What happens above, within, and under your skin is a maelstrom of fascinating biological processes.
Skin is of course your body's largest organ, but what are the functions of that organ? What happens within and under your skin? Leading dermatologist Dr. Robert Norman answers these questions in The Blue Man and Other Stories of the Skin (University of California Press, 2014), a compelling and accessible introduction to the life of your skin, while also recounting his experiences with patients and their memorable and mysterious skin maladies. Excerpted from "What Covers Us?" this selection goes into the basics of what's going in around and under your skin.
The finest clothing made is a person’s own skin, but, of course, society demands something more than this.
— Mark Twain
Our skin, at the most basic level, defines us.
The skin is the body’s largest organ, averaging twenty square feet and nine pounds; it makes up 16 percent of the body’s weight. The skin is complicated but amazing in structure; it can be the target and dwelling place of thousands of tiny viruses, bacteria, or yeasts, yet does a stellar job of living with the good and keeping out the bad, all to protect the inner environment.
The epidermis, the outermost layer of skin, is a major part of the immune system. It is filled with Langerhans cells that form a first line of defense against environmental threats, identifying foreign materials and dangerous substances and ridding us of them. The epidermis is also part chemical plant, synthesizing vitamin D in the presence of sunlight, transforming a variety of helpful chemical compounds that interact with it, and inactivating substances that could be dangerous for us to absorb.
The epidermis protects the body from all kinds of insults. As Arthur and Loretta Balin write, “It seems fitting that the organ that defines the boundary between outside and inside worlds would be involved in the essential immune-system task of distinguishing between self and other.” Poison ivy is a common example: it is known to affect over 350,000 people in the United States annually, and demonstrates the wide range of possible sensitivities and reactions to exposure. Here’s how the reaction to poison ivy works. Urushiol is a chemical within the sap of the poison ivy plant that binds to the skin on contact. Urushiol shimmies its way into the skin and is broken down by T lymphocytes (or T-cells) that recognize it as a foreign substance, or antigen. The T-cells send out inflammatory signals called cytokines and the immune system pumps up the volume and calls in the troops—white blood cells. Still under the command of cytokines, the white blood cells turn into macrophages (super Pac Men) that eat up the foreign urushiol but also cause collateral damage to the normal tissue skin, resulting in inflammation and a dermatitis. A severe allergic reaction and blistering and oozing may occur in susceptible individuals; the fluid is produced by the body as blood vessels develop gaps and leak fluid through the skin. Approximately a quarter of the people exposed to poison ivy have no allergic reaction, while in extreme cases a anaphylactic reaction can occur. With age and repeated exposure, the sensitivity usually decreases.
The epidermis has a top layer called the stratum corneum, composed of closely packed cells that protect the skin from external abuse. The stratum corneum keeps the skin hydrated, both absorbing water and preventing water evaporation by means of a dense network of the protein keratin. The stratum corneum’s thickness varies throughout the body. On the palms of the hands and the soles of the feet, this layer is thicker to provide additional protection. Generally, the stratum corneum has fifteen to twenty layers of dead cells in addition to the layers of proteins, for a total thickness of between ten and forty micrometers—very thin.
Every move you make results in showers of skin particles from the epidermis released into the air. Every twenty-four hours an estimated ten thousand million skin scales or squames peel off each of our bodies, accounting for one to one and a half grams of skin each day, or about one pound each year. These scales are the desiccated remnants of skin cells that continually form at the base of the epidermis and travel slowly toward the surface. After forty to fifty-six days a newly formed cell reaches the surface and it is now called the stratum corneum, the same horny components that make up our hair and fingernails.
At high magnification this surface of dead skin appears as irregular patches of rough and curly cornflakes. House dust consists of 80–90 percent skin; squames are the motes in the sunbeam filtering into our rooms.
Just beneath the stratum corneum live the keratinocytes or squamous cells, which mature and move toward the surface to form the stratum corneum. Below them, in the deepest layer of the epidermis, is the basal layer, containing cells that continually divide and form new keratinocytes, replacing the old ones shed from the skin’s surface. This constant upward migration characterizes the epidermis.
Also in the basal layer are the cells known as melanocytes, which determine differences in skin color. These cells produce the pigment melanin, which protects the skin from sunlight and determines the intensity of skin and hair color. Each of us has the same number of melanocytes. The difference between darker and lighter skin tones is a result of the type, amount, and arrangement of the melanin produced by our melanocytes. Those with darker skin color, such as African Americans, have more melanin and are much better adapted to the harsh conditions of sun exposure. Carotenes, mostly located a level deeper down in the dermis, may contribute to the yellowish cast characteristic of Asian skins. Hemoglobin, the oxygen-carrying pigment in blood, gives pinkness to some fair skins. Freckles are due to increased melanin production, while nevocellular nevi, or moles, are caused by tightly packed groups of melanocytes. Solar lentigines, the flat, brown “liver spots,” occur because of an abnormal increase in the number of melanocytes. Those with vitiligo have a decrease in melanocyte function and albinos are genetically unable to produce any melanin at all.
But the epidermis does not only protect and color us. It also is host to some of the marks of aging and sun exposure. If you look closely at the skin of the elderly, you may notice the acquired spots and “barnacles of life” (seborrheic keratosis) that accumulate in the epidermis. Scaly actinic, or solar, keratosis can be detected by feeling its sandpaper texture.
Below the epidermis is the dermis, the middle layer of the skin. It contains blood vessels, lymph vessels, sweat glands, collagen bundles, fibroblasts, and nerves. Held together by a protein called collagen made by the fibroblasts, the dermis is a major contributor to the skin’s flexibility and strength and also contains pain and touch receptors.
The dermis also contains the hair follicles; infection or inflammation associated with infection in the vicinity of the roots results in folliculitis. As the Balins have pointed out, we humans call ourselves “naked apes,” yet we are covered with fine, unpigmented hairs that are actually ultrasensitive touch sensors. As the only mammals with such highly sensitive touch receptors all over our bodies, we require an enormous brain to process this constant sensory input from the skin.
The dermis can be marked by dilated blood vessels called telangiectasias, or spider veins, brought on by chronic sun exposure, by estrogen, or in some cases by an underlying liver or blood disorder. (Every skin disorder has its anatomical correlate; the field of dermatopathology specializes in connecting clinical skin findings to underlying anatomy.)
The subcutis (also known as the subcutaneous layer) is the deepest layer of skin. It consists of a network of collagen and fat cells. This layer helps conserve the body’s heat and protects the body from injury by acting as a “shock absorber.”
When we are babies, our skin is elastic and resilient—and it becomes less so every day from then on. We lose about 1 percent of our collagen, as well as elastic fibers and blood vessels that attach to the epidermis, every year after age thirty. The result is crinkles and wrinkles, a rather unfair exchange. The skin becomes sallow and pale. We increase fat deposition in the areas we don’t like, and we lose fat and therefore insulation in other body areas such as the face, arms, and legs. The underlying tissue depletion makes us more prone to injury, and the loss of nerves decreases our tolerance for cold.
Reprinted with permission from The Blue Man and Other Stories of the Skin by Dr. Robert Norman and published by University of California Press, 2014.