Rejecting Tooth Decay and Combating Corrosion: From Low-Corrosion Sweeteners to Anti-Aging Antioxidant Philosophy

Sucrose isomers are new food ingredients produced from sucrose under enzymatic action. They have a similar sweetness to sucrose but are less likely to cause tooth decay and can be used as a source of energy. Therefore, these sweeteners can be used as a sucrose substitute in the manufacture of candies targeting growing children. Sucrose is composed of one molecule of glucose and one molecule of fructose. However, not all sugars formed by the combination of one molecule of glucose and one molecule of fructose are sucrose, because there are various ways in which molecules can combine.

This sugar is formed by the combination of one molecule of glucose and one molecule of fructose, but its physical and biochemical properties are quite different from sucrose. A type of bacterial cell isolated from beet wash water is immobilized, and then sucrose is passed through a bioreactor containing these immobilized cells. The sucrose is then converted into this isomer sugar, and after separation and purification, the refined product of this sugar can be obtained. Tooth decay is caused by the interaction of three factors: food, microorganisms, and tooth enamel. Among these, the main microorganism is a mutant strain of streptococcus (S-mutant) in the oral cavity.

When the S-mutant encounters sucrose, it causes many glucose molecules to link together, forming a water-insoluble, adhesive dextran. This water-insoluble dextran aggregates on the tooth surface, forming plaque. Besides the S-mutant, other bacteria also multiply in plaque. These bacteria break down sugars to form organic acids such as lactic acid and acetic acid, making the area around the plaque acidic. With the pH value of plaque and its surroundings below 5.5, calcium in the tooth enamel is dissolved, a process known as demineralization. This repeated process leads to tooth decay.

Adding 1% of this sugar barely changes the pH, while adding other sugars quickly makes it acidic. Besides the S-mutant, Lactobacillus and Streptococcus also cannot utilize this sucrose isomer to form organic acids. When culturing the S-mutant in a medium with added sucrose, a layer of white bacterial aggregate adheres to the inner wall of the petri dish, but this phenomenon does not occur when culturing in a medium with this sucrose isomer. When sucrose reacts with the glucan synthase of the S-mutant, it forms insoluble glucan and precipitates, while this sucrose isomer does not precipitate upon reaction.

In addition, animal experiments were conducted to study the relationship between diet and tooth decay. Young mice were first fed breast milk for 15 days, then fed regular feed for 3 days, and finally fed the experimental diet for 55 days. The results showed that nearly half of the mice in the group with 56% sucrose added to their feed developed tooth decay, while less than 10% of the group with 56% of this sucrose isomer developed tooth decay. Based on these experimental results, it can be concluded that this sucrose isomer is a sweetener that is less likely to induce tooth decay. However, this sucrose isomer is less soluble in water than sucrose and is more prone to discoloration upon heating.

Therefore, caution is needed during the manufacturing and processing of foods. Candies, pastries, and other foods using this sucrose isomer as a sweetener are already on the market. When cyclodextrin gluconate transferase is added to a mixture of starch and sucrose, a reaction occurs, causing several glucose molecules at the glucose terminus of the sucrose molecule to combine in an α-1,4 form to generate glucosyl sucrose. This mixture is called a mixed sugar. This component has been found in honey and ginseng. It has been reported that in the human body, this substance can also be generated from a mixture of starch and sucrose through the action of amylase.

The sweetness of the mixed sugar is 50%–55% that of sucrose, with a mild and delicate taste. It is understood that this component with a similar structure can inhibit the synthesis of insoluble dextran from sucrose by S-mutants. From 1975 onwards, dental research institutions across the country conducted detailed studies on the efficacy and safety of the mixed sugar in preventing tooth decay over a five-year period. The results showed that the mixed sugar can be digested, absorbed, and metabolized in the body like sucrose, but it cannot be utilized by S-mutants to form plaque. Furthermore, it can prevent sucrose from being used to form plaque, and it produces less acid.

In summary, mixed sugars can be considered a low-cariogenic sweetener. Given their low cariogenicity, they have been approved for use in JSD foods certified by the Japan Nutrition Food Association. From a nutritional perspective, especially for rapidly growing children, mixed sugars are widely used in foods such as jellies, candies, jams, and bread. On the other hand, mixed sugars are also a type of maltose with relatively high viscosity; like sucrose, they are unstable to acid, but rarely brown.

Due to its unique water-retention properties, erythritol can prevent starch retrogradation and sucrose crystallization, making it a popular substitute for sucrose or maltose in the manufacture of various Japanese and Western-style pastries and confectionery. Erythritol is widely distributed in the plant kingdom. It is found in lichens, edible fungi, fruits, and fermented foods such as wine, sake, and soy sauce. It is a tetracarbon sugar alcohol. Erythritol is three-quarters as sweet as sucrose, has a refreshing taste, and is a low-calorie sweetener that produces almost no energy. It does not cause tooth decay.

Nikken Chemical Co., Ltd., in collaboration with the National Food Research Institute of the Ministry of Agriculture, Forestry and Fisheries, has isolated a high-yield erythritol-producing bacterium using glucose as a raw material and bred a mutant strain with practical value. They have successfully produced erythritol in large quantities using fermentation. In the food industry, erythritol is already being used as a low-calorie sweetener in chocolate, chewing gum, candy, cookies, and as a table condiment. Furthermore, its potential applications in medicine are also being considered. Everyone desires immortality. However, life is ultimately finite.

It would be wonderful to stay young as long as possible. All living things age. While various theories exist regarding why living things age, none have fully elucidated the mechanism of aging. Among these theories, the theory of free radical-induced peroxidation of unsaturated fatty acids has recently become one of the most compelling. Diseases accompanying aging include cancer, arteriosclerosis, hypertension in the elderly, Parkinson's disease, Alzheimer's disease, amyloidosis, and immune dysfunction.

The mechanisms underlying these diseases require further investigation, but it is believed that lipid peroxidation caused by free radicals plays a significant role. Oxidation refers to the combination of one oxygen molecule; the combination of two oxygen molecules is called peroxidation. During peroxidation, oxygen is activated. This activated oxygen is unstable and readily reacts chemically with other functional groups. Oil used for frying shrimp or fish becomes sticky and darkens after a few uses; this is due to oil peroxidation. This process can also occur in the body.

Unsaturated fatty acids are found in the cell membrane and other areas surrounding the cell. These unsaturated fatty acids can undergo peroxidation. Once peroxidized, these unsaturated fatty acids react with other components within the cell, such as proteins, to form special compounds. These compounds lack the properties of the original fats and the functions of proteins; they are fluorescent pigments called aging pigments. An increase in aging pigments prevents cells from performing normal functions; as cells age, the amount of aging pigments also increases.

Measuring blood levels of lipid peroxides reveals that their concentration increases with age, particularly rapidly after age 40. Aging is accompanied by the accumulation of lipid peroxides and is also related to the progression of hypertension and arteriosclerosis. Furthermore, patients with myocardial infarction, diabetes, and hyperlipidemia all have high levels of lipid peroxides in their blood. Thus, aging and many diseases are closely related to lipid peroxides. Therefore, it can be said that by eliminating lipid peroxides, which act as "rust" in the body, it may be possible to prevent aging and various diseases.

Furthermore, lipid peroxidation is also considered one of the causes of arteriosclerosis and vascular aging. Lipid peroxidation also frequently occurs in cancer cells. Vitamin E can effectively prevent cancer. There are reports that vitamin E also has a role in preventing arteriosclerosis. This is because vitamin E inhibits oxygen activation, eliminating some activated oxygen and thus protecting biological membranes. Peroxidation is a chain process, and vitamin E can break this chain.

Unsaturated fatty acids on cell membranes combine with activated oxygen to generate free radicals. Vitamin E reacts with these free radicals, stabilizing them and thus breaking the lipid peroxidation chain, while vitamin E itself is converted into vitamin E groups. Unsaturated fatty acids such as linolenic acid, linoleic acid, and arachidonic acid are essential for humans. However, excessive intake of unsaturated fatty acids can lead to the accumulation of lipid peroxides. When consuming large amounts of foods rich in unsaturated fatty acids, it is necessary to simultaneously consume a large amount of vitamin E.

Lipid peroxides are like rust, causing the body to become "rusty," while vitamin E can be considered a "rust remover" in the body. Based on this understanding, adequate intake of vitamin E and vitamin C, which can eliminate free radicals generated in the body, may potentially inhibit aging. Vitamin E is fat-soluble and exists in membranes, while water-soluble vitamin C exists in its water-soluble portion outside the membrane. Vitamin C can reduce vitamin E groups back to vitamin E, thereby enhancing the effects of vitamin E.

Experiments have shown that vitamin E deficiency can significantly accelerate aging, and people who take vitamin E have a survival rate about 2.5 times higher than those who don't, with fewer deaths from cerebrovascular diseases and cancer. Generally speaking, excessive intake of fat-soluble vitamins is harmful. Although vitamin E is a fat-soluble vitamin, excesses like those of other fat-soluble vitamins such as vitamins A and D are rarely reported. Don't wait until you're older to start taking vitamin E. To prevent "rust" in your body and slow down the aging process as early as possible, you should start taking appropriate amounts of vitamin E from a young age. It can be said that this is the only wise approach.