DGL: A Special Licorice Extract for Peptic Ulcers

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DGL: A SPECIAL LICORICE EXTRACT FOR PEPTIC ULCERS

(duodenal & gastric)

 

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.

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.

 

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.

 

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.

 

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.

 

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.

 

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.

 

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

documented as having remarkable success.

 

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.

 

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.

 

How does DGL work?

 

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

protective factors which protect against ulcer formation.

 

This mechanism of action is much different than antacids and drugs like Tagamet,

Zantac, and Pepcid which work by neutralizing or suppressing gastric acid.

 

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.

 

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.

 

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.

 

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.

 

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.

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?

 

I strongly recommend avoiding antacids which contain aluminum.

 

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.

_________________

 

JoAnn Guest

mrsjoguest

DietaryTipsForHBP

http://www.geocities.com/mrsjoguest

 

 

 

 

 

 

 

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