According to a report in Reuters in 1999, the death rate from complications from diabetes, already the third-most common cause of death in the U.S., has risen 30% since 1980.
In the first article in this anti-aging series, "The Basic Theories of Aging"(DC, Nov. 1, 1999, online at chiroweb.com/archives/17/23/16.html), I stated:
"There are many theories of aging...(including) oxidation reactions and suboptimal hormone levels.
"... As we age, some hormones begin a precipitous decline that strongly parallels the onset of aging signs and symptoms. These include human growth hormone (HGH), melatonin, DHEA, pregnenolone, androstenedione (made famous by Mark McGwire), testosterone, estrogen and progesterone.
"Conversely, insulin levels tend to rise, culminating in adult-onset diabetes. Also, a relative rise in cortisol, the stress hormone, is all too common." (In men, estrogen levels tend to also rise.)
In this article, we will focus on the age-related tendency for insulin levels to rise. The understanding of this tendency is fundamental to anti-aging and longevity.
To understand the rationale of the anti-aging protocols I will present, we need to understand a little bit about how the brain (neuro) controls the hormones (endocrine) and how they relate to aging.
The modern neuroendocrine theory of aging was first conceived by Russian gerontologist Vladamir Dilman in 1954. His precocious theories were not appreciated here in the West until his works were translated in 1992! His theory is that aging is caused by a progressive loss of sensitivity by the hypothalamus and related structures in the brain to negative feedback inhibition.
The hypothalamus is part of the brain from which the "master hormone gland" (the pituitary) hangs, as it were, by a stalk in the middle of our craniums. It is the primary organ of homeostasis. Its function is much like that of a thermostat. Among the many and complex functions, known and unknown, of the hypothalamus is that it senses the levels of circulating hormones and tells the other glands, via the pituitary, to release certain hormones and stop releasing others. This is a major part of homeostasis, which physiologically speaking, is akin to holding the status quo.
Homeostasis and Aging
Fortunately, true hormonal homeostasis is never attained. If it were, growth and development (as best typified by the hormonal changes at puberty) would never happen. Maturation seems to occur in part via a progressive loss of hypothalmic sensitivity from infancy. Thus, the progressive loss of hypothalmic sensitivity may be the basis of all hormone-related maturation and aging processes.
The problem occurs when puberty ends in complete maturation at about 20 to 25, as there is no mechanism to shut off or reverse this progressive loss of sensitivity and resultant "aging" of the hypothalamus. To revisit our thermostat analogy: as the thermostat "ages," the room has to get hotter and hotter before the thermostat turns on the air conditioner, and colder and colder before it turns on the heat. This could be called "thermostat insensitivity."Dilman theorized that the hypothalamus "ages" because of:
- reduced levels of brain messenger proteins (neurotransmitters, particularly catecholamines and serotonin);
- death of hypothalmic cells, which as nerve cells do not replicate or regenerate;
- pineal secretion declines; (The hypothalamus' regulatory functions are strongly allied with the pineal gland, which secretes melatonin and other pineal peptides and regulates 24-hour circadian "sleep-wake" cycle.)
- fat accumulation;
- reduced glucose getting inside the nerve cells (hyperglycemia);
- prolonged stress with high cortisol levels;
- cholesterol accumulation in nerve cell membranes.
The Disease of Aging
Dilman intuited that all of the diseases of aging are characterized by three similar metabolic changes. The most prevalent of these changes are:
- reduction in glucose tolerance and the ability of muscle tissue to utilize glucose;
- hyperinsulinemia or high blood insulin, in response to #1;
- hyperlipidemia (high cholesterol and triglycerides, related to atherosclerosis and hardening of the arteries) resulting from #1 and 2.
All three of these metabolic changes, along with high blood pressure, increased abdominal fat, and elevated uric acid, are characteristic of the ominous-sounding "syndrome X."
- The high blood insulin levels seen in syndrome X are the result of insulin resistance.
- Insulin resistance is related to the age-related loss of sensitivity of cell membranes to insulin.
- Insulin is needed to transport glucose to the inside of cells. In special organelles called mitochondria, insulin is utilized along with oxygen to make energy.
- As the cells desperately need energy, they signal for more glucose. The body responds with more insulin, resulting in hyperinsulinemia.
- Among insulin's many functions is to signal liver enzymes to make cholesterol, leading to hypercholesterolemia.
- Insulin also tells the body to burn sugar, not fats. Therefore, fatty acids known as triglycerides rise in the blood.
- Insulin tells the body to store fat, not burn it, promoting obesity, particularly as "central" or abdominal fat.
- The above cluster of signs leads to greatly increased incidence of heart disease and stroke, leading some authorities to call syndrome X "the silent killer."
Eventually, even the super-high levels of insulin are not enough to overcome the insulin resistance and the blood sugar begins to rise. We call this condition diabetes!
The excess blood sugar leads to a kind of sugar blood poisoning with advanced glycation end-products (AGEs). These AGEs produce free radicals and cause cross-linking of the molecules in body proteins. These undesirable reactions result in many serious complications of diabetes mentioned in our introduction.
Jeffrey Bland,PhD, suggests we no longer call type-2 diabetes "maturity onset." He suggests this based on the fact that the greatest increase in type-2 diabetes is in children and adolescents! Dr. Bland presents what he describes as "a more appropriate description for the disease ...hyperinsulinemia/insulin resistance."3
I will try to present the new model of diabetes not so much as a separate disease someone "gets," but as the end stage of a cluster of related aging processes. We can call these processes neuropause (brain aging with loss of hypothalmic sensitivity), somatopause (pituitary aging with HGH decline) and/or pancreopause (hyperinsulinemia/insulin resistance/ diabetes). These three organs, the hypothalamus, the pituitary and the pancreas, make up part of what Dr. Ward Dean calls the "energy homeostat."4
We will focus on the part of the energy homeostat that concerns the interrelationship between: (1)growth hormone (HGH); (2) insulin; (3) glucose; and (4) fatty acids, generally in the form of triglycerides.
This four-component system regulates the interrelationship of the body's two main energy-producing substances (glucose and fatty acids), and the two main hormones that control sugar and fatty acids: human growth hormone (HGH) and insulin.
The workings of this four-component system are as follows: When the stomach is empty and blood sugar levels are low, as at night, HGH stimulates fat burning. However, after eating, as is normal during the day, blood sugar rises, which inhibits growth hormone secretion and stimulates insulin release.(This is why it is best to take HGH enhancers at night just before bed on an empty stomach.)
Age-Related Changes in the Four-Component Energy Homeostat
From age 10 to 35, our HGH levels decline dramatically. (This may in turn be caused by hypothalmic aging as hypothesized above.) This results in a dysfunctional post-maturational "three-component" energy homeostat as lowered HGH levels cease to exert as strong an influence, resulting in chronically elevated levels of insulin, triglycerides, and glucose.
These three conditions culminate in syndrome X, obesity (generally central or around the waist) and diabetes, respectively. Indeed, insulin levels are a major bio-marker of aging.
Insulin Level Two Hours after Eating5
Age Level 20 10 30 40 50 60 70 120
This can be interpreted to mean that nearly everyone over the age of 20 is a "pre-diabetic." It also explains why adult-onset diabetes is likely postponable, but nonetheless inevitable.
Such understanding of the physiology of aging leads to the above model of "neuropause." In this case, the age-related loss of sensitivity of the hypothalamus leads to "somatopause." The age-related dropping of HGH levels triggers "pancreopause" and the age-related hyperinsulinemia, hyperlipidemia, and maturation-onset diabetes.
In the new therapeutic model, the 21st-century doctor does not wait for the 60-year-old patient to develop diabetes. The doctor understands the "disease" called aging and provides interventions to slow this admittedly ultimately irresistible process by supporting a more youthful physiology. The doctor does not merely prevent disease but significantly expands the "youth-span."
Approaches to Improve Age-Related Alterations in the Energy Homeostat
- Exercise is "the ultimate anti-aging pill." It restores hypothalmic activity, increases insulin sensitivity, and increases HGH secretion.
- Proper diet, especially low glycemic and low carbohydrate eating strategies, along with certain salutary foods like cold-water fish, cruciferous vegetables and legumes (especially soy), helps hold down the age-related rise in insulin and blood sugar levels. This ever-earlier rise with each generation is strongly associated with our high-sugar, high-(poor quality) fat, nutrient-poor, low-fiber standard American diet (SAD), which, through massive advertising, the world rushes to emulate.
- Restore insulin sensitivity by taking chromium; niacin; vanadyl sulfate; zinc, magnesium; alpha-ketoglutarate; omega-3 fats; EPA/DHA; alpha lipoic acid; bitter melon; fenugreek; gymnera sylvestre; Metaformin (or its OTC herbal counterpart, goat's rue); either substance works best with L-carnitine tartrate.
- Restore nighttime growth hormone to optimum levels.
- Stress management/adrenal support. Prolonged periods of stress results in chronically elevated stress hormones (cortisol) which leads to hypertension, insulin insensitivity and increased hypothalmic cell death.
- Restore testosterone levels to optimum. Raising testosterone in middle-aged men does not lower HDL-cholesterol and may reduce visceral adiposity ("the spare tire"), hyperglycemia and insulin resistance.6
- Balance the neurotransmitters (brain messengers) dopamine and norepinephrine by utilizing their amino acid precursors, tyrosine, phenlyalanine and L-pyroglutamate.
- Utilize EDTA chelation to reverse mitochondrial membrane dysfunction secondary to cholesterol infiltration and reverse/inhibit arteriosclerosis.
- DHEA enhancement, as DHEA release is inhibited by insulin. (Indeed, DHEA-S levels have been proposed as a biomarker of insulin sensitivity. However, hyperinsulinemia stimulates the shunting of estrogen to testosterone in females, associated with polycystic ovary syndrome, with outward signs of acne, facial hair and deepening voice. DHEA is the promotional choice in such cases.)
- Maximize brain antioxidants to delay irreplaceable hypothalmic cell death, i.e.; vitamin C, glutathione (whey), N-acetyl cystiene, green tea, OPCs, alpha lipoic acid, NADH, acetyl-carnitine, etc.
As we age, the hypothalamus becomes less sensitive to feedback, and growth hormone levels dramatically decline. This results in:
1) elevated levels of blood insulin (hyperinsulinemia) and blood fats (hyperlipidemia);2) less-efficient utilization of glucose for energy, thus fatigue;3) an increase in conversion and storage of glucose as fat, thus obesity;4) hypertension, atherosclerosis and coronary artery disease, a.k.a. syndrome X;5) ultimately, diabetes and depression (the brain is starved for glucose).
By creating a properly timed nutritional, supplemental, lifestyle and hormone enhancement program based on the above 10 factors decades before the onset of heart disease, stroke, diabetes and depression, this admittedly inevitable process can be delayed dramatically with great potential for extending both the life-span and the youth-span. Understanding the diseases of aging in this new paradigm will be integral to the transformation of the "sick care" reactive interventions of the 20th century to the proactive true health care prescriptions of the 21st century.
1. Bach J. (1997). Prescription for National Healing. Garden City Park, NY: Avery Publishing.
2. Bland J, PhD. Functional medicine approach to managing syndrome X and type 2 diabetes. Int'l Journal of Integrative Medicine 11/12 1999, p 42.
3. Ibid, pp. 39-40.
4. Dean W. The neuro-endocrine theory of aging, part III: Energy homeostatic dysfunction. Vitamin Research News, June 1999, p.2.
5. Ibid, p.3, fig. 5.
6.Lane L. Boosting testosterone levels for cardiovascular health. Vitamin Research News 12/99, p. 8.
About the author: Dr. Maher is a postgraduate instructor for the New York Academy of Anti-Aging, which prepares doctors for their certification by the American Board of Anti-Aging Health Professionals through A4M. Call 1-888-354-6528 for more information.
Click here for previous articles by John Maher, DC, DCBCN, BCIM.