Whether incorporated into food bars, beverages or other nutritional delivery systems, harnessing nutrients to increase overall human energy capacity and day-to-day activities is the next great frontier in functional foods development. Developing products using ingredients that naturally increase energy in healthful ways will pave the way to these next generation consumer products. In this article we will discuss the source of human energy and the nutrients that can be included into our daily diet to promote a greater sense of vitality into our experience of life.
All energy production starts at the cellular level. Your vitality and energy is totally dependant on whether the production and utilization of the internal resources can be converted into a bio-energetic source of fuel (ATP). This is done by a small component of the cell called the “mitochondria”. The mitochondrion is the energy producing power house of the cell and ultimately, in combination with other cells, produces the energy that defines your vitality. The mitochondrial produces over 90% of all cellular bio-energy (ATP). ATP bio-energy virtually powers every activity of our cells.
Mitochondrial damage is one of the main causes of the age-related decline of cellular energy production (“bio-energetic decline”). In addition to being the principal source of energy for all cells, mitochondria (Fig.1) are also the primary site of free radical production. Free radicals are highly reactive molecules that damage cellular structures such as membranes, proteins, and mitochondrial DNA. Because of their limited capacity for self-protection and repair, mitochondrial DNA are particularly susceptible to free radical damage.
Mitochondrial dysfunction is now well recognized as a cause of energy declining conditions as well as aging itself. As evidence implicating mitochondrial dysfunction in the aging process continues to accumulate, the question becomes: What—if anything—can we do about it?
Improving Mitochondrial Function
Fortunately, a growing body of research suggests that a number of interventionist strategies may help to reduce mitochondrial damage, enhance mitochondrial repair, and restore mitochondrial energy producing processes to more youthful levels. These strategies include lifestyle changes, such as diet and exercise, as well as supplementation with nutritional substances that may minimize age-related mitochondrial changes and enhance mitochondrial function.
Coenzyme Q10 for example, is probably the most widely used cofactor for treating mitochondrial related health conditions. Basically, CoQ10 functions as the electron carrier in the inner mitochondrial membrane. In addition to increasing biosynthesis of ATP (the universal energy molecule), and acting as a potent free radical scavenger, CoQ10 also reduces lactic acid levels, improves muscle strength, and decreases muscle fatigability. In particular it has an infinity with the heart muscles and is often used to improve recovery from cardiovascular disease. CoQ10 is an important antioxidant component of the lipid (fatty) membranes that surround all cells, as well as the lipid membranes surrounding the various organelles ("little organs"), such as mitochondria and microsomes, inside the cells.
Studies of CoQ10 have mostly focused on its role in improving certain types of heart disease, including congestive heart failure. However evidence suggests that CoQ10 may benefit brain function, help maintain healthy blood pressure, assist in elevating energy for suffers of chronic fatigue syndrome, muscular dystrophy, periodontal disease, breast cancer and allergies.
Acetyl-L-carnitine is derived from the lysine and methionine amino acids. It is mainly synthesized in the liver and kidneys, and must be transported for use to other tissues in the body. It is found in highest concentration in tissues that use fatty acids as fuel, such as the skeletal and cardiac muscles.
When mitochondrial damage occurs, the organelle structure show changes which include alteration of mitochondrial membrane potential, a reduction in membrane levels of cardiolipin (an important phospholipid that serves as a cofactor for a number of critical mitochondrial transport proteins); a reduction in Coenzyme Q10 levels (an important factor in the electron transport chain); and a decrease in the concentration of carnitine (an important factor in the beta oxidation of fatty acids).
Dr. Tory Hagen, in the Molecular and Cell Biology Laboratory of Dr. Bruce Ames at the University of California, proposed that dietary supplementation of acetyl-L-carnitine (ALC) might reverse some of these age-related mitochondrial changes. Dr. Hagen and his associates demonstrated that ALC restores mitochondrial membrane potential and cardiolipin levels, facilitates fatty acid transport into mitochondria, and increases overall cellular respiration. The researchers also noted that ALC enhances cognitive performance, increased production of neurotransmitters, and restores levels of certain hormone receptors to more youthful levels. They concluded that ALC reverses many aspects of age-related cellular dysfunction, principally through maintenance of mitochondrial function.
Alpha Lipoic Acid
Alpha lipoic acid (ALA), also known as lipoic acid is a powerful, natural antioxidant. Alpha lipoic acid can be found in foods such as meats, and veggies (ie. spinach). Alpha lipoic acid is also easily absorbed into the blood stream, and it can also cross the blood brain barrier.
Its main function is to increase production of glutathione, which helps dissolve toxic substances in the liver. An antioxidant helps neutralize free radicals in our bodies and protects our cells from damage. Alpha-lipoic acid (ALA) plays an important link in mitochondria respiration, in particular glycolosis and the Kreb’s cycle. Most of the metabolic reactions in which ALA participates occur in mitochondria.
Alpha-lipoic acid has been shown to increase ATP synthesis (bio-energy) in the mitochondria of heart cells. It is believed that increased ATP production occurs because of ALA’s role in the oxidation of pyruvate and the alpha-ketoglutarate in the mitochondria. For energy metabolism to progress to the Kreb’s cycle, pyruvate must be converted into acetyl-CoA. Alpha-lipoic acid is one of four coenzymes required by the body in order to create acetyl-CoA. Oxidative phosphorylation completes the complex procedure of capturing energy and ultimately enhancing energy production which contributes to our sense of vitality.
Omega-3 Fatty Acids
The use of omega-3 fatty acids is well documented and researched and has become a popular supplement for the health conscious particularly those concerned about there cardio-vascular system which includes the heart. Fish are rich sources of omega-3 fatty acids, specifically eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are present in fatty fish.
More recently research on omega 3 fatty acids has shown to benefit the health of the mitochondria. As the body ages mitochondrial calcium levels increase and mitochondrial membrane cardiolipin content decrease. Scientists at the National Institute on Aging found that omega-3 fatty acids from fish oils are cardio-protective in aging animals, in that they minimized the increase in mitochondrial calcium content, prevented the decrease in cardiolipin content, and increased levels of phosphatidylcholine.
Dr. Salvatore Pepe of the Alfred Hospital Cardiac Surgical Research Unit in Melbourne, Australia, reported similar findings. Dr. Pepe demonstrated that an omega-3 rich diet directly increases mitochondrial membrane cardiolipin concentrations, increases the ratio of mitochondrial membrane omega-3 to omega-6, and increases tolerance of the heart to Ischemia and infarction (heart attack).
Elderly subjects tend to use more glucose and less fat during exercise than young subjects. However, endurance training increases muscle respiratory capacity, decreases glucose production and oxidation, and increases fat oxidation, thereby correcting or compensating to some degree the age-related alterations in substrate oxidation and energy production.
One argument that is put forth by some scientists as an excuse for their sedentary lifestyles is the fact that exercise increases the production of free radicals. However, scientists at the Guangzhou Institute of Physical Education in Canton, China, showed that endurance training actually increases the production of mitochondrial manganese superoxide dismutase (MnSOD) and glutathione peroxidase (GSH px), resulting in an overall increase in antioxidant activity and decrease in lipid peroxidation. Simply, regular exercise contributes to health and longevity.
Mitochondrial dysfunction has been identified as one of the principal causes of age-related bio-energetic decline. Although there is no single “silver bullet” or even combination of substances that will unfailingly resuscitate all aspects of aging mitochondria, anti-aging physicians and scientists have discovered a number of nutrients that alleviate or completely restore many aspects of mitochondrial failure. Some of these substances have been discussed in this article, and their sites of action and specific mitochondrial resuscitating properties are summarized in Table 2. Combinations of these nutrients, acting on multiple targets, may normalize mitochondrial function, increase cellular and systemic energy production, alleviate mitochondrial-related disease, and delay age-related decline in many organs and systems of the body.