Firmicutes/Bacteroidetes Ratio Test Summary

Description/Background Information

A healthy gut microbiota is vital to our wellbeing—it helps to establish and maintain our immune system, fend off opportunistic pathogens, extract nutrients and energy from foods we cannot digest (e.g., dietary fiber), produce vitamins, and stimulate communication between the gut and brain.^1-5 The beneficial end-products of fiber fermentation are short-chain fatty acids (SCFAs), which nourish the gut lining and regulate food intake, inflammatory tone, and insulin signaling.^1,6 Microbiota diversity is dependent on both diet and colonic transit time, and may confer resilience to stress.^2,7 Overall microbial composition affects the structural integrity of the gut lining and, although influenced by our genetic background and maternal flora, also reflects what we eat.^5,8

Dysbiosis is an undesirable shift in the microbiota composition—an imbalance between protective and potentially harmful microbes—that can damage the gut lining and lead to chronic diseases.^2,9 In addition to pathogens and toxins, a high-fat, high-sugar, low-fiber (standard Western) diet may induce dysbiosis and reduce microbial diversity.^2,10 Over time, dysbiosis can cause impaired glucose and lipid metabolism, aberrant immune responses, intestinal permeability, and metabolic endotoxemia,^3,9  paving the way for cardiometabolic, autoimmune, and other inflammatory disorders.^1-3 Gastrointestinal imbalance is compounded by other, all-too-common factors: a sedentary lifestyle, high stress levels, excessive alcohol intake, and gut-damaging medications.^4,11-13 Chronic dysbiosis can alter gut pH and disrupt the epithelial mucus layer, creating space for pathogens to flourish.^2,14

In humans, ~90% of the gut bacteria are represented by two phyla—Firmicutes (60–80%) and Bacteroidetes (15–30%).^15,16 The Firmicutes phylum encompasses more than 250 genera, including Lactobacillus and Clostridium, while Bacteroidetes includes around 20 genera, the most abundant being Bacteroides. Both phyla produce beneficial SCFA from indigestible carbohydrates that reach the colon, with Firmicutes being the main butyrate-producers and Bacteroidetes producing mainly acetate and propionate.¹⁶ The ratio of Firmicutes to Bacteroidetes in the stool is a gauge of overall gut microbiota balance.

Clinical Utility & Indications

Untreated intestinal dysbiosis may underpin a variety of chronic diseases^1,2,9:

• Inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), and colon cancer
• Gastric ulcers, nonalcoholic fatty liver disease, and cardiometabolic diseases
• Allergic disorders and autoimmune disorders (e.g., celiac disease, rheumatoid arthritis, eczema)
• Mood disorders (e.g., anxiety, depression)

A shift in the Firmicutes to Bacteroidetes ratio (F/B ratio) may be influenced by various factors and conditions:

• Various factors such as changes in nutrition, digestive secretions, use of prescription medications, and alterations in gut transit time all contribute to a decrease in the F/B ratio and microbial diversity with age.^16,17
• Higher F/B Ratios have been associated with a standard Western diet.¹⁷Evidence suggests that Bacteroidetes communities can shift according to dietary modulation and weight change, whereas Firmicutes numbers are more dependent on one’s genetic makeup.^15,17
• Antibiotic-associated diarrhea, Crohn’s disease, and ulcerative colitis have been correlated with decreases in Firmicutes strains, a concomitant increase in Bacteroidetes (low F/B ratio), and a reduced gut biodiversity.^9,18
• Although obesity and energy intake can affect the microbiota, studies fail to demonstrate a consistent relationship with the F/B ratio.¹⁹However, metabolic comorbidities have been associated with a higher ratio in obese patients.²⁰
• Dysbiosis has been suggested to play a role in the development of type 2 diabetes (T2D).^1-3 Patients with T2D have a lower F/B ratio than nondiabetic controls with worsening glucose tolerance as the F/B ratio decreases.²¹

F/B Ratio Cut Points and Interpretation

	Low	Mildly Decreased	Optimal	Mildly Elevated	High
F/B ratio	≤ 0.5	0.6 – 0.9	1.0 – 5.6	5.7 – 9.1	≥ 9.2
Firmicuteslog10 CFU/g	≤ 8.6		8.7 – 11.7		≥ 11.8
Bacteroideteslog10 CFU/g	≤ 8.1		8.2 – 11.6		≥ 11.7

Firmicutes and Bacteroidetes are reported as log₁₀ CFU/g. This means that the Firmicutes/Bacteroidetes Ratio can be high or low when the individual values of both bacterial phyla are within the optimal range.

– For example, if the Firmicutes result is 10 and the Bacteroidetes result is 9 (a 1-unit difference) the Firmicutes/Bacteroidetes ratio will be 10 (mildly elevated), but if the Firmicutes result is 11 and the Bacteroidetes result is 9 (a 2-unit difference) the Firmicutes/Bacteroidetes ratio will be 100 (high).

All Salveo Diagnostics materials are provided for educational purposes and should not be taken as medical advice. No action or inaction should be taken solely on the basis of the contents herein. It is important that readers consult their healthcare provider on health-related concerns. Diagnosis and treatment decisions are the responsibility of the practitioner.

Sample Type/Collection/Stability/ Shipping

It is recommended that patients refrain from taking probiotics for 14 days and antibiotics for 28 days prior to sample collection or as directed by the healthcare provider.

Stool samples should be refrigerated immediately after collection and shipped with cold icepacks to Salveo Diagnostics.

STOOL SAMPLE SHOULD NOT BE FROZEN.

Treatment Considerations

For optimal balance of the gut microbiota, consider a diet that is low in refined carbohydrates and processed foods, rich in fiber, essential fatty acids, and phytonutrients, with a wide variety of fresh fruits and vegetables, beans (legumes), nuts, and whole grains.1,17,22,23 Depending upon clinical context, the following suggestions may also help restore the microbiota:

• Specific pharmaceutical or botanical medications may be taken under the guidance of a qualified clinician for the treatment of bacterial, fungal, or parasitic infections.
• Abstinence from gut-damaging medications (e.g., antibiotics, nonsteroidal anti-inflammatory drugs, proton-pump inhibitors, oral contraceptives) and alcohol.^12,13
• Probiotics, especially Lactobacilli and Bifidobacteria, help restore GI balance; they activate anti-inflammatory pathways, regulate gut contractility and calm IBS symptoms, improve weight control and insulin sensitivity, and reinforce intestinal barrier integrity.^24,25“Reseeding” the dysbiotic gut with these friendly bacteria may preclude pathogens taking up residence. Probiotics can be found in fermented foods (e.g., yogurt, miso, tempeh, and sauerkraut) or taken as supplements.
• Prebiotics, food ingredients that feed the gut flora, can augment the benefits of probiotics and include bran, resistant starch, and oligosaccharide-containing foods such as onions, garlic, leeks, chicory, asparagus, tofu, and bananas.²³ Supplemental prebiotics may help patients with low levels of beneficial SCFA.
• Low stomach acid (often resulting from treatment with gastric acid suppressants) and pancreatic insufficiency may exacerbate the effects of dysbiosis by impairing digestion and assimilation of food.⁴ If fecal elastase levels are low, consider supplemental pancreatic enzymes. Drinking warm water containing fresh lemon juice before meals may aid digestion by stimulating gastric acid secretion.
• Patients with dysbiosis may benefit from vitamin and mineral supplements to address associated nutrient deficiencies.
• Regular physical exercise lowers inflammation, and can increase microbial diversity and decrease transit time.¹¹

References

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2. Chan YK, et al. Ann Nutr Metab 2013;63(Suppl 2):28–40
3. Nicholson JK, et al. Science 2012;336:1262–1267
4. Cresci GA, et al. Nutr Clin Pract 2015;30:734–746.
5. Di Mauro A, et al. Ital J Pediatr 2013;39:15.
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8. David LA, et al. Nature 2014;505(7484):559–563.
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13. Engen PA, et al. Alcohol Res 2015;37(2):223–236.
14. Duncan SH, et al. Environ Microbiol2009;11(8):2112–2122.
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16. Mariat D, et al. BMC Microbiol 2009;9:123.
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18. Ott SJ, et al. Gut 2004;53:685–693.
19. Tagliabue A, Elli M. Nutr Metab Cardiovasc Dis2013;23:160–168.
20. Louis S, et al. PLoS One 2016;11(2):e0149564.
21. Larson N et al. PLoS One 2010;5(2):e9085.
22. Martinez I, et al. ISME J 2013;7:269–280.
23. Conlon MA, Bird AR. Nutrients 2015;7:17–44.
24. Ebner S et al. World J Gastroenterol2014;20(43):16095–16100.
25. Le Barz M, et al. Diabetes Metab J 2015;39:291–303.