defects present prior to birth, internal physiology and cellular biochemistry
determine an individual's level of health and capabilities. Damage at the
cellular level causes groups of cells to function abnormally, eventually leading
to chronic disease.
Within the scientific community, the theories of cellular aging, based on
advances in cellular biology, explain not only the factors that accelerate the
aging of our cells, but also the destructive processes that lead to disease.
These mechanisms of cellular damage often express themselves in chronic
degenerative illnesses, especially autoimmune diseases, and work to accelerate
our death.
In medical research today the cellular congestion theory is the leading
theory of biologic aging. A few other respectable theories also have advocates
in the scientific community. They are presented here because it is likely that no
single idea adequately explains all the mechanisms involved in the loss of
cellular function that leads to disease or premature aging. When we can
comprehend the science supporting many of these most respected theories, we
can gain a clearer understanding of cellular function. It then becomes easy to
understand how fasting can lead to cellular rejuvenation and why scientific
experimentation on animals reveals that fasting prolongs the life span.
The Cellular-Congestion Theory of Aging
Many scientists believe this theory explains why aging occurs. Waste material
gathers inside the cell, and eventually accumulates to the point of internal cell
damage. The amassing of unwanted and often toxic substances explains the
gradual decline in cellular function and therefore body function in general.
The waste products of cellular breakdown and cellular metabolism include
excesses and unrestrained free radicals, as well as hundreds of other toxic
metabolites. The more stress or the more use demanded from the cell, the
more metabolic wastes will be produced.
The Free-Radical Theory of Aging
Free radicals are reactive elements. They contain an unpaired electron, making
them chemically reactive. They can break apart other chemical bonds they
come in contact with. Free radicals have both negative and positive functions
within the cell. Though they are an important toxin, they also function as part
of the detoxification machinery of the cell. Cells contain free radicals in order to
utilize their reactive and destructive properties to chew up and destroy other
wastes. It is only when the production of free radicals becomes excessive and
their activity continues outside the confines of the specific areas of the cell that
are designed to process waste that free radicals cause cellular damage.
We know now that there are hundreds of other cellular toxins besides free
radicals; therefore, it is more precise to include the free-radical theory of aging
as part of the cellular-congestion theory. Since the free-radical theory of aging
was proposed in 1956 by Harmon,
3 many attempts have been made to use
antioxidants, vitamins, and free-radical-scavenging drugs to see if they extend
the life span in lab animals. These interventions have not been effective at
extending life spans, though periodic fasting of animals has consistently shown
the ability to do so. This failure does not provide strong evidence against the
free-radical theory for three reasons: 1) The administered antioxidant may not
be distributed to the cellular site of production of the free radical; 2) each
antioxidant is specific for a particular free radical species and thus is unlikely to
have a global effect; and 3) significant damage to cellular structures, especially
the mitochondria, occurs from other nonradical toxins such as
malondialdehyde, ceroid, lipofuscin, and other related substances.
.
On the other hand, fasting (and food restriction in general) has a powerful
effect on modulating free-radical production, repairing free-radical damage,
and facilitating removal or detoxification of the products of free-radical
damage. Fasting aids in the removal of other toxins, and has been shown to
maintain the integrity of the cellular structure even at advanced ages.
4 Food restriction also decreases the rate of free-radical generation by reducing the
rate of electron transport and oxygen utilization.
The Cross-Linkage Theory of Aging
Tissues in our body, especially collagen, develope cross-links at the cellular
level as the tissue ages. These cross-linkages cause tissue to become less
elastic and interfere with normal function. Internally produced waste products
that are the leading cause of these cross linkages are intermediate metabolites.
Intermediate metabolites are waste products that increase in quantity as a
result of excess nutrient intake, especially excessive protein intake.
When a product the body needs, such as a hormone, is manufactured by the
cellular machinery, it is put together by enzymes in numerous steps. The more
proteins and other excess raw materials are fed into our system, the more
these enzymes will be activated to produce products. Since the body regulates
its production of end-products very carefully, it must have a means of
controlling this production so that too much product will not be produced. For
example, can you imagine if too much insulin was produced?
The body accomplishes this regulation by slowing the activity of the enzymes
in the pathway as more fuel (typically protein) is available. As these ratecontrolling
enzymes slow down, less final product is produced and more
partially constructed products, also known as intermediate metabolites,
increase in quantity. This explains one clearly defined mechanism via which
excess proteins and a few other nutrient precursors are converted into harmful
substances within the cells.
Studies have shown that the process of cross-linkage can be retarded in rats
by restricting food intake. Overeating and nutrient excesses cause the
accumulation of intermediate metabolites, many of which are potent crosslinking
agents.
When animals are fasted, the aging of collagen is prevented.
Fasting inhibits production of cellular intermediates and enables the body either
to eliminate such retained wastes or to utilize them as fuel. It was observed
that fasting in animals prevented the aging-related stiffening of the blood
vessels as well.
This theory of aging is not very different from the cellular-congestion theory.
This theory describes further endogenous toxins besides free radicals and
shows the powerful effect they can have by cross-linking connective tissue. By
combining the above leading theories we can have a more accurate picture of
biologic damage on the cellular level.
Genetic-Code-Error Theory of Aging
The genetic code theory is based on the overuse of the cell's genetic
machinery, or DNA. The nucleus of the cell contains the architectural blueprint
(DNA) for all activity the cell is called on to perform. If the DNA suffers
sufficient damage, the cell will not be able to function normally, and could even
become cancerous. The more the cell is called on to function, the more the DNA
is utilized. Unessential usage of the genetic machinery of the cell encourages
more errors to occur in the genetic code and leads to cellular breakdown.
Each cell has a DNA repair team of enzymes that is continually working to
repair damage to the cell's vital DNA; however, a cell's ability to repair itself is
limited. Free radicals and cellular congestion are known to contribute to DNA
damage. This is known as the genetic-code-error theory.
Other theories of aging focus on the function of endocrine glands, growth
rate, and rate of immunologic breakdown. Whichever theory we look at can be
applied to our model and shows that a nutritionally adequate diet containing no
excess nutrients (especially proteins and fats) and no overeating will prolong
structure and function at the cellular level.
What these theories all have in common is that we age prematurely when
we place our body under stress and drive cellular machinery to overwork in the
attempt to process unessential waste. These theories, because they are based
on modern scientific knowledge of cells combined with experimental studies on
both animals and humans, indicate that food intake is the most crucial factor
that determines aging.
It is remarkable to consider the number of scientific studies illustrating the
effect of food restriction on life span. Hundreds of studies have found that in
many species dietary restrictions can increase longevity by approximately 50
percent. These studies also show that any fat at all on an animal's body has the
effect of shortening life span.
Fasting animals not only extends their life
but also, by blunting most physiologic mechanisms of aging, dismantles
immune system imbalances that contribute to disease.
It is also evident that fasting powerfully opposes all the processes that lead
to aging at the cellular level. This prolongs life even in healthy individuals. The
restorative effects of fasting have been observed in many species of animals
(including primates), and have been clinically observed in humans by doctors
such as myself who regularly conduct therapeutic fasts.
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