The subject of hypoglycemia reactions in aspartame disease and the mechanisms involved will be considered in Chapter XIV.
Excessive insulin may be released by aspartame through a reflex mechanism involving the cephalic phase of insulin release. This is exaggeration of normal physiology relative to anticipating the arrival of food. It could result in hypoglycemic symptoms or aggravation of diabetes mellitus when the binding of more insulin at cell membranes creates "insulin resistance."
Severe caloric restriction and other forms of metabolic stress in noninsulin-dependent diabetics increases the release of endorphins and enkephalins. These endogenous peptides with opiate-like activity have been shown to have important glucose-regulating effects in humans - notably, significant increases in plasma insulin and glucose concentrations (Giugliano 1987). Such effects can also lead to clinical hypoglycemia and insulin resistance.
Diabetic patients who receive increased doses of insulin for "tight control," as occurred while using aspartame, are at greater potential risk for the adverse cerebral consequence of hypoglycemia. This problem is compounded by reduced release of counter regulatory hormones (epinephrine; growth hormone; cortisol; glucagon) in response to severe hypoglycemia. These altered counter regulatory hormonal thresholds in well controlled Type II diabetics, even at normal blood glucose concentrations (Spyer 2000), can further compound complications by aspartame-induced hyperinsulinemia.
- Widom and Simonson (1990) demonstrated that diabetic patients may develop cognitive impairment before the onset of symptoms attributable to the release of epinephrine and norepinephrine.
- Amiel et al (1991) reported a threefold increase in the incidence of both severe and asymptomatic hypoglycemia among diabetic patients treated intensively with insulin. Furthermore, they are more likely to develop EEG abnormalities during hypoglycemia.
Criticism of Related Research (see Chapter XXVIII)
The administration of aspartame as capsules to evaluate its effect on diabetic control, rather than "real world" products, is relevant. This introduces the deficiency of not invoking the cephalic phase of insulin release associated with the taste of sweet (see above). If insulin production is already strained, such superimposed stimulation could result in a state termed "high-output failure of insulinogenesis" (Roberts 1964, 1965).
Professional Confusion and Disagreement (see Chapter XXVIII)
Many physicians and other health care professionals disagree with the author's concerns about aspartame use by diabetics.
- Filer and Stegink (1989) reviewed aspartame metabolism in diabetic subjects, and concluded "aspartame may be safely ingested at projected levels of use." (These investigators received considerable corporate support).
- John D. Fernstrom, Ph.D. (1987) opined that the "pros" of aspartame in improving the quality of life for "millions of diabetics in the population" far outweigh "any imagined cons" of this and related products. He argued against wasting effort by "being obsessive about something that isn't really there."
- Dr. F. Xavier Pi-Sunyer, a physician-representative of the American Diabetes Association, reaffirmed this organization's approval of the safety of aspartame - both for diabetics and the general population in testimony given in an U.S. Senate hearing on Nov 3, 1987. He asserted that there had been no significant input from physicians concerning problems in managing diabetics related to aspartame use. Moreover, he expressed concern over the unwarranted anxiety created by this hearing, and objected to spending any more money for research "already done."
Furthermore, most physicians accept the assertion by diabetologists that aspartame is harmless for diabetics.
- Horwitz and Bauer-Nehrling (1983) concluded that there is "no evidence of alteration of diabetic control because of aspartame ingestion."
- Visek (1984) stated that aspartame does not interfere with the basic treatment of diabetic patients.
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