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

Crux

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I experienced symptoms that were identical to what Dr Lawrence Wilson describes in copper detoxing. My doctor thought I had a copper issue because my Zinc is low and so is my Ceruloplasmin.
My question is - were the symptoms really copper detoxing, or were they copper deficiency?
My experience was similar a few years ago. I had symptoms of zinc deficiency, then started taking some higher dosages without copper.

Recently, I've been having low copper symptoms including, peripheral neuropathy, optic neuropathy, etc. After a month of copper supps., I tested ceruloplasmin and serum copper. The copper was in lower normal range, but the ceruoplasmin was barely in range. Ceruloplasmin is a copper protein. If it's low, it could mean copper deficiency.

Anyway, I brought this up because, when I tried resistant starch and starchy foods, I began to feel worse after a time.
Eventually, I couldn't tolerate carbs. at all. I started ketogenic diet about 2 mnths. ago, and have begun to feel much better.

I started copper supps. about 6wks. ago because, even with the diet, there were issues. I wonder if some of the resistant starch intolerance I had was because of the copper deficiency.
 

Sidereal

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My question is - were the symptoms really copper detoxing, or were they copper deficiency?
My experience was similar a few years ago. I had symptoms of zinc deficiency, then started taking some higher dosages without copper.

Recently, I've been having low copper symptoms including, peripheral neuropathy, optic neuropathy, etc. After a month of copper supps., I tested ceruloplasmin and serum copper. The copper was in lower normal range, but the ceruoplasmin was barely in range. Ceruloplasmin is a copper protein. If it's low, it could mean copper deficiency.

Anyway, I brought this up because, when I tried resistant starch and starchy foods, I began to feel worse after a time.
Eventually, I couldn't tolerate carbs. at all. I started ketogenic diet about 2 mnths. ago, and have begun to feel much better.

I started copper supps. about 6wks. ago because, even with the diet, there were issues. I wonder if some of the resistant starch intolerance I had was because of the copper deficiency.
Those symptoms sound more likely to be attributable to thiamine depletion which is a known consequence of suddenly increased carb intake.
 

Crux

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Those symptoms sound more likely to be attributable to thiamine depletion which is a known consequence of suddenly increased carb intake.
That could be true, thiamine deficiency is possible.
I take a low dose B complex and get plenty of thiamine in diet. ( yes, I eat pork.)
 

Eastman

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I tried to read through the early portions of this thread (Ripley's posts) but am pretty brain-fogged. I'm on a heavily carb-restricted diet and have also been diagnosed with a Candida problem. Yet, due to my 'adrenal fatigue', I was experiencing blood-sugar crashes every 1-2 hours prior to adopting the Keto diet. So, according to him, it accelereates fungal/yeast overgrowths .. yet, my fear is that stopping it will just regress me back to my previous state of having to eat throughout the day to feel vaguely normal. It's a catch-22. I used to really benefit from resistant starch, but when I tried adding it in post-CFS, it 'crashes' me .. I never use it for more than 1-2 days in a row, so perhaps it's a Herx?

My gut is quite heavily dysbiotic, so I know I need to try and address that with my doctor. But it makes me concerned about being on Keto ..
I think the original concern with being on a ketogenic diet while having candida came from Paul Jaminet, who suggested that low-carb diets can actually promote fungal infections, one reason being that fungus can feed on ketones. He also reported that fungal infections often go away with increased starch consumption

Have you looked at the mercury angle? Supposedly, it can also cause candida overgrowth.
 

South

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@outdamnspot I've seen on numerous blogs that a transition from low-carb ketogenic back to eating carbs (even slow carbs and resistant starch) should be done quite slowly, otherwise the body can't handle the blood sugar changes and the change in gut microbiome too quickly.

I don't have links anymore though, to the blogs I've seen. But maybe making the change much more slowly would help you?
 

jepps

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Last edited:

jepps

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Interesting @jepps , did you try it?
Hi @Asklipia I´m happy to hear from you:) Are you still fine?
No, I did not try it, because I have enough proteobacteria:D
But I still take prescript assist, that has actinos+bacteroidetes+proteos+firmicutes.
I would take Equilibrium, if I had too little proteobacteria, as proteos in healthy levels and high diversity are good in treating infections.
 

Gondwanaland

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Although polyphenols aren't RS per se, they too can affect the gut bugs
https://www.ncbi.nlm.nih.gov/pubmed/26619254
Acta Biochim Pol. 2015;62(4):895-901. doi: 10.18388/abp.2015_1154. Epub 2015 Nov 30.
The impact of polyphenols on Bifidobacterium growth.
Gwiazdowska D1, Juś K1, Jasnowska-Małecka J1, Kluczyńska K1.
Author information
  • 1Department of Natural Science and Quality Assurance, Faculty of Commodity Science, Poznań University of Economics, Poznań, Poland.
Abstract
Polyphenols are a common group of plant based bioactive compounds, that can affect human health because of their antioxidant and antimicrobial properties as well as free-radical scavenging activity. An increasing interest is observed in the interaction between polyphenols and microbiota occurring in food and the human gut. The aim of the work presented here, was to evaluate the effect of some polyphenolic compounds on the growth of two strains of Bifidobacterium: B. adolescentis and B. bifidum. The influence of some flavonoids: naringinin, hesperidin, rutin, quercetin as well as phenolic acids: gallic, caffeic, p-coumaric, ferulic, chlorogenic, vanillic and sinapic was determined by a 96-well microtiter plate assay. In the experiments the effect of three different concentrations of polyphenols: 2, 20 and 100 µg/ml on the growth of Bifidobacterium strains was investigated. All tested compounds influenced the growth of the examined bacteria. Both stimulatory and inhibitory effects were observed in comparison to the positive control. The strongest impact on the growth of bifidobacteria was observed during the first hours of incubation. The constant inhibitory effect was observed for hesperidin and quercetin addition and was dose-dependent. B. bifidum showed a stronger dependence on phenolic acids content in the medium than B. adolescentis during the first hours of incubation.
PMID: 26619254

DOI: 10.18388/abp.2015_1154
[PubMed - indexed for MEDLINE] Free full text
 

Gondwanaland

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4943740/
PLoS One. 2016 Jul 13;11(7):e0159236. doi: 10.1371/journal.pone.0159236. eCollection 2016.
The Gut Microbiota from Lean and Obese Subjects Contribute Differently to the Fermentation of Arabinogalactan and Inulin.
Aguirre M1,2,3, Bussolo de Souza C3,4,5, Venema K1,2,6.
Author information
  • 1Top Institute of Food & Nutrition (TIFN), Wageningen, The Netherlands.
  • 2Maastricht University, School of Nutrition and Translational Research in Metabolism (NUTRIM), Faculty of Health, Medicine and Life Sciences, Department of Human Biology, Maastricht, The Netherlands.
  • 3The Netherlands Organization for Applied Scientific research (TNO), Zeist, The Netherlands.
  • 4CNPq, Brasilia, Brazil.
  • 5University of Groningen, Groningen, The Netherlands.
  • 6Beneficial Microbes Consultancy, Wageningen, The Netherlands.
Abstract
BACKGROUND:
An aberrant metabolic activity or a compositional alteration of the gut microbiota has been proposed as a factor that makes us more prone to disease. Therefore, we explored the effect of two dietary fibers (arabinogalactan and inulin) on the microbiota from lean and obese subjects during 72 h in vitro fermentation experiments using the validated TNO dynamic in vitro model of the proximal colon: TIM-2. Metabolically, arabinogalactan fermentation showed a higher production of propionate when compared to n-butyrate in the obese microbiota fermentations. In general, lean microbiota produced more n-butyrate from the fermentation of both substrates when compared to the obese microbiota. Furthermore, the obese microbiota extracted more energy from the fermentation of both fibers.

RESULTS:
Compositionally, bacteria belonging to Gemmiger, Dorea, Roseburia, Alistipes, Lactobacillus and Bifidobacterium genera were found to be highly abundant or stimulated by the prebiotics in the lean microbiota suggesting a potential role in leanness. Furthermore, a significant correlation between known butyrogenic strains including B. adolescentis, an unclassified Bifidobacterium and F. prausnitzii with this metabolite in the fermentation of inulin in both microbiotas was found.

CONCLUSIONS:
Although supplementary in vivo studies are needed, the current study provides more evidence for the consumption of specific ingredients with the aim of modulating the gut microbiota in the context of obesity.

PMID: 27410967

PMCID: PMC4943740

DOI: 10.1371/journal.pone.0159236
Free PMC Article
 

Gondwanaland

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I wonder if some of the resistant starch intolerance I had was because of the copper deficiency.
My experience with it was that RS raised uric acid, and copper helps with oxidizing excess UA.

I think the original concern with being on a ketogenic diet while having candida came from Paul Jaminet, who suggested that low-carb diets can actually promote fungal infections, one reason being that fungus can feed on ketones. He also reported that fungal infections often go away with increased starch consumption
It is possible that estrogen disruption is whay underlies candida flares, and low carb lowers estrogen.
 

Gondwanaland

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Microbiome. 2017 Feb 7;5(1):12. doi: 10.1186/s40168-017-0230-5.
Resistant starch can improve insulin sensitivity independently of the gut microbiota.
Bindels LB1, Segura Munoz RR1, Gomes-Neto JC1, Mutemberezi V2, Martínez I3, Salazar N4, Cody EA1, Quintero-Villegas MI1, Kittana H1, de Los Reyes-Gavilán CG4, Schmaltz RJ1, Muccioli GG2, Walter J3,5, Ramer-Tait AE6.
Author information
1 Department of Food Science and Technology, University of Nebraska-Lincoln, Lincoln, NE, USA.
2 Bioanalysis and Pharmacology of Bioactive Lipids Research Group, Louvain Drug Research Institute, Université catholique de Louvain, Brussels, Belgium.
3 Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada.
4 Department of Microbiology and Biochemistry of Dairy Products, Instituto de Productos Lácteos de Asturias-Consejo Superior de Investigaciones Científicas (IPLA-CSIC), Asturias, Spain.
5 Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada.
6 Department of Food Science and Technology, University of Nebraska-Lincoln, Lincoln, NE, USA. aramer-tait2@unl.edu.
Abstract
BACKGROUND:
Obesity-related diseases, including type 2 diabetes and cardiovascular disease, have reached epidemic proportions in industrialized nations, and dietary interventions for their prevention are therefore important. Resistant starches (RS) improve insulin sensitivity in clinical trials, but the mechanisms underlying this health benefit remain poorly understood. Because RS fermentation by the gut microbiota results in the formation of physiologically active metabolites, we chose to specifically determine the role of the gut microbiota in mediating the metabolic benefits of RS. To achieve this goal, we determined the effects of RS when added to a Western diet on host metabolism in mice with and without a microbiota.

RESULTS:
RS feeding of conventionalized mice improved insulin sensitivity and redressed some of the Western diet-induced changes in microbiome composition. However, parallel experiments in germ-free littermates revealed that RS-mediated improvements in insulin levels also occurred in the absence of a microbiota. RS reduced gene expression of adipose tissue macrophage markers and altered cecal concentrations of several bile acids in both germ-free and conventionalized mice; these effects were strongly correlated with the metabolic benefits, providing a potential microbiota-independent mechanism to explain the physiological effects of RS.

CONCLUSIONS:
This study demonstrated that some metabolic benefits exerted by dietary RS, especially improvements in insulin levels, occur independently of the microbiota and could involve alterations in the bile acid cycle and adipose tissue immune modulation. This work also sets a precedent for future mechanistic studies aimed at establishing the causative role of the gut microbiota in mediating the benefits of bioactive compounds and functional foods.

KEYWORDS:
Adipose tissue macrophages; Gut microbiota; Insulin sensitivity; Resistant starch

PMID: 28166818 PMCID: PMC5294823 DOI: 10.1186/s40168-017-0230-5
Review
Health effects of resistant starch

DOI: 10.1111/nbu.12244

Abstract

The merits of a fibre-rich diet are well documented. Resistant starch (RS) is a form of starch that resists digestion in the small intestine and, as such, is classified as a type of dietary fibre. RS can be categorised as one of five types (RS1–5), some of which occur naturally in foods such as bananas, potatoes, grains and legumes and some of which are produced or modified commercially, and incorporated into food products. This review describes human evidence on the health effects of RS consumption, with the aim of identifying any benefits of RS-rich foods and RS as a functional ingredient. The reduced glycaemic response consistently reported with RS consumption, when compared with digestible carbohydrate, has resulted in an approved European Union health claim. Thus, RS-rich foods may be particularly useful for managing diabetes. There appears to be little impact of RS on other metabolic markers, such as blood pressure and plasma lipids, though data are comparatively limited. Promising results on markers of gut health suggest that further research may lead to the classification of RS as a prebiotic. Microbial fermentation of RS in the large intestine to produce short-chain fatty acids likely underpins some of its biological effects, including increasing satiety. However, effects on appetite have not resulted in notable changes in bodyweight after long-term consumption. Emerging research suggests potential for RS as an ingredient in oral rehydration solutions and in the treatment of chronic kidney disease. Overall, RS possesses positive properties as a healthy food component.
 

NotThisGuy

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I'm currently reading this thread and it looks very promising.
Im still at page 30, so there still is a lot to read. I will read the rest the next days,
Anyway I hoped I can ask a few questions to the people here who already read the whole thread:

Is potato starch still the best choice for RS2? Is there a brand of potato starch from organic grown potatos?

There is also banana flour RS2, but it is rich in potassium.
Is this potassium trapped in the flour and won't be released? Don't tolerate high potassium, thats why im asking.

Is RS2 good for people like me with candida (possibly other yeast), SIBO and IBS-D?

Is the d-lactate free probiotic from custom probiotics 100% safe for people with MCAS and histamine intolerance?
 

sflorence

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Not really looking forward to fliping through 180 pages of this entire thread.

Could anyone let me know if there is anyone within those 180 that saw improvements from RS? Is there still merit to this approach or have we left it in the dust?
 

aquariusgirl

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Just want to give you guys a heads up.

Dr. Grace and Tim Steele have been digging more and more into the RS2 and RS3 research over the past few months, and they are taking a bit of a course correction. I expect them to clarify this in a post sometime next week and apparently their upcoming book downplays potato starch as well.

http://freetheanimal.com/2014/05/magazine-interview-presentation.html#comment-614784

Have folks tried this?


Tim also gave this simple cheat sheet in another comment:
 
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I came across resistant starch recently after experiencing less symptoms after freezing and defrosting carb rich foods like bread. https://www.thesun.co.uk/fabulous/food/6465485/freezing-white-bread-toasting-less-sugar/

It's early days but I do think it helps with overall symptoms including digestion and energy, although am suspecting I may have blood sugar issues/hypoglycemia and so I'm coming at the RS angle from a point of view that freezing means slower release carbs and therefore more stable energy.

Would be interested to hear any recent updates from anyone who's been experimenting with RS :)