Most diabetics desire sweets. This may represent an inborn characteristic, an acquired habit, or both.
- A survey of 500 diabetic patients conducted in West Germany (cited by Horwitz 1983) revealed that only 84 could abstain from sweets.
- A comparable situation exists among juvenile diabetics. Court (1976) found that 72 percent of mothers used artificial sweeteners in preparing the meals of their diabetic children to achieve compliance.
The hazards of aspartame for diabetics require further clarification in light of statistics concerning premature mortality. The years of potential life lost (YPLL) increased only for the categories of diabetes mellitus and chronic obstructive pulmonary disease in the Morbidity and Mortality Weekly Report (December 1986 Supplement).
Mechanisms of Aspartame's Diabetognic Potential
The adverse metabolic, hormonal, toxic, and other undesirable effects of aspartame and its components are detailed in Section 5. Many could contribute to the aggravation of diabetes and its complications. They encompass the wasting of insulin, impaired insulin-stimulated glucose transport, increased growth hormone and glucagon release after phenylalanine administration, other effects of its amino acids (see below), and additional pharmacologic activities. Another mechanism whereby aspartame-induced stimulation of insulin could aggravate diabetes involves the generation of insulin receptor antibodies capable of blocking the access of insulin to liver receptors (Dozio 2001).
With reference to aspartame-induced insomnia (Chapter VI-F), sleep debt has a detrimental impact on carbohydrate metabolism and endocrine function - including decreased glucose tolerance, and altered thyrotropin and cortisol concentrations (Spiegel 1999).
Some of the scientific observations that pertain to the effects of aspartame and its amino acid components on insulin release, other hormones, and metabolism are briefly reviewed.
- Phenylalanine and aspartic acid might enter the brain of diabetics more readily due to altered permeability of the blood-brain barrier. They could then aggravate fetal development during gestational diabetes in conjunction with elevated sorbitol concentrations because of increased polyol metabolism (Eriksson 1986) - conducive to eye and neurologic complications
- Limited insulin reserves could be further depleted by pancreatitis (Chapter IX) or phenylalanine-induced pancreatitis stimulation (Chapter XXIV). This and other amino acids, as well as protein, increase insulin and blood glucose levels. Years ago, Conn and Newburgh (1936) demonstrated comparable elevations of the blood sugar in diabetic patients consuming either dextrose or beefsteak.
- Schusdiziaria et al (1981) reported that digested gluten elicited a more rapid and significantly greater rise in postprandial (after a meal) peripheral vein insulin and glucagon levels than undigested gluten.
- Wahren et al (1972) found accelerated splanchnic uptake of amino acids in diabetic patients (24 hours after withdrawal of insulin), compared to healthy controls. This increase was most notable for phenylalanine, glycine, serine, threonine, methionine, and tyrosine.
- Atawa et all (1990) noted the high frequency of aspartic acid at 57 of the HLA -DQ Beta-chain in Japanese patients with insulin-dependent diabetes mellitus.
- Another influence of phenylalanine and its analogs on glucose and insulin metabolism involves the binding and activation of glucose-dependent insulinotropic polypeptide (GIP) receptors by the photoactivable p-benzyl-L-phenylalanine (Yip 1999). GIP, an important regulator of insulin receptor of the insulin receptor as well as insulin action on target issues.
Sardesai et al (1987) concluded on the basis of experimental data that aspartame may adversely influence the control of diabetics. They found that a single dose of aspartame administered to both normal and streptozotozin-induced diabetic rats increased liver tryptophan oxygenase by 12 percent. Furthermore, aspartame decreased blood and brain tryptophan, and increased serum glucose and glucagon in the diabetic animals. The chronic administration of aspartame to both groups also resulted in increased tryptophan oxynase activity, hyperglycemia, and a further rise of glucose in the diabetic animals.
Insulin/Hypoglycemia Reactions
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