A reader write a comment on one of my earlier posts

“I’ve had CFS since I was 11. I, at 46, just had a gut microflora test from ubiome. The analysis below is from ubiome data, through the metagenomics RAST server. I note that the Faecalibacterium prausnitzii are rather abundant, as well as various butyrate producing bacterium. E. coli is nonexistant, and bifidobacterium are quite sparse.”

and then provide details from ubiome.

I responded (see above) with a quick first past of what I found on PubMed for Faecalibacterium prausnitzii. Below is a greater dive. REMEMBER this appears to be a SMALL subset of CFS patients, without uBiome results, do no assume it applies to you. Most CFS patients are LOW for Faecalibacterium prausnitzii [see this post], as is also seen with Crohn’s Disease and UC, there is a very low level of Faecalibacterium prausnitzii.

• Abundance and diversity of GI microbiota rather than IgG4 levels correlate with abdominal inconvenience and gut permeability in consumers claiming food intolerances. “The abundance and diversity of microbiota significantly correlates with low Calprotectin values (R=-0.35; p=0.01) and with higher abundance of Faecalibacterium prausnitzii (R=0.78; p<0.01) and Akkermansia (R=0.82; p<0.01). ” (http://www.ncbi.nlm.nih.gov/pubmed/24502607 ). For your none statistical types, R=0.78 is almost a straight line relationship!!
• “One study demonstrated a strong association between high abundance of Faecalibacteriumprausnitzii and decreased levels of butyrate and propionate, and established eczema.” [2016]
• “F. prausnitzii phylotypes[strains] differed in obese with and without developed diabetes type two.” [2016]
• “In particular, subject 137 was a standout example whereF. prausnitzii was found to contribute less than 5% to the overall community, whereas its metaproteome exceeded more than 10% of all proteins, indicative of the very high gene expression activity of this bacterial group. The majority of the F. prausnitzii KOs were involved in amino acid metabolism, but almost half of theF. prausnitzii peptides could not be designated to any specific function”
• “whereas depletion of Faecalibacterium prausnitzii and reduced butyrate biosynthesis are shared in each of the metabolic [gout] syndromes.” [2016]
• “Rifaximin appeared to influence mainly potentially detrimental bacteria, such as Clostridium, but increasing the presence of some species, such as Faecalibacterium prausnitzii.” [2015]
• “In the metabolic syndrome patients, red wine polyphenols significantly increased the number of fecal bifidobacteria and Lactobacillus (intestinal barrier protectors) and butyrate-producing bacteria (Faecalibacterium prausnitzii and Roseburia) at the expense of less desirable groups of bacteria such as LPS producers (Escherichia coli and Enterobacter cloacae).” [2016] i.e. Grape Seed Extract
• Faecalibacterium prausnitzii subspecies-level dysbiosis in the human gut microbiome underlying atopic dermatitis[2016].
• “Phylogroup I was found in 87% of Healthy subjects but in under 50% of IBD patients (P = 0.003). In contrast, phylogroup II was detected in >75% of IBD patients and in only 52% of H subjects (P = 0.005). This study reveals that even though the main members of the F. prausnitzii population are present in both H subjects and individuals with gut diseases, richness is reduced in the latter and an altered phylotype distribution exists between diseases.” [2015] – Different strains impacts the gut differently. A shift to the bad strains results in IBD.

Treatment Options

• “However, fast non-preferential degradation of all chain length fractions of oligofructose (extracellularly) and efficient degradation of the short chain length fractions of inulin by B. angulatum LMG 11039(T) and B. longum LMG 11047 made it impossible for F. prausnitzii DSM 17677(T) to compete for the available substrate.” [2016]
• “numbers of lactobacilli, bifidobacteria (P<0.001) and Faecalibacterium prausnitzii (P<0.05) were higher in the low-fat/high-fiber pigs  than in high-fat/low-fiber pigs,” [2016]
  • “The aim of this study was to test the effect of consuming two healthy diets: a Mediterranean diet and a low-fat high-carbohydrate diet, for 2years in the gut microbiota of MetS patients and those in the control group….Our results suggest that the Mediterranean diet could be a useful tool to restore potentially beneficial members of the gut microbiota, although the stability of these changes over time still remains to be assessed.” [2016] — note Low Fat may be the dominant cause of the study result (instead of the Med. diet).
  • “Association between Faecalibacterium prausnitzii and dietary fibre in colonic fermentation in healthy human subjects[2010].
  • ” Faecalibacterium prausnitzii, reported to be an efficient butyrate producer and a highly metabolically active bacterium in the human intestinal microbiota, was more abundant in the raffinose diet and the chickpea diet compared to the control diet.” [2010]
  • “Effect of inulin on the human gut microbiota: stimulation of Bifidobacterium adolescentis andFaecalibacterium prausnitzii.[2009]”
• “This case study investigated changes of gut microbiota with an omega-3 rich diet. Fecal samples were collected from a 45-year-old male who consumed 600 mg of omega-3 daily for 14 days. After the intervention, species diversity was decreased, but several butyrate-producing bacteria increased. There was an important decrease in Faecalibacterium prausnitzii and Akkermansia spp. Gut microbiota changes were reverted after the 14-day washout.” [2016]
• “In particular, several experiments involving downshifts to pH 5.5 resulted in Faecalibacterium prausnitzii replacing Bacteroides spp. as the dominant sequences observed.” [2016]  i.e. increasing pH in stomach…
• “he aim of this study was to test the effect of consuming two healthy diets: a Mediterranean diet and a low-fat high-carbohydrate diet, for 2years in the gut microbiota of MetS patients and those in the control group….Our results suggest that the Mediterranean diet could be a useful tool to restore potentially beneficial members of the gut microbiota, although the stability of these changes over time still remains to be assessed.” [2016] — note Low Fat may be the dominant cause of the study result (instead of the Med. diet).
• “correlation to vacuum cleaning frequency, with an increase in Faecalibacterium prausnitzii for mothers” [2015] — vacuum less often!
• Increased gut microbiota diversity and abundance of Faecalibacterium prausnitzii and Akkermansia after fasting: a pilot study[2015]. – do not fast
• “The optimal pH for growth [for F P] ranged between 5.5 and 6.7, while most isolates were inhibited by of the lowest concentration of bile salts tested (0.1%)… Antimicrobial resistance profile showed that most isolates of Faecalibacterium sp. were resistant against ciprofloxacin and sulfamethoxazole-trimethoprim. More than 50% of the isolates were resistant to tetracycline, amikacin, cefepime and cefoxitin. A total of 19 different combinations of multidrug resistance were observed among the isolates.” [2014]
  • “A relatively higher resistance to chotosan hydrolyzates was detected in F. prausnitzii” [2012]
  • “The relative abundance of Faecalibacterium prausnitzii was unaffected except with thymol [Thyme Oil] at 500 p.p.m. of essential oils tested”

Bottom Line Suggestions

This is explicit to those with major Faecalibacterium prausnitzii overgrowth and assuming that is target #1. 

• Do not bother asking for antibiotics, they are likely to have little effect and will likely cause greater harm.
• Change you diet to low fiber and high fat (contrary to the typical “healthy eating” advice). Do not fast.
• Thyme oil is your best choice.
• Supplement with bile salts, for example Swanson Iron Bile Salts, which should increase your pH also.
• 600 mg of Omega 3 daily

As always, consult with your knowledgeable medical professional, before starting.