Over the past decade, a WNPRC longitudinal study on aging and caloric restriction-one of only two such studies in the world-has provided a wealth of new information about the biology of aging and how the manipulation of diet can influence the process of growing old. Rhesus monkeys eating 30 percent less of a nutritionally complete diet than normal are exhibiting better health all around than study controls. Reduced intake seems to slow basic aging processes and may extend ultimate life span in primates, as has been shown in rodents.
Some of the findings so far include:
The next five years of the study should be even more insightful as the monkeys in the study enter late middle age: During this phase, age-related diseases and disorders appear more frequently, including adult-onset diabetes, osteoporosis, cancers, obesity, the loss of skeletal muscle mass and hypertension.
A potential long-term application of this study may come through the development of drugs that slow aging by mimicking the biological effects of caloric restriction.
Osteoporosis is a common disease in which bones become weak and consequently fracture occurs. Nutritional deficiencies, potentially including vitamin K, contribute to osteoporosis and unappreciated nutritional vitamin K insufficiency is extremely common in humans. We have been evaluating in both monkeys and humans the possibility this may be a heretofore-unrecognized contributor to bone loss.
We are continuing a pilot study evaluating the possibility that a vitamin K dependent protein osteocalcin contributes to maintenance of normal serum calcium concentration.
In addition, we are assessing the effect of anticoagulant-induced (warfarin) vitamin K insufficiency on bone masses. Preliminary results suggest that doses of warfarin commonly utilized for human anticoagulation do not produce adverse skeletal effects. This has direct human clinical importance given the large anticoagulant treated population.
Improved understanding of the ocular focusing mechanism and it's age-related functional impairment, derived from our rhesus monkey model, is suggesting possible approaches to alleviate this most common human ocular affliction.
The pathways by which fluid flows out of the eye are partially obstructed with aging. Improved understanding of this age-related decline, especially in the lesser-used pathway, deriving from our monkey model, may be lead to new glaucoma therapies.
Visual function declines during aging. Although some age-related deficits are due to optical changes (e.g., the formation of a cataract), careful sensory testing in humans suggests that the visual pathways in the brain are also likely to be affected. As the older portion of the human population increases it will be necessary to recognize and potentially treat neurally-based visual deficits of senescence. The goal of this research is to better understand the neural bases of visual deficits during normal aging using the aged non-human primate as a model. We have used non-invasive evoked potentials to show that acuity and speed of neural response declines in old rhesus monkeys.