We need blood.

We need it to travel to all tissues and organs—all the time. It delivers nutrients, signals molecules, and removes wastes & other metabolic byproducts. However, there is considerable evidence that during human aging, the network of the smallest blood vessels—collectively called the microvasculature—atrophy with age.

These tiny tubes tend to branch into and penetrate tissues that are the greatest distance from the heart. This includes the skin, where the density of the blood supply is particularly important for thermoregulation. Blood vessels in the skin contract when it’s cold, keeping the heated blood closer to the heart and less exposed to the elements. Conversely, when it’s especially hot outside, they dilate, allowing more blood to flow to the surface of the skin, which acts like a radiator in a car, releasing excess heat into the environment.

One age-related dysfunction of the skin microvasculature is called senile purpura—purple spots on the skin, often on the hands, arms, face, and neck. On a microscopic level, senile purpura appears to be characterized by disintegration of the microvasculature, where capillaries basically rupture or fall apart, and blood continues to be pumped into the intercellular spaces outside of the capillaries. That’s why senile purpura looks like bruising; structurally, it’s very similar.

The research group in this paper reported that topical application vitamin C to the skin caused significant regression of senile purpura. How could this be? As you might know, vitamin C is involved in the synthesis of collagen, a connective tissue that is prevalent in the walls of blood vessels. While the condition was not completely cured, the degree of improvement is remarkable enough to make us wonder.

If topical vitamin C improves senile purpura—in other words, enabled the microvasculature to better maintain itself—what is happening to cause the purpura in the first place? Is this a case of nutritional deficiency, in which years-long dietary deficiency of vitamin C manifests in older people not necessarily because of their extra years, but because of their extra years of insufficient vitamin C? Perhaps vitamin C simply acts as an antioxidant, which helps to counteract a presumed age-related increase in reactive oxygen species, which in-turn enables the microvasculature to regenerate itself to a significant degree.

The answers are not yet clear. One prudent option available right now is to ensure consumption of adequate vitamin C (one small study of elderly hospitalized patients reported 88% of them were vitamin C deficient).

For the sake of our mission to Renew the Rivers, we hope to see more research on the aging human microvasculature and what we can do about it.

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