Will the Real Diabetic Please Stand

ABSTRACT: This article examines some of the epidemiology of noninsulin dependent diabetes mellitus (NIDDM). Instead of regarding diabetes as a discrete and specific disease entity or syndrome, the condition is approached more correctly as a spectrum of abnormality with varying shades of grey from normal to progressively more abnormal.

Introduction

Diabetes has been mapped and measured. However, as unusual as it may sound, it can be expressed analogically as an illusory box. Pictured within the box is good health and obviously this excludes diabetes. Outside the box is the general phenomenon of illness which includes the diabetic state. Obviously, there are also those patients who can be plotted “on the demarcating line.” They are variously referred to as prediabetes, borderline, subclinical, marginal and/or chemical diabetes mellitus. The centerpiece for this viewpoint is “the size of the box.” The more rigid the criteria for health, the smaller is the box.

The diagnosis of diabetes is based on two sets of requirements. The first, the clinical, is derived from prevailing symptoms and signs. There is a plethora of largely qualitative information that defines diabetes mellitus in terms of its symptomatology. These include polyphagia, polyuria, polydipsia, weight loss, weakness and pruritus, among others.^1-5 Beaser⁶ presented them with some degree of objectivity (Table 1).

Polydipsia was the most common symptom and was reported in about half the patients. More importantly, it was suggested by Beaser, from the title of his paper, that these were early symptoms.

Few physicians are aware that there are scores of articles concerning the oral manifestations of diabetes mellitus, which may appear very early in the disease process.⁷ One of these is dry mouth which is one of the commonest early symptoms (Table 2). Barach compared the number of teeth in aging diabetics with a group of a similar age who were considered to be healthy (Table 3).

There is no evidence that healthy individuals lose their teeth, but tooth loss convincingly parallels the health status of diabetic patients, there being a difference of 4 teeth in those under 30 and as many as eight in those over 60 years, as compared with age matched healthy controls.

Usually some measure of blood glucose is part of the biochemical diagnosis. Various investigators vicariously emphasize the fasting state, postprandial levels, or different temporal points in glucose tolerance patterns. A review of the medical literature^8-14 underscores the presently employed arbitrary norms. For example, Davidson¹³ considered that a fasting plasma glucose level repeatedly greater than 140 mg/dl was universally accepted as being diagnostic. In contrast, other clinicians⁵ claim that the fasting nondiabetic level should be 70-110 mg/dl. One might well ask what happens to those with a blood glucose between 110 and 140 mg/dl. It seems that this indicates confusion and conventional studies of the epidemiology of the disease are based on very autocratic and haphazard biochemical and clinical assumptions.^15-23 The data that we review here suggest that there is an alternative.

Discussion

For purposes of this discussion, three data sources are derived from 3 groups of patients. Group A consisted of 100 randomly chosen clinically non-diabetic dental patients who received a three-hour oral glucose tolerance test (OGTT).^24-28 Group B consisted of 170 randomly selected and clinically non diabetic patients who were examined by means of the cortisone glucose tolerance test (CGTT).²⁹ Group C consisted of 38 age- and sex-matched clinically nondiabeticsubjects with a chief complaint of dry mouth.³⁰

Group A

These patients completed a detailed questionnaire with particular emphasis on 3 common oral symptoms, dry mouth, burning tongue, and gingival tenderness. We reported a significant linear correlation between these symptoms, both singly and in combination and blood glucose concentration. This suggested, without drawing a specific line, the possibility that these three oral findings may represent early evidence of diabetic symptomatology. What was perhaps of even greater interest was that the same 3 oral symptoms tended to occur also in those with hypoglycemic responses. We are the only investigators, to our knowledge, to have observed this. It suggests that an intermediate concentration of blood glucose may be a barometer for homeostasis (Cheraskin E. Unpublished observation).

Group B

These patients with gingival tenderness²⁷ received a cortisone glucose tolerance test (CGTT). Like those patients in group A, there was a similar correlation in both hypo- and hyper-glycemic responses. We found a similar correlation in group C patients²⁸ between dryness of the mouth and dysglycemia.

We reported these correlations 30 years ago^31-37 and similar studies in relation to periodontal state, tooth mobility and dental loss which were confirmed by roentgenographic studies.^38-40 We found that the classic early symptoms of diabetes, namely polyphagia, polyuria and polydipsia had a much weaker correlation with blood sugar than the oral symptomatology.⁴¹

Much is still poorly understood in diabetes^42-47 There is general agreement that the disease phenomenon has a familial pattern though the old question of nature versus nurture remains unresolved.⁴⁸ It is generally accepted as a disorder involving both carbohydrate and lipid metabolism due to an absolute or relative insulin deficit. Finally, there seems to be unanimous acceptance of the fact that, even in the face of increasingly sophisticated control, the problem has not yet been solved.

Recent figures are available from the National Health Interview Survey of the Centers for Disease Control.⁴⁹ During the years 1980 through 1989, diabetic incidence among persons 75+ years increased 12-fold. That this is simply not a geriatric explosion is underlined by a rise of three-fold in those less than 45 years. Additionally, diabetes is commonly associated with devastating sequelae in the circulatory system, the kidney, and the eye. End-stage renal disease has increased fivefold during this same decade.

It is time, therefore, for rethinking the nature of diabetes mellitus. For example, there is growing interest in the observations that the microangiopathy in this disease and in scurvy are at least similar if not identical.⁵⁰ The history of maturity-onset diabetes and the label NIDDM bring into focus many shortcomings. There is reason to believe that the process should be recognized for what it is–a disturbance in energy metabolism and, as such, a deviation in homeostasis which requires much more exploration.

So, who should rise to the question, “Will the real diabetic patient please stand?” There is no single answer. The reason is based purely and simply on different philosophies. Actually, there are three broad possibilities. First, in this day and age, in the minds of the public, and unfortunately even many physicians, illnesses in general and diabetes in particular are considered to be highly specific in nature. The critical element in who is to be tagged diabetic or nondiabetic is determined by the size of the imaginary box. It is currently estimated that one to five percent of Americans suffer with NIDDM. For the elderly this may well be higher.

A concept exists that there is change from health to disease that follows a spectrum, eloquently described many years ago by Leo Krall.⁵¹ He said that the detection of diabetes can be compared to fishing with a small mesh net that increases the catch of fish but also seines some nonfish or the wrong variety of fish, as opposed to using a larger mesh which would be more specific for the size and type of fish sought, but bring a smaller yield.

Utilizing the “smaller fish” concept obviously raises the prevalence of diabetes. Hence, we are provided with progressively more restricted boxes. Recognizing the hazards of extrapolation, the prevalence problem increases to possibly 50 or more percent of the population. Perhaps, one day it may be possible to identify this metabolic imbalance at its inception and remove the “fish eggs.” Such laudable efforts are presently considered, and largely through studies of the genetics of diabetes mellitus. What is even more promising is the possibility of affecting the earliest stages of the disease since the demonstration of the effect of ascorbate on chromosomal damage.⁵²

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