Abstract

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Background: This is a hypothesis based on an observation made by the author when he was a rotating intern in the department of internal medicine. It was observed by the author that some patients admitted in the ward with peptic ulcer disease had their blood sugar levels above normal and their blood sugar levels came down to be within normal limits with anticholinergics containing hyoscine. The author explains it through the hypothesis of Hyperactive Vagus Syndrome.

Conclusion: In some people vagus nerve is hyperactive and causes peptic ulcer disease together with hyperglycemia. This hyperglycemia can be corrected with the use of anticholinergics drugs. This aspect needs further experimental exploration.

Hypothesis

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Background: This hypothesis is based on an observation made by the author when he was a rotating intern in the department of internal medicine at Bankura Sammilani Medical College, Bankura, India. It dates back to November – December 1981. It was observed by the author that some patients admitted in the ward with peptic ulcer disease had their blood sugar levels above normal. Furthermore their blood sugar levels came down to be within normal limits with anticholinergics containing hyoscine. This was the usual treatment done at that time. The author observed it as a student intern. He had no role in the therapeutic intervention. The observation was not in accordance with the earlier findings as follows:

1. Peptic ulcer was found only rarely in diabetics [1].

2. Achlorhydria was more commonly present in diabetics than would be expected [2].

It’s obvious that peptic ulcer disease and hyperglycemia should not normally coexist. But the author’s observation was contrary so he explained it through the hypothesis of Hyperactive Vagus

Syndrome:‘In some people vagus nerve is hyperactive and causes peptic ulcer disease together with hyperglycemia. This hyperglycemia can be corrected with the use of anticholinergics drugs’.

Explanation: The blood glucose level is maintained by a dynamic equilibrium between it and insulin. Insulin hypoglycemia causes vagus stimulation and gastric secretion [3]. By ill understood mechanism vagus stimulation also causes hypoglycemia [4].

In diabetics the effect of insulin is negligible and the higher glucose depresses the vagus [1] which then further increases glucose- a vicious cycle. This depressed vagus also decreases the gastric secretion conforming to the observations of Hosking et.al [1] and Rabinowitch [2].

In case of hyperactive vagus tending to cause hypoglycemia, this equilibrium is disturbed but as the effect of insulin is not absent (contrary to diabetics) glucose is maintained by interplay of three factors, namely glucose, insulin and vagus (Illustration.1).  As the hyperactive vagus tends to cause hypoglycemia, this equilibrium is adjusted so that the glucose is maintained at higher levels. Thus glucose is maintained at higher than normal level so that the hyperactive vagus if ever lowers the glucose there will be no chances of hypoglycemia taking place.

Discussion: Not all the patients having peptic ulcer disease have higher blood sugar levels, because the disease has several etiologies. Common exogenous causes of peptic ulcer are Helicobacter pylori infection and administration of ulcer causing drugs. The endogenous cause of hyperactive vagus may be emotional or may be due to excessive stimulation of autonomic ganglion caused by nicotine (partly exogenous). The men who were observed were also smokers and their diastolic blood pressures were mildly elevated. This hypothesis was not further developed by the author because he took another specialty after graduation. But he conjectures if anticholinergics be a part of therapy for diabetes as glucose and vagus are involved in a vicious cycle! This aspect needs further experimental exploration. Though it may appear bit old, yet old views sometimes come out with new evidence if re-explored.

References

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1. Hosking DJ, Moody F, Stewart IM, Atkinson M. Vagal impairment of gastric secretion in diabetic autonomic neuropathy. Br Med J 1975; 2:588-590.
2. Rabinowitch IM. Achlorhydria and its clinical significance in diabetes mellitus.  Am J Dig Dis 1949; 16: 322-332.
3. Kneller AW, Nasset ES. Relationship of insulin hypoglycemia to intestinal secretion. Am J Physiol 1949; 159: 89-94.
4. Best CH and Taylor NB eds. The Physiological Basis of Medical Practice . The Williams & Wilkins Company, Baltimore, Maryland, 1966:1104.

Source(s) of Funding

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No funding was required.

Competing Interests

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None.

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