The Resistant Starch Challenge: Is It The Key We've Been Looking For?

JPV

ɹǝqɯǝɯ ɹoıuǝs
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And the baddies themselves must be trying with all their might to make us stop the reconquest of our microbiome!
I think this is a very important observation.

Much the same way that candida can cause sugar cravings in the host, in order to insure it's survival, many pathogens seem to use the tactic of causing discomfort in order to discourage any actions that may threaten it's existence. We are definitely dealing with intelligent organisms that are able to literally manipulate our minds and bodies as a part of their defense mechanism. It's truly a symbiotic relationship.

This is also one of the most frustrating aspects of implementing any of the interventions proposed on this forum. It's often so hard to differentiate a negative reaction, that is genuinely harmful to our well being, from a transitory phase that may eventually lead to significant and lasting improvements.
 
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ariel

Senior Member
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119
@Sleeping Beauty - well that's great that you've improved by focusing on diet and RS alone! Maybe it has had a bigger effect than you thought, even though you didn't have strong reactions to the pre and probiotics when you started them.

Even just earlier today I was thinking this RS thing is really not helping me so much either, my energy levels are still pretty much unchanged, and maybe I've been deluding myself into thinking that this really is the way forward. :( Especially after Jepps wrote that she knows some people who are totally healthy and they can't tolerate RS either... that really did make me pause and make me wonder... :thumbdown:
Like Adreno, a part of me had started to give up, I've tried a million and one things but never really got anywhere.
BUT.... I feel better right now, and even though my energy levels have only slightly improved, I do honestly think this is the way forward for me. And potentially for many others here. I feel like different parts of my brain have switched on. And the amount of stuff that has come out has been shocking.
And we are ALL getting better. I can read it in the posts and the way everybody is communicating, either more clearly or simply being more expressive. It is just taking quite a bit longer than any of us ever thought possible!
:hug:
 

alicec

Senior Member
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1,572
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Australia
Well a lot has been happening here in the day or so when I wasn't reading!

I won't go over the same ground that others have already covered, except to say this is far and away the most useful and interesting thread on PR. Keep going everyone, including @Sidereal.

Although I never had strong gut symptoms I have always thought that dysbiosis was at the heart of my problems and have tried many gut treatment programs. While some things have certainly helped, the dismal results on CDSA tests never improved much and I had decided that as soon as I felt a bit stronger I was going to have an FMT at the Centre for Digestive Diseases in Sydney. There didn't seem to be any other effective way to influence the gut flora.

Towards the end of last year I belatedly caught up with this thread. It's not that I wasn't familiar with the notion of pre and probiotics, indeed I had tried many, but somehow the much more nuanced and targeted discussion here, along with the valuable reports of self-experiments, suddenly presented me with a whole new way of thinking about how I could tackle the gut and really make a difference. As well as hope, it has given results, set-backs yes which I would never have understood without this thread, but also moderate but noticeable improvements.

Based on my experiences so far I can see it is going to be a long haul but in the end I think it will be much more permanent than FMT.

With best wishes
Alice
 

JPV

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@Sidereal is very knowledgeable about a lot of pertinent health issues and has contributed a tremendous amount of valuable information to this forum. It would be a shame to lose her input because of a misunderstanding that I believe could be easily resolved.
 
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Valentijn

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15,786
There are other patients on this forum with mental-only or mental-predominant PEM, and such patients are recognized in the CCC, since the CCC defines PEM as arising from physical or mental exertion.

And a lot of patients with physical PEM do also get mental PEM. Perhaps you are one of them?

I would have thought, though, that the ratio of physical-predominant PEM to mental-predominant PEM patients would be something like 20 to 1.
Atypical and mild ME patients have just as much to contribute to the forum as typical and severe patients, and frequently patients, doctors, and advocates without ME do as well.

There's nothing wrong or inherently insulting in pointing out differences, when relevant to specific treatments, symptoms, or experiences. When a problem does arise in that context it's usually because someone new to the forum does not know what ME actually is, and is equating it to their chronic fatigue, mood disorders, and/or uncomplicated orthostatic intolerance. Some are quite happy to learn the difference, but others persist in in making inappropriate comparisons and making harmful recommendations - in which case they deserve to get smacked on the nose.

Anyhow, I've not seen any atypical patients get upset about having their atypical-ness mentioned in a constructive context. It's not an attack, just a relevant statement in a discussion. And in my experience, the atypical patients or non-ME patients who are contributing on a regular basis are also very upfront and proactive in pointing out their own atypical status when necessary. They'll usually say something like "this worked for me in resolving this symptom we're discussing, BUT I'm not an ME patient so your experience might be very different."
 
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Hip

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18,148
Atypical and mild ME patients have just as much to contribute to the forum as typical and severe patients, and frequently patients, doctors, and advocates without ME do as well.

I agree there's nothing wrong with pointing out the differences, but I am not sure this notion of an "atypical patient" has much meaning.

ME/CFS as defined by the CCC includes a whole raft of symptoms. Very few patients will have all the symptoms. Nearly all patients will be missing several symptoms when compared to all the possible symptoms listed in the CCC.

So given that physical PEM and mental PEM are just one of many symptoms listed in the CCC, you cannot consider an ME/CFS patient atypical if they are missing one of these.

Similarly, some studies have shown the majority of ME/CFS patients have psychiatric symptoms, or psychiatric comorbidities. But you wouldn't assume an ME/CFS patient without psychiatric symptoms was an "atypical patient".
 
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Location
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This is really interesting. This thread has been going on for months, and with RESULTS. And I think this is what is happening. Subtly we are not the same sick people as before!!! In the fight against the baddies we can become more aggressive or see slight when there is none.
And the baddies themselves must be trying with all their might to make us stop the reconquest of our microbiome!

Very encouraging! Hang on everybody! We need all hands on deck against the pirates!
Lots of love
Asklipia :hug::balloons::hug:

I will respond to other posts later, too tired tonight. Just wanted to say, though, that I wish I could like your post 1001 times, @Asklipia ! You always know how to put a positive spin on things. Thanks for that :balloons::beer::heart:!
 

Asklipia

Senior Member
Messages
999
I came across a very interesting article by Mark Lyte :
Probiotics function mechanistically as delivery vehicles for neuroactive compounds. Microbial endocrinology in the design and use of probiotics.
http://www.ncbi.nlm.nih.gov/pubmed/21732396
In which there is a Table 1. showing a diversity of neurochemicals isolated from various species.
Lactobacillus, Bifidobacterium > GABA
Escherichia, Bacillus, Saccharomyces > Norepinephrine
Candida, Streptococcus, Escherichia, Enterococcus > Serotonin
Bacillus, Serratia > Dopamine
Lactobacillus > Acetylcholine

This whole subject of Microbial Endocrinology is fascinating!
 

adreno

PR activist
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4,841
@Vegas

I got the flaxseed you recommended, optimistically took 1 ts, and it absolutely destroyed me. The immune activation was intense. It's been three days now, and I'm still not back to baseline. Potent stuff, I must say.

I also got a breakout of shingles rash. Do you know the mechanism behind this? When I read about, it is usually stated that this reactivation occurs in immunosuppression, but I feel like my immune system is anything but suppressed!
 

Gondwanaland

Senior Member
Messages
5,100
@Vegas

I got the flaxseed you recommended, optimistically took 1 ts, and it absolutely destroyed me. The immune activation was intense. It's been three days now, and I'm still not back to baseline. Potent stuff, I must say.

I also got a breakout of shingles rash. Do you know the mechanism behind this? When I read about, it is usually stated that this reactivation occurs in immunosuppression, but I feel like my immune system is anything but suppressed!
It is anti-testosterone :eek: I get immediate FM onset from it.
 

adreno

PR activist
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4,841
It is anti-testosterone :eek: I get immediate FM onset from it.
I thought it wasn't that bad, but perhaps it is. In this case study, flaxseed all but obliterated test (in a woman). Of course, this was 30g daily, compared to the 5g I took:

This clinical case study describes the impact of flaxseed supplementation (30 g/day) on hormonal levels in a 31-year old woman with PCOS. During a four month period, the patient consumed 83% of the flaxseed dose. Heights, weights, and fasting blood samples taken at baseline and 4-month follow-up indicated the following values: BMI (36.0 vs. 35.7m/kg2); insulin (5.1 vs. 7.0 uIU/ml); total serum testosterone (150 ng/dl vs. 45 ng/dl); free serum testosterone (4.7 ng/dl vs. 0.5 ng/dl); and % free testosterone (3.1% vs. 1.1%).
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2752973/

What might be even worse, flax is also a DHT inhibitor. I think @mariovitali will tell us this causes ER stress.
 
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mariovitali

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1,216
I thought it wasn't that bad, but perhaps it is. In this case study, flaxseed all but obliterated test (in a woman). Of course, this was 30g daily, compared to the 1.5g I took:


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2752973/

What might be even worse, flax is also a DHT inhibitor. I think @mariovitali will tell us this causes ER stress.



Hi there @adreno,


Upon looking this message i entered 'flaxseed' on my software to see associations. This is the output :


*********Topic : butyrate ***************
butyrate.csv : 28.71 %
resistant_starch.csv : 11.99 %
microbiome_humans.csv : 1.59 %

l_carnitine.csv : 0.29 %
monosodium_glutamate.csv : 0.29 %
caspase_human.csv : 0.28 %
rar.csv : 0.23 %
d-limonene.csv : 0.21 %
resveratrol.csv : 0.20 %
vitamin_d3.csv : 0.19 %
irritable_bowel.csv : 0.15 %
hsp70.csv : 0.12 %
rxr.csv : 0.12 %
nadh_human.csv : 0.11 %
triiodothyronine_levels.csv : 0.11 %
curcumin.csv : 0.10 %
heat_shock_protein.csv : 0.09 %
calcium_homeostasis.csv : 0.08 %
glutamate.csv : 0.08 %
taurine.csv : 0.07 %
er_stress.csv : 0.07 %
lipoic_acid.csv : 0.07 %
inflammatory_response.csv : 0.07 %
cyp2e1.csv : 0.07 %

So i looked in PubMed about Flaxseed and Butyrate :


Incremental amounts of ground flaxseed decrease milk yield but increase n-3 fatty acids and conjugated linoleic acids in dairy cows fed high-forage diets.


with 14 d for diet adaptation and 7 d for data and sample collection. Treatments were fed as a total mixed ration (63:37 forage-to-concentrate ratio) with corn meal and soybean meal replaced by incremental levels (i.e., 0, 5, 10, or 15% diet dry matter) of GFX. The ruminal molar proportions of acetate and butyrate decreased linearly with GFX supplementation, whereas the ruminal molar proportion of propionate increased linearly resulting in decreased acetate-to-propionate ratio. Apparent total-tract digestibilities of nutrients either decreased (dry matter) or tended to decrease (organic matter, neutral detergent fiber, acid detergent fiber) linearly in cows fed GFX.


Perhaps this happens to humans as well? Unfortunately i do not have time at this moment to research this properly but it maybe a start.


Regarding Flaxseed :


Flaxseed suppressed prostatic epithelial proliferation in a rat model of benign prostatic hyperplasia.
Said MM1, Hassan NS, Schlicht MJ, Bosland MC.
Author information
Abstract

Benign prostatic hyperplasia (BPH), a disease occurring frequently among elderly males, is a slow progressive enlargement of the fibromuscular and epithelial structures of the prostate gland. Dietary factors may influence the prostate and exert an influence on prostatic growth and disease. The current study was undertaken to investigate the protective effect of dietary flaxseed supplementation against testosterone-induced prostatic hyperplasia in male rats. Forty male Wistar rats were divided into 5 groups: (1) untreated control; (2) treatment with testosterone propionate (TP) to induce prostate enlargement; (3) TP-treated group fed a diet containing 5% milled flaxseed; (4) TP-treated group fed a diet containing 10% milled flaxseed; and (5) TP-treated group fed a diet containing 20 ppm finasteride. Treatment with TP significantly increased the absolute and relative weights of different prostatic lobes, serum testosterone (T), and testosterone/estradiol ratio, as well as prostatic vascular endothelial growth factor (VEGF) expression, RNA synthesis per cell, and epithelial cell proliferation, detected as Ki67 labeling. Histopathological examination did not reveal marked differences in acinar morphology in ventral prostate, whereas morphometric analysis showed significantly increased epithelial cell height. Co-administration of flaxseed or finasteride with TP significantly reduced prostatic VEFG, epithelial cell proliferation, and RNA/DNA ratio, along with a significant increase in serum T and testosterone/estradiol ratio compared with TP-only-treated rats. Our results indicate that flaxseed, similar to the 5α-reductase inhibitor finasteride, blocked TP-induced prostate enlargement in a rat model of BPH, likely through suppression of prostatic VEFG and cellular proliferation.
 
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Gondwanaland

Senior Member
Messages
5,100
The ruminal molar proportions of acetate and butyrate decreased linearly with GFX supplementation, whereas the ruminal molar proportion of propionate increased linearly resulting in decreased acetate-to-propionate ratio. Apparent total-tract digestibilities of nutrients either decreased (dry matter) or tended to decrease (organic matter, neutral detergent fiber, acid detergent fiber) linearly in cows fed GFX.
Hmmm so this might be the mechanism making me gluten intolerant. I get the same outcome from eating wheat, flax, quinoa, etc. I thought vitamin B15 would be implied as well, depleting B12.

I wonder if it is possible to replenish all the butyrate needed to be healthy again and be able to eat those foods without being harmed again. Of course those foods are linked to glyphosate and then the vicious circle restarts...
 
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Asklipia

Senior Member
Messages
999
I wonder if it is possible to replenish all the butyrate needed to be healthy again and be able to eat those foods without being harmed again. Of course those foods are linked to glyphosate and then the vicious circle restarts...
Well, we can eat pretty much anything now, and we had severe intolerances before.
Not that we eat bad stuff, but if we go to dinner with friends, we can eat and have absolutely no problems after.
In fact we can also drink pretty much anything in any quantity.
Strange….
This is not 'being healthy again'. This is a new kind of health.
Good luck to all!
The week-end is over, all goes as planned and Reality is easy to stir.
:hug:
 

mariovitali

Senior Member
Messages
1,216
Since this is the Resistant Starch Thread, here goes :


*********Topic : resistant starch ***************
resistant_starch.csv : 76.79 %
butyrate.csv : 0.25 %
microbiome_humans.csv : 0.24 %
hmgcoa.csv : 0.04 %
insulin_resistance.csv : 0.03 %
zinc_supplementation.csv : 0.02 %
curcumin.csv : 0.01 %
irritable_bowel.csv : 0.01 %
oxidative_stress_protection.csv : 0.01 %
l_carnitine.csv : 0.01 %
oxidative_stress_markers.csv : 0.01 %
taurine.csv : 0.01 %
inflammatory_response.csv : 0.01 %
glycosylation.csv : 0.00 %
vitamin_d3.csv : 0.00 %
heat_shock_protein.csv : 0.00 %


So we have an association of HmG-CoA between RS and HmG-CoA. Please note that the Software shows the Hits (%) but does not tell us anything about the context.

In our example above we see hits that are expected (resistant_starch.csv,butyrate.csv) but what was interesting was that RS was found with HmG-CoA (a key step in Mevalonate Pathway and Ketogenesis) articles in PubMed.

It appears that Resistant Starch lowers HmG-CoA activity therefore -in theory- it should also lower Cholesterol levels.

Note that Statins work in the same way (i.e. by inhibiting HmG-CoA), although i do not believe that RS lowers HmG-CoA so much as statins.
 

Violeta

Senior Member
Messages
3,227
Same thing happens with sleep in those who take acetylcholinesterase inhibitors. AD patients commonly take these, but my experience is with traumatic brain injured patients who use these to promote wakefulness/cognition/memory. It certainly interrupts their sleep and it can't be taken too early in the day. I remember reading about the effects of LAG and recall seeing that its maximal effects on microbial populations is more delayed than I would have expected, 6 hours, perhaps. (I don't remember exactly) Of course this will vary with the product. Perhaps someone has some info on this.

I may have mentioned that I noticed a huge increase in focus with one of my children initially; afterwards, it seemed to provoke exactly what I get...inflammation likely mediated by endotoxin displacement, and an ADHD child to the extreme. Anyway, the sleep interruption like the myoclonus symptoms, I think this is a case of cholinergic hyperstimulation. Did I say I hate this feeling! I believe, potato starch may oppose this somewhat, not sure yet. Of course too much at one time is going to cause adverse effects regardless. The parasympathetic nervous system which is largely regulated by acetylcholine plays a big role in neutralizing the inflammatory response to endotoxins, so the response is also surely related to the "overmobilization" of these bad molecules. Take it slow.

I am trying to understand the subject of inhibition of acetylcholinesterase by organophosphates such as pesticides
and remembered this thread touched on the subject. Do you know if there is any hope for restoring whatever needs to be restored in the case of organophosphate poisoning? You can probably tell by my question that I only have a surface knowledge of the subject so far, so if my question doesn't even make sense, any help in that arena would also be appreciated.

And also, this sounds similar to what I'm reading about myasthenia gravis.



Thanks
 
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