NaturaLift MD Review Blog

Free radicals are toxic molecules resulting from exposure to ultraviolet radiation. Oxygen, the essential element to life, is damaged and contributes to the creation of reactive oxygen species. Hydroxy ions (-OH) abound, missing an electron that, in an attempt to become whole again, they create holes in other molecules.

Free radicals can oxidize fatty molecules, a process known as lipid peroxidation. That’s a catastrophe because the cell needs a functional plasma membrane to sustain life.

It is through this membrane that nutrients and oxygen needed for life and body function pass. Most waste produced by the cel s, including carbon dioxide pass through each cell’s membrane, and into the microscopic capillaries. From there, they enter the main bloodstream to be removed by the kidneys, liver, and lungs. The remaining waste that passes through the cel membrane enters the fluid between the cells (interstitial fluid) and from there into the lymphatic channels where they eventually enter the bloodstream in the upper chest.

But, when the membrane is damaged by lipid peroxidation, the cell begins to age rapidly and die. This membrane is composed of two layers of fatty substances, which, when oxidized, fail to function. These oxidation bullets” attack at random, but the more unblocked sunlight hitting the skin, the more free radicals are generated in all layers of the skin.

Note: Free radicals are generated not only by ultraviolet sunlight: weather, and other pollutants such as smoke, chlorine, harsh detergents, and cosmetics also create them.
Reactive Oxygen Species

Studies have clearly shown that reactive oxygen species, such as superoxide anion (O2-), hydroxyl radical (-OH), and hydrogen peroxide (H2O2), are responsible for ultraviolet-induced oxidative damage. Reactive oxygen species also directly contribute to the cause of skin cancers, photoaging, and many skin and inflammatory disorders.

Reactive oxygen species damage cell membranes by the peroxidation of fatty acids in the phospholipid structure of the membrane. Unfortunately, the process doesn’t stop there. Peroxidation forms lipid peroxide radicals, lipid hydroperoxides, and other lipid fragmentation products, which are active oxidizing agents. This chain reaction, in which electrons are removed from lipids such as cell membrane phospho-lipids, give rise to more lipid radicals. As long as there is oxygen in the system, this chain reaction will continue and lipid peroxides will continue to accumulate until they are reduced by antioxidants in the skin.

Free radical reactivity generates a chain reaction of many free radical species production, enhancing skin aging and skin cancer.

Loss of Fat-Soluble Nutrients

The top of the skin is covered by natural protective secretions called skin surface lipids (SSL). These are: “… a very complex mixture of sebum mixed with small amounts of epidermal lipids, which mantle the human epidermis, thus representing the outermost protection of the body against oxidative insults.” The body of a well-nourished, healthy, and non-stressed child or an older person may make an adequate amount of coenzyme Q-10. However, exposure to four times the amount of sunlight that causes just some redness of the skin depletes protective SSLs by 70% of coenzyme Q-10 and 84% of vitamin E.

Cumulative Ultraviolet Light Exposure

Sub-chronic sunlight (UV-A and UV-B radiation) exposure is the sum of what you’ve been getting all your life. It does not result in sunburn or a noticeable tan, but it wreaks havoc on the skin. In 2002, scientists finally examined this problem histologically and found these harmful effects:

• After just one month, there was obvious epidermal hyperplasia (thickening of the outer layer of the skin). In three months, that progressed to “… epidermal thickening and formation of epidermal ingrowths projecting into the dermis.”
• The “… keratinocytes were somewhat pleomorphic.” These keratinocytes developed “… cytoplasmic projections which migrated into the dermis.” What should have been a well-defined junction between the epidermis and dermis, the basement membrane,” began to “… disappear along with the development of edema spreading from the upper dermis to the epidermis.”
• Furthermore, “… [i]n the dermis, in addition to edema, fibroblast proliferation and mast cell infiltration progressed with time, and degranulation was obvious at two and three months. In the upper dermis, especially beneath the epidermis, decrease in diameter and disintegration of collagen fibrils (the main structural protein compound of the skin) were observed.”