Summary of Kombucha
Primary Information, Benefits, Effects, and Important Facts
Kombucha, sometimes called mushroom tea (though it does not contain Bioactive Mushrooms) is a fermented tea from the plant Camellia sinensis. Kombucha is a green or black tea that is fermented for a week after sugars, fungi, and bacteria have been added to it.
The fermentation process produces a variety of acidic compounds that are claimed to benefit health through detoxification and anti-oxidation. Kombucha is also thought to promote longevity.
Though kombucha is a popular product, its actual effects on health are lacking. Kombucha contains more anti-oxidants than other teas, but there is not enough evidence to compare it against other standards like Green Tea Catechins and vitamin c.
Hypothetically, kombucha can aid detoxification through its main bioactive, which is called saccharolactone, but this has not been tested in people.
Improper sanitation and too long of a fermentation period can contribute to kombucha’s toxicity, which can result in death. Usually, this is because an individual was brewing their own kombucha, but death has also resulted from drinking too much kombucha (more than 14oz). Most of the evidence supporting kombucha's potential benefits is limited to rodents, while much of the evidence demonstrating its risks extends to humans. Therefore, it is not recommended to drink kombucha for its health benefits.
Things To Know & Note
Improper preparation has been noted to cause adverse effects, sometimes resulting in death
How to Take Kombucha
Recommended dosage, active amounts, other details
There are several case reports of adverse effects occuring following Kombucha consumption. This may be due to toxins, pathogens, or excess acid, as a result of over-fermentation. Due to this potential harm, regular kombucha consumption is not recommended.
Although rare, most adverse effects occurred after a person drank more than 4 ounces (125mL). Therefore, it is not recommended to ingest more than 4 ounces of kombucha a day, in order to minimize the chance of an adverse effect. If kombucha is brewed at home, it must be properly prepared in a sanitized environment and fermented for less than a week to be safe to drink.
Scientific Research on Kombucha
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Kombucha is a fermented beverage made from tea and sugar, where the addition of inoculum and subsequent fermentation is thought to produce unique health bioactives. This inoculum is commonly referred to as 'tea fungus' and contains a mixture of bacteria and fungi which act during the fermentation process. A pellicle which forms during this process is referred to as the 'fungus', and the fungus produces alcohol which helps the bacteria produce the aforementioned bioactives.
The tea used is from the Camellia sinensis plant and usually refers to the black tea, although green tea is sometimes used. When black tea is used (as black tea itself requires fermentation to be produced) the final kombucha product is sometimes referred to as being doubly fermented.
Kombucha is produced by making a tea from the plant Camellia sinensis (basic extraction being called 'green tea'), fermenting it initially to make black tea, and then fermenting it again with a mixture of bacteria and fungi and sugars to produce kombucha; in this sense, it is doubly fermented.
The essential organisms that make up the tea "fungus" are an acetic-acid producing strain of bacteria (usually the Acetobacter genus, both and being identified) and yeast. Strains of lactic acid-producting (Lactobacillus) and gluconic acid-producing (Gluconobacter oxydans being identified) bacteria can also be present.
There are various yeast fungi that are seen, including Brettanomyces/Dekkera, Candida, Kloeckera, Pichia, Saccharomyces, Saccharomycoides, Shizosaccharomyces, Torulospora and Zygosaccharomyces. Although most have been unidentified, up to 163 strains of yeast have been detected, with four major yeasts being Zygosaccharomyces bailii, T.delbrueckii, C.stellata, and S.pombe.
Although kombucha contains a variety of bacteria and fungi, it appears to be safe for human consumption when properly processed and consumed in moderation (details in the safety and toxicology section).
The strains of bacteria used in kombucha fermentation are those that are acid-resistant and produce acids upon metabolizing ethanol and sugars, and while there are no standard yeast fungi used during this process, the ones that are most-often found also tend to also be acid-resistant and acid-producing.
Components of kombucha that are preexisting in the tea (Camellia sinensis) prior to fermentation include:
Green tea catechins, which experience variable degradation rates (18-48%) with less degradation seen with green tea relative to black tea and less with EGCG relative to other catechins; epigallocatechin (EGC) and epicatechin (EC) were noted to be markedly (30-50%) elevated after 12 days fermentation, thought to be due to the degragation or their gallated forms (EGCG and ECG, respectively).
Thearubigins found in black tea, where 11% is lost during 18 days fermentation
The standard tea polyphenols found in the Camellia sinensis plant and those produced during the intitial fermentation to get black tea (theaflavins and thearubigins) persist in kombucha, with the losses during the second fermentation being fairly minimal.
Components of kombucha tea produced during the fermentation process include:
Acetic acid (produced from the alcohol via bacteria) reaching 1.6g/100mL after 10 days; this may be a high estimate, as other studies have noticed a plateau at 0.95g/100mL after 15 days followed by a decline
D-Saccharic acid 1,4-lactone (saccharolactone)
Succinic acid reaching 0.65g/100mL after 10 days
Citric acid has been noted to transiently occur after three days fermentation (less than 0.01g/100mL) although it's undetectable after 12 days
Carbon dioxide (produced from the acetic acid via bacteria), produced which separates the pellicle from the broth and creates an anaerobic/serum-starved environment
Studies comparing the fermentation of green tea and black tea by the same fungal and bacterial colonies have failed to find any significant differences in the production of acids, aside from possibly more acetic acid with green tea relative to black tea.
The fungal fermentation that produces kombucha creates a large variety of small acidic compounds, with the most notable one (thought to mediate the 'detoxification' effects) being D-Saccharic acid 1,4-lactone (Saccharolactone)
Kombucha is known to have a somewhat specific processing method, and similar to most fermentation products (requiring heat) there is a possibility for contamination during the cooling phase.
The formation of alcohol during the fermentation process is necessary for the production of acetic acid, and while the alcohol content of kombucha is usually under 1% after fermentation, excessive fermentation for one month has been noted to raise it up to 3%; commercial products tend to have less than 0.5% alcohol content (to avoid being mandated as an alcohol-containing product).
Overfermentation of kombucha during the standard 7-10 day period is possible if not refrigerated soon after, which may cause an elevation of acetic acid levels above what is desirable. Acetic acid has the potential to leech metals from the container in which kombucha is fermented, so care should be taken to ferment kombucha in nonmetallic containers.
Improper processing of kombucha, either contamination or by needlessly prolonging the fermentation period, is known to cause bacterial and fungal overgrowth and has been noted to covert kombucha into a toxic food product.
The brewing of kombucha from teas of Camellia sinensis (green or black) results in a pH around 5, which can be reduced to around 2.5 (variable between 2.3-2.8) after one week. The increase in acidity (occurring within one day of fermentation) is due to production of organic acids during bacterial fermentation (although a perfect correlation does not exist between pH and organic acid content, thought to be due to some buffering agents in the medium). This is necessary for proper fermenting since it, as well as antimicrobial metabolites produced from the tea, are thought to prevent competing bacterial and fungal strains from contaminating the final product.
The pH of the final product is increased (acidity reduced) after 12 days, perhaps explaining why traditional fermentation is halted at around this time. It is also around this time that sucrose, continually produced into increasing quantities of fructose and glucose, reaches peak levels where afterwards they decline.
The standard processing of kombucha starts with boiling of water and adding both the tea and sugar to steep for 10 minutes, although unlike other teas which would be drunk at this stage, manufacturing kombucha requires that the tea leaves be removed and an inoculum (bacteria and fungi which would conduct the fermentation) be added. This is then left to ferment at room temperature over the course of 7-10 days and then refrigerated.
The yeast tends to proliferate after two to four days fermentation when the pH drops, with levels of yeast in the pellicle (removed from final product) spiking after four days and remaining steady until the end of standard fermentation (10 days), where a slight decline is seen.
If not consumed locally, kombucha is then packaged with additional measures taken to prevent excessive microbial growth (pasteurization or addition of sodium benzoate and potassium sorbate, for example).
It has been hypothesized that kombucha can increase glucuronidation in the body after ingestion, either directly by providing dietary glucuronic acid or secondary to inhibiting the β-Glucuronidase enzyme (which hydrolyzes the bond between glucuronide and its conjugation target). D-saccharic acid 1,4-lactone (saccharolactone) is a competitive inhibitor of β-Glucuronidase with an IC50 of 3.6µM and exerts complete inhibition at 1mM. Fecal β-Glucuronidase is inhibited in both healthy controls and in subjects with colon cancer (who have elevated β-Glucuronidase concentrations) at a concentration of 30-150µg/mL.
The inhibition of β-Glucuronidase and supposed augmentation of glucuronic acid's conjugation ability seen with saccharolactone is thought to also underly the 'detoxifying' anticancer properties of kombucha by facilitating the elimination of toxic substances from the body, similar to the mechanism of calcium-D-glucarate.
The 'detoxifying' properties of kombucha refer to the ability of some acids produced during the fermentation process to increase glucuronidation in the human body, which is involved in eliminating some drugs and xenobiotics from the body by conjugating them.
When tested in vitro in lymphocytes exposed to γ-radiation, kombucha at 250-1000µL in whole blood samples prior to irradiation appeared to dose-dependently preserve lymphocyte chromosomal structure, reaching approximately 50% preservation relative to control. Kombucha at 1000µL by itself did not alter lymphocyte structure without any irradiation relative to control.
The antioxidative properties of kombucha appear to preserve white blood cell integrity in vitro when exposed to radiation, which is an expected effect from antioxidant compounds; practical significance of this information is not known.
A study of male rats examined the protective effects of black tea (from Camellia sinensis) or kombucha prepared from the aforementioned batch of black tea to CCl4-induced hepatotoxicity; it found that doses of both black tea and kombucha of 2.5mL/kg for 30 days prior to (preventative) or alongside (curative) induced hepatotoxicity were protective, as assessed by liver enzymes and malondialdehyde in the liver, but the reductions noted with black tea (50-74% in preventative and 61-65% in curative) were less than kombucha (75-83% and 70-76%, respectively).
Protective effects from kombucha have been noted elsewhere in rats against acetominophen-induced liver toxicity and isolated liver cells subject to oxidative death via TBHP, thought to be due to the D-Saccharic acid 1,4-lactone content of the tea which may function through antioxidation or by increasing the glucuronidation and elimination of toxic substances through inhibiting β-glucuronidase. This substance alone is also known to exert hepatoprotective effects.
Kombucha, at least when given to rodents, appears to be beneficial in reducing toxicity of known stressors on the liver. This is likely due to the saccharolactone content, and is thought to be due to either antioxidative mechanisms or increased glucuronidation of toxins (perhaps a combination of both).
While the protective effects are thought to be due to a combination of antioxidative mechanisms plus the potential increase in glucuronidation of the toxins via saccharolactone, the toxic effects of kombucha (thought to be due to improper preparation) can manifest themselves as hepatotoxicity or gastrointestinal toxicity.
When kombucha is improperly processed, the potential benefits are lost and ingestion will result in hepatotoxicity instead of hepatoprotection.
Kombucha in general appears to be associated with numerous case studies where the subject was harmed. These instances include an increase in oral intake from 4oz to 14oz in a person making kombucha at home (this person may have had a predisposition to acidosis), resulting in death. Death has been reported in other instances, and there exist numerous cases of nonlethal hepatoxicity, instances of gastrointestinal toxicity with and without jaundice, cutaneous anthrax, unspecified acute illness (resulting in hospitalization), and acute renal failure.
Kombucha tea can be produced safely, but even then the recommended intake of safely-produced tea is still quite low (half of a metric cup); such a low dose may preclude the health benefits seen in rat studies and expected to occur with the D-Saccharic acid 1,4-lactone content. Kombucha also carries the possibility to exert a wide variety of negative effects due to mishandling of the fungal and bacterial strains used in its production.
- Teoh AL1, Heard G, Cox J. Yeast ecology of Kombucha fermentation. Int J Food Microbiol. (2004)
- Jayabalan R, Marimuthu S, Swaminathan K. Changes in content of organic acids and tea polyphenols during kombucha tea fermentation. Food Chem. (2007)
- Liu C-H, et al. The isolation and identification of microbes from a fermented tea beverage, Haipao, and their interactions during Haipao fermentation. Food Microbiol. (1996)
- Murugesan GS1, et al. Hepatoprotective and curative properties of Kombucha tea against carbon tetrachloride-induced toxicity. J Microbiol Biotechnol. (2009)
- Pauline T1, et al. Studies on toxicity, anti-stress and hepato-protective properties of Kombucha tea. Biomed Environ Sci. (2001)
- Wang K1, et al. Determination of D-saccharic acid-1,4-lactone from brewed kombucha broth by high-performance capillary electrophoresis. J Chromatogr B Analyt Technol Biomed Life Sci. (2010)
- Petrović SE1, et al. Biosynthesis of glucuronic acid by means of tea fungus. Nahrung. (2000)
- Blanc PJ. Characterization of the tea fungus metabolites. Biotechnol Lett. (1996)
- Nummer BA. Kombucha brewing under the Food and Drug Administration model Food Code: risk analysis and processing guidance. J Environ Health. (2013)
- Mayser P1, et al. The yeast spectrum of the 'tea fungus Kombucha'. Mycoses. (1995)
- LEVVY GA. The preparation and properties of beta-glucuronidase. IV. Inhibition by sugar acids and their lactones. Biochem J. (1952)
- Sperker B1, et al. Regulation of human beta-glucuronidase by A23187 and thapsigargin in the hepatoma cell line HepG2. Mol Pharmacol. (2001)
- Kim DH1, Jin YH. Intestinal bacterial beta-glucuronidase activity of patients with colon cancer. Arch Pharm Res. (2001)
- Kim DH1, et al. Purification and characterization of beta-glucuronidase from Escherichia coli HGU-3, a human intestinal bacterium. Biol Pharm Bull. (1995)
- Oleson L1, Court MH. Effect of the beta-glucuronidase inhibitor saccharolactone on glucuronidation by human tissue microsomes and recombinant UDP-glucuronosyltransferases. J Pharm Pharmacol. (2008)
- Cavusoglu K, Guler P. Protective effect of kombucha mushroom (KM) tea on chromosomal aberrations induced by gamma radiation in human peripheral lymphocytes in-vitro. J Environ Biol. (2010)
- Wang Y1, et al. Hepatoprotective effects of kombucha tea: identification of functional strains and quantification of functional components. J Sci Food Agric. (2014)
- Bhattacharya S1, Gachhui R, Sil PC. Hepatoprotective properties of kombucha tea against TBHP-induced oxidative stress via suppression of mitochondria dependent apoptosis. Pathophysiology. (2011)
- Bhattacharya S1, et al. Prophylactic role of D-Saccharic acid-1,4-lactone in tertiary butyl hydroperoxide induced cytotoxicity and cell death of murine hepatocytes via mitochondria-dependent pathways. J Biochem Mol Toxicol. (2011)
- Perron AD, Patterson JA, Yanofsky NN. Kombucha "mushroom" hepatotoxicity. Ann Emerg Med. (1995)
- Srinivasan R1, Smolinske S, Greenbaum D. Probable gastrointestinal toxicity of Kombucha tea: is this beverage healthy or harmful. J Gen Intern Med. (1997)
- Centers for Disease Control and Prevention (CDC). Unexplained severe illness possibly associated with consumption of Kombucha tea--Iowa, 1995. MMWR Morb Mortal Wkly Rep. (1995)
- Ernst E. Kombucha: a systematic review of the clinical evidence. Forsch Komplementarmed Klass Naturheilkd. (2003)
- SungHee Kole A1, et al. A case of Kombucha tea toxicity. J Intensive Care Med. (2009)
- No authors listed. Is Kombucha tea safe to drink. Mayo Clin Womens Healthsource. (2011)