DGL: A SPECIAL LICORICE EXTRACT FOR PEPTIC ULCERS (duodenal & gastric)

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DGL: A SPECIAL LICORICE EXTRACT FOR PEPTIC ULCERS (duodenal & gastric) JoAnn

Guest May 10, 2005 14:50 PDT

 

A special extract of licorice known as DGL is a remarkable medicine for

peptic ulcers. The term peptic ulcer refers to ulcers that occur in the

stomach (gastric ulcer) or the first portion of the small intestine

(duodenal ulcer). Duodenal ulcers are more common with an estimated

frequency rate of 6 to 12% of the adult population in the United States.

In other words, approximately 10% of the U.S. population has clinical

evidence of duodenal ulcer at some time in their lifetime. Duodenal

ulcers are 4 times more common in men than in women and 4 to 5 times

more common than gastric ulcers.

 

What are the symptoms of an ulcer?

 

Although symptoms of a peptic ulcer may be absent or quite vague, most

peptic ulcers are associated with abdominal discomfort noted 45-60

minutes after meals or during the night. In the typical case, the pain

is described as gnawing, burning, cramp-like, or aching, or as

" heartburn. " Eating or using antacids usually results in great relief.

 

What causes an ulcer?

 

Even though duodenal and gastric ulcers occur at different locations,

they appear to be the result of similar mechanisms. Specifically, the

development of a duodenal or gastric ulcer is a result of some factor

damaging the protective factors which line the stomach and duodenum.

 

In the past, the focus has primarily been on the acidic secretions of

the stomach as the primary cause of both gastric and duodenal ulcers.

However, more recently the focus has been on the bacteria Helicobacter

pylori and non-steroidal anti-inflammatory drugs.

 

Gastric acid is extremely corrosive. The pH of gastric acid (1 to 3)

would eat an ulcer right through the skin. To protect against ulcers,

the lining of the stomach and small intestine has a layer of mucin. In

addition, the constant renewing of intestinal cells and the secretion of

factors which neutralize the acid when it comes in contact with the

stomach and intestinal linings also protect against ulcer formation. The

acid is designed to digest the food we eat, not the stomach or small

intestine.

 

Contrary to popular opinion, over-secretion of gastric acid output is

rarely a factor in gastric ulcers. In fact, patients with gastric ulcers

tend to secrete normal or even reduced levels of gastric acid. In

duodenal ulcer patients, almost half have increased gastric acid output.

This increase may be due to an increased number of acid producing cells

known as parietal cells. As a group, patients with duodenal ulcers have

twice as many parietal cells in their stomach compared to people without

ulcers.

 

Even with an increase in gastric acid output, under normal

circumstances, there are enough protective factors to prevent either

gastric or duodenal ulcer formation. However, when the integrity of

these protective factors is impaired, an ulcer can form. A loss of

integrity can be a result of H. pylori, aspirin and other non-steroidal

anti-inflammatory drugs (NSAIDs), alcohol, nutrient deficiency, stress,

and many other factors. Of these factors, H. pylori and NSAIDs are by

far the most significant.

 

Are ulcers really caused by a bacteria?

 

The role of the bacteria H. pylori in peptic ulcer disease has been

extensively investigated. It has been shown that 90-100% of patients

with duodenal ulcers, 70% with gastric ulcers, and about 50% of people

over the age of 50 test positive for this bacteria.1 Physicians can

determine the presence of H. pylori by measuring the level of antibodies

to H. pylori in the blood or saliva, or by culturing material collected

during an endoscopy (the process of examination of the stomach or

duodenum with a fiberoptic tube with a lens attached to it).

 

Predisposing factors for H. pylori infection are low gastric output as

well as low antioxidant content in the gastrointestinal lining. H.

pylori infection increases gastric pH, thereby setting up a positive

feedback scenario.2 In other words, H. pylori infection leads to ulcer

formation and ulcer formation leads to H. pylori infection.

 

Probably more important causes of ulcers than H. pylori are aspirin and

smoking. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs)

are associated with a significant risk of peptic ulcer. While most

studies documenting the relative frequency of peptic ulcers as a

consequence of aspirin and NSAIDs have focused on their use in the

treatment of arthritis and headaches, recently the risk of

gastrointestinal bleeding due to peptic ulcers was evaluated for aspirin

at daily dosages of 300 mg, 150 mg, and 75 mg--dosages commonly

recommended to prevent heart attacks and strokes.3

 

One study, conducted at five test hospitals in England, found an

increased risk of gastrointestinal bleeding due to peptic ulcer at all

dosage levels. However, the dosage of 75 mg per day was associated with

a 40% less bleeding than 300 mg per day and 30% less than 150 mg per

day. The researchers concluded " No conventionally used prophylactic

aspirin regimen seems free of the risk of peptic ulcer complications. "

 

The combination of NSAID use and smoking is particularly harmful to the

ulcer patient.4

 

Smoking is a significant factor in the occurrence and severity of peptic

ulcers. Increased frequency, decreased response to peptic ulcer therapy,

and an increased mortality due to peptic ulcers are all related to

smoking. Smoking causes ulcers by at least three mechanisms. First of

all, increases the backflow (reflux) of bile salts into the stomach.

Bile salts are extremely irritating to the stomach and initial portions

of the duodenum, bile salt reflux induced by smoking appears to be the

most significant factor responsible for the increased peptic ulcer rate

in smokers. Smoking also decreases the secretion of bicarbonate by the

pancreas - an important neutralizer of gastric acid - and accelerates

the passage of food from the stomach into the duodenum.5 In addition,

the psychological aspects of smoking are also important, since the

chronic anxiety and psychological stress associated with smoking appear

to worsen ulcer activity.

 

What about stress? Can it cause an ulcer?

 

Stress is universally believed to be an important causative factor in

peptic ulcers. However, this link is quite controversial in the medical

literature. One of the big problems is that studies attempting to

examine this assumption about stress and ulcers have been poorly

designed.6 The data suggests that it is not simply the amount of stress,

but rather the patient's response to it that is the significant factor.

Also, as a group, ulcer patients have been characterized as tending to

repress emotions. At the very least, I encourage my patients with ulcers

to discover enjoyable outlets of self-expression and emotions.

 

Are their any foods that a person with ulcers should avoid or eat more

of?

 

Yes. A diet eliminating food allergies has been used with great success

in treating and preventing recurrent ulcers.7,8 It is ironic that many

people with peptic ulcers soothe themselves by consuming milk, a highly

allergic food. Milk should be avoided on this basis alone. However,

there is additional evidence suggesting that milk should be avoided in

patients with peptic ulcers such as population studies show the higher

the milk consumption the greater the likelihood of ulcer and milk

significantly increases stomach acid production.9

 

A diet rich in fiber is associated with a reduced rate of ulcers as

compared with a low-fiber diet. The therapeutic use of a high-fiber diet

in patients with recently healed duodenal ulcers reduces the recurrence

rate by half.10 Although several fibers often used to supplement the

diet (e.g., pectin, guar gum, psyllium, etc.) have been shown to produce

beneficial effects, a diet rich in plant foods is best.11,12

 

As far as a specific food to help heal ulcers - raw cabbage juice has

been well documented as having remarkable success.13-15 One liter per

day of the fresh juice, taken in divided doses, resulted in total ulcer

healing in an average of only ten days. Further research has shown that

the high glutamine content of the juice is probably responsible for the

efficacy of cabbage in treating these ulcers. In a double-blind clinical

study of 57 patients, 24 using 1.6 grams of glutamine a day, with the

rest using conventional therapy (antacids, antispasmodics, diet, milk,

and bland diet), glutamine proved to be the more effective treatment.

Half of the glutamine patients showed complete healing (according to

radiographic analysis) within 2 weeks, and 22 of the 24 showed complete

relief and healing within 4 weeks.15 Although the mechanism for these

results is not known, it is postulated by the authors to be due to the

role of glutamine in the manufacture of compounds which line and protect

the stomach and small intesine.

 

What is the best natural medicine for ulcers?

 

A special extract of licorice known as DGL. Licorice has historically

been regarded as an excellent medicine for peptic ulcer. However, due to

the side effects of the licorice compound glycyrrhetinic acid (it causes

elavations in blood pressure in some cases), a procedure was developed

to remove this compound from licorice and form deglycyrrhizinated

liquorice (DGL). The result is a very successful anti-ulcer agent

without any known side effects.16-21

 

How does DGL work?

 

The proposed mechanism of DGL is that it stimulates and/or accelerates

the protective factors which protect against ulcer formation.16 This

mechanism of action is much different than antacids and drugs like

Tagamet, Zantac, and Pepcid which work by neutralizing or suppressing

gastric acid. A obvious question related to DGL is " Does DGL have any

effect on Heliobacter pylori? " The answer appears to be yes as DGL is

composed of several flavonoids which have been shown to inhibit H.

pylori.23

 

How does DGL compare to antacids or drugs like Tagamet and Zantac?

 

Numerous studies over the years have found DGL to be an effective

anti-ulcer compound. In several head to head comparison studies, DGL has

been shown to be more effective than either Tagamet, Zantac, or antacids

in both short term treatment and maintenance therapy of peptic

ulcers.17,18 However, while these drugs are associated with significant

side effects, DGL is extremely safe and is only fraction of the cost.

For example, while Tagamet and Zantac typically cost well over $100 for

a month's supply, DGL is available in health food stores at $15.00 for a

month's supply.

 

What has the research shown with DGL in gastric ulcers?

 

Very good results. For example, in a study of DGL in gastric ulcer, 33

gastric ulcer patients were treated with either DGL (760 mg, three times

a day) or a placebo for one month.19 There was a significantly greater

reduction in ulcer size in the DGL group (78%), than in the placebo

group (34%). Complete healing occurred in 44% of those receiving DGL,

but in only 6% of the placebo group.

 

Subsequent studies have shown DGL to be as effective as Tagamet and

Zantac for both short term treatment and maintenance therapy of gastric

ulcer. For example, in a head to head comparison with Tagamet, one

hundred patients received either DGL (760 mg, 3 times a day between

meals) or Tagamet (200 mg, 3 times a day and 400 mg at bedtime).17 The

percentage of ulcers healed after 6 and 12 weeks were similar in both

groups. Yet, while Tagamet is associated with some toxicity, DGL is

extremely safe to use.

 

Gastric ulcers are often a result of the use of alcohol, aspirin or

other nonsteroidal anti-inflammatory drugs, caffeine, and other factors

that decrease the integrity of the gastric lining. As DGL has been shown

to reduce the gastric bleeding caused by aspirin, DGL is strongly

indicated for the prevention of gastric ulcers in patients requiring

long-term treatment with ulcer-causing drugs, such as aspirin, other

NSAIDs, and corticosteroids.20

 

What about DGL in duodenal ulcers?

 

DGL is also effective in duodenal ulcers. This is perhaps best

illustrated by one study in patients with severe duodenal ulcers. In the

study, forty patients with chronic duodenal ulcers of 4 to 12 years

duration and more than 6 relapses during the previous year were treated

with DGL.21 All of the patients had been referred for surgery because of

relentless pain, sometimes with frequent vomiting, despite treatment

with bed rest, antacids, and powerful drugs. Half of the patients

received 3 grams of DGL daily for 8 weeks; the other half received 4.5

grams per day for 16 weeks. All 40 patients showed substantial

improvement, usually within 5 to 7 days, and none required surgery

during the one year follow-up. Although both dosages were effective, the

higher dose was significantly more effective than the lower dose.

 

In another more recent study, the therapeutic effect of DGL was compared

to that of antacids, or cimetidine in 874 patients with confirmed

chronic duodenal ulcers.18 Ninety-one percent of all ulcers healed

within 12 weeks; there was no significant difference in healing rate in

the groups. However, there were fewer relapses in the DGL group (8.2%)

than in those receiving cimetidine (12.9%), or antacids (16.4%). These

results, coupled with DGL protective effects, suggest that DGL is a

superior treatment of duodenal ulcers.

 

How do I take DGL?

 

The standard dosage for DGL in acute cases is two to four 380 mg.

chewable tablets between or 20 minutes before meals. For more mild

chronic cases or for maintenance the dosage is one to two tablets 20

minutes before meals. Taking DGL after meals is associated with poor

results. DGL therapy should be continued for at least 8 to 16 weeks

after there is a full therapeutic response.

 

It appears that in order to be effective in healing peptic ulcers, DGL

must mix with saliva. DGL may promote the release of salivary compounds

which stimulate the growth and regeneration of stomach and intestinal

cells. DGL in capsule form has not been shown to be effective.

 

Antacids seem to help my symptoms, should I continue to use them or will

they interfere with the effectiveness of DGL?

 

Antacids can be used as part of the initial treatment for symptomatic

relief. All antacids are relatively safe when used on an occasional

basis, but I strongly recommend avoiding antacids which contain

aluminum. I recommend following label instructions and avoiding the

regular use or overuse of antacids. Taken regularly antacids they can

lead to malabsorption of nutrients, bowel irregularities, kidney stones,

and other side effects.

 

References:

 

Berstad K and Berstad A: Helicobacter pylori infection in peptic ulcer

disease. Scand J Gasroenterol 28:561-7, 1993.

Sarker SA and Gyr K: Non-immunological defense mechanisms of the gut.

Gut 33:987-93, 1992.

Weil J, et al.: Prophylactic aspirin and risk of peptic ulcer bleeding.

BMJ 310:827-30, 1995.

Gray GM: Peptic ulcer diseases. In, Dale DC, Federman DD: Scientific

American Medicine. Sci Am, New York, NY, 1995.

Anda RF, Williamson DF, Escobedo L, et al: Self-perceived stress and the

risk of peptic ulcer disease. Arch Int Med 152:829, 1992.

Feldman EJ and Sabovich KA: Stress and peptic ulcer disease.

Gastroenterol78:1087-9, 1980.

Andre C, Moulinier B, Andre F, and Daniere S: Evidence for anaphylactic

reactions in peptic ulcer and varioliform gastritis. Ann Allergy

51:325-8, 1983.

Siegel J: Immunologic approach to the treatment and prevention of

gastrointestinal ulcers. Ann Allergy 38:27-9, 1977.

Kumar N, Kumar A, Broor SL, et al: Effect of milk on patients with

duodenal ulcers. Brit Med J 293:666, 1986.

Rydning A, Berstad A, Aadland E, and Odegaard B: Prophylactic effects of

dietary fiber in duodenal ulcer disease. Lancet 2:736-9, 1982.

Kang JY, et al.: Dietary supplementation with pectin in the maintenance

treatment of duodenal ulcer. Scand J Gastroenterol 23:95-9, 1988.

Harju E, and Larme TK: Effect of guar gum added to the diet of patients

with duodenal ulcers. J Parenteral Enteral Nutr 9:496-500, 1985.

Cheney G: Rapid healing of peptic ulcers in patients receiving fresh

cabbage juice. Cal Med 70:10-14, 1949.

Cheney G: Anti-peptic ulcer dietary factor. J Am Diet Assoc 26:668-72,

1950.

Shive W, Snider RN, DuBiler B, et al: Glutamine in treatment of peptic

ulcer. Tex J Med 53:840-3, 1957.

Marle, J, et al.: Deglycyrrhizinised liquorice (DGL) and the renewal of

rat stomach epithelium. Eur J Pharm. 72:219, 1981.

Morgan Ag, et al.: Comparison between cimetidine and Caved-S in the

treatment of gastric ulceration, and subsequent maintenance therapy. Gut

23:545-51, 1982.

Kassir ZA: Endoscopic controlled trial of four drug regimens in the

treatment of chronic duodenal ulceration. Irish Med J 78:153-6, 1985.

Turpie AG, Runcie J and Thomson TJ: Clinical trial of deglycyrrhizinate

liquorice in gastric ulcer. Gut 10:299-303, 1969.

Rees WDW, et al.: Effect of deglycyrrhizinated liquorice on gastric

mucosal damage by aspirin. Scand J Gastroent 14:605-7, 1979.

Tewari SN and Wilson AK: Deglycyrrhizinated liquorice in duodenal ulcer.

Practitioner 210:820-5, 1972.

Zhou H and Jiao D: 312 cases of gastric and duodenal ulcer bleeding

treated with 3 kinds of alcoholic extract rhubarb tablets. Chung Hsi I

Chieh Ho Tsa Chih 10:150-1, 131-2, 1990.

Beil W, Birkholz and Sewing KF: Effects of flavonoids on parietal cell

acid secretion, gastric mucosal prostaglandin production and

Helicobacter pylori growth. Arzneim Forsch 45:697-700, 1995.

 

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AIM Barleygreen

" Wisdom of the Past, Food of the Future "

 

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