I've begun to wonder whether potato starch is actually helping me, or whether it's been placebo.
Others have reported strong reactions, positive and negative, to small amounts. I started at 1 tsp to zero effect, and it wasn't until I hit 3 tbsp that I felt "something". I seemed to feel better - maybe a little more energy, a little less PEM. However, it has not improved my sleep, not caused me any gas (associated with the fermentation we're after) and honestly not done anything that I can definitively associate with potato starch intake.
I wonder if, as
Dr. Grace/BG says, I'm feeding empty zoo cages.
Dr. Ayers agrees that RS is "inert fiber" if you don't have the right microbiota, specifically Clostridium. I may need to supplement the right bugs.
Also, I'm trying the larch arabinogalactan today. Interested to see how, if at all, this stuff effects me. According to Dr Ayers "...
resistant starch can be digested by a couple of enzymes into glucose that can be used by most gut flora. Arabinogalactan, on the other hand, requires a dozen enzymes for plant synthesis and an equal number of hydrolytic enzymes to produce arabinose and galactose, which require further enzymes for metabolism in a select few of species of gut flora bacteria."
Isn't self-experimentation fun?
I've been thinking about this, why someone wouldn't react to RS.
The first possibility is that RS cannot produce the effects that have been ascribed to it. I have over the years learned to become wary of such things, because failures have been numerous and false hopes plentiful. My wife sceptically refers to these interventions as "the next great thing that is going to bring about my recovery."
I'm not going to go into great detail about the legitimacy of RS, but there are some things that I have witnessed that defy any other obvious explanation. Little things, like seeing my wife exhausted by the end of the day and going to bed an hour and half earlier every time she takes 1 tsp of RS in the morning. I find that three of my children have lymphatic pain in some of the areas that have long been known to me, beginning several days after the RS. I see the changes in mood, changes in bowel habits, and some slow and nonlinear improvement in some things that are more subjective, like sleep and anxiety, which is trending in the right direction.
The bottom line is that these are inflammatory features, they are quite clearly features of endotoxins: Fatigue, lymph soreness/pain, mood disturbance. I have reviewed the studies describing LPS effects on humans, the research regarding endotoxins effects, how these molecules are neutralized, how they travel the body, what parts of the immune system they impact, etc. If we had lab studies, they would, in all likelihood demonstrate changes in IL6, IFN-gamma, TNF-alpha, etc. depending upon the concentration in the peripheral tissues. If you don't have the characteristic symptoms of endotoxin exposure though, these measures will not change.
The second obvious explanation is that you have a viable and even an optimal concentration of the organisms that can utilize this substrate and/or no pathogenic organisms that would be effected by a significant increase in these commensals. I'm skeptical about this explanation given your report of significant GIT dysfunction, which includes the need to use yucca schidigera, which inhibits bacterial urease (enzyme) and thus inhibits the conversion of urea (via hydrolysis) and lessens the concentration of gaseous ammonia. The organisms that I know that are really good at turning urea into ammonia are gram-negative pathogens.
(As a quick aside, this is where I think ME/CFS physicians need to understand this dynamic a bit better. The Gram-negative pathogens are there for a reason, and that is because the environment is hospitable for them. This is due to many factors, including a lack of commensals, pH, they have access to a substrate, there is a particular concentration of SCFA, there is a scarcity or abundance of particular nutrients, etc. They are also executing roles that benefit the host, so indiscriminate modification of the GIT is not advisable. Some of the gram-negative urea-splitting bacteria are not just great at turning urea into ammonia, they also produce hydrogen sulfide. The hydrogen sulfide dampens the immune response caused by LPS and the ammonia serves the purpose of alkalizing the environment. Often, I see physicians blindly use antibiotics thinking they are going to shift the underlying microbiota toward more favorable conditions. Many of these antibiotics have no activity against many of these gram-negative pathogens yet they have very pronounced effects on these commensals. The best I can determine is that the antibiotics that have may have a role only do so because they can neutralize the toxicity of the endotoxins either via improving intestinal epithelial integrity--rifaximin--or diminishing the immune response induced by LPS--tetracyclines.)
I agree with you that, in all likelihood, you don't have any or sufficient numbers of the specific organisms that can access this substrate, I would have expected a response before now based upon how much and how long you have used the potato starch. Changes in the GIT should be obvious, I think. Did you ever try any of the yogurt that I recommended? That might be something to consider. I think you need species that can utilize amylopectin. I think this starch has some very special properties, which match it perfectly with certain Bifidobacterial organisms. I certainly can't discount the need for commensal clostridial species, though from a chemical and molecular perspective, PS has some very special qualities that would effect the survivability of Bifidobacterial strains. Without the bacteria able to utilize this, amylopectin is of no particular value to you.
usually means that our immune system isn't functioning well.