Abstract
Aging can increase cancer incidence because of accumulated mutations that initiate cancer and via compromised body control of premalignant lesions development into cancer. Relative contributions of these two factors are debated. Recent evidence suggests that the latter is rate limiting. In particular, hyperglycemia caused by compromised body control of blood glucose may be a factor of selection of somatic mutation-bearing cells for the ability to use glucose for proliferation. High glucose utilization in aerobic glycolysis is a long known characteristic of cancer. The new evidence adds to the concepts that have been being developed starting from mid-1970ies to suggest that age-related shifts in glucose and lipid metabolism increase the risk of cancer and compromise prognoses for cancer patients and to propose antidiabetic biguanides, including metformin, for cancer prevention and as an adjuvant means of cancer treatment aimed at the metabolic rehabilitation of patients. The new evidence is consistent with several effects of glucose contributing to aging and acting synergistically to enhance carcinogenesis. Glucose can affect (i) separate cells (via promoting somatic mutagenesis and epigenetic instability), (ii) cell populations (via being a factor of selection of phenotypic variants in cell populations for higher glucose consumption and, ultimately, for high aerobic glycolysis); (iii) cell microenvironment (via modification of extracellular matrix proteins), and (iv) the systemic levels (via shifting the endocrine regulation of metabolism toward increasing blood lipids and body fat, which compromise immunological surveillance and promote inflammation). Thus, maintenance of youthful metabolic characteristics must be important for cancer prevention and treatment.
Highlights
Relationships between aging and cancer is a focus of longstanding attention in biomedical research [1,2,3,4,5,6]
Else assuming that aging attenuates the resistance of body to any causes of death, one may suggest that these causes include cancer, i.e., aging attenuates the ability of organism to counteract carcinogenesis, e.g., because cell immunity and/or the ability of normal tissue cells to compete with transformed cells for resources available to a tissue become increasingly compromised in the course of aging
Nondiabetes-related points derived from both source figures are consistent with a common exponential trend, which suggests that when fasting blood glucose increases from 4 to 6 mmol/l, i.e. within the range assumed as normal, the risk of death from cancer increases by 20%
Summary
Relationships between aging and cancer is a focus of longstanding attention in biomedical research [1,2,3,4,5,6]. One of them (Figure 2A in [50]) shows indexes of cancer-related mortality vs baseline fasting blood glucose in initially non-diabetic subjects having fasting glucose levels from less than 4.0 up to 7.5 mmol/l.
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