I am looking for links between this finding and my me/cfs symptoms and possible treatments.
 

Richard7

Senior Member
Messages
772
Location
Australia
@RustyJ 1st I think its great that you have this evidence. I do not know if @ChrisArmstrong needs any confirmation but I have tagged him anyway.

My progress has been uneven. I had considerable improvement in late 2017 and in the beginning of 2018, but still had occasional diarrhoea, was tested for parasites, found positive and took antibiotics and lost my mind to fog and stupidity for most of the year.

And my understanding of the issues has evolved.

I would say that from the time I got ME/CFS till late 2017 I suffered from malabsorption diarrhoea, which is a kind of slurry, not watery. Taking Creon, Sibb Zymes, ox bile and betaine HCL with pepsin dealt with malabsorption diarrhoea, but it did not solve digestion.

I also think that for all or much of that time my gut has favoured SCFA production. I suspect that this is a ME/CFS adaptation, that the SCFAs are a work around to getting energy to the brain and other organs. My idea being that the gut has ways of favouring some bacteria and types of fermentation over others.

That I was producing SCFAs was pretty apparent from the smell, and measurements using a
Ketonix breath acetone metre.

That I depended upon them is pretty evident from the way I declined when I tried a GAPS diet (very low fibre) or had antibiotics.

Late last year I went back onto a ketogenic diet, but one with a lot of fibre and found myself in a cycle where I would have some days with reasonable stools, then produce a lot of SCFAs and get rather acidic watery diarrhoea and start the cycle again.

At the moment I am on a paleoketogenic diet, or almost - I am on the PKD + coffee, enzymes, Betaine hcl, ribose, inositol, ox bile, electrolytes, vitamin k2 and L rhamnosus*. https://www.paleomedicina.com/en discussed here https://forums.phoenixrising.me/threads/carnivore-diet-for-me.57009/page-5

I am not consuming sugars or starches so I am not taking an invertase or maltase. I eat one or twice a day and, very roughly, my meals tend to be about 40-50g protein and 80 -100g fat at the moment, and they are taken with 3x Creon 25,000, 3x Best Naturals betaine HCL with Pepsin, 0.5x Houston Enzymes AFP Peptizyde and 1x Houston Enzymes Lypazyme. At the moment I seem to need about 250mg of ox bile a day, which I take about 30mins to and hour after one of my meals.

I bought empty gelatin capsules and use them to make half doses of the protease and ox bile.

links https://au.iherb.com/pr/Houston-Enzymes-Lypazyme-120-Capsules/46117
https://au.iherb.com/pr/Houston-Enzymes-AFP-Peptizyde-90-Capsules/43339
https://au.iherb.com/pr/Best-Naturals-Betaine-HCL-648-mg-250-Capsules/84544
https://au.iherb.com/pr/Nutricology-Ox-Bile-500-mg-100-Vegicaps/3451

I mention the brands because the paleomedicina people report problems with medicines and supplements increasing gut permeability and include the links so you can see what they contain.

I use Creon as a base because I have it on subscription and it is subsidised. I use the petizyde because the proteases in Creon are inactive and need a exopeptidase to activate them. I use the lypazyme because I needed more lipase than the creon provided and felt uncomfortable (burning sensations) when I had higher doses of creon.

I am hoping that this approach will provide me with plenty of ketone bodies, without propionate or any other SCFAs that may prove problematic. I have fluctuated a bit as I have tried to work this out, but my urine readings are pretty regularly between 1.5 and 4mMols, my exhalations turn the Ketonix Red most of the time, and my bowl movements no longer smell of SCFAs.

I am thinking more clearly and am more vertical. I have gone from being mostly horizontal (say 22hrs) and having to wait several days before I was well enough to sit up and think clearly enough to order food online or pay bills; to sitting most of the day and being able to put the clothes on the line, put the bin out and check the mail without having to steel myself up to the task.

I have only being doing the modified PKD since January and there is more to tell, but I will make a post about L rhamosus and then take a break.

* I will write about this in a separate post
 

Richard7

Senior Member
Messages
772
Location
Australia
L rhamnosus, L casei and L paracasei are so closely related that they were all thought to be l casei until the 90s.

The commercial names for strains of probiotics do not always match the scientific name. Yakult says it is l casei shirota, but it actually L paracasei, and it is actually a mixture of strains. I saw a paper that identified 10 strains of l paracasei in samples of Yakult.

There is a rather poor Canadian paper on pwme/cfs, anxiety and a powedered version of Yakult . The measure that they used for anxiety measures symptoms that sound a lot like PoTS. I found that taking Yakult or a cheaper supermarket equivalent improved my anxiety/PoTS. However, these probiotics contain a lot of glucose and are incompatible with a ketogenic diet, so I played around with other strains of l rhamnosus, l casei and l paracasei.

I found that this l rhamnosus worked well for me https://www.ebay.com.au/itm/Probiot...Billion-CFU-GRAM-High-Quality-23/263780184812 as did l paracasei LP 33 (which was much more expensive).

I tried several other strains, most were pretty bad: ie no positive effect or worse - sometimes much worse.
 

Richard7

Senior Member
Messages
772
Location
Australia
It is a bit hard to explain all of this journey.

(1) Inflammation

When I was on a high fibre version of keto - high fibre because my carbs were coming from chinese broccoli, bok choy, spinach and other foods with a high fibre to available carb ratio. I found that ketosis + vitamin k2 (Mk4)+ ubiquinol supplementation reduced the sense of inflammation in my head and made it easier to think.

Now, 2.75 months into PKD I have been able to maintain the clearer head while dropping the ubiquinol and taking smaller, less frequent doses of Mk4.

I have also lost a lot of water. This was evident too dramatic to be anything else drops in weight. I regularly see a physio and she has noted that my muscles feel more normal now, she can feel the reduction in inflammation/retained water.

(2) Anxiety/PoTS

For some years now I have been taking L Rhamnosus ( or an equivalent probiotic) and Hip's combination of turmeric, flaxseed oil and NAG everyday for baseline anxiety and taking large doses of innositol when I needed to deal with acute anxiety(sometimes daily, sometimes fortnightly).

This worked mostly, unless I overdid things and got major issues with PoTS, or I was put in a stressful environment (migraine triggers mostly).

I now find that I do not need Hip's mix, I take a lot of inositol. It is now almost an everyday need, but I am not sure that it is for anxiety - the trigger to take it is a feeling of need. I have also reduced my L Rhamnosus dose.

My PoTS has also improved. In December a heart rate peak of 180 - 220 was pretty common, these days I am more vertical and on the odd occasion where I get lightheaded and notice that I have an elevated heart rate it is under 120 BPM. PoTS still limits my movement, but I do not have to push myself to 180 or 220 to cook or some other essential task.

(I am still drinking electrolytes all day.)

(3)Digestion.

On the earlier version of Keto I was able to endogenously produce bile if I had lots strong hibiscus tea (say a litre made with three handfuls of dried hibiscus/day), or lots of liver (say 200g of pate/day). On PKD I stopped taking these things because I no longer felt like liver and hibiscus was contrary to the diet. So I now use exogenous bile: ox bile.

Bile is a little complicated. We have circulating bile that is released by the gallbladder when we eat and mostly reabsorbed in the cecum and recycled. Usually a small amount passes into the colon and colours our stools, but if too much bile gets into the colon it will cause diarrhoea.

So on my version of the PKD I started with supplementary ox bile, and moderated my intake by paying attention to the colour of my stools. It is basically a matter of increasing the dose till things look right and then reducing it immediately, because you are at first building up the reservoir of cycling bile until it spills over and then you should just need the spill over amount.

Only I might have been improving my ability to recycle bile and produce it. I have gone from 2g/day to 250mg/day. And I have done this while increasing my consumption of fat.

I have also made adjustments to the enzymes I take, so that I can break the fats down and absorb them.

I am still having some diarrhoea. This is pretty common in transition to ketogenic diets. To consume the amount of fat needed for such a diet people need to produce more lipases, more bile, and make changes to their cecums to absorb more fat. And most of the advice I have found online focuses on the first two of these problems.

I do not have the link, but somewhere amongst Dr. Boz's vast number of introductory videos https://www.youtube.com/user/annettebosworthmd/videos I saw one where she talked about issues with absorption, explaining that cecum can be damaged by years of SIBO.

I gather that her practice is mostly focused on cancer patients who are fasting part of each week and eating a ketogenic diet for the remainder. And she seemed to favour fasting, and giving the cecum a break during which it can be repaired as a solution. She also mentioned something about some research showing that people took 6months to recover from this sort of damage (I assumed that this was without fasting).

Whatever is going on, it seems to be becoming less of an issue. At the beginning I could not manage the 2:1 fat to protein ratio set by paleomedicina (which is standard ketogenic ratio when measured by weight instead of kCal). Now I can. Over time I have increased the proportion of fat in my diet while slowly reducing the frequency of diarrhoea.

I will continue in another post
 

Richard7

Senior Member
Messages
772
Location
Australia
(4) Sleep

Sleep has been a bit of an issue. When I get inter deeper levels of ketosis (towards 8mmol). I find myself overbreathing, and I assume regulating blood acidity by blowing off a lot CO2 to make up for the acidity of the BHOB. This can be painful painful. There where a few days in December where I was unable to sleep for as much as hour before the pain woke me. I booked the first available appointment with my doctor and went there contemporaneous notes for three days I could not remember. Fun.

I have worked around this problem by changing my electrolyte solution so that it now contains bicarbonate of soda (NaHCO3). Some nights (last for example) I start getting pains in my legs and take a little extra bicarb and find that that does the trick.

I have not read up enough on acid base homeostasis. But I gather that the reduced respiration in ME/CFS is part of the problem, so the need for Bicarb may be long term.

When changing my diet I knew I was also changing my gut microbiome so I was not surprised to have several nights of excess and painful gas which woke me up.

At the moment I do have some issues with having an over active mind either when I am trying to get to sleep, or when I wake up at some point in the night. I am not sure what to do about this, I have tried GABA, which seems to help but not always. And after seeing Mark Donohoe's presentation at EmergeCFS I have ordered l tryptophan and plan to give it a go when it arrives.

But since getting ME/CFS sleep has always been an issue, so the changes in sleep an issue that niggles not a major problem from my point of view.
 

Richard7

Senior Member
Messages
772
Location
Australia
Loose ends.

(1)I find that I need coffee. I was kind of OK for 6 weeks without it, but found that I was feeling quite exhausted/sleepy during the middle of the day and overeating in a vain attempt to get energy.

In last weeks Emerge ME/CFS conference I think Neil McGregor said something about pwme/cfs having a different cortisol pattern to normal. Normal starting high and then decreasing over the day. Pwme/cfs starting at about the low level of the normals and staying there all day. I do not know but wonder if this explains/ justifies my use of coffee.

(2) I forgot to mention in the top post that I was using ALCAR. I will also note that I seem to be less dependent on it. I have typically had it first thing of late I have occasionally forgotten till noon or early afternoon.

(3) I have on a few of occasions felt a need for vitamin C and taken about .25tsp ascorbic acid.

(4) my electrolyte mix is about .5tsp salt, .33tsp potassium chloride .25tsp bicarb, a pinch of tricalcium phosphate, and a pinch of magnesium sulphate to 750ml water. When I need extra bicarb I take .33tsp in about a cup of water, or in half a bottle of this solution.

I also have a mineral mix that I add sometimes when I feel the need.

(5) there were some occasions where I had a sore throat/thyroid. So I now take a drop or two of lugols solution once a week.
 

RustyJ

Contaminated Cell Line 'RustyJ'
Messages
1,200
Location
Mackay, Aust
Loose ends.

Wow, thanks for going into so much detail. It will take a couple of days to assimilate ;) I know what you mean about coffee... I am battling with getting off it as any creamer has the disacs. I'm also intolerance for gluten, so it's been a confusing 30 years. Milk was the big surprise, since I would have it whenever I was having grain (even gluten-free grain). And I would keep having coffee even when I had gone off grain completely.

Going off grain made a significant difference to my reflux and bloating and allowed me to cease medication. I am still in the process of winnowing out the disacs and trying to establish some sort of manageable diet so I probably won't stabilise till then. I'll probably follow the SCD diet, (but even then the advice is contradictory depending on the website) and kick off with an elimination diet.
 
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