Juvenon Health Journal volume 2 number 11 november 2003
By Benjamin V. Treadwell, Ph.D.
The physiological events associated with aging are, as a colleague once stated, barbaric. Although harsh, this statement is not far off the mark, especially when one considers the following characteristics of healthy aging:
- Mild decreases in memory, mental alertness, and cognitive functions
- Loss of physical strength, and ability to quickly recover after injury
- Loss of skeletal mass
- Loss of flexibility; skin, blood vessels, tendons, and connective tissue in general lose their resiliency and elasticity
- Mild decreases in vision and hearing capabilities.
How does all this happen? Scientists have developed numerous hypotheses over the years to guide our inquiry into why our bodies deteriorate with age. One of the most durable and respected explanations is the Mitochondrial Theory of Aging.
Regular readers of this newsletter know that themitochondria are the power plants within each cell. The Mitochondrial Theory of Aging states that the mitochondria are the source not only of energy production but also of destructive oxidants, or free radicals, which act on and destroy components of the cell. Evidence indicates the mitochondria are one of the more susceptible cellular components to free radical attack, for two primary reasons: their proximity to the source of the oxidants, and their relatively inefficient machinery to repair free radical-damaged components. A third reason is the mitochondria contain naked DNA – naked in that mitochondrial DNA lacks a protective protein coat (histones) present on DNA contained in the cell’s nucleus. This coat helps protect the DNA from free-radical damage.
When the mitochondria are not functioning at optimal level, decreased capacity of the cell to produce energy is not the only result. The mitochondria also suffer from an age-associated accumulation of errors in the mitochondrial DNA, protein and membranes.
Energy loss is one thing, but how do free-radical-damaged mitochondria translate into mildly decreased memory and cognitive function and all those other “barbaric” effects?
The brain contains some of the tissues most susceptible to damage from a lack of a steady energy supply. This organ can consume an equivalent of 1/4 pound of glucose per day, just to keep the wheels moving and our minds working optimally. Much of the glucose-derived energy is utilized in the movement of electrolytes, such as potassium, sodium, and calcium from one cellular compartment to another during the continuous transmission of nerve impulses. This electrolyte transport requires energy in the form of the chemical ATP, which is produced – you guessed it – in the mitochondria.
The movement of electrolytes in the brain is an extraordinarily complex and fine-tuned process. It begins with the mobilization of the amino acid, glutamate, the major excitatory neurotransmitter in our brains. The glutamate-initiated neurotransmission involves the transport of calcium from the cell’s exterior to the interior of the nerve cell. This, in turn initiates additional events. However, excessive calcium in the cell can cause structural damage to the nervous tissue, and an over excited state. (Remember the headache after eating food laced with an excess of monosodium glutamate -“the Chinese restaurant syndrome?”)
The influx of calcium must be carefully regulated so as not to reach toxic levels. Here again, it’s our friendly mitochondria that provide the regulation. Thus the mitochondria not only provide the energy to run the pumps, but they also serve as reservoirs to help buffer the cellular calcium to prevent it from reaching toxic levels.
Therefore, the consequence of unhealthy mitochondria in the nervous system is age-related decline of both nerve cells and of the capacity of the brain and nervous system in general to function optimally. The same is true of other tissues of the body, especially muscular tissue, as it too is highly dependent on a sound energy source for optimum health. Significant evidence suggests that the type of cellular decline described above occurs at an increased rate as we age. The mitochondria appear to be a major contributor to the aging process.
This type of regulation of electrolytes, most importantly calcium regulation by the mitochondria, pertains to other tissues besides nervous tissue. Heart and circulatory health are at risk as a result of dysfunctional mitochondria that are incapable of efficiently performing the activities described above.
Can we prevent mitochondrial decay? Can we reverse it?
Laboratory experiments with aged animals have clearly demonstrated a loss of structural integrity of the mitochondria, and concomitant functional decline with age. This decline has been postponed and even reversed by supplementing the animal’s diet with the compounds, acetyl-L-carnitine and alpha lipoic acid
These two natural compounds are involved as key cofactors required for energy production in the mitochondria. Unfortunately, our cells don’t produce enough of these cofactors for optimal mitochondrial health, especially in the aged. In this regard, they can be considered conditionally essential nutrients requiring supplemental amounts for maximum health.
Examination of the mitochondria from aged animals after a diet supplemented with the two compounds for a 14-day period demonstrates a remarkable recovery of both structure and function. The mitochondria from the aged animals supplemented with the compounds appear to resemble the mitochondria of the young animals both in structure and in their capacity to generate energy. Tests on these animals demonstrated enhanced activity levels and improved cognitive function compared to similarly aged but unsupplemented animals.
A very recent (October 2003) article sheds new light on the role of the mitochondria in the death of our cells. In fact, the article implicates the mitochondria as “central executioners of cell death.” This European research study delves into the complex processes that begin with excitotoxicity and overload of mitochondrial calcium and culminate many steps later in cell demise. Studies such as this add one more increment to scientists’ growing knowledge of the aging process. For further information, click here.
This Research Update column highlights articles related to recent scientific inquiry into the process of human aging. It is not intended to promote any specific ingredient, regimen, or use and should not be construed as evidence of the safety, effectiveness, or intended uses of the Juvenon product. The Juvenon label should be consulted for intended uses and appropriate directions for use of the product.
Dr. Treadwell answers your questions about Juvenon™ Cellular Health Supplement
QUESTION: My husband and I are on the Atkins diet and watch our carb intake closely. Will Juvenon™ Cellular Health Supplement affect this diet, or will the diet’s efficacy be compromised?
L & K, via email
ANSWER: Juvenon™ Cellular Health Supplement should not interfere with the Atkins diet. In fact it may act synergistically with the Atkins diet as part of a weight loss plan. The compounds in the formula function as cofactors in the production of energy in the mitochondria. One of the compounds in the formula is specifically involved in the transport of fat constituents, fatty acids, into the mitochondria to be utilized as fuel. Since the Atkin’s diet stresses a higher than normal amount of fat in the diet, Juvenon™ Cellular Health Supplement may help facilitate the metabolic conversion of the fat to energy. Furthermore, since the conversion of fat to energy always produces toxic by-products, this same component in the formula combines with and removes those by-products from the mitochondria to be excreted.
Benjamin V. Treadwell, Ph.D., is a former Harvard Medical School associate professor and member of Juvenon’s Scientific Advisory Board.