The person involved has a strong personal interest, which although not a discounting factor, means that they are much more likely to seek something definitive and reach further to find that.
The study specifically focused on people that have CFS and IBS, which, although somewhat related, are not perfectly correlated. It's a confounding factor that makes me wonder why he chose it. It's entirely possible that he was unable to find a significant effect unless he included it, which is a huge red flag. I'd be curious to see what the results are for people with only CFS or IBS. There's a lot of things associated with CFS given the vague criteria, and if you cast a net wide enough, you're bound to find something worth publishing, even if it's a false connection
It's a correlational study, not a causal study. The best it can say if done perfectly is that there exists a correlation between the two syndromes, but that doesn't discount a common or indirect cause.
IBS is related to improper absorbance of nutrients, which could cause very similar symptoms to CFS. Was there any work done to differentiate between these two causes? CFS can exist without IBS, and vice versa.
The final conclusion, that "such metabolic disruptions could impair cells’ ability to generate energy in response to stress, explaining the findings from his nanofabricated cube," comes out of left field. All his research showed is that people with both CFS and IBS respond differently to his test method, and that there was a statistically significant correlation to certain gut bacteria. That's a lot of variables for this sort of study. Even the linked study showing a correlation between PDH levels and CFS makes absolutely no mention of microbiota.
If this is due to a metabolic disruption in the production of essential nutrients, what happens in a controlled study where patients are supplied with these nutrients? Do people exist with similar microbiota profiles without symptoms? Do people have CFS, IBS, or both without such a profile?
I did like how he wants to study the consistency of his hypothesis. This is an exploratory study, and he knows it. If anything, this is more about the reporting than it is the actual research. I would bet that if you asked the researcher, he would advise caution about making interpretations this early. If I had to guess, I would say the subject of the article would agree with every one of my points, and bring up even more. That's science. You have to be your own devil's advocate before you get torn apart in peer review.
Tl;dr: A guy that has no history of studying metabolic diseases or microbiota has a family member with CFS, creates an untested device which measures something uncorrelated with any disease, finds a correlation between his device and CFS, but only when they have another loosely related syndrome, draws an untested hypothesis of causation that hasn't been proven for either syndrome, then says that he needs to do much more testing to verify his results.
I'm not saying there isn't merit to the study. I'm saying it raised a whole lot of questions that need to be addressed before it rises above the noise. There was stronger evidence for XMRV and CFS, and that ended up being untrue.