Monday, August 31, 2009



Mastic is a resin, or gum, that is extracted from a tree from the Mediterranean or Middle Eastern regions. Long used as a chewing gum and a traditional medicine, mastic resin also has been developed for use in numerous industrial applications (Milov et al., 1998). Preliminary clinical evidence has confirmed mastic resins use to be useful in the treatment of ulcer. Mastic has been further shown to exhibit antibacterial activity against Helicobacter pylori, explaining its efficacy in ulcers. Mastic has also shown antibacterial, antiplaque and antigingival activity in the saliva and on the teeth (Takahashi et al., 1998).


Although it has not yet been well-studied as an herbal medicine, mastic resin has a long history of use and the preliminary clinical evidence is promising for its use in ulcers.

Scientific Support

Duodenal Ulcer

Al-Habbal et al. (1984) performed a double-blind clinical study on mastic for treatment of duodenal ulcer. Mastic was given (1 gram daily) to twenty patients and placebo (lactose, 1 gram daily) to eighteen for 2 weeks. Mastic showed highly statistically significant improvements in both the symptomatic relief (80% of the treatment group vs. 50% of the placebo group) and the clinical manifestation of disease as proven by endoscopic examination (70% of the treatment group vs. 22% of placebo patients). Additionally, mastic was found to be well tolerated with no side effects.

Antiplaque, Antigingival and Antibacterial Activity of Mastic Chewing Gum

A chewing gum of mastic resin was tested in two double-blind, randomized, placebo-controlled studies for the control of dental plaque. In the first study, the saliva of was collected from the mouths of participants after mechanical brushing and chewing gum and examined for its antibacterial activity by mastic or placebo gum. The mastic chewing gum group showed statistically significant reduction in the bacterial growth as compared to the placebo group during the 4 hours of chewing gum. In the second study, mastic or placebo gum chewing (and no brushing) was tested over the period of 7 days for their ability to control new plaque formation on tooth surfaces and on gingival inflammation. The mastic group showed significantly reduced plaque index measures, and gingival index compared to placebo (Takahashi et al., 1998).

Safety / Dosage

One gram daily is used for treating ulcers and gastrointestinal discomfort. Mastic is not known to product any side effects, and is thought to be safe (Al-Habbal et al., 1984).


1.Al-Habbal MJ, Al-Habbal Z, Huwez FU. A double-blind controlled clinical trial of mastic and placebo in the treatment of duodenal ulcer. Clin Exp Pharmacol Physiol. 1984 Sep-Oct;11(5):541-4.

2.Huwez FU, Al-Habbal MJ. Mastic in treatment of benign gastric ulcers. Gastroenterol Jpn. 1986 Jun;21(3):273-4.

3.Milov DE, Andres JM, Erhart NA, Bailey DJ. Chewing gum bezoars of the gastrointestinal tract. Pediatrics. 1998 Aug;102(2):e22.

4.Takahashi K, Fukazawa M, Motohira H, Ochiai K, Nishikawa H, Miyata T.

5.A pilot study on antiplaque effects of mastic chewing gum in the oral cavity. J Periodontol. 2003 Apr;74(4):501-5.

EDITOR'S NOTE: This monograph can be found in The Health Professional's Guide to Dietary Supplements (Lippincott, Williams & Wilkins) by Shawn M. Talbott, PhD and Kerry Hughes, MS.

Milk Thistle


Milk thistle is a common weed that has a long history as a traditional medicine and food. Its potent activity in restoring and protecting the liver has been confirmed in a number of studies, and it is often included in herbal medicines intended to act as “detoxification” formulas. The main active constituents of milk thistle are the flavonolignans, and the bioactive flavonolignans are generally called silymarin as an umbrella term. Silymarin has 3 isomers: silybin (also called silibinin), silydianin, and silychristin (McKenna et al., 2001).

Silymarin has exhibited cholesterol lowering and normalizing activity, reduced high blood pressure in hypertensive patients, antiproliferative activity in cancer cells, and chemoprotective activity. However, the preclinical data that most relates to the traditional use and current herbal use of milk thistle is focused on hepatic functions and its antioxidant activity (McKenna et al., 2001). Some highlights of this preclinical data follows:

•Silymarin has shown hepatoprotective activity against a number of toxins, including carbon tetrachloride, galactosamine, ethanol, paracetamol, Amanita toxins, thioacetamide, microcystin-LR, heavy metals, poisons of lanthanden, sulfur acetamide, and the FU3 virus (a hepatotoxic virus of cold blooded animals) (Morazzoni and Bombardelli, 1995; Bone, 1996).

•Silymarin has shown activity against peroxidation in liver microsomes of the rat (Bosisio et al., 1992).

•Silymarin has hepatorestorative properties, and the primary mechanism it is thought to accomplish this through is the stimulation of protein synthesis. Silymarin stimulates the activity of RNA polymerase which synthesizes ribosomal RNA (Sonnenbichler and Zetl, 1986).

•In the process of liver cirrhosis and damage caused by ethyl alcohol and paracetamol, the depletion of glutathione levels causes most of the damage to the liver. Silymarin has been found to increase glutathione levels, thus protecting the liver (Valenzuela et al., 1985).

•Also involved in the hepatoprotective activity of silymarin, certain cytosol enzymes (including alanine amino transferase (ALT/GPT) and lactic dehydrogenase (LDH)) are inhibited by silymarin, preventing the destruction of the cell membranes. In addition, certain intoxicants have been found to block phospholipid synthesis on rat livers, and silymarin is capable of counteracting this effect (Castigli et al., 1977).

•Silybin was found to partially or completely block the toxic effects of cisplatin on the kidney functions of rats (Gaedeke et al., 1996).

•Silymarin (especially silybin) acts as free radical and reactive oxygen species (ROS) scavengers. Free radical formation is known to be one of the key processes in hepatotoxicity, contributing to lipid peroxidation on the cellular membranes (Valenzuela et al., 1989).


Milk thistle is safe and efficacious leading herb in a therapeutic area that lacks many good pharmaceutical alternatives: liver restoration and protection. Although the major public has been slow to catch on, liver health may be one of the most pertinent issues to our evolving unhealthy lifestyles, and the growing concern of toxins from the environment affecting our health.

Scientific Support

A study by Lang et al. (1990) investigated the effect of milk thistle extract (Legalon, 140 mg p.o., three times daily) in cirrhotic patients (from alcohol consumption). The study was conducted in 4-weeks, and was a randomized, double-blind, placebo-controlled design, and also used a second active treatment for comparison (Acia-P, Chinoin, Budapest, 200 mg p.o., three times daily). Both of the active treatments showed significant improvements in hepatic functions, and no change was found for the placebo group. In the milk thistle group, bilirubin (SEBI), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) had all normalized during treatment (they were moderately elevated before the study). Another study by Lang et al. (1990a) found similar results.

A two-year, double-blind, placebo-controlled study examined the effect of an oral dose of 200 mg 70% silymarin extract, three times daily, in cirrhotic patients (91 due to alcohol, and 79 not related to alcohol). At the termination of the study, there was a 23% mortality rate, and a cumulative survival rate of 58% in the treatment group, compared to a 33% mortality rate, and a 38% cumulative survival rate in the placebo group (Ferenci et al., 1989).

Further studies have found that silymarin exhibits a hepatoprotective action in people prior to alcohol consumption, and improves hepatic function in alcoholic patients. Silymarin has been found to be most effective for milder cases of alcohol cirrhosis (Salmi and Sarna, 1982; McKenna et al., 2001).

In a double-blind, crossover clinical study on the effect of silymarin (420 mg daily) vs. ursodeoxycholic acid (UDCA- 600 mg daily) in chronic hepatitis patients, significant improvements were found in both treatment groups. Significant declines in the serum levels of several elevated liver enzymes were noted for both groups, and the group receiving UDCA also had a significant reduction in γ–GT levels. The crossover phase of the study used a combination therapy of UDCA and silymarin vs. placebo, but the combined treatment showed no advantage over either single treatment (Lirussi and Okolicsanyi, 1992).

A review of clinical studies performed by Hikino and Kiso (1988) found silymarin to work therapeutically through three main activities in protecting the liver from toxic agents. Silymarin is able to stabilize the cell membrane and stimulate protein synthesis, while accelerating the regeneration of damaged liver tissue.

An open-label study involving 975 patients with various causes of liver damage examined the effect of 140 mg of a 70% standardized milk thistle extract (p.o., 2-3 times daily for 12 weeks). Five hundred and seventy of the patients were diagnosed with a fatty liver, with 143 confirmed to have fatty liver hepatitis and 214 confirmed to have hepatic cirrhosis. A mean reduction in the levels of serum liver enzymes (SGOT dropped from 46.0 µg/L to 28.8 µg/L; SGPT from 48.0 µg/L to 31.0 µg/L; and γ–GT from 112.0 µg/L to 60.6 µg/L) and a normalization of total bilirubin concentration was found at the end of the study (Grungreiff et al., 1995).

A double-blind study using silymarin (800 mg p.o daily for 90 days) found therapeutic effects in female patients with hepatopathies who had been taking psychopharmaceutical drugs such as phenothiazines or butrophenones for 5 years. A decline in the level of malodialdehyde (MDA) levels were found in the treatment group (Palasciano et al., 1994).

A study involving 2,169 patients with hepatotoxicities found improved or normalized clinical readings after taking silymarin orally for 8 weeks (at an average of 264 mg daily) (Frerick et al., 1990).

A study involving 49 workers who had been exposed to toluene and/or xylene vapors on the job for 5-20 years tested the therapeutic effect of silymarin on liver function. All the patients had low blood platelet counts and abnormal liver function before the study, and after taking silymarin for 30 days (at 140 mg p.o., three times daily) showed significant improvement in the liver and hematological tests. Symptoms reported as headaches were ameliorated after treatment, as well as parameters of leukocytosis, relative lymphocytosis, serum, γ–GT , ALT, and AST. In addition, platelet counts were increased after treatment (Szilard et al., 1988).

A 12 month open controlled study involving diabetic patients with alcoholic liver cirrhosis examined the therapeutic effect of silymarin (600 mg/day) with standard therapy for 4 months. Significant improvements in those receiving silymarin were found: a significant decrease in fasting and daily blood glucose levels, daily HbA1c levels, and glucosuria levels. Levels of MDA were also decreased. In addition, blood insulin levels were improved significantly, as well as the amount of insulin needed by injection (Velussi et al., 1997).

Safety / Dosage

Dosage of milk thistle is usually based on an 80% standardized (silymarin flavonoids- silybin, silydianin and silychristin) extract and is 175 mg daily. Other dosage recommendations vary depending on the preparation, for example: 200-400 mg (70% silymarin standardized extract- calculated as silybin); 600 mg/day (for advanced cirrhosis of a 70:1 extract); or 3-5 mL (1:1 liquid extract) (McKenna et al., 2001).

Milk thistle is safe and well tolerated, as it also has a long history as a food. Most of the side effects that have been reported in clinical trials are thought to be not significantly different from placebo or of a mild and transient nature. There have been a few cases reported of a mild laxative effect and a pruitic skin rash produced by milk thistle (McKenna et al., 2001).


1.Bone K. Silybum marianum. MediHerb 1996; 2: 22-23. ISSN: 1322-2775.

2.Bosisio E, Benelli C, and Pirola O. Effect of the flavonolignans of Silybum marianum L. on lipid peroxidation in rat liver microsomes and freshly isolated hepatocytes. Pharmacological Research 1992; 25: 147-154.

3.Castigli E, Montanini I, Roberti R. et al. The activity of silybin on phospholipid metobolism of normal and fatty liver in vivo. Pharmacological Research Communications 1977; 9: 59-69.

4.Ferenci P, Dragosics B, Dittroch H. et al. Randomized controlled trial of silymarin treatment in patients with cirrhosis of the liver. Journal of Hepatology1989; 9: 105-113.

5.Frerick H, Kuhn U, Strenge-Hesse A. Silymarin – ein phytopharmakon zur behandlung von toxischen leberschäden. Der Kassenarzt 1990; 33/34: 36-41.

6.Gaedeke, J.; L.M. Fels; C. Bokemeyer et al. 1996. Cisplatin nephrotoxicity and protection by silibinin. Nephrology, Dialysis, Transplantation 11:55-62.

7.Grungreiff, K.; M. Albrecht; and A. Strenge-Hesse. 1995. The value of drug therapy for liver disease in general practice. Medizinische Welt 46:222-227.

8.Hikino, H and Y. Kiso. 1988. Natural products for liver disease, in: Wagner, H.; H. Hikino and N.R. Farnsworth (eds.), Economic and Medicinal Plant Research, 2. London, England: Academic Press.

9.Láng I, Nékám K, Deák G. et al. Immunomodulatory and hepatoprotective effects of in vivo treatment with free radical scavengers. International Journal of Gastroenterology 1990; 22: 283-287.

10.Láng I, Nékám K, Gonzalex-Cabello R. et al. 1990a. Hepatoprotective and immunological effects of antioxidant drugs. Tokai Journal of Experimental and Clinical Medicine 1990; 15:123-127.

11.Lirussi F, Okolicsanyi L. 1992. Cytoprotection in the nineties. Experience with ursodeoxycholic acid and silymarin in chronic liver disease. Acta Physiologica Hungarica 80:363-367.

12.McKenna DJ, Jones K, Hughes K (eds). Botanical Medicines: A Desktop Reference for the Major Herbal Supplements. 2001 Haworth Press: New York

13.Morazzoni P, Bombardelli E. Silybum marianum (Carduus marianus). 1995; Fitoterapia 66: 3-42.

14.Palasciano G, Portincasa P, Palmieri V. et al. The effect of silymarin on plasma levels of malondialdehyde in patients receiving long-term treatment with psychotropic drugs. Current Therapeutic Research 1994; 55:537-545.

15.Salmi H, Sarna S. Effect of silymarin on chemical, functional and morphological alterations of the liver: a double-blind controlled study. Scandinavian Journal of Gastroenterology 1982; 17:517-521.

16.Sonnenbichler J, Zetl, I. Specific binding of a flavonolignane derivative to an estradiol receptor, in: Cody, V.; E. Middleton, Jr. and J.B. Harborne. (eds.), Plant Flavonoids in Biology and Medicine: Biochemical, Pharmacological and Structure-activity Relationships. 1988; New York, NY: Alan R. Liss, pp. 319-331.

17.Szilard S, Szentgyorgyi D, Demeter D. Protective effect of Legalon® in workers exposed to organic solvents. Acta Medica Hungarica 1988; 45:249-246.

18.Valenzuela A, Aspillaga M, Vial S. et al. Selectivity of silymarin on the increase of the glutathione content in different tissues of the rat. Planta Medica 1989; 55:420-442.

19.Valenzuela A, Lagos C, Schmidt K. et al. Silymarin protection against hepatic lipid peroxidation induced by acute ethanol intoxication in the rat. Biochemical Pharmacology 1985; 34:2209-2212.

20.Velussi M, Cernigoi CM, Viezzoli L. et al. Silymarin reduces hyperinsulinemia, malondialdehyde levels, and daily insulin need in cirrhotic diabetic patients. Current Therapeutic Research 1993; 53:533-545.

EDITOR'S NOTE: This monograph can be found in The Health Professional's Guide to Dietary Supplements (Lippincott, Williams & Wilkins) by Shawn M. Talbott, PhD and Kerry Hughes, MS



Fructo-oligosaccharides (FOS) also called “prebiotics” are a group of non-digestible compounds that stimulate the growth of beneficial microflora (note: this is different than PRO-biotics, or the actual beneficial bacteria such as acidophilus and bifidum). In terms of chemistry, a fructo-oligosaccharide (FOS) is a glucose molecule bonded to multiple fructose molecules. These bonds cannot be broken down by enzymes in the human small intestine - allowing the FOS to reach the large intestine intact, where it becomes a substrate for colonic bacteria. The effects of short-chain FOS have been studied for nearly two decades. Groups of oligosaccharides can be found in foods such as beans, blueberries, and onions; a liquid supplement is available in Japan, and FOS is available in capsule form in the U.S.


Prebiotics have been shown to selectively stimulate the growth and activity of benefical bacteria in the colon. The prebiotic, fructooligosaccharide (FOS), is found naturally in many foods, such as wheat, onions, bananas, honey, garlic, and leeks – and FOS can also be isolated from chicory root or synthesized enzymatically from sucrose (both more commonly found in FOS dietary supplements). Fermentation of FOS in the colon results in a large number of physiologic effects including increasing the numbers of bifidobacteria in the colon, increasing calcium absorption, increasing fecal weight, shortening of gastrointestinal transit time, and possibly lowering blood lipid levels.

Based on the available scientific evidence, FOS supplements are generally claimed to boost levels and activity of beneficial gut bacteria and thus promote general gut health, reduce serum lipids, increase intestinal calcium absorption, alleviate antibiotic-induced diarrhea, and reduce both the severity of irritable bowel syndromes and the risk of colon cancer.

Scientific Support

Short-chain FOS is metabolized in the colon (by colonic bacteria) into short-chain fatty acids (Giacco et al. 2004). These short-chain fatty acids cause a drop in pH, which may inhibit the growth of pathogenic bacteria, facilitate intestinal calcium absorption, and act as an energy substrate for colonic epithelial cells (Bouhnik et al. 1999, Tahiri et al. 2001). By manipulating colonic pH and microflora content, FOS may also play a protective role against colon cancer (Giacco et al. 2004, Swanson et al. 2002, Ten Bruggencate et al. 2003 and 2004). Research also points to a reduction in liver fatty acid synthesis as a possible mechanism for serum lipid reduction (Giacco et al. 2004, Swanson et al. 2002).

Human studies have shown significant increases in bifidobacteria (beneficial bacteria in the gut) from ingestion of as little as 6-8 grams of short-chain FOS per day (Chow 2002). Research has also shown decreases in pathogenic colonic bacteria from FOS ingestion (Chow 2002). There is evidence that short-chain FOS can lower cholesterol and triglycerides, but most of this research has involved animal models. Colon tumors and indicators of cancer have also been reduced in animal models. Although animal studies have given promising results, relatively few human studies have shown that mineral absorption can be enhanced from FOS ingestion (Tahiri et al. 2001).


Since the bonds of FOS are not digestible, bacterial metabolism in the large intestine produces gas and bloating. Flatulence is a common symptom associated with FOS ingestion and can be worse in people who are lactose intolerant (depending on how the FOS is processed). Studies have shown that the severity of symptoms is dose-dependent (less FOS = less symptoms). Ingestion of 20-30 grams per day has been associated with the onset of severe discomfort – but symptoms may be alleviated by starting with a small dose and increasing gradually to the desired amount (Bouhnik et al. 1999). Ten grams of FOS per day appears to be the “optimal” dose, since this amount produces a significant increase in bifidobacteria and is fairly well-tolerated.


1.Alles MS, Hautvast JG, Nagengast FM, Hartemink R, Van Laere KM, Jansen JB. Fate of fructo-oligosaccharides in the human intestine. Br J Nutr. 1996 Aug;76(2):211-21.

2.Bouhnik Y, Flourie B, Riottot M, Bisetti N, Gailing MF, Guibert A, Bornet F, Rambaud JC. Effects of fructo-oligosaccharides ingestion on fecal bifidobacteria and selected metabolic indexes of colon carcinogenesis in healthy humans. Nutr Cancer. 1996;26(1):21-9.

3.Bouhnik Y, Vahedi K, Achour L, Attar A, Salfati J, Pochart P, Marteau P, Flourie B, Bornet F, Rambaud JC. Short-chain fructo-oligosaccharide administration dose-dependently increases fecal bifidobacteria in healthy humans. J Nutr. 1999 Jan;129(1):113-6.

4.Chow J. Probiotics and prebiotics: A brief overview. J Ren Nutr. 2002 Apr;12(2):76-86.

5.Djouzi Z, Andrieux C. Compared effects of three oligosaccharides on metabolism of intestinal microflora in rats inoculated with a human faecal flora. Br J Nutr. 1997 Aug;78(2):313-24.

6.Flickinger EA, Hatch TF, Wofford RC, Grieshop CM, Murray SM, Fahey GC Jr. In vitro fermentation properties of selected fructooligosaccharide-containing vegetables and in vivo colonic microbial populations are affected by the diets of healthy human infants. J Nutr. 2002 Aug;132(8):2188-94.

7.Giacco R, Clemente G, Luongo D, Lasorella G, Fiume I, Brouns F, Bornet F, Patti L, Cipriano P, Rivellese AA, Riccardi G. Effects of short-chain fructo-oligosaccharides on glucose and lipid metabolism in mild hypercholesterolaemic individuals. Clin Nutr. 2004 Jun;23(3):331-40.

8.Gibson GR. Dietary modulation of the human gut microflora using prebiotics. Br J Nutr. 1998 Oct;80(4):S209-12.

9.Luo J, Van Yperselle M, Rizkalla SW, Rossi F, Bornet FR, Slama G. Chronic consumption of short-chain fructooligosaccharides does not affect basal hepatic glucose production or insulin resistance in type 2 diabetics. J Nutr. 2000 Jun;130(6):1572-7.

10.Moore N, Chao C, Yang LP, Storm H, Oliva-Hemker M, Saavedra JM. Effects of fructo-oligosaccharide-supplemented infant cereal: a double-blind, randomized trial. Br J Nutr. 2003 Sep;90(3):581-7.

11.Piche T, des Varannes SB, Sacher-Huvelin S, Holst JJ, Cuber JC, Galmiche JP. Colonic fermentation influences lower esophageal sphincter function in gastroesophageal reflux disease. Gastroenterology. 2003 Apr;124(4):894-902.

12.Rao AV. Dose-response effects of inulin and oligofructose on intestinal bifidogenesis effects. J Nutr. 1999 Jul;129(7 Suppl):1442S-5S.

13.Roberfroid M. Dietary fiber, inulin, and oligofructose: a review comparing their physiological effects. Crit Rev Food Sci Nutr. 1993;33(2):103-48.

14.Roberfroid MB, Van Loo JA, Gibson GR. The bifidogenic nature of chicory inulin and its hydrolysis products. J Nutr. 1998 Jan;128(1):11-9.

15.Roberfroid MB. Prebiotics and synbiotics: concepts and nutritional properties. Br J Nutr. 1998 Oct;80(4):S197-202.

16.Schaafsma G, Meuling WJ, van Dokkum W, Bouley C. Effects of a milk product, fermented by Lactobacillus acidophilus and with fructo-oligosaccharides added, on blood lipids in male volunteers. Eur J Clin Nutr. 1998 Jun;52(6):436-40.

17.Swanson KS, Grieshop CM, Flickinger EA, Bauer LL, Wolf BW, Chow J, Garleb KA, Williams JA, Fahey GC Jr. Fructooligosaccharides and Lactobacillus acidophilus modify bowel function and protein catabolites excreted by healthy humans. J Nutr. 2002 Oct;132(10):3042-50.

18.Tahiri M, Tressol JC, Arnaud J, Bornet F, Bouteloup-Demange C, Feillet-Coudray C, Ducros V, Pepin D, Brouns F, Rayssiguier AM, Coudray C. Five-week intake of short-chain fructo-oligosaccharides increases intestinal absorption and status of magnesium in postmenopausal women. J Bone Miner Res. 2001 Nov;16(11):2152-60.

19.Ten Bruggencate SJ, Bovee-Oudenhoven IM, Lettink-Wissink ML, Katan MB, Van Der Meer R. Dietary fructo-oligosaccharides and inulin decrease resistance of rats to salmonella: protective role of calcium. Gut. 2004 Apr;53(4):530-5.

20.Ten Bruggencate SJ, Bovee-Oudenhoven IM, Lettink-Wissink ML, Van der Meer R. Dietary fructo-oligosaccharides dose-dependently increase translocation of salmonella in rats. J Nutr. 2003 Jul;133(7):2313-8.

21.van Dokkum W, Wezendonk B, Srikumar TS, van den Heuvel EG. Effect of nondigestible oligosaccharides on large-bowel functions, blood lipid concentrations and glucose absorption in young healthy male subjects. Eur J Clin Nutr. 1999 Jan;53(1):1-7.

EDITOR'S NOTE: This monograph can be found in The Health Professional's Guide to Dietary Supplements (Lippincott, Williams & Wilkins) by Shawn M. Talbott, PhD and Kerry Hughes, MS.



“Probiotics” is a term used to refer to a group of “beneficial” bacteria that help maintain the health and function of the gastrointestinal tract. Probiotics have been defined as viable microorganisms that (when ingested) have a beneficial effect in the prevention and treatment of specific pathologic conditions. These microorganisms are believed to exert biological effects through a phenomenon known as colonization resistance, whereby the indigenous anaerobic flora limits the concentration of potentially pathogenic (mostly aerobic) flora in the digestive tract. Other modes of action, such as supplying enzymes or influencing enzyme activity in the gastrointestinal tract, may also account for some of the other physiologic effects that have been attributed to probiotics.

Acidophilus (Lactobacillus acidophilus) and Bifidus (Bifidobacterium lactis) of varying strains are popular forms of “good” bacteria found in dietary supplements. By displacing other bacteria and yeast, Acidophilus and other lactic acid bacteria may also play an important role in immune system function and prevention of gastrointestinal problems, including cancer. A wide variety of beneficial bacterial strains can be found in cultured yogurts and in freeze-dried form as dietary supplements. Claims for these products are generally made to reduce cholesterol levels (marginal evidence), support immune system function (solid evidence), maintain a healthy digestive system (solid evidence), and prevent colon cancer (preliminary evidence).


Dietary supplements providing Acidophilus in combination with some of the other beneficial probiotic bacteria are fairly inexpensive. Given the strong evidence for their beneficial effects on immune system function and the possibility that regular consumption may reduce colon cancer risk, these supplements would be a good choice for anybody looking for a general immune system booster.

Scientific Support

The digestive system is home to millions of bacteria that help digest, modify and convert the food we eat. Any alteration in the gastrointestinal environment is likely to influence the activity of these beneficial bacteria – sometimes posing health problems. Maintaining the “normal” populations of these good bacteria in the intestines, through consuming them as supplements or in cultured yogurt, can help displace disease-promoting bacteria and yeast that may gain a foothold when the levels of good bacteria drop.

Acidophilus and other beneficial bacteria are both acid- and bile-resistant, and thus capable of surviving transit through the gastrointestinal tract after they are ingested. These bacteria are sometimes called “probiotics” because regular consumption is linked to health benefits such as reducing cholesterol, preventing microbial growth, modulation of the immune system and, possibly, prevention of colon cancer.

Both human and animal studies have shown direct benefits of regular consumption of acidophilus and other beneficial bacteria on immune system function (Arunachalam et al. 2000, Gill et al. 2000 and 2001, Shieh et al. 2001). Overall, the probiotic bacteria tend to result in an enhanced ability of the immune system to recognize and destroy invading organisms. Several key components of the immune system, including macrophages, immunoglobulins and cytokines are altered by regular intake of beneficial bacteria. Populations of white blood cells are known to increase in number and activity following 1-2 weeks of consuming beneficial bacteria (Gill et al. 2001, Shieh et al. 2001). Importantly, resistance to viral and bacterial infections is significantly improved following regular intake of probiotics.

Epidemiological studies support the possibility that consumption of beneficial bacteria (from fermented milk and yogurt) may play a role in the prevention of colon cancer and inflammatory conditions (Gill et al. 2000 and 2001, Isolauri et al. 2000, Shieh et al. 2001). Test tube studies have shown that Acidophilus can decrease the cancer-causing potential (mutagenic activity) of various carcinogens – possible due to a direct interaction between the carcinogens and the bacteria. Consumption of acidophilus (and other lactic acid bacteria) has also been shown to reduce levels of cancer-causing enzymes in the digestive tract, supporting the possibility that probiotics do indeed play a role in the prevention of colon cancer.


There are no safety issues associated with regular consumption of Acidophilus or other probiotic bacteria at recommended levels, although those individuals with severe gastrointestinal ailments (Crohn’s disease or ulcerative colitis) should consult with their personal physician prior to consuming probiotic supplements. Most probiotic products will typically list the type of bacteria and the number of “live cells” on the label or side panel. There are no strict guidelines for dosage intake, but 1-10 billion CFUs (colony forming units) is a general rule of thumb and corresponds to effective levels used in human studies.


1.Agerholm-Larsen L, Raben A, Haulrik N, Hansen AS, Manders M, Astrup A. Effect of 8 week intake of probiotic milk products on risk factors for cardiovascular diseases. Eur J Clin Nutr. 2000 Apr;54(4):288-97.

2.Arunachalam K, Gill HS, Chandra RK. Enhancement of natural immune function by dietary consumption of Bifidobacterium lactis (HN019). Eur J Clin Nutr. 2000 Mar;54(3):263-7.

3.Arunachalam K, Gill HS, Chandra RK. Enhancement of natural immune function by dietary consumption of Bifidobacterium lactis (HN019). Eur J Clin Nutr. 2000 Mar;54(3):263-7.

4.Bengmark S. Bacteria for optimal health. Nutrition. 2000 Jul-Aug;16(7-8):611-5.

5.Bengmark S. Colonic food: pre- and probiotics. Am J Gastroenterol. 2000 Jan;95(1 Suppl):S5-7.

6.Bengmark S. Ecological control of the gastrointestinal tract. The role of probiotic flora. Gut. 1998 Jan;42(1):2-7.

7.Brady LJ, Gallaher DD, Busta FF. The role of probiotic cultures in the prevention of colon cancer. J Nutr. 2000 Feb;130(2S Suppl):410S-414S.

8.Chin J, Turner B, Barchia I, Mullbacher A. Immune response to orally consumed antigens and probiotic bacteria. Immunol Cell Biol. 2000 Feb;78(1):55-66.

9.Collins MD, Gibson GR. Probiotics, prebiotics, and synbiotics: approaches for modulating the microbial ecology of the gut. Am J Clin Nutr. 1999 May;69(5):1052S-1057S.

10.Cunningham-Rundles S, Ahrne S, Bengmark S, Johann-Liang R, Marshall F, Metakis L, Califano C, Dunn AM, Grassey C, Hinds G, Cervia J. Probiotics and immune response. Am J Gastroenterol. 2000 Jan;95(1 Suppl):S22-5.

11.D'Argenio G, Mazzacca G. Short-chain fatty acid in the human colon. Relation to inflammatory bowel diseases and colon cancer. Adv Exp Med Biol. 1999;472:149-58.

12.Davidson GP, Butler RN. Probiotics in pediatric gastrointestinal disorders. Curr Opin Pediatr. 2000 Oct;12(5):477-81. Roos NM, Katan MB. Effects of probiotic bacteria on diarrhea, lipid metabolism, and carcinogenesis: a review of papers published between 1988 and 1998. Am J Clin Nutr. 2000 Feb;71(2):405-11.

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EDITOR'S NOTE: This monograph can be found in The Health Professional's Guide to Dietary Supplements (Lippincott, Williams & Wilkins) by Shawn M. Talbott, PhD and Kerry Hughes, MS.