While we have boosted average life span substantially, with the help of antibodies and improved hygiene and sanitation, strictly speaking the aging process has scarcely been challenged. The chances of dying are high around birth, but they steadily decline until around 10 years of age. Mortality only starts to increase again at puberty, when aging begins in earnest. From then on it is a gentle but slippery slope all the way to the grave.

One of the cell’s in our body, the germ cell—sperm or egg—and the DNA they carry, trace their ancestry right back in an unbroken line to the first organism that swarmed over the earth more than 4 billion years ago. The other cells, somatic cells, are mainly the disposable slaves of these immortal DNA.

Cells in the outer layer of the skin-the epidermis-die faster than they can be replaced with fresh cells coming up from below. This leads to thinning and wrinkle formation. Furthermore, these new cells become increasingly disorganized. In the layer just below-the dermis-strength is supplied by collagen fibers. But with increasing age, the formation of cross-links between these molecules renders them less flexible. Over the years, there is a stiffening of the skin’s elastin, the protein that gives skin the flexibility. Sebaceous and sweat glands become less active, making the skin more vulnerable to drying out and overheating. In the fatty layer beneath the dermis-the hypodermis-the total number of fat cells declines, but they accumulate in particular areas resulting in bags under the eyes, enlarged ear lobes and a double chin. Elsewhere in the face, blood vessels and bone are increasingly visible as a result of the overall loss of fatty tissue. The skin becomes paler because there are fewer capillaries near the surface, and pigment cells enlarge and gather, creating age spots. No one has found a way to reverse this process or to stop the aging process of the skin. There is a lot of interindividual variation in this process that is suggestive of some underlying control mechanism, which is still not clearly understood.

Thanks to the constant work of bone building cells called osteoblasts, and bone destroying cells called osteoclasts, our entire skeletons are replaced every 7 years or so. As we age, the balance between bone formation and resorption is upset, leading to a loss over a lifetime of about 15% of the total skeletal mass in men and 30% in women. The loss is particularly dramatic in post-menopausal women. In both men and women, bones become more prone to fracture as a result of mineral depletion and increased porosity. The flexibility of joints starts to decline from about age 20, and by old age mobility can be severely restricted by arthritis and inflammation that ensues.

Exercise can help elderly people to maintain bone density, and the same is true of muscle strength. But no matter how much you exercise, there is an inevitable slow decline in strength. This is due to a poorer blood supply to muscles and low effective nervous stimulation. Mitochondria, the powerhouse of cells, may also become less efficient in muscle cells.

Up to 50% of the variation in bone mass is genetically determined. Targeting high-risk daughters of women affected by osteoporosis for advice on modifiable risk factors and consideration of HRT would appear to be a fundamental part of the family based services provided by the general practitioner. This could retard some of the difficulty encountered in the aging process i.e. reducing joint inflexibility. 

Our brains shrink as we age, losing 5 to 10% in weight between the age of 20 and 90 years. One tenth of all brain cells we have when we are in our 20’s will be lost by the age of 65. While we may lose a lot of neurons, the density of synapses-the connections between nerve cells-may actually increase, offsetting much of the loss of mental agility.

The loss of primary immunity results from a decline in the body’s limited stock of "virgin" T-cells- immune cells responsible for spotting foreign molecules (antigens) that the body has never come across before. At the same time, elderly people are more prone to autoimmune diseases, when the immune system attacks the body i.e. rheumatoid arthritis
.

At the molecular level the two most important substances for life, oxygen and sugar, do most of the damage.

Aerobic respiration, in which oxygen is used to break down complex organic molecules such as fat and carbohydrates to release energy, produces highly reactive by-products called free radicals. These have the capacity to wreck havoc particularly in the vicinity of mitochondria, where respiration occurs. As a result, the small but vital amount of DNA inside mitochondria is especially vulnerable.

Less reactive radicals, such hydrogen peroxide, diffuse through the cell and into the nucleus, where they damage the DNA in chromosomes as well. Fats also come under attack whenever they occur in the body, for example in membranes or as part of a hormone and eye pigments.

The harmful form of blood-borne cholesterol, low-density lipoprotein, is also attacked-which might seem like a good thing. But when LDL is oxidized by free radicals, it changes into a form, which cannot be recognized as "self" by the immune system making it a target for autoimmune attack. This process may contribute to the development of fatty plaques in arteries.

Fortunately, antioxidant vitamins, such as E and C can soak-up free radicals. Enzymes, such as catalase, covert hydrogen peroxide into water. It has been estimated that there are as many as 10000 instances of free radical damage per cell per day. Most of these chemical dents are patched-up by the body’s repair mechanism, but not all. Over the years, the damage accumulates and the aging process accelerates.

Sugars can also harm vital molecules. Glucose binds to proteins in a process called glycosylation. For example, the cross-links that make collagen less flexible are the result of glycosylation. When collagen in the walls of arteries is glycosylated, it tends to trap passing proteins and this may be another in accumulation of LDL cholesterol. All proteins are prey to glycosylation, which makes them less soluble and less likely to be broken down

Error accumulation theory argues aging is due to build-up over a lifetime of unrepaired damage, lipids and proteins, particularly that caused by free-radical attack and glycosylation.

A protein called APOE helps to remove cholesterol from the blood and the genes that code for it in three different varieties, e 2, e 3, e 4. People who carry e 4 gene are more prone to high cholesterol levels, heart disease and Alzheimer’s disease, but e 2 seems to protect against these diseases. Research suggests that people who carry e 4 and also suffer from hyperglycemia (high blood sugar levels) in the middle age experience greater decline in mental functioning that those who have hyperglycemia and e 4 alone.

Go Back to Article I of Articles on Aging-Mortality risk factors
The Aging Process-Part II-Gender Difference
The Aging Process-Part III-Cellular Senescence
The Aging Process-Part IV-Biological Aging
Go to Article V of Articles on Aging-Arteriosclerosis
The Aging Process-Part VI-Aging in Males
The Aging Process-Part VII-Aging in Women
The Aging Process-Part VIII-Infectious Disease
Process of Aging-Part IX-DHEA
The Aging Process:-Part XI-Apotosis and the Elderly
The Aging Process-Part XII-Biomarkers for Aging
The Aging Process- Part XIII- Body Odors

FOR AN INFORMATIVE AND PERSONAL ARTICLE ON PRACTICAL SUGGESTIONS WHEN SELECTING A NURSING HOME SEE OUR ARTICLE "HOW TO SELECT A NURSING HOME".

Harold Rubin, MS, ABD, CRC, Guest Lecturer
posted January 4, 2003

Email: hrubin12@nyc.rr.com or rubin@brainlink.com

http://www.therubins.com