AT THE TIPPING POINT
Navin M. Geria, Doctors Skin Prescription (DSP),
Senior Technical Advisor & Principal
DSP- Doctors Skin Prescription
34 Mountainview Road, Warren, NJ 07059
ABSTRACT
The skin is the largest, most complex immune organ. The skin is exposed to both endogenous and environmental oxidizing agents leading to its premature aging and impaired cellular function. All vital organs begin to lose some function as you age. Aging changes have been found in all of the body’s cells, tissues, and organs. These changes affect the functioning of all body systems. Aging is common to all living organisms, yet there is no universal agreement as to its biological mechanisms. If the underlying cause of aging can be determined, it might be possible to interfere with the process, thus extending human longevity. To date more than 300 molecular biological mechanisms have been described in an effort to explain human aging. Biologists define aging as a genetic process associated with morphological and physiological process-functional changes in cellular and extracellular components aggravated by injury throughout life and resulting in a progressive imbalance of the control and regulatory systems of the organism, including hormonal, autocrine, neuro-endocrine, and immune homeostatic mechanisms (1). In short, aging is a process in which both intrinsic and extrinsic determinants lead progressively to a loss of structural integrity and physiological function (2). Aging theories basically can be separated into two fundamental groups. DNA damage theories advocate that aging is caused by accumulated damage to DNA, which in turn inhibits cells’ ability to function and express the appropriate genes. This leads to cell death and overall aging of the skin. Another group is in favor of built-in breakdown theories, which advocate that aging is a direct consequence of genetic programming. The causes for aging are directly built into the genome and cellular structure as a sort of molecular clock. This chapter will examine a few mainstream theories of aging.
a. Wear and Tear Theory (Immunological Theory)
m. Mutation Accumulation and DNA/RNA Damage
n. Deficient Immune System/Autoimmune Theory
a. Wear and Tear Theory (immunological theory)
This theory assumes that the body and its cells are damaged by constant use, causing minor damage to cells, which remain unrepaired. There are changes in the immune system as it begins to wear out and the body is more prone to infections and tissue damage. As the system breaks down, the body becomes more apt to have autoimmune reactions in which the body’s own cells are mistaken for foreign material and are destroyed by the immune system. It is generally agreed that the body and its cells are damaged by abuse, neglect, and overuse. The organs such as liver, stomach, kidneys, and skin are worn down by toxins in our diet, environment, excessive consumption of fat, sugar, caffeine, alcohol, nicotine, ultraviolet rays, and by many other physical and emotional stresses to which we subject our bodies every day. Wear and tear is not confined to organs, but also takes place at the cellular level (1). As a result, the system becomes worn or damaged, adding more stress on other organs and causing a downward spiral in body functioning. These are nonreversible physical or chemical changes within cells that gradually alter the cellular function. This theory supports the concept that aging is a programmed process. Each cell has a specific amount of metabolic energy available to it, and the rate at which this energy is used determines an individual’s length of life. Besides depletion of available energy, this theory includes other contributing factors, such as effects of accumulation of harmful by-products of metabolism and of faulty enzymes due to random errors. This is one of the oldest and most outdated theories of aging.
The neuro-endocrine system is a complicated network of biochemicals that govern the release of hormones by the hypothalamus, located in the brain. The hypothalamus controls and instructs other organs and glands to release their hormones. Aging endocrine glands secrete a progressively reduced level of hormones leading to decline in the body’s ability to repair and regulate itself, and the circadian rhythms of hormone in the blood become progressively more irregular. Furthermore, hormone effectiveness is also reduced due to the receptors’ downgrading.
Life-span determining genes are inherited and are called longevity assurance genes, and they determine the process of aging. Furthermore, aging is genetically programmed by some sort of neurological center that functions as a biological clock. It specifically focuses on the genetic programming encoded within our DNA. We are all born with a unique genetic code, and a predetermined tendency to certain types of physical and mental functioning. The genetic inheritance has a great deal to tell about how long we live. Each of us has a biological clock ticking away, set to go off at a particular time. When that clock goes off, it signals our body first to age and then to die. The timing of this genetic clock is subject to enormous variation (2). Certain cell components specifically limit the number of divisions of that particular cell type. This raises the question: How can there be lifelong division of many cell types in the body if each cell type is capable of only a limited number of cell divisions? Well, there are present in the body several generations of dormant “renewal cells” in each tissue that begin dividing at different rates. These are, in effect, reserve embryonic cells. Only when these are used up, the tissue begins to show signs of aging. It is safe to speculate that aging results from the loss of capacity to divide, rather than the finite division capacity of cells, which is rarely, if ever, reached in the human body. Thus the reaction of at least some cells in the body is different than when they are cultured. Other functional losses occur in the cells, producing physiological dysfunctions. This causes the cells to show aging changes before they reach their finite limits to divide.
Free radicals are unstable molecules that damage most other kinds of molecules in the body. This starts a chain reaction that disrupts cell function, accelerating the aging process. This is the most commonly held theory of aging. Free radical theory was discovered in 1954 by Dr. Denham Harman. “Free radical” describes any molecule that has a free electron, which causes the rogue molecule to react with the healthy molecule in a destructive manner. It is based on the fact that ongoing chemical reactions in the cells produce free radicals. In the presence of oxygen, these free radicals cause the cells of the body to break down. While free radicals are required for physiological functions, they also attack the structure of our cell membranes, generating metabolic waste products like lipofuscins. Such toxic accumulations interfere with cell communication, disturb DNA, RNA, and protein synthesis, lower the energy levels, and generally impede vital chemical processes. An excess of lipofuscins in the body manifests as a darkening of the skin in certain areas, also known as “aging spots.” Lipofuscins in turn interfere with the cells’ ability to repair and reproduce themselves. Cell metabolism is disturbed by free radicals, and this is partly responsible for the aging of our cells (3). As time goes on, more cells die or lose the ability to function, and the body soon ceases to function as a whole. Essentially, free radicals cause irreversible damages such as: DNA damage, cross-linking of proteins, and formation of age pigments.
The mitochondria organelles are found in most cells and are considered to be the weakest link in aging. The role of mitochondria is to utilize oxygen in the production of energy. Many researchers have linked mitochondrial DNA damage to virtually all degenerative diseases. With time, toxins, or by-products of energy generation, accumulate in the mitochondria. This poisons the mitochondria and allows it to make less and less energy. This is known as the mitochondrial theory of aging. The primary cause of mitochondrial damage is its exposure to oxygen radicals. Free radicals or oxygen radicals on the other hand are by-products of mitochondrial metabolic functions, which then attack and damage their own DNA. Failure of cellular/mitochondrial DNA repair mechanism is usually assumed to play a role in cellular aging. Mitochondria are one of the easiest targets of free radical injury because they lack most of the defenses found in other parts of the cell. Although mitochondria do suffer damage from free radicals, such damage seldom triggers wholesale cell death. The connection between free radical damage to the mitochondria and the broader aging process remains unclear.
Related posts:
– THE CELLULAR WATER PRINCIPLE
– STRESS, SLEEP AND EPIGENETIC ORTHODONTICS: NEW DIRECTIONS FOR NONSURGICAL SKIN ANTI-AGING
– CHRONOBIOLOGY OF THE SKIN SKIN CIRCADIAN RHYTHM AND CLOCK GENES: A NEW APPROACH TO SLOWING DOWN THE AGING PROCESS
– GLYCATION, PROTEASOME ACTIVATION, AND TELOMERE MAINTENANCE
– SKIN WHITENER INGREDIENTS
– AMINO ACIDS
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