Fasting and Eating for Health by Joel Fuhrman; Neal D. Barnard
Authors: Joel Fuhrman; Neal D. Barnard
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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 rate-controlling 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 cross-linking agents.5 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.6
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 57
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 al on an animal's body has the effect of shortening life span.7,8,9,10 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.
The body accomplishes this regulation by slowing the activity of the enzymes in the pathway as more fuel (typically protein) is available. As these rate-controlling 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 cross-linking agents.5 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.6
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 57
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 al on an animal's body has the effect of shortening life span.7,8,9,10 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.
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