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Life Extension Magazine

LE Magazine September 2003
New Study Indicates that Diabetics Might Get Worse on Certain NSAIDs

It is only experimental at this point, but a new study suggests that, except for aspirin, people with diabetes should choose their non-steroidal anti-inflammatories carefully. Researchers at the University of Michigan tested the effects of two different kinds of NSAIDs on diabetic rats, and found that the standard variety that suppresses both COX-1 and COX-2 can make nerve-related complications of diabetes worse. Selective COX-2 inhibitors did not have the negative effects. Aspirin does not appear to have negative effects either.1

The two drugs used in the study were flurbiprofen (Ansaid, a COX-1 and COX-2 inhibitor) and meloxicam (Mobic, a COX-2 inhibitor). In assessing the effects on diabetic neuropathy (a degeneration of nerves that causes abnormal and painful sensations in diabetics such as “pins-and-needles”), it was discovered that the non-selective NSAID, Ansaid worsened the underlying chemistry of nerve problems (nerve blood flow, nerve myo-inositol content, motor nerve conduction velocity, reduced taurine levels, and reduced Na,K-ATPase activity). Surprisingly, the drug had the same negative effects on the nerves of non-diabetic rodents. The study dose is approximately the equivalent of what a human would take. Meloxicam, the COX-2 inhibitor, didn’t have these effects. In the case of nerve blood flow, Meloxicam actually reversed diabetes-related deficits.

The research helps explain reports that non-specific NSAIDs can cause neuropathy in people without diabetes. Indomethacin is one of the NSAIDs reported to cause neuropathy in non-diabetics.3,4 The antibiotic, Cipro, and its fluoroquinolone relatives, have also been reported to cause neuropathy in people without diabetes.2,5 The negative effects of Ansaid in the above study could be reversed with supplemental acetyl-L-carnitine, a readily-available, non-toxic supplement that has multi-benefits for nerve, heart and brain health.1

–Terri Mitchell


1. Pop-Busui R, et al. Dissection of metabolic, vascular and nerve conduction interrelationships in experimental diabetic neuropathy by cyclooxygenase inhibition and acetyl-l-carnitine administration. Diabetes 2002. 51:2619-28.

2. Cohen JS. Peripheral neuropathy associated with fluoroquinolones. Ann Pharmacother 2001. 35:1540-7.

3. Eade OE, et al. Peripheral neuropathy and indomethacin. Br Med J 1975. 2:66-67.

4. Argov Z, et al. Drug-induced peripheral neuropathies. Br Med J 1979. 1:663-66.

5. Rollof J, et al. Neurologic adverse effects during concomitant treatment with ciprofloxacin, NSAID, and chloroquine: possible drug interation. Ann Pharmacother 1993. 27:1058-9.

Live Longer, Healthier, Without Drugs

Fasting every other day is a sure-fire way to good health according to new research in rats. Experiments done at the National Institute on Aging show that skipping meals causes significant and lasting reductions in blood sugar, blood pressure and heart rate. The program worked even if it was started in adulthood. And that’s not all. Resistance to stress, weight-loss and increased life span (by one-third) were part of the reward of skimpy eating. Researchers have known for decades that calorie restriction extends life span—as long as the restricted diet meets nutrient requirements, but the findings about enhanced stress-resistance are new.

The study is the first to report that even though the rats skipping meals were just as active during the day as those getting three squares, they were less active at night. This coincides with reports that people on fasts sleep better, have better concentration, more vigor and are less likely to get upset during the day. Some of this may occur because fasting elevates growth hormone (GH) in aging people. Two days of fasting can elevate GH 400%. The hormone is impressive with regard to its ability to turn flab into muscle, restore an optimistic mind-set and reverse other signs of aging.

Every-other-day eating greatly improves the body’s ability to cope with stress. It reduces levels of stress-activated hormones of the kind that trigger heart attacks, and activates proteins designed to protect the body against stress. What happens when the anti-stress proteins are activated is that individual cells go into a “shutdown” mode until the stress blows over. The more stress proteins activated, the better the anti-stress protection. An everyday example of stress proteins in action is what happens when a plant doesn’t get watered. Dehydration causes the production of stress proteins in individual cells. These proteins cause normal processes like growth to stop. The plant wilts. When it’s watered, stress proteins degrade and the plant “comes alive” again–i.e., normal processes are restored.

The numbers on insulin and glucose in the fasting rat study are impressive. At three months, the levels of blood glucose in the animals not fasting were about 143 mg/dL compared to 118 for the fasting animals. By six months, levels had risen to 160 in the non-fasting animals compared to 120 in the fasting animals. There was a big difference in insulin levels. Non-fasting animals had approximately 120 nmol/L at three months compared to 70 for fasting animals. At six months, levels had risen to 133 for non-fasting animals, but remained steady for fasting animals at 74.

Weight loss is one of the benefits of fasting. The animals in the fasting study lost significant weight during the first four weeks of the study. Their weight then rebounded slightly but stayed fairly stable into old age when it again dropped. Age-related weight gain was significantly greater for the non-fasting rats, and throughout the study they weighed more than their fasting friends. At the point where the fasting rats’ body weight dropped in old age, non-fasting rats’ weight went up.

(When mice were put on the same regimen in another study, however, they made up for the lost calories on the eating day, and maintained their weight. They still, however, got the other benefits of caloric restriction (resistance to stress, lower glucose, etc.). This indicates that it’s not the calories per se that increase longevity in caloric restriction, it’s the fasting).

The heart rate, blood pressure and core body temperature of the rats in the fasting study was much lower than in rats eating everyday. This difference was maintained when the animals were exposed to stress. The fasting animals were also able to recover more quickly, and normalize their blood pressure and heart rate more efficiently.

Going without food every other day appears to have the same benefits as eating 30% less everyday. Both types of caloric restriction significantly extend life span and improve health. Other studies show that in addition to the benefits mentioned here, caloric restriction increases the resistance of brain cells to stress and provokes the formation of new neurons from stem cells. It increases the resistance to toxins and upregulates beneficial genes. It reduces the risk of cancer and reverses age-related declines in DHEA and melatonin, two important anti-aging hormones.

Does it work in people? Yes. UCLA researcher, Dr. Roy Walford, one of the pioneers in longevity research, did a two-year stint in the environmentally enclosed Biosphere. Caloric restriction had the same effects on the humans in the Biosphere as it does in rodents and monkeys. Weight loss, lower blood pressure, lower insulin and lower cholesterol were among the many benefits. All without drugs.

–Terri Mitchell


Michalsen A, et al. Effects of short-term modified fasting on sleep patterns and daytime vigilance in non-obese subjects: results of a pilot study. Ann Nutr Metab 2003. 47:194-200.

Wan R, et al. Intermittent food deprivation improves cardiovascular and neuroendocrine responses to stress in rats. J Nutr 2003. 133:1921-29.

Hartman ML, et al. Pulsatile growth hormone secretion in older persons is enhanced by fasting without relationship to sleep stages. J Clin Endocrinol Metab 1996. 81:2694-701.

Walford RL, et al. Alterations in physiologic hematologic hormonal, and biochemical parameters in humans restricted for a 2-year period. J Geront A: Biol Sci Med Sci 2002. 57:B211.

Mattison JA, et al. Calorie restriction in rhesus monkeys. Exp Gerontol 2003. 38:35-46.

Anson RM, et al. Intermittant fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake. Proc Natl Acad Sci USA 2003. 100(10):6216-20.

Mai V, et al. Calorie restriction and diet composition modulate spontaneous intestinal tumorigenesis in Apc(Min) mice through different mechanisms. Cancer Res 2003. 63:1752-5.

Duan W, et al. Brain-derived neurotrophic factor mediates an excitoprotective effect of dietary restriction in mice. J Neurochem 2001. 76:619-26.

Bruce-Keller, et al. Food restriction reduces brain damage and improves behavioral outcome following excitotoxic and metabolic insults. Ann Neurol 1999. 45:8-15.