Theories of Aging

The DNA and Genetic Theories

We are born with a unique code and a predetermined tendency to certain types of physical and mental functioning that regulate the rate at which we age. But this type of genetic clock can be greatly influenced with regard to its rate of timing. For example, DNA is easily oxidized and this damage can be accumulated from diet, lifestyle, toxins, pollution, radiation and other outside influences.

Thus, we each have the ability to accelerate DNA damage or slow it down.

The Neuroendocrine Theory

Hormonal Damage. The neuroendocrine system is a complicated network of biochemicals that govern the release of hormones which are altered by the hypothalamus located in the brain.

One theory for the hypothalamus loss of regulation is that it is damaged by the hormone cortisol. If cortisol damages the hypothalamus, then over time it becomes a vicious cycle of continued hypothalamic damage, leading to an ever increasing degree of cortisol production and thus more hypothalamic damage. A catch-22 situation.

The Free Radical Theory

The term free radical describes any molecule that has a free electron, and this property makes it react with healthy molecules in a destructive way.

Free radicals are known to attack the structure of cell membranes, which then create metabolic waste products. Such toxic accumulations interfere with cell communication, disturb DNA, RNA and protein synthesis, lower energy levels and generally impede vital chemical processes.

The Membrane Theory of Aging

According to this theory it is the age-related changes of the cells ability to transfer chemicals, heat and electrical processes that impair it.

As we grow older the cell membrane becomes less lipid (less watery and more solid). This impedes its efficiency to conduct normal function and in particular there is a toxic accumulation. This cellular toxin is referred to as lipofuscin and as we grow older lipofuscin deposits become more present in the brain, heart and lungs and also in the skin. Indeed some of the skin age-pigments referred to as liver or age-spots are composed of lipofuscin. It is known that Alzheimer Disease patients have much higher levels of lipofuscin deposits than compared to their healthy controls.

The Hayflick Limit Theory

suggests that the human cell is limited in the number of times it can divide. Nutrition has an effect on cells, with overfed cells dividing much faster than underfed cells. Calorie restriction in animals significantly increases their life-span. In essence less fed animals live longer. Is this because they are subject to less free radical activity and therefore less cellular damage? Or is it that insulin and glucose damage is less prevalent in them than in overfed animals?

The Hayflick Limit indicates the need to slow down the rate of cell division if we want to live long lives.

The Mitochondrial Decline Theory

The mitochondria are the power producing organelles found in every cell of every organ. Their primary job is to create Adenosine Triphosphate (ATP). ATP is literally the life giving chemical because every movement, thought and action we make is generated from it. Yet very little ATP can be stored in the body.

Under normal conditions the mitochondria are fiery furnaces and subject themselves to a lot of free radical damage. They also lack most of the defenses found in other parts of the body, so as we age the mitochondria become less efficient, fewer in number and larger. Accordingly, ATP production declines.

Enhancement and protection of the mitochondria is an essential part of preventing and slowing aging.

The Cross-Linking Theory

In this theory it is the binding of glucose (simple sugars) to protein, (a process that occurs under the presence of oxygen) that causes various problems.

Once this binding has occurred the protein becomes impaired and is unable to perform as efficiently. Living a longer life is going to lead to the increased possibility of oxygen meeting glucose and protein and known cross-linking disorders include senile cataract and the appearance of tough, leathery and yellow skin.

Diabetes is often viewed as a form of accelerated aging and the age related imbalance of insulin and glucose tolerance leads to numerous problems; these have been called Syndrome X. In fact, diabetics have 2-3 times the numbers of cross-linked proteins when compared to their healthy counterparts.

The cross-linking of proteins may also be responsible for cardiac enlargement and the hardening of collagen, which may then lead to the increased susceptibility of a cardiac arrest.

Cross linked proteins have also been implicated in renal disorders.

It is also theorized that sugars binding to DNA may cause damage that leads to malformed cells and thus cancer.

The modern diet is of course a very sweet one and we are bombarded with simple sugars from soft drinks and processed foods etc. One obvious example to reduce the risk of cross-linking is to reduce sugar (and also simple carbohydrates) in ones diet.