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From the Book: Healing Factor Vitamin C Against Disease – by Irwin Stone, Linus Pauling, Albert Szent-Gyorgyi 1972.
Source on-line: https://vitamincfoundation.org/stone/
Source download book: https://welib.org/md5/35609ae8abf6e1dcb1cc701374943358
Peptic ulcers may be the butt of many jokes, but as any ulcer sufferer can testify, having one is not funny. Ulcers are a painful, chronic disease affecting about 14 million Americans during their productive years. Every day some 4,000 individuals develop an ulcer and each year about 10,000 people die of complications from peptic ulcer. The drain on the economy is estimated to be 500 million dollars in lost man-hours and cost of medical treatment. A simple, inexpensive, successful preventive and therapeutic regime is needed.
Our stomach is the second stop in the processing of food for digestion and absorption. It is a tough, strong, muscular, spheroidal-shaped bag with an opening at the top (inlet) and at the side (outlet). Each opening is surrounded by a circular muscle, the sphincter, controlled by nerve impulses for opening and closing. The top opening is connected to the esophagus, which carries the food from the mouth; the side opening is connected to the duodenum, the first section of the intestines. The lining of the stomach secrets strong hydrochloric acid and a powerful enzyme, pepsin, which dissolves and digests proteins.
The stomach contents are normally highly irritating, corrosive, and erosive. This can be seen when the stomach contents sometimes back up into the esophagus producing the distressing sensations of "heartburn" and in the sour, irritating taste of vomit. Since the stomach walls are themselves made of protein, they must in some way be protected against the corrosive action of their own secretions. Sometimes this equilibrium is disrupted and open sores and lesions in the lining result. If they are in the stomach, they are called gastric ulcers; if in the adjacent intestine, duodenal ulcers. In the United States, duodenal ulcers are about eight times more common than gastric ulcers.
The secretion of hydrochloric acid and the enzyme, pepsin, is also under nervous control. The stimulation of these nerves is caused by food entering the mouth or even by the thought of food, so that the stomach will be ready for processing the food when it reaches there. In nervous people, smokers, excessive drinkers, or individuals under stress, this nervous stimulation does not turn off at the proper sequence or turns on when there is no food in the stomach. When no food is present to take the full brunt of the corrosive chemical attack of the stomach juices, gastric distress is felt and, if long continued, actual attack of the lining may result.
Animal experiments have been conducted since the early 1930s on ascorbic acid and its relation to gastric and duodenal ulcers. In 1933, Smith and McConkey (1), working in a New York State tuberculosis hospital, performed autopsies on 1,000 guinea pigs that had been fed a normal diet and failed to find a single spontaneous stomach ulcer. Of seventy-five guinea pigs fed a diet deficient in ascorbic acid, twenty, or approximately twenty-six percent, developed ulcers. In eighty guinea pigs fed the same deficient diet but supplemented with added ascorbic acid, only one developed ulcers. In other experiments, they found that diets deficient in vitamins A, B, and D did not produce ulcers if the ascorbic acid supply was adequate. Mechanical injury to the duodenum lining of guinea pigs fed an adequate diet was followed by rapid and complete healing, while similar injury to guinea pigs on an ascorbic acid-deficient diet resulted in the formation of duodenal ulcers. They also gave a small group of their tuberculous patients with chronic duodenal ulcers tomato juice supplements (their only source of ascorbic acid in those early days) with favorable responses. They also advised adding tomato juice or orange juice to the scurvy-producing Sippy or Lenhartz diets used for ulcer treatment. Hanke (1), in Germany in 1937, confirmed this work.
There is an extensive medical literature on clinical tests going as far back as 1934 correlating deficiency of ascorbic acid with high incidence of gastric and duodenal ulcers, bleeding ulcers, and poor healing after surgery. Many of the papers point out that the ulcer patient should receive adequate amounts of ascorbic acid.
Over the years, the author has collected over fifty medical research papers on this subject with no claim that this represents all the papers which have been published. Complete reference to all these papers is obviously beyond the scope and space of this book. Instead, a limited illustrative selection of twelve papers is included in the bibliography covering the period from 1936 to 1968 (2). The earliest papers show that ulcer patients have higher requirements for ascorbic acid than normal subjects. The patients have low, inadequate intakes of ascorbic acid and are in a state of subclinical scurvy and there is poor healing of the ulcers and the wounds after surgery. The papers recommend that ulcer patients receive plenty of ascorbic acid. The following are quotes from a few of these early papers:
It is important for the clinician to make sure that patients with peptic ulcers are receiving an adequate amount of vitamin C... The severest degrees of vitamin C deficiency were found in the patients with haematemesis (vomiting of blood). It is suggested that large doses of vitamin C should be given to all subjects of peptic ulcerations and haematemesis in order to saturate them as rapidly as possible (2).
The results and suggestions contained in these early references have been repeated in the later papers and have continued up to the present time.
In 1968, Russell and coworkers (2) compared a series of sixty hospitalized patients with gastrointestinal hemorrhage -- 2 with peptic ulcer -- with a group having uncomplicated peptic ulcer and with healthy controls. They found significantly lower ascorbic acid levels in the bleeding group than in the uncomplicated peptic ulcer group, which was much lower than the healthy controls. The differences were more striking with advancing age over forty-five. They stated That only six of the bleeders had any clinical evidence of scurvy but that the ret suffered from a subclinical form of the disease. They believed this subclinical scorbutic state prevented healing of the bleeding ulcers and maintained hemorrhage in the gastric erosions precipitated by other factors such as aspirin or alcohol.
Certain drugs, such as aspirin, cortisone, and other anti-inflammatory agents, and cinchophen, are known to provoke ulcers and gastric hemorrhage. This is especially the case when a deficiency of ascorbic acid is present. In animal experiments, the administration of ascorbic acid along with the toxic drug reduced the incidence of peptic ulcer and gastric hemorrhage to such an extent that it prompted one author (Aron) to suggest, "Therefore it would seem judicious in human therapeutics to include ascorbic acid in every prescription for an anti-inflammatory drug" (3).
In any surgery, the importance of ascorbic acid has long been known (see Chapter 27). Patients undergoing surgery for ulcers are no exception. In a 1947 paper, Zerbini (4) discusses two surgical cases of patients with ascorbic acid deficiency. One patient exhibited severe surgical shock during the operation and the other patient showed no evidence of healing of the surgical wounds when the stitches were removed on the seventh postoperative day. This latter patient had been given a daily injection of 200 milligrams of ascorbic acid, but obviously this low, vitaminlike dosage was insufficient to supply the patient's high demands and as a result the wounds did not heal.
Williamson, in 1967, again confirmed the low ascorbic acid levels in patients subjected to gastric surgery and said that in these patients, "the administration of ascorbic acid would seem obligatory." Cohen, in the same year, stated that all patients with gastrointestinal disorders should be suspected of having subclinical scurvy. He also pointed out that this concept was proposed by Lazarus in 1937 but was "not yet generally acknowledged." This was over three decades ago -- the medical mills certainly grind slowly. Three other papers and a review added further confirmation to the pathogenetic role played by low levels of ascorbic acid in gastrointestinal disorders. In the paper by Cohen and Duncan they state:
[Patients should] be given routine ascorbic acid supplements before surgery and during the phase of early wound healing ... There are no known hazards of ascorbic acid therapy, and overdosage is therefore of no practical importance (4).
In a thirteen-page government bulletin (5) entitled "Peptic ulcer, " prepared by The National Institute of Arthritis and Metabolic Diseases of the National Institutes of Health, there is not a single mention of ascorbic acid in the entire booklet. Nothing is said of its possible role in ulcer formation or in the ulcer treatment, in spite of the worldwide background of nearly four decades of research, some of which has been cited above. This is a bulletin sold to the general public for its information on the causes and treatments of this disease. "The Medical Letter, " which is a semimonthly publication for doctors and is designed to convey authoritative recommendations for current medical treatments, devoted a large part of its December 26,1969 issue to a discussion of the "Medical Treatment of Peptic Ulcer" (5). Here again no mention is made of ascorbic acid in the two and a half pages of discussion. It seems rather fantastic that, in both these publications, all of the suggestive work reported in the medical literature on ascorbic acid in ulcer therapy, can be so blatantly ignored. It also indicates that the use of ascorbic acid in ulcer therapy is not widely practiced and that ulcer patients are generally denied the possible benefits indicated in the above review of medical literature.
The following clinical research proposal is made in the hope that it will be picked up and tested by the government health agencies, by the publicly endowed health foundations with clinical testing facilities, or by doctors in the gastrointestinal field. The proposed rationale for the use of sodium ascorbate instead of ascorbic acid in ulcer prevention and therapy at megascorbic levels combines the antacid and buffering capacity of sodium ascorbate with its wound healing and antihemorrhagic effects. The research protocol would include the use of 0.5 to 1 teaspoonful (1.5 to 4 grams) of sodium ascorbate, dissolved in a glass of milk, taken before meals and at bedtime. For gastric distress at other times, 0.5 teaspoon of sodium ascorbate, dissolved in about 2 ounces of water, will usually provide immediate relief. This simple regime was very successful in several ulcer volunteers who were thus able to avoid surgery. The use of sodium ascorbate should be subjected to large-scale clinical testing to determine its value as a new approach to peptic ulcer prevention and therapy.
