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War I decreased dramatically in countries where the food supply was inadequate from shortages brought on by the war.55

that obesity, atherosclerosis, and diabetes declined from lack of dietary sugar.56

consumption could explain signicant increases in these chronic disorders prior to the war when a remarkable boost in intake of sweets had taken place.12,55

the interpretation, both sugar and fat, neither one alone, were in short supply during wartime.12,13,55

proposed that fats, especially saturated fats, were the major culprit.57,58

for his sugar hypothesis, the theory that dietary fats by increasing circulating levels of cholesterol and augmenting body fat mass via enhanced calorie consumption are most accountable for increased prevalence of diabetes and cardiovascular diseases received much more backing from academicians, clinicians, and the public.9-11

many supported the fat hypothesis believing that only modest evidence existed to favor that sugar consumption causes any health hazards except dental caries.59-61

sugar consumption can promote insulin resistance and various components of the metabolic syndrome by at least two signicant mechanisms that are somewhat interdependent: rst, by direct effects of circulating glucose on insulin sensitivity and second, by producing fat accumulation that indirectly is associated with insulin resistance.1,2

mentioned, although excess sugar intake leads directly to insulin resistance, accumulation of body fat from the surplus caloric intake also is associated with insulin resistance.73

As further depicted in Fig.2, increased glucose levels enhance non-enzymatic glycation of proteins and


then, numerous studies in rats have reconrmed sugar- induced metabolic disturbances produced by sucrose feeding occur regularly despite no weight gains.68-72


Sweets like table sugar are frequently eaten in excess and increased calories portend accumulation of body fat.1,2,74

increased systolic blood pressure occurred with sucrose in the drinking water of spontaneously hypertensive rats (SHR) despite no weight gain.67


Rodent studies substantiate the rst mechanism clearly. In a 1980 publication foretelling the recent awareness paid sugar-containing soda beverages and elevated blood pressure,65,66

Our group has long believed that the results of excess intake of dietary sugars, especially sucrose, high fructose corn syrup, and other rapidly absorbed rened carbohydrates are more deleterious to overall health than even saturated fat intake and hypercholesterolemia due to their inuence on glucose-insulin balance  insulin resistance.1,2,26,35,62-64 Figure 2 is an updated composite of numerous gures and slides developed on our part over many years in an attempt to elucidate a sound hypothesis.1,34

Excessive In addition,

From 1957 on, a series of noteworthy papers by John Yudkin et al. championed the theory that consumption of too much sugar was largely responsible for the increasing incidence of diabetes and coronary heart disease.12,14-16,55 Disturbances in the glucose-insulin system were key to the theory.31

While Yudkin received moderate backing

Confusing So, many

With this knowledge in mind, Paton proposed Paradoxically, augmented sugar

the compensatory hyperinsulinemia can lead to direct damage, particularly to the cardiovascular system.62 Hyperglycemia and hyperinsulinemia, in turn, are further associated with increased free radical formation, alterations in electrolyte transport, and various serious hormonal derangements.62

report of Masoro that showed lower circulating levels of glucose and insulin in longer-living caloric restricted rats,32


words, might circulating glucose and/or insulin, especially in the higher end of the non-diabetic range (125 mg/ dl), bring forth the risk for metabolic disturbances and provide clues to the causes behind various elements of the metabolic syndrome? Based largely on Yudkin’s clinical observations,12,14-16,55,78,79

the straightforward

and our own early reports in rodents on the ability of insulin sensitizers to overcome various manifestations of the metabolic syndrome and prolong life span,71,80 possibility of positive ndings appeared to be realistic.

This prole, elevated glucose and insulin concentrations, suggests insulin resistance caused by sucrose intake.31,78,79 In response to insulin resistance from whatever source, circulating levels of glucose increase and bring about, at least initially, a compensatory upsurge in insulin concentrations.83

glucose and insulin concentrations rise. Consequently, we believe insulin resistance, even in relatively mild forms, can be approximated, at least to some extent, by examining circulating glucose levels. The challenge to this hypothesis is whether circulating glucose levels, measured routinely by practitioners, can be linked closely with common age-related health disturbances in order to use these levels as guides.

A number of methodological limitations are found with the current study. The subject population is heterogeneous in terms of gender and age, for instance, with its dening characteristic being serum glucose levels at or below 125 mg/dl. In the proposed follow-up study, which will have available thousands of subject datum sets, stratifying subsets based on gender, age and a small number of other parameters will be possible due to the luxury of large numbers. However, it is not clear that the present pilot data necessarily are especially weakened for our purposes by its heterogeneous subject pool. In terms of years, the preponderance of subjects runs from middle -to late-middle age. With the targeted fasting glucose cut- off, this suggests that our data is drawn from a healthier than normal population. One implication may be that our positive correlations between fasting glucose levels and various elements of the metabolic syndrome likely would be even more robust in a more representative cross section of the population, i.e., including more younger subjects. Our follow-up could begin to address this by looking at subgroups and determining whether correlations are (Continued on next page)

81 The eventual result of this is that both

Isocaloric exchanges of dietary sucrose for starch have long been known to characteristically produce increases in circulating glucose and insulin in both humans81

and rats.82

We questioned in previous communications whether circulating glucose and insulin even at levels not considered to be in the diabetic range could be linked to risks for future, more severe health problems.33,34

In other

DNA, often with subsequent deranged function75-77


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