Decreasing food intake, reducing inflammation and free radical formation, and taking multivitamins and supplements can help slow the aging process and extend the life of your patients

Aging is characterized by a general decline in physiological functions that affects many tissues and increases the risk of death. Aging appears to begin while people are in their 20s and 30s. Conversely, chiropractors often encounter 40- and 50-year-olds who look like they are in their 20s and 30s, respectively. Why is this? I do not think anyone knows for sure; however, genetics and lifestyle choices seem to be the determining factors.

In recent years, a significant amount of research has been directed at aging. Some research offers a simple recommendation for extending life and slowing the aging process—eat less. Extensive gerontological research¹ has confirmed that calorie restriction imposed on laboratory animals extends their mean and maximum lifespans, and it is generally thought this applies to humans.

For example, an epidemiologic study showed that elderly people in Okinawa, who are known for their longevity, consume only 75% of the recommended energy intake, and a recent study examined the dietary patterns of age-matched patients with Alzheimer’s disease (AD), vascular dementia (VD), and normal controls.² In males, AD patients consumed 25% more calories than they expended, and VD patients consumed 35% more calories, while controls’ energy intake matched energy expenditure.

How easy is it to live longer and feel better? All we have to do is eat less, especially fewer desserts and unnecessary snacks. Avoiding grains is important as they are known to promote inflammation.³

We should focus our diets on vegetables, high-quality protein (meat, fish, fowl), and fruits. We should also avoid grains, and take a multivitamin, magnesium, EPA/DHA, and coenzyme Q10 (CoQ10). This approach should be viewed as part of a healthy lifestyle, not only for the purpose of treating aged patients. This lifestyle should be adopted as early as possible.

Go Up In Flames
It is now clear that subclinical, chronic inflammation drives numerous conditions, including pain, heart disease, cancer, endometriosis, AD, osteoporosis, diabetes, and most chronic diseases. Chronic inflammation is very different than acute inflammation.

Acute inflammation occurs after injury, with the telltale signs, such as heat, redness, swelling, and pain. We can either see or feel these so-called cardinal signs of inflammation. We also learned that various chemical mediators are responsible for driving the acute response, such as bradykinin, histamine, serotonin, and the family of pro-inflammatory eicosanoids, such as prostaglandin E2. These same meditors can drive chronic inflammation when released in smaller amounts, or so it appears—and this is especially true for the eicosanoids. Additional mediators are also involved in the chronic response, such as the family of pro-inflammatory cytokines, including tumor necrosis factor (TNF), interleukin- (IL-1), and interleukin-6 (IL-6).

The inflammatory damage that occurs due to subclinical release of eicosanoids and cytokines takes place as we age. For example, IL-6 is known to play a central role in inflammation, and its basal output increases with age.4 Researchers state that inflammation is a component of many age-associated chronic diseases, which often cause disability, and high circulating levels of IL-6 may contribute to functional decline in old age (>2.5 pg/mL).⁴

Higher circulating levels of IL-6 predict disability onset in older persons. This may be attributable to a direct effect of IL-6 on muscle atrophy and/or to its pathologic role played in specific diseases, such as atherosclerosis, postmenopausal osteoporosis, congestive heart failure, major depression, rheumatoid arthritis, and dementia.⁴

Kushner states that “a substantial number of conditions that are not apparently inflammatory, as we ordinarily understand the term, are associated with a minimal acute phase response.”⁵ The acute phase response is associated with obvious signs or symptoms including fever, fatigue, malaise, and loss of appetite, ie, flu-like symptoms. It is well known that the acute phase response is driven by TNF, IL-1, and IL-6.

A minimal acute phase response, or subclinical inflammatory state, remains subclinical until sufficient tissue damage has been done to create symptoms of disease. Kushner lists the following conditions as being associated with subclinical inflammation: obesity, diabetes mellitus, uremia, hypertension, marked physical exertion, sleep disturbance, chronic fatigue, low levels of physical activity, and depression. He states that aging is accompanied by a profile of gene expression that characterizes an inflammatory response and oxidative stress.^4,5

Proper diet is the only way to effectively modulate the expression of pro-inflammatory eicosanoids and cytokines. Adequate intake of bioflavonoids, magnesium, and omega-3 fatty acids seems to be most important.^6-9 I suggest getting your flavonoids from vegetables; spices such as ginger and turmeric; fruit; and green tea; and supplementing your diet with 400 mg to 1,000 mg of magnesium and 1 g to 2 g of EPA/DHA from fish oil.

Collateral Damage
We make tissue-damaging, inflammation-promoting free radicals during many bodily processes, but one of the bigger producers of free radicals is the respiratory chain, from which ATP is produced during oxidative phosphorylation (OXPHOS). Tissues highly dependent on oxygen, such as the cardiac, skeletal, and smooth muscles, central and peripheral nervous systems, kidneys, and insulin-producing pancreatic beta-cells, are especially susceptible to defective OXPHOS. There is evidence that defective OXPHOS plays an important role in atherogenesis, in the pathogenesis of AD, Parkinson’s disease, diabetes, and aging.¹⁰ In short, without ATP synthesis, aging and various chronic diseases are promoted. There are numerous drugs available for each condition. Never, however, are cell viability considered in the medical care, with respect to augmenting cell function, ie, ATP synthesis.

CoQ10 is one of the most important drivers of ATP synthesis, and plays a pivotal role in slowing the aging process. Linnane explains that human aging is a slow process that takes place over decades; it is a cellular process in a dynamic equilibrium of continuing damage and repair.11 He refers to tissues as “damage mosaics.” A case is made for the encompassing role for CoQ10 in the regulation of systemic disease, cellular metabolism, and aging.¹¹ In addition to the functions of CoQ10 in ATP synthesis, it also acts as a potent antioxidant.¹² While these functions impact the tissues that we treat, CoQ10 is known to have an even more direct effect on the musculoskeletal system and has been shown to regulate global gene expression in skeletal muscle.¹²

Human subjects about to undergo hip replacement surgery received 300 mg of CoQ10 per day for 25–30 days before surgery, whereas control subjects received placebo treatment.¹² At the time of surgery, samples of vastus lateralis muscle were taken from the same region, and gene and protein expression patterns and muscle fiber type profiles were compared between placebo and CoQ10-treated subjects. It was found that CoQ10 regulates the expression of numerous genes and proteins. Furthermore, a dramatic change in muscle fiber types toward profiles of young people was observed in subjects treated with CoQ10.

Achieving adequate levels of dietary CoQ10 is difficult as it is highly concentrated in pig and beef heart. The normal level in blood is around 1 µg/mL. To increase the concentration significantly requires at least 100 mg/day which increases the level in blood to around 2 µg/mL. An increase to 2 µg/mL in blood can be therapeutic for various conditions; this may indicate that a high blood level is needed to get coenzyme into deficient tissues.¹³

Supplemental lipoic acid should also be considered if you want to augment ATP synthesis and provide free radical defense. Research¹⁴ has demonstrated that administration of alpha-lipoic acid is beneficial to a number of oxidative stress models, such as diabetes, cataract, HIV activation, neurodegeneration, and radiation injury in animals. Furthermore, lipoic acid functions as a redox regulator of pro-inflammatory cell signaling molecules. Lipoic acid has neuroprotective effects in neuronal cells.

One possible mechanism for the antioxidant effect of lipoic acid is its metal chelating activity. Lipoic acid can increase ambulatory activity, improve memory in aged animals, and partially restore age-associated mitochondrial decay in liver and heart. Lipoic acid is used to treat or prevent peripheral neuropathy and cardiac autonomic neuropathy, insulin resistance in type II diabetes, retinopathy and cataract, glaucoma, HIV/AIDS, cancer, liver disease, Wilson’s disease, cardiovascular disease, and lactic acidosis caused by inborn errors of metabolism. It has also been used for treating Alzheimer-type dementia.¹⁴ Associates of Bruce Ames, who have done the lion’s share of research with lipoic acid in animals, suggest that humans need to take about 400 mg of lipoic acid per day to derive the same benefit (personal communication with Ames).

In recent years, so-called antiaging medicine has become a popular area, such that antiaging clinics and medical organizations are common. Much of the effort is directed at increasing growth hormone output. From a physiological and pathophysiological perspective, it makes much more sense to focus on the drivers of aging—inflammation and reduced ATP synthesis.

Protect cells by eliminating grains from the diet, and dramatically increasing vegetable and fruit intake. Eat high-quality meat, fish, and fowl, and consider supplementing with a multivitamin, magnesium, EPA/DHA, CoQ10, and lipoic acid. When decreasing calories, make absolutely sure to follow these recommendations, to ensure adequate nutrients. CP

David R. Seaman, DC, MS, DABCN, is an assistant professor at Palmer College of Chiropractic, Fla, is on the postgraduate faculties of several chiropractic colleges, and presents postgraduate seminars for chiropractic colleges and associations. He has written a textbook on nutrition and published several articles in JMPT. Seaman can be reached at seaman_d@palmer.edu.

References
1. Chung HY, Kim HJ, Kim JW, Yu BP. The inflammation hypothesis of aging molecular modulation by calorie restriction. Ann NY Acad Sci. 2001;928:327–335.
2. Otsuka M, Yamaguchi K, Ueki A. Similarities and differences between Alzheimer¹s disease and vascular dementia from the viewpoint of nutrition. Ann NY Acad Sci. 2002;977:155–61.
3. Cordain L. Grains: man’s double edge sword. World Rev Nutr Diet. 1999;84:19–73.
4. Ferrucci L, Harris TB, Guralnik JM, et al. Serum IL-6 level and the development of disability in older persons. J Am Geriatr Soc. 1999;47:639–46.
5. Kushner I. C-reactive protein can be caused by conditions other than inflammation and may reflect biologic aging. Cleve Clin J Med. 2001;68(7):535–37.
6. Nijveldt RJ, Van Nood E, Van Hoorn DE, Boelens PG, Van Norren K, Van Leeuwen PA. Flavonoids: a review of probably mechanisms of action and potential applications. Am J Clin Nutr. 2001;74:418–25.
7. Middleton E, Kandaswami C, Theoharides TC. The effects of plant flavonoids on mammalian cells: implications for inflammation, heart disease, and cancer. Pharmacol Rev. 2000;52:673–751.
8. Durlach J, Bac P, Bara M, Guiet-Bara A. Physiopathology of symptomatic and latent forms of central nervous hyperexcitability due to magnesium deficiency: a current general scheme. Magnes Res. 2000;13(4):293–302.
9. Simopoulos AP. Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr. 2002;21:495–505.
10. Fosslien E. Mitochondrial medicine—molecular pathology of defective oxidative phosphorylation. Ann Clin Lab Sci. 2001;31(1):25–67.
11. Linnane AW. Cellular CoQ10 redox poise constitutes a major cell metabolic and gene regulatory system. Biogerontology. 2002;3:3–6.
12. Linnane AW. Human aging and global function of coenzyme Q10. Ann NY Acad Sci. 2002;959:396–411.
13. Crane FL. Biochemical functions of coenzyme Q10. J Am Coll Nutr. 2001;20(6):591–598.
14. Liu J, Atamna H, Kuratsune H, Ames BN. Delaying brain mitochondrial decay and aging with mitochondrial antioxidants and metabolites. Ann NY Acad Sci. 2002;959:133–66.David R. Seaman, DC, MS, DABCN