The Durk Pearson & Sandy Shaw®
Life Extension News™

"It is this recognition of the individual as the ultimate judge of his ends, the belief that as far as possible his own views ought to govern his actions, that forms the essence of the individualist position."

"By giving the government unlimited powers, the most arbitrary rule can be made legal; and in this way a democracy may set up the most complete despotism imaginable."

"Even if you're on the right track, you'll get run over if you just sit there."

Table of Contents This Issue

Cognitive Function
Noradrenaline in Exertion and Mental Load

Most people experience a slowdown and increasing fatigue and inefficiency in the afternoon after a day's work. Most studies of the excretion of the catecholamine noradrenaline, the brain's version of adrenaline, have been over short periods, 1 to 2 hours, and have reported increases in urinary excretion of adrenaline, but not noradrenaline, in human subjects doing mental arithmetic. A day long study of mental work (an anagram task), however, reports a marked increase in noradrenaline excretion in the afternoon, coinciding with self-rated assessments of fatigue and stress. The subjects were 18 healthy college studients, 16 male and 2 female, with average age of 22.3 years.[1]

We initially created a family of formulations (which includes Blast™, Fast Blast™, and Rise & Shine™, and other names) to provide nutrients our brains could use to make more noradrenaline. We had discovered how mentally debilitating and energy depleting a long day of book promotion activity on TV and radio could be during our first book tour in 1982 and wanted to improve our performance. (You had to answer questions fast -- which uses noradrenaline -- and accurately -- rapid memory requires noradrenaline.) This group of formulations provides nutrients that your brain can use to make noradrenaline, including the essential amino acid phenylalanine, vitamins B-6, folic acid, and C, and copper, plus (except for the Rise & Shine, which contains no caffeine) either 40 mg. or 80 mg. of caffeine per serving. One of the effects of caffeine is to stimulate the brain's release of noradrenaline and to increase the brain's sensitivity to noradrenaline. (Caffeine doesn't help the brain make more noradrenaline, however, which is what the other ingredients are for.) It worked so well that we continue to use it daily -- we prefer the version containing 40 mg. caffeine per serving.

1 Miki and Sudo, "An Increase in Noradrenaline Excretion during Prolonged Mental Task Load," Industrial Health 35:55-60 (1997)

Some Effects of Medium Chain Triglycerides
on Body Weight

Some recent studies have reported new and interesting differences (in relation to mechanisms governing body weight) between the effects of medium chain triglycerides as opposed to long chain triglycerides (LCTs). Medium chain triglycerides (MCT) contain fatty acids of carbon chain length 6-12 (LCTs have fatty acids with length greater than 12 carbons), found naturally in butter, coconut oil, and other palm kernel oils; commercial MCTs are derived from coconut oil.1 Due to their shorter chain length, the energy content of MCTs is less than that of LCTs2 (roughly 90%, depending upon which of the particular fatty acids are compared).

The literature on the effects of MCTs is large and complex, with a diversity of experimental designs and sometimes apparently contradictory results from different studies. Hence, this discussion is not intended as a general review of MCTs and body weight. We simply want to bring to your attention some particularly striking findings that have been reported recently.

Gastric Inhibitory Polypeptide Signaling Fosters Obesity

A recent paper in Nature Medicine3 reported that inhibition of signaling by gastric inhibitory polypeptide (GIP), a duodenal hormone primarily induced by absorption of ingested fat and of glucose, prevents obesity in a mouse model. When these mice, which had their receptors for GIP knocked out, were fed a high fat (not MCT) diet, they were protected from both obesity and insulin resistance. Wild type mice (did not have receptors knocked out) that were fed a high fat (not MCT) diet hypersecreted GIP and had extreme visceral and subcutaneous fat deposition with insulin resistance. The GIP receptor knockout mice had a lower respiratory quotient and used fat as the preferred energy substrate, thus avoiding obesity.

In a separate paper[1], scientists reported earlier studies in which one of the physiological effects of LCTs is to increase baseline levels of several hormones, including GIP, CCK, neurotensin and pancreatic polypeptide, while MCTs did not increase levels. MCT increased the release of the hormone PYY4 less than LCT. It is possible that the non-release of GIP in response to MCTs may be a regulatory mechanism that results in MCTs being useful in weight maintenance.

MCTs and a Ketogenic Diet

Some people have found that the most effective method for their losing weight and keeping it off is a ketogenic diet, a very low carbohydrate diet (the basis for the Atkins Diet). A ketogenic diet has been used in the treatment of children with intractable epileptic seizures.5 In the treated children, MCT oil was mixed with diet soda, low-fat milk, and foods. Patients were instructed to sip the oil slowly throughout the meal. The oil was given in divided portions at the three meals and sometimes with snacks. Slow ingestion can help avoid possible side effects (diarrhea, vomiting, gastric irritability) that may be experienced when MCTs are ingested in too great a quantity and/or too quickly.

Both MCT and LCT are ketogenic, but MCT are much more ketogenic than LCT.6 In one rat study6, rats fed a high fat diet of either LCT or MCT had extremely elevated blood ketones, especially in the MCT group. Some adaptation to this diet may have gradually occured, as the blood ketone body concentration in the rats declined over the course of the experiment so that by the 44th day, the concentration had decreased by about 50%. The amount of nitrogen retained in the rats fed the LCT and MCT diets was similar but 25% less than in rats fed a low fat diet. This is probably because the high fat diets contained very little carbohydrate and in order to maintain blood glucose homeostasis, it was necessary to use some of the ingested proteins for gluconeogenesis. Thus, it would probably be a good idea for those on a ketogenic diet to eat high protein foods.

Possible Increase in Energy Expenditure with MCTs

There have apparently been no long-term studies of humans consuming high-MCT diets. The longest duration reportedly published to date was of 14 days on a diet containing 40% of energy as fat, either in the form of butter and coconut oil or beef tallow.1 Hence, it is not known whether the effects on energy expenditure of high MCT diets found in humans in short term studies persist. These human studies do show an increase in energy expenditure, especially in men. When data were extrapolated from trials conducted in men, the average energy expenditure was approximately 460 kJ/d greater with MCT than with LCT consumption. In contrast, data from one study in women found differences in energy expenditure of 138 kJ/d between MCT and LCT. The authors1 reported a difference of approximately 188 kJ/d in energy expenditure between MCT and LCT. Using the most optimistic scenario for men (calculating from the greatest difference between MCT and LCT in energy expenditure), they determined that a weight gain of 1.35 kg./month could be avoided by substituting MCT for LCT. At the low end, men and women could avoid a weight gain of 0.45 kg./month.

In another study7, it was reported that Dulloo et al fed 30 g. of MCT in addition to a maintenance diet with about 15% of energy as protein, 40% as fat, and 45% as carbohydrate. The difference in energy expenditure over 24 hours (for 30 grams of MCT versus 30 g. LCT) was 471 kJ, or 113 kcal. This would be about one pound of fat over approximately 36 days if the effects persisted over that period.

We have available for license a highly purified MCT oil (containing only C8 and C10 fatty acids that cannot be lengthened to LCTs). We use it for salads and cooking (except frying, which requires an oil that can withstand very high temperatures).

1 St-Onge and Jones, "Physiological Effects of Medium-Chain Triglycerides: Potential Agents in the Prevention of Obesity," J. Nutr. 132:329-332 (2002)

2 Bach et al, "The usefulness of dietary medium-chain triglycerides in body weight control: fact or fancy?," Journal of Lipid Research 37:708-726 (1996)

3 Miyawaki et al, "Inhibition of gastric inhibitory polypeptide signaling prevents obesity," Nature Medicine 8(7):738-742 (2002)

4 Peptide YY3-36 is a gut hormone, released from the gastrointestinal tract in proportion to the calorie content of a meal. It subsequently decreases appetite and reduces food intake. (In humans, infusion of normal postprandial concentration of the hormone reduces food intake by 33% over 24 hours). See Batterham et al, "Gut hormone PYY3-36 physiologically inhibits food intake," Nature 418:650-654 (2002).

5 Trauner, "Medium-chain triglyceride (MCT) diet in intractable seizure disorders," Neurology 35:237-238 (1985)

6 Crozier et al, "Metabolic Effects Induced by Long-term Feeding of Medium-Chain Triglycerides in the Rat," Metabolism 36(8):807- 814 (1987)

7 Papamandjaris et al, "Medium Chain Fatty Acid Metabolism and Energy Expenditure: Obesity Treatment Implications," Life Sciences 62(14):1203-1215 (1998)

Estrogens, Not Just Androgens,
Play an Important Role in Human Prostate Cancer

A new study in The Journal of Clinical Investigation[1] reports that estrogen receptor signaling contributes to telomerase activation, an early event in prostate tumorigenesis. Normal human prostate epithelial cells were treated with 17beta-estradiol, which resulted in an increase in both the mRNA encoding the catalytic subunit of human telomerase and telomerase activity. The same results were obtained in cells from human benign prostate hyperplasia and prostate cancer explants and cell lines.

Telomerase has been detected in over 95% of prostate tumor samples tested[1] and is, therefore, a commonly used evaluation (in addition to prostate-specific antigen, PSA) of prostate malignancy. The authors of this paper had previously shown that estrogens can reverse the telomerase silencing in normal telomerase-negative ovary epithelial cells. They note that the age-dependent decline of androgens-to-estrogens ratio has been suggested as a factor in prostate tumor development. However, local conversion of androgens to estrogens by the aromatase enzyme may stimulate telomerase activity in the prostate. Indeed, in this study, the researchers found that treatment with the aromatase inhibitor letrozole prevented the testosterone-mediated interaction between the estrogen receptor and telomerase estrogen response element.

Aromatization is the last step in estrogen formation, in which three consecutive hydroxylating reactions form estrone and estradiol from their precursors androstenedione and testosterone, respectively.[2] In addition to the ovaries, aromatase activity has also been detected in muscle, fat, nervous tissue, and the Leydig cells of the testes.[2]

Nutritional Inhibitors of Aromatase

While for the purposes of treating prostate cancer, powerful aromatase inhibiting drugs may be necessary, nutritional inhibitors of aromatase may help prevent the development of prostate cancer. There are a number of these. Phytoestrogens, including flavones, isoflavones, and lignans derived from whole grains, fruits, berries, and soy are plant compounds that bind to the estrogen receptor and may function as anti-estrogens or estrogens.[3] Recent studies are reported to suggest that isoflavones and flavones suppress aromatase.[3] Other studies show that red seedless grape juice, green seedless grape juice, and black grape juice contain chemicals that inhibit aromatase. They appear to work by competing for the binding to aromatase of the substrate androstenedione.[3] In fact, a study using a nude mouse model of breast cancer (with aromatase-transfected MCF-7 cells) showed that tumor size in mice fed (by gavage) 0.5 ml. of grape juice/day for 5 weeks was reduced 70% as compared to animals that were not fed grape juice.

The same researchers who performed the grape juice studies also examined heat stable extracts from several vegetables, including green onion, celery, carrot, bell pepper, broccoli, spinach, and white button mushrooms for aromatase inhibition. The white button mushroom (Agaricus bisporus) was the most effective aromatase inhibitor. The authors suggest that "a diet that includes grapes and mushrooms, therefore, would be considered preventative against breast cancer."[3] We would add that it might also help to prevent prostate cancer.

The vitamin riboflavin also inhibits aromatase. One nice thing about taking riboflavin is that it is regulated such that when it saturates the gut's ability to absorb it and the bloodstream's ability to carry it, the rest is eliminated in the urine and feces, coloring the urine a bright yellow. That lets you know when you are taking saturating levels of riboflavin. We have available for license a booster to our daily mulinutrient supplement that contains (in the recommended daily dosage) the amount of riboflavin that will saturate its absorption and carrying capacity.

1 Nanni et al, "Signaling through estrogen receptors modulates telomerase activity in human prostate cancer," The Journal of Clinical Investigation, 110(2):219-227 (2002)

2 Gruber et al, "Production and Actions of Estrogens," New England Journal of Medicine 346(5):340-352 (2002)

3 Chen et al, "Prevention and Treatment of Breast Cancer by Suppressing Aromatase Activity and Expression," in "Hormone-Related Tumors" edited by Castagnetta et al, Annals of the New York Academy of Sciences, Volume 963, 2002, pp. 232-233

Riboflavin is Cofactor for Enzyme Involved
in Reducing Plasma Homocysteine Levels

Homocysteine metabolism is controlled by two pathways -- one in which it is catabolized to cysteine and another in which it is remethylated to methionine. The function of these pathways depends upon adequate supplies of folic acid, vitamin B-6, and vitamin B-12. A new study now suggests that for some people, riboflavin (vitamin B-2) is a limiting factor.[1]

The enzyme methylenetetrahydrofolate reductase is required for the production of 5-methyltetrahydrofolate, necessary in the remethylation of homocysteine to methionine. A commonly found variant of the enzyme (the so-called thermolabile variant, involving a 677C to T transition, carried by about 12% of healthy people) has been found to be approximately ten times as likely as the wild-type enzyme to become deactivated because of inappropriate loss of its riboflavin cofactor. The authors found that individuals with the variant were indeed sensitive to riboflavin status, which could be remedied by riboflavin supplementation. They note that previous studies have found that there is a prevalance of 49% to 78% of suboptimal riboflavin status in noninstitutionalized elderly people. The new study found 28.6% of its sample of young people to be outside the normal range for riboflavin.

The authors suggest that public health officials considering food fortification strategies to lower homocysteine levels should not neglect riboflavin.

1 McNulty et al, "Impaired functioning of thermolabile methylenetetrahydrofolate reductase is dependent on riboflavin status: implications for riboflavin requirements," Am. J. Clin. Nutr. 76:436-41 (2002)

Blood Pressure, Renin-angiotensin, and Vitamin D

A recent editorial in The New England Journal of Medicine said that "...inhibitors of the renin-angiotensin system should be preferred agents for treating hypertension because they have proved effective in causing regression of left ventricular hypertrophy, preventing diabetes, preventing heart failure, and reducing mortality and vascular morbidity among high-risk patients with hypertension, diabetes, and vascular disease."[1] Moreover, evidence from clinical studies has shown an inverse relationship between circulating vitamin D levels and blood pressure and/or plasma renin[2], but the mechanism has not heretofor been understood.

It is exciting, then, to consider the findings of a new study reporting negative regulatory effects of 1,25-dihydroxyvitamin D3 on renin expression and blood pressure.[2] Li and colleagues hypothesized that the vitamin D3 receptor (VDR3) may be a primary negative regulator of the renin gene expression. They therefore studied mice that had VDR3 knocked out and found that these mice had elevated levels of both renin mRNA and also protein in their kidneys. They then tested the effects of strontium, an inhibitor of vitamin D3 synthesis, and found increased kidney renin mRNA levels even in normal mice. Administration of vitamin D3 reduced these levels.

The authors report that renin secretion is stimulated by factors such as prostaglandins, NO, and adrenomedullin, and inhibited by factors such as angiotensin II (feedback), endothelin, vasopressin, and adenosine. Although vitamin D is a primary regulator of calcium homeostasis, it is also important in immune function, the cardiovascular system, the reproductive system, and even hair growth. The authors were intrigued by reports over the past two decades showing an inverse relationship between plasma 1,25(OH)2D3 and blood pressure and/or plasma renin activity in both normal men and patients with essential hypertension. Moreover, ultraviolet light exposure, required for the endogenous production of vitamin D, is also inversely related to the prevelance of high blood pressure and has been shown to have blood-pressure reducing effects[2].

You might want to take between 800 units and 2000 units of vitamin D daily, unless you have parathyroid cancer, in which case you should discuss a possible vitamin D supplement with your doctor before taking it.

1 Massie, "Obesity and Heart Failure -- Risk Factor or Mechanism?" New England Journal of Medicine 347(5):359 (2002)

2 Sigmund, "Regulation of renin expression and blood pressure by vitamin D3," The Journal of Clinical Investigation 110(2):155-156 (2002); Li et al, "1,25-dihydroxyvitamin D3 is a negative endocrine regulator of the renin-angiotensin system," The Journal of Clinical Investigation 110(2):229-238 (2002)

Nicotinamide May Reverse Certain Aspects of
Cellular Aging

Nicotinamide may reverse certain aspects of the aging of human diploid fibroblasts.[1] These fibroblasts lose the ability to proliferate after a certain number of cell divisions (the number depends upon the particularities of the medium in which they are grown). The aging of cells nearing the limiting number of cell divisions, often called the Hayflick limit, is associated with size enlargement, shape change and senescence-associated beta-galactosidase activity as compared to young cells. Senescence is the termination of proliferation, but not the end of the life of a cell.

A protein, Sir2, is a gene silencer and putative longevity regulator in yeast.[2] It alters the histone proteins surrounding DNA that regulate gene expression, acting as a histone deacetylase inhibitor dependent upon NAD (nicotinamide adenine dinucleotide). Moreover, Sir2 gene homologs have been found in diverse organisms from bacteria to humans.[3] In the course of the authors' studies1 on the effects of Sir2 on the aging of mammalian cells, they found that nicotinamide (the precursor of NAD) was able to reverse the cellular aging phenotypes (changes in size, shape, and beta-galactosidase activity) without extending cellular proliferative lifespan. (This is reminiscent of the
study in which repeated mild heat shock of cell cultures throughout their lifespan extended their youthful phase, but did not increase cellular lifespan.[4]) The reversal of the aging phenotypes lasted only as long as the nicotinamide treatment. Nicotinamide was found to elevate histone acetyltransferase activity (HAT) in vivo; HAT activity and histone H4 acetylation are lowered in aged cells. The authors tried several other compounds that proved to be ineffective, including nicotinic acid, l-ascorbic acid, alpha-tocopherol, 3-aminobenzoamide, and 3 acetylpyridine.

A recent study[5] found that Sir2alpha (the mammalian homolog of Sir2) physically interacts with p53 (a tumor suppressor gene) and attentuates p-53 mediated functions. Sir2alpha also suppressed p-53 dependent apoptosis (programmed cell death) in response to DNA damage and oxidative stress, whereas the expression of a Sir2alpha point mutant increases the sensitivity of cells in the stress response. This is interesting in relation to a recent study finding that increased expression of p53 in mice led (as expected) to increased resistance to cancer, but (unexpectedly) reduced longevity. The fine tuning of p53 for longevity in mammals may include the Sir2alpha gene.

Hence, another clue to the DNA regulatory trail leading from youth to aging has emerged and nicotinamide may play a role in the retention of cellular youthfulness.

One of our formulations is an especially good source of nicotinamide (for specifics, see last paragraph of article above on the effect of estrogen receptors on prostate cancer).

Our thanks to Will Block for sending us copies of many papers on Sir2, which stimulated our interest in this regulatory gene.

1 Matuoka et al, "Rapid reversion of aging phenotypes by nicotinamide through possible modulation of histone acetylation," Cellular and Molecular Life Sciences 58:2108-2116 (2001)

2 Kaeberlein, McVey, Guarente, "The SIR2/3/4 complex and SIR2 alone promote longevity in Saccharomyces cerevisiae by two different mechanisms," Genes & Development 13:2570-2580 (1999)

3 Guarente, "Sir2 links chromatin silencing, metabolism, and aging," Genes & Development 14:1021-1026 (2000)

4 Rattan, "Repeated Mild Heat Shock Delays Ageing in Cultured Human Skin Fibroblasts," Biochem. and Molec. Biol. Internat'l. 45(4):753-759 (1998)

5 Luo et al, "Negative Control of p53 by Sir2alpha Promotes Cell Survival under Stress," Cell 107:137-148

Loss of Ovarian Function Decreases Lepin Transport
into Mouse Brain

Many women have weight gain and increased fat mass after menopause. Ovariectomy in mice after at least five weeks was reported to be associated with increased fat mass (and by 30 weeks, with both increased fat and weight) along with decreased blood-to-brain transport of leptin.[1] In fact, the entry of leptin into the brain in the ovariectomized mice was reduced by five weeks to a level not significantly different from zero. As leptin has been reported to be more effective when injected directly into the brain than into the blood, the researchers propose that decreased amounts of leptin reaching the brain centers controlling energy regulation may explain, in part, increased body weight in the mice. Although serum concentrations of leptin in women are not changed by menopause, hormone replacement therapy, or changes in serum levels of estradiol, if decreases in leptin's crossing the blood-brain barrier occur, it may account in part for the weight gain and increased fat mass experienced by many postmenopausal women.[1] Therefore, it could be that estrogens/estrogen receptors are involved in the passage of leptin into the brain in postmenopausal women.

1 Kastin et al, "Chronic loss of ovarian function decreases transport of leptin into mouse brain," Neuroscience Letters 310:69-71 (2001)

Hidden Agendas in Research Papers

A recent paper in the Journal of the American Medical Association[1] sought to "determine whether the views expressed in a research paper are accurate representations of contributors' opinions about the research being report."

This was a small study, in which ten papers were chosen from The Lancet that were published in 2000. The author deliberately chose papers with varying numbers of contributors, across a range of subject areas, and including a diversity of research methods. He then obtained permission to contact all of each paper's contributors to ask them several questions concerning the strengths and weaknesses of each study, the implications, etc. In all, 36 (67%) of 54 contributors contacted replied to the survey.

The results were reported to show that a research paper rarely represents the full range of opinions of those scientists whose work it claims to report. There was censored criticism and, noted as striking to the author, inconsistency in publishing evaluations, especially regarding weaknesses. As the author summed it, "[a] scientific research paper is an exercise in rhetoric; that is, the paper is designed to persuade or at least convey to the reader a particular point of view. When one probes beneath the surface of the published report, one will find a hidden research paper that reveals the true diversity of opinion among contributors about the meaning of their research findings."

The implications of this study, small though it was, is even more suggestive when you consider that the papers chosen for this study were not particularly political in their implications. Hence, when you attempt to interpret the "hidden" paper behind those on frankly political scientific issues such as global warming, there is (in our opinion) likely to be a world of censored criticism and inadequate discussion of uncertainties all covered under the misleading label of "consensus."

1 Horton, "The Hidden Research Paper," Journal of the American Medical Association, 287(21):2775-2778 (2002)

It's Better to Have Health Insurance Than Not
Institute of Medicine Reports

A recent report "Care Without Coverage: Too Little, Too Late," the second of six reports from the Institute of Medicine, with support from the Robert Wood Johnson Foundation) compares various health outcomes of those who have health insurance to those who don't have it and concludes (surprise, surprise), it's better to have insurance than not.

Among the findings on uninsured patients with high blood pressure (eg., they are less likely to be screened and have worse clinical outcomes than those with high blood pressure who have health insurance) is that they are less likely to take prescription drugs if such drugs are diagnosed. We wonder to what extent health outcomes might be predicted by such a behavioral difference (if it exists generally) between the insured and non-insured. Studies have found that compliance in taking medication improves outcome, and is true even if one is taking only a placebo (i.e. those compliant in taking a placebo do better than those non-compliant in taking placebo).

-- Marwick, "For the Uninsured, Health Problems are More Serious," Journal of the Nat'l Cancer Institute 94(13):967-968 (2002)

European Union Directive on Food Supplements

The European Union directive was published on July 12, 2002 in the "Official Journal of the European Communities." The bad news for freedom-loving and supplement-using Europeans is that member countries have until July 31, 2003 to designate "maximum levels " of vitamins and minerals and regulate how they can be sold. D & S Comment: Our guess is that, assuming this is really carried out, it will merely result in a large black market of vitamins and minerals that meet the customers' standards, not necessarily those of the central European government. Customers do not necessarily always make wise choices in their purchases, but a one-size-fits-all government choice that is generally made to avoid risks to the government's political exposure rather than serving individual health goals, is unlikely to be either wise or enforceable. A better role for the government would be to provide information and let consumers make their own decisions.

-- from the July 2002 Director's Report of the American Association for Health Freedom (formerly the American Medical Preventive Association)

Paging Dr. Mengele...

"Beginning in the mid-1990s, a Kennedy Krieger Institute study -- overseen by JHU [Johns Hopkins University] and funded through a $200,000 grant from the U.S. Environmental Protection Agency -- sought to identify easy and cost-effective methods to clean up lead-contaminated homes. The study asked poor families with young, healthy children to move into lead-contaminated houses in a Baltimore, MD neighborhood. Landlords were given incentives to recruit subjects, who then were placed randomly into homes that received varying levels of lead abatement or contained no lead contamination whatsoever. The subject families signed JHU-approved consent forms that allegedly failed to disclose the study's inherent risks, and were then given T-shirts, food stamps, and payments of $5-$15 for their 'participation.' Researchers subsequently tested the children's blood lead levels over time and thus assessed the various cleanup technologies." Judge Dale R. Cathell of the Maryland Court of Appeals on August 21, 2001 found (in a lawsuit by two of the parents), among other things, that test results showing low lead contamination levels were given to families, whereas test results indicating higher levels were not. One of the two children involved in the suit allegedly suffered from lead poisoning contracted during the study.

-- Vogelsen, "Rules and ethics betrayed," Modern Drug Discovery, pp. 17-19, August 2002

ERRATA: "Web Sites List Ongoing Clinical Trials"

We received an e-mail from Darrin Kiessling, Medical Editor, Acurian, Inc. (darrin.kiessling@acurian.com) regarding our earlier discussion (March/April 2002 Life Extension News™) of web sites for those looking for ongoing clinical trials. He notes:

Thanks very much for the clarification.

© 2002 by Durk Pearson & Sandy Shaw