Life span is 25 percent inherited and 75 percent determined by exposure to environmental toxins, accidents, injuries and chance. That helps explain how Calmet’s brothers and sisters lived into their 90s, as did her parents.1 Her daughter, however, died of pneumonia at only 36. While Calmet’s life span seems impressive in light of the statistics showing that the life expectancy is about 76 years, it pales in comparison to some other planetary life forms.
One bristlecone pine tree, situated in California’s White-Inyo Mountains and dubbed Methuselah, is 4,767 years old. Other trees live a thousand years or more. The secret of tree longevity is that, unlike humans, trees can regenerate. If humans could do that, they could replicate their old hearts, lungs and perhaps brains for newer versions and live indefinitely.
The longevity of other species is more ambiguous; that is, science hasn’t yet figured out their secret. The red sea urchin lives an average of 200 years with no signs of aging. Rockfish and some types of sturgeon can survive for 200 years.
Then there’s the Galapagos tortoise, surviving to an average 177 years. A tortoise at an Australian zoo died last year at age 176. Adwaita, a tortoise in India, died of liver failure last year; she was born in 1750, some four decades before the French Revolution. The tortoise Tu’l Malia, presented to the royal family in Tonga by Captain Cook, lived to age 219 before passing away in 1966.
No human on record has ever remotely approached the longevity of the Galapagos tortoise; we seem programmed to die after our allotted threescore and 10 and then some. Or are we? Some speculate that science will eventually find a way to extend human life to a considerable degree. Others suggest that children born now will live to at least age 150 because of good genetics and scientific advancements in gerontology, the study of aging.
One such optimist is Ray Kurzweil. A well-known computer maven who has won prestigious awards in that field, he’s invented a number of devices, such as the computer scanner and various text-reading machines. A self-described futurist, Kurzweil became intensely interested in health after both his grandfather and father died prematurely of heart disease. Kurzweil himself was diagnosed with type 2 diabetes in his 30s and seemed to be following his family’s genetic fate. Rather than acquiesce in that fate, he applied his analytical intelligence to come up with a solution that evolved into a lowfat diet that enabled him to get off insulin injections. Ultimately his diabetic symptoms disappeared.
Buoyed by his initial success, Kurzweil embarked on a long-term personal study of longevity and ways to achieve it. Eventually he came up with a concise plan, which he describes in his book Fantastic Voyage: Live Long Enough to Live Forever.
According to Kurzweil, there are three bridges to immortality. The first is his current health regimen, designed to enable him to live long enough to reach the second bridge, a biotechnology revolution featuring common use of such therapies as stem cells and gene therapy to repair and replace worn-out tissues and organs in a manner that mimics what trees do naturally.
Kurzweil gets the most flak from his description of the third bridge, which features nanotechnology and artificial intelligence, whereby minuscule robots, called nanobots, will enter the blood, just as in the 1966 film “Fantastic Voyage,” and repair all damaged cells from the inside out. The nanobots will be capable of curing currently incurable diseases, rebuilding organs and even increasing the range of human intelligence. Improvements to genetic coding will be*downloadable from the Internet, and you won’t have to worry about heart attacks, since human hearts will have become obsolete (come to think of it, I already know many people who seem to have no hearts). He even talks about transferring brains into machines, thus making us immortal, or perhaps real-life Terminators.
Many scientists who’ve examined Kurzweil’s ideas call them more whimsical than pragmatic. That’s particularly true when Kurzweil confidently predicts the second bridge will be here within a mere 25 years. Kurzweil’s immediate goal is to survive long enough to make it to the second bridge.
The first bridge is a daily routine that includes taking more than 250 supplement pills and drinking eight to 10 glasses of only alkaline water, along with 10 cups of green tea. He tracks 40 to 50 “fitness indicators” and makes adjustments to his program accordingly. Along with his book, Kurzweil offers anyone the chance to join him on the first bridge with a line of food supplements that he sells over the Internet. That bridge is apparently not toll-free. And no, he does not yet offer a download to tweak your genetic coding.
What Causes Aging?
That’s the problem with aging—there is no one specific cause, regardless of what you hear or read on the Internet. Aging is what scientists refer to as multifactorial. Even if you overcome one factor, another one will just as certainly turn out your lights forever—at least in this world. What science is realizing, however, is that many gerontological theories overlap; that is, aging may not be as complicated as originally believed.
With that in mind, here are the current leading theories of aging:
• Mutation accumulation. As you age, cells develop mutations that aren’t blocked by the body. In a worst-case scenario, that means cancer and explains why the majority of cancer patients are older—their bodies have lost the ability to block incipient tumor formation. Mutations mean that cellular DNA, which governs cellular replication, begins turning out bad copies of cells that just don’t work right, much as a Xerox machine makes the original copy look great, while successive copies look a bit hazy.
• Disposable soma. The primary goal of nature is perpetuation of the species through reproduction. After you reach the prime reproductive age (about 30), it’s all downhill. Nature takes a cue from Ray Kurzweil and doesn’t have a heart; it doesn’t care about the golden years. Just make a genetic copy of yourself and then drop dead, declares Mommy-dearest Nature. A recent study, however, found evidence of the “grandmother effect,” in which the descendants of women who survive longer after menopause had increased reproductive fitness.2
• Antagonistic pleiotropy. That’s a five-dollar term meaning that genes beneficial when you’re younger become deadly when you’re older. One example is the P53 gene. When you’re young, it helps prevent cancer. With age it turns against the cells, promoting cell death, or apoptosis. Resveratrol, which is discussed below, inhibits the P53 gene.
• Gene regulation. Changes occur in genes that are involved in development and aging.
• Error catastrophe. A drop in gene expression reliability results in abnormal protein and tissues. An example is crosslinking of tissue, resulting in the accumulation of what are called advanced glycosylation end products. AGEs involve an abnormal bond between sugar and protein structures in tissues, leading to brittleness and stiffening in affected tissues. An increase in AGEs is common in diabetes. When AGEs accumulate in connective tissue based on collagen, arthritis results. Abundant AGEs are also linked to Alzheimer’s disease, hypertension, atherosclerosis and cataracts.
• Somatic mutation. An accumulation of molecular damage, especially to DNA and cellular genetic material. An example of how gene mutations in DNA repair mechanisms can affect aging is seen in Werner syndrome and Hutchinson-Gilford syndrome, both of which are characterized by accelerated aging. Those with Hutchinson-Gilford, also known as progeria, appear normal at birth but wizened by the time they are about eight years old. They show many of the same degenerative aspects of advanced age, such as cardiovascular disease, and usually die of cardiovascular disease complications by age 14. Their brains remain unaffected, however. They experience no dementia, which somehow makes it even more tragic.
• Cellular senescence. A preponderance of old cells interferes with total cell activity. Related to this is a gradual shortening of the ends of chromosomes called telomeres that are required for cellular replication. Telomeres shorten with each cell replication, though that doesn’t occur in some cells, such as neurons in the brain. Telomere shortening is linked to cell death and cancer.
Telomere length is inherited. One rare genetic defect that results in premature telomere shortening leads to premature aging. People with shorter telomeres are three times more likely to die of heart disease and eight times more likely to die of an infectious disease. Those with age-related conditions, such as atherosclerosis, vascular dementia, Alzheimer’s disease and cancer, have shortened telomeres. Telomeres are longer in women than men.
Obesity and smoking shorten telomeres, as does oxidative damage. Cancer cells are immortal because they produce an enzyme, telomerase, that repairs telomeres. Those who suffer from mood disorders, such as depression, also have shortened telomeres, as do those under high stress conditions. Some athletes have a condition characterized by shortened telomeres in muscle that results in premature fatigue during exercise and sports activity.3 And yet mice tend to have long telomeres but brief life spans, so clearly telomeres aren’t the whole story behind the aging process.
• Free radicals. The free-radical theory, first presented in 1957, states that unpaired electrons lock onto paired electrons—the normal state—and interfere with cellular function. The body neutralizes them with built-in antioxidants, such as superoxide dismutase, catalase and glutathione, all of which decline with age. Oxidative stress is associated with an increase in inflammatory mediators, resulting in a rise in inflammation-related diseases, such as arthritis, atherosclerosis, osteoporosis and dementia.
• Neuroendocrine. Declines in various hormones, such as growth hormone and testosterone, impair functioning. With age, hormone secretion declines or target organs become less receptive to hormonal stimulation. Growth hormone drops by an average of 14 percent per decade. By age 60, GH is lower by 50 to 70 percent than at ages 30 and 40. Estrogen promotes telomerase activity, while testosterone decreases it (another reason women usually outlive men).
• Decreased immunity. When you hear that a person “died of old age,” it usually means that death resulted from immune failure. Diseases that can easily be dealt with in younger years, such as pneumonia and influenza, become fatal with age.
• Mitochondrial decay. Mitochondria are the organelles in cells that produce energy in the form of ATP through the electron transport system that fuels all cellular function, including cell repair and replication. The mitochondria are the site of the greatest production of free radicals, as a by-product of the energy-producing process. The free radicals interact with mitochondrial fatty membranes and DNA, destroying mitochondria and, subsequently, cells. Female more than male mitochondria are resistant to oxidative stress—another reason for women’s longer average life span.4 Studies show that mitochondrial DNA mutation begins around age 30, and the mutant cells produce less ATP but release more free radicals. Tissues particularly affected are those with high energy requirements, such as neurons, heart cells and skeletal muscle.
It all seems overwhelming, until you consider a few facts. For one, exercise, such as weight training, can activate genes that maintain youthful muscles. Another is that most theories of aging center on out-of-control oxidative reactions related to excess free-radical activity, as well as the DNA mutations that lead to faulty cell replication. People you read about who live to 115 or older are mutants in a way, genetically gifted with advanced DNA repair and cell-defense mechanisms, such as heat shock proteins, and lowered cellular oxidation or heightened defense against it. Kurzweil thinks the key to delaying the rate of aging is controlling the factors of oxidation and DNA mutations. His method is the strategic deployment of food supplements.
I would add another controllable factor of aging: lowering inflammation. While inflammation is integral to the healing process, out-of-control inflammation is at the core of such aging-related maladies as cardiovascular disease, brain degeneration, diabetes and cancer. In short, all the leading causes of death and infirmity linked to aging are related in one way or another to excess inflammation. Everybody knows that having inflamed joints and muscles makes you feel old. The good news is that inflammation is the most controllable age acceleration factor of all.
Inflammation Control
In fact, the only method currently considered feasible for extending longevity is calorie restriction. Various studies of animal species show that when you reduce food but not nutrient intake, inflammation declines, and so do the physical problems associated with it. Human-subject proof is strictly theoretical, but many people who follow the stringent guidelines for restricting calories experience less body inflammation in the form of reduced blood pressure, lower insulin levels and so on.
Even so, they often appear gaunt and may feel cold and depressed. They have no energy to exercise, and even if they did, it wouldn’t do them much good, since they have elevated cortisol and a deficit of anabolic hormones, including growth hormone, thyroid hormone and testosterone.
The key to calorie restriction may involve nothing more than reduced oxidation through eating less, along with reduced inflammation because of the lack of bodyfat. Reduced bodyfat, however, may be achieved more healthfully through exercise and a diet rich in nutrients.
Which leads to the question: Are there food supplements that will help attain longevity and reduce inflammation? I believe there are.
Here are my top 10 supplements and the rationale or mechanism for their use. In no particular order, they are:
1) Lipoic acid and acetyl-L-carnitine. You recall the theory that links aging to mitochondrial damage in cells. Studies with mice conducted at Stanford University found that the combination of lipoic acid and ALC regenerated aged mitochondria to an appearance comparable to teenage years. The combo works because lipoic acid is a potent antioxidant that helps temper the oxidation produced in mitochondria.
Lipoic acid helps promote the uptake of glucose into cells, which would lower insulin resistance. The lower the insulin level, the slower the rate of aging. Lipoic acid is also synergistic with ALC because ALC can promote oxidation in the mitochondria, and lipoic acid blocks the effect.
The question is, What’s the most effective supplemental form of lipoic acid? Most supplements come as a mixture of the R and S isomers and are sold as alpha lipoic acid. Only the R form, however, is active in the mitochondria. While some studies suggest that the S form, which is synthetic, is converted into the R form, others say that the S form interferes with the function of the R form. What is known is that the R form is much more expensive than the more common alpha lipoic acid.
ALC is simply L-carnitine with an acetyl group attached to it. That acetyl group, however, helps the ALC enter the brain, where it helps synthesize neurotransmitters that often decline with age, such as acetylcholine and dopamine. ALC protects the vulnerable mitochondrial membranes and may help regenerate mitochondria in that manner. For supplemental purposes, take 1,000 milligrams of ALC, along with 200 milligrams of lipoic acid.
2) Resveratrol. The French paradox refers to the fact that people in France, who take in a lot of saturated fat, have lower rates of cardiovascular disease. At first it was attributed to the French habit of drinking red wine with meals. The active ingredient in the red wine was thought to be resveratrol. More recent studies, however, found that the amount of resveratrol in red wine is too small to have any significant health effect. Instead, other antioxidants in wine, called procyanidins, are likely to produce the health effects, mainly by promoting nitric oxide synthesis in the body.
Resveratrol has received extensive publicity lately because animal studies show that it activates a protein called Sirtuin-1, or SIRT-1, that seems to protect cells from aging. SIRT-1 has a gene-silencing property that blocks the death of cells and aids cellular survival. Resveratrol proved the most active among more than 20,000 tested compounds. In fact, stimulating the protein duplicates the effect of calorie restriction—minus the eating restriction.
A 2006 study found that resveratrol extended the life span of a type of short-lived fish by 59 percent. Another study found that it mitigated the adverse health effects of high-fat diets in mice. Obese mice given resveratrol lived 15 percent longer than fat mice that didn’t get it. The mice were given 22.4 milligrams per kilogram of bodyweight. That would amount to a human dose of 150 to 200 milligrams a day.
One problem with comparing mice to humans is that mice metabolize resveratrol far more slowly than do humans. In humans it’s rapidly degraded after oral intake, and its bioavailability is low. Another mouse study provided far larger doses of resveratrol, with a human equivalent dose being 4,571 milligrams daily. The mice in the study showed a significant increase in endurance and fat oxidation during exercise. The author commented, “Resveratrol makes you look like a trained athlete without the exercise.” Resveratrol was thought to work by increasing the number of mitochondria in muscle. A study of 123 Finnish adults found that those with more active SIRT-1 genes had faster metabolisms, indicating that this mechanism may be active in humans as well as mice.
Because of the extensive publicity about these studies, resveratrol is now a popular—and expensive—supplement. While there are no toxicity indications thus far, there are also no studies that prove the effectiveness of supplemental resveratrol in humans. That doesn’t faze the primary researchers of the compound, all of whom are taking human-equivalent doses of those shown effective for animals.
Resveratrol in small amounts acts like a phytoestrogen, meaning it has weak estrogenic effects. Larger doses, however, provide a reverse effect; that of inhibiting estrogen synthesis. If you use resveratrol supplements, you’d be wise not to take them close to when you take supplements containing nicotinamide, a B-complex vitamin. Some emerging research shows that nicotinamide inhibits the function of the protein that resveratrol activates.
3) Vitamins C and E and antioxidants. While some studies show that dietary antioxidants have few or no antiaging properties, the body’s built-in antioxidant system dims with age. One study showed that a lack of vitamins and minerals can accelerate mitochondrial decay.6 The brain, which is mostly fat, is particularly prone to oxidation, and research demonstrates that older people who take in the most antioxidants from supplements or food are also the healthiest. The fact that antioxidants may help preserve brain function is reason enough to take them. In addition, they help defend the body against such age-related diseases as cancer, atherosclerosis and brain degeneration.
4) Omega-3 fatty acids. The brain is composed of 40 percent DHA, an omega-3 fatty acid. If you don’t eat fatty fish, such as salmon, halibut or sa rdines, at least three times a week, you’ll likely be deficient in omega-3 fats. Omega-3 fats help decrease depression, protect the cardiovascular system, increase insulin sensitivity and decrease the incidence of cancer.
Don’t depend on flaxseed oil for omega-3 fats. Flaxseed contains alpha linoleic acid, which is a precursor of the omega-3 fatty acids DHA and EPA, but the body can convert only about 2 percent of the precursor into the active omega-3s. Stick with fish oils, which contain the active omega-3 fatty acids. Also, avoid omega-6 fats, such as vegetable oils. Not only are they far more ubiquitous in the diet than omega-3 foods, but they also convert into inflammatory substances in the body and interfere with omega-3 function.
5) Creatine. It may seem strange to see creatine listed as an antiaging substance. But a recent animal study found that when mice were fed a diet that was 3 percent creatine, their life spans increased by 9 percent.7 While we are men and women, not mice—although I’ve met quite a few rats out there too—creatine has antiaging effects. It protects neurons in the brain by blocking the overstimulation of neurons that result in neuronal death. By maintaining ATP levels in neurons, it also protects against such diseases as Parkinson’s.
In the research lab creatine improved mouse memory and thinking skills and lowered the degree of brain-damaging pigments that build up in aging brains. Creatine also prevented noise-induced hearing loss, which is important because hearing is commonly impaired with age.8
6) Green tea. Green tea contains potent antioxidants that protect cells. It also offers cardiovascular and anticancer effects along with a thermogenic effect that helps burn excess bodyfat. For true antiaging benefits, you’d need the equivalent of at least 10 cups of green tea daily. Sounds like a lot, but you can get that amount in supplement form. It’s far more concentrated in the active green tea antioxidants than the tea itself, and the dosage is standardized.
7) Carnosine. Carnosine is a dipeptide composed of two amino acids, histidine and beta-alanine. It functions as the primary intramuscular buffer, reducing acid accumulation that leads to premature exercise-related fatigue. Muscle levels of carnosine decline 63 percent from age 10 to age 70. Carnosine may reduce a process linked to accelerated aging involving the cross-linking of proteins. This process, known as glycation, damages cell proteins and connective tissue and may cause much of the stiffness associated with aging.
One study found that supplying carnosine to connective tissue cells called fibroblasts extended cell life, an effect thought to occur because of carnosine’s beneficial slowing of telomere attrition. The only reliable food source of carnosine is red meat. Those who don’t eat red meat can take carnosine supplements in doses of 1,000 milligrams or more daily. An alternative is to use beta-alanine, which is the primary nutrient precursor of carnosine synthesis.
8) Ginkgo biloba. This herb offers several useful features related to longevity. It promotes circulation and oxygen use in the brain while blocking the effects of cortisol. Cortisol is a major cause of brain aging because it destroys neurons, especially in the hippocampus, where learning and memory occur.9 A study found that ginkgo prevented mitochondrial aging caused by excess oxidation.10 Recent studies also show that ginkgo exerts anti-estrogenic effects.
People who take statin drugs to treat cardiovascular disease may be low in Q10 because the drugs interfere with Q10 metabolism, inhibiting the liver enzyme that produces both cholesterol and Q10, lowering Q10 plasma levels as much as 40 percent. The primary side effect that occurs is excess muscle breakdown. One study of aged people given CoQ10 found that supplementation with 300 milligrams a day for four weeks reduced type 1 muscle fibers but promoted the growth of type 2 fibers. That’s a reversal of what usually happens with age: Smaller and weaker type 1 fibers are more numerous than type 2 fibers, which are associated with increased muscle size and strength. The mechanism was thought to be a gene regulation effect exerted by coenzyme Q10.11 You’d need to eat 1.5 kilograms of sardines to get 100 milligrams of Q10, so supplements are an easier option.
10) Alpha GPC. This is a form of choline that can enter the brain far more easily than ordinary choline. In the brain it’s rapidly converted into acetylcholine, the primary neurotransmitter linked to memory and learning. Alzheimer’s disease is marked by a selective destruction of neurons that produce acetylcholine, and drugs used to treat Alzheimer’s help prevent excessive breakdown of it. Some studies show that alpha GPC may help promote growth hormone release.
Honorable mention goes to other supplements, all of which blunt the effects of aging, including turmeric, glucosamine and chondroitin, whey and branched-chain amino acids, DHEA, melatonin, lycopene, grapeseed extract, garlic, phosphatidyserine, multiminerals and HMB.
While there is no true antidote to the aging process, you can improve your quality of life now with proper exercise and nutrition that includes the best supplements. The pathway is yours to follow, and the bridge is there to cross.
References
2 Hawkes, K. (2003). Grandmothers and the evolution of human longevity. Am J Human Biol. 15:380-400.
3 Collins, M., et al. (2003). Athletes with exercise-associated fatigue have abnormally short muscle telomeres. Med Sci Sports Exerc. 35:1524-28.
4 Borras, C., et al. (2003). Mitochondria from females exhibit higher antioxidant gene expression and lower oxidative damage than males.Free Rad Biol Med. 34:546-52.
5 Bitterman, K.J., et al. (2006). Inhibition of silencing and accelerated aging by nicotinamide, a putative negative regulator of yeast Sir2 and human SIRT-1. J Biol Chem. 277(47):45099-107.
6 Ames, B, et al. (2005). Mineral and vitamin deficiencies can accelerate the mitochondrial decay of aging. Mole Aspects Med. 26:363-78.
7 Bender, A., et al. (2007). Creatine improves health and survival of mice. Neurobiol Aging. In press.
8 Minami, S., et al. (2007). Creatine and tempol attenuate noise-induced hearing loss. Brain Res. 1148:83-89.
9 Mercilhac, A., et al. (1998). Effect of chronic administration of ginkgo biloba extract or ginkgolide on the hypothalamic-pituitary-adrenal axis in the rat. Life Sci. 63:2329-2340.
10 Sastre, J., et al. (1998). A ginkgo biloba extract prevents mitochondrial aging by protecting against oxidative stress. Free Rad Biol Med. 24:298-304.
11 Linnane, A.W., et al. (2002). Cellular redox activity by coenzyme Q10: Effect of CoQ10 supplementation on human skeletal muscle. Free Rad Re. 36:445-53.
9) Coenzyme Q10. Q10 is produced in the body from the amino acid tyrosine through the same pathway that produces cholesterol, but the synthesis becomes less efficient with age.
Q10 is involved in energy production within the mitochondria and acts as an antioxidant. Some studies show that Q10 offers brain protection, especially in the portion that produces dopamine, and may help protect against Parkinson’s disease. Q10 concentrates in high-energy tissue, such as muscle and brain.
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
