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The Durk Pearson & Sandy Shaw®
Life Extension News™

Vol. 6 No. 4 November 2003

"My goal is to cut government in half, to get it down to the size where we can drown it in the bathtub."

— Grover Norquist

We couldn’t agree more, especially after reading the 547 pages of the FDA’s proposed rule imposing druglike Good Manufacturing Practices on dietary supplements. At the end of this newsletter, we include a special section of the 16 pages of comments we filed with the FDA concerning this proposed rule. Bottom line for consumers is that, if these rules are put in practice, most very small and small dietary supplement companies will be put out of business, and the price of dietary supplements will dramatically increase, without our being any healthier or safer and with less innovation because of decreased competition. We and others in the dietary supplement business also filed comments jointly through our attorney, Jonathan Emord, which you can read at www.emord.com.

Table of Contents This Issue

1. If Only It Worked When the Government Stole Your Cattle . . .
2. Aspirin to the Rescue
3. Ketone Bodies in Energy, Neuroprotection, . . .
4. Coming Soon! To Your Kitchen from Ours!
5. Curcumin in Phase I Clinical Trial Prevention of Cancer
6. Xanthine Oxidase and Endothelial Dysfunction
7. Xanthine Oxidase Mediates Cytokine-Induced Bone Resorption
8. Xanthine Oxidase Inhibition by Flavonoids
9. Quercetin and Kaempferol Inhibit in Vitro Osteoclastic Bone Resorption
10. When Shopping for High-Polyphenol Cocoa, All Cocoas Are Not Alike
11. Ecology and Bias in Scientific Media
12. Ain't FDA Regulations Fun?
13. Reforming the FDA
14. Bioengineering Healthier Corn


If Only It Worked When the Government Stole Your Cattle . . .

Cattle Rustler Corralled Yakima, Washington (AP) – For the first time, the state of Washington has used DNA testing to solve an old-time, Wild West crime—cattle rustling. The analysis occurred in a Spokane-area case of a man accused of stealing seven calves from a Cheney rancher. The calves were too young to have been branded, so the question of ownership was one man’s word against another’s. By matching DNA obtained from blood or hair from the stock at the Cheney ranch, however, investigators were able to prove the calves were the offspring of the rancher’s cows.

Elko Daily Free Press, June 4, 2003

Aspirin to the Rescue: Salicylic Acid Attenuates Virulence in Staphylococcus aureus

This is another case of an old drug (aspirin) being discovered to do a new trick—attenuating the virulence of a common bacterial infection, Staphylococcus aureus.

A new paper1 reports that salicylic acid, the major metabolite of aspirin (acetylsalicylic acid), mitigated two important virulence phenotypes in both clinical and laboratory S. aureus by interfering with the function of alpha-hemolysin secretion and fibronectin binding in vitro, reducing the expression of the alpha-hemolysin gene promoter hla and the fibronectin gene promoter fnbA. Expression of the sigB-repressible global regulon sarA and the global regulon agr were also mitigated by salicylic acid, corresponding to the reduced expression of the hla and fnbA genes in vitro. The paper notes that studies in experimental endocarditis confirmed the key roles of both sarA and sigB in mediating the antistaphylococcal effects of salicylic acid in vivo.

As S. aureus (which is often antibiotic-resistant) is a leading cause of a diversity of infections (including endocarditis, pneumonia, abscesses, septicemia, and osteomyelitis) that may be serious or even deadly, this effect of salicylic acid may be useful in the treatment of such infections. The authors1 showed in a 1999 paper2 that treatment of an invasive experimental S. aureus infection (endocarditis) with intravenous aspirin caused a significant reduction in bacterial densities within target tissues and that the latter effects are mediated by salicylic acid.

We would suggest using magnesium salicylate (Doan’s) at the manufacturer’s suggested dose as an adjunct to antibiotic treatment of S. aureus infection; it is the salicylate that is active, not aspirin per se, and the risk of gut bleeding would probably be less. If your ears are ringing, whining, or hissing, you are taking too much.

  1. Kupferwasser et al. Salicylic acid attenuates virulence in endovascular infections by targeting global regulatory pathways in Staphylococcus aureus. J Clin Invest 112(2):222-33 (2003).
  2. Kupferwasser et al. Acetylsalicylic acid reduces vegetation bacterial density, hematogenous bacterial dissemination, and frequency of embolic events in experimental Staphylococcus aureus endocarditis through antiplatelet and antibacterial effects. Circulation 99:2791-7 (1999).

Ketone Bodies in Energy, Neuroprotection, and Possibly in the Effects of Dietary Restriction

Ketone bodies, natural metabolites produced from fatty acids, are sources of energy that can be used when there is insulin deficiency (which may be pathological, as in diabetes, or as a result of consuming low dietary carbohydrate) or mitochondrial senescence. Ketone bodies are found in moderate amounts in prolonged human fasting and in type 2 diabetes.

Interestingly, ketones are very efficient sources of energy. One paper1 reports that the efficiency of cardiac hydraulic work (in rat hearts) was 10.5% in hearts perfused with glucose alone, and increased to 28% in combination with insulin, to 24% with ketones, and to 36% on addition of the combination. Addition of insulin, ketones, and the combination increased acetyl CoA (in the tricarboxylic acid cycle) 9-fold, 15-fold, and 18-fold, respectively, with corresponding decreases in CoA. “Addition of insulin increased the efficiency of hydraulic work per mole of oxygen consumed in [rat] heart 28% by decreasing oxygen consumption by 14% and increasing cardiac work 13%. Addition of ketones, on the other hand, increased the efficiency mainly by increasing hydraulic work, at the same time decreasing oxygen consumption by only a small percentage.”

The authors propose that “The increase in efficiency caused by ketones therefore was compatible with a decrease in proton leakage across mitochondrial membrane due simply to a decrease in potential, as has been previously suggested.” We have written earlier in this newsletter on the hypothesis that increased mitochondrial membrane potential (which increases free radical production in mitochondria) is a mechanism of aging.

The authors propose that “. . . the functional and energetic effects of insulin and ketone bodies may have important clinical consequences.” For instance, they note that elevation of blood ketones to levels that are observed after a 48-hour fast almost completely reverses the mitochondrial abnormalities associated with insulin deficiency. They thus suggest that mild ketosis might be considered a beneficial adaptation to insulin deficiency. They also suggest that ketones might be a beneficial treatment for elderly patients or others suffering from oxidative damage to mitochondria.

The second paper2 found that d-beta-hydroxybutyrate, a ketone naturally found in rat and human metabolism, protected neurons in cell-culture models of Alzheimer’s and Parkinson’s diseases. Addition of a 4-mM solution of the ketone to cells exposed to the cytotoxic amyloid-beta protein1-42 doubled the number of surviving cells and increased cell size and neurite outgrowth compared to cells exposed to the amyloid-beta protein1-42 but not treated with d-beta-hydroxybutyrate. The authors propose that the ketones may ameliorate the amyloid-beta protein1-42 toxicity by overcoming a block at mitochondrial pyruvate dehydrogenase (PDH) that occurs as a result of glycogen synthase 3 beta kinase activation by the amyloid-beta protein. As they put it, “Ketones are the physiological means of overcoming PDH, resulting from a lack of insulin stimulation, and ensure the continuing function of the TCA cycle and hence the provision of NADH, the major substrate required for electron transport and ADP phosphorylation.”

We wonder what the usual dietary restriction (30% below ad libitum levels) does to ketone levels in rodents and in monkeys. We know that insulin and glucose levels are reduced due to dietary restriction. We wouldn’t expect to see the same levels of ketones that occur in prolonged fasting or even in very-high-fat, very-low-carbohydrate diets (medical ketogenic diets, which are sometimes used to treat intractable epilepsy). Yet it may be that ketones contribute to the protective effects of dietary restriction, though we haven’t seen anything on this.*


*After writing this, we received a PubMed search on the subject of ketones and calorie restriction carried out by Will Block (thanks, Will!). One paper reported that a 90% calorie-restricted diet in rats did not increase ketone levels [Cheng et al. A ketogenic diet increases brain insulin-like growth factor receptor and glucose transporter gene expression. Endocrinology 144(6):2676-82 (2003)]. Another found that in male Sprague-Dawley rats fed a normal rodent-chow diet calorie-restricted to 90% or 65%, ketones were elevated in approximate proportion to the degree of calorie restriction [Eagles et al. Calorie restriction of a high-carbohydrate diet elevates the threshold of PTZ-induced seizures to values equal to those seen with a ketogenic diet. Epilepsy Res 54(1):41-52 (2003)]. Yet another paper reported that ketone bodies increased by 65% in old, but not young, CR mice [Hagopian et al. Influence of age and caloric restriction on liver glycolytic enzyme activities and metabolite concentrations in mice. Exp Gerontol 38(3):253-66 (2003)]. Another paper found that mild calorie restriction (15%) in EL mice induced changes in blood glucose levels that were predictive of both blood ketone levels and seizure susceptibility [Greene et al. Caloric restriction inhibits seizure susceptibility in epileptic EL mice by reducing blood glucose. Epilepsia 42(11):1371-8 (2001)].


Moreover, the lower gastrointestinal tract is depleted of carbohydrates, since these are converted to sugar in the small intestine by amylase and then absorbed. The fiber (which includes resistant starch) that reaches the lower GI tract is broken down into short-chain fatty acids, such as butyric acid, which, when oxidized, become ketones, such as d-beta-hydroxybutyrate, that can then be used as energy. Ketones may therefore play a role in the lower-GI-tract anticancer protective properties of butyric acid.

  1. Sato, Kashiwaya, Keon, et al. Insulin, ketone bodies, and mitochondrial energy transduction. FASEB J 9:651-8 (1995).
  2. Kashiwaya, Takeshima, Mori, et al. d-Beta-hydroxybutyrate protects neurons in models of Alzheimer’s and Parkinson’s disease. Proc Natl Acad Sci 97(10):S440-4 (2000).

Coming Soon! To Your Kitchen from Ours!

The Durk & Sandy low-carbohydrate, high-protein, high-fiber, high-tech, and 100% delicious and nutritious snack cakes and bars are soon to be released to the market, after meeting all our rigid standards and, of course most importantly, the approval of our very picky taste buds.


Curcumin in Phase I Clinical Trial Prevention of Cancer

A 2001 paper1 reported on the results of a phase I clinical trial of curcumin to reduce the risk of or prevent cancer in patients with high-risk conditions, including: (1) recently resected urinary bladder cancer; (2) arsenic Bowen’s disease of the skin; (3) uterine cervical intraepithelial neoplasm; (4) oral leukoplakia; and (5) intestinal metaplasia of the stomach. Thus, this was not a trial of the ability of curcumin to prevent cancer in healthy individuals, but in those who have already had cancer (and are at risk of recurrence) or have premalignant lesions.

Curcumin is the major component (about 40%) of turmeric, a spice commonly used in foods, especially those of India. In India and China, curcumin has been said to be long used as a medicinal herb. Evidence suggests that curcumin acts on stages of initiation, promotion, and progression of carcinogenesis.1

A total of 25 patients were enrolled in this study. The subjects took curcumin once in the morning on an empty stomach. Since a previous small-series human study used 500 mg/day for 7 days without observing any toxicity, and a commonly consumed diet in India may contain as much as 100 mg/day of curcumin, the authors chose 500 mg/day as the starting dose. The patients were then moved up into the next dose level (1000, 2000, 4000, 8000, and 12,000 mg/day) as soon as at least two patients at a given level had completed the 3-month treatment and no more than one patient had experienced any equal to or greater than grade II toxicity. Tissue samples were taken from the indicator lesions before and at completion of the 3-month treatment with curcumin.

No toxicity was observed up to 8000 mg/day. However, it was not possible to increase patients to the next level (12,000 mg/day) because the bulky volume of the tablets was unacceptable.

The authors found that curcumin was not well absorbed from the GI tract. The peak serum concentration was only 1.77 µM even at the 8000-mg/day dose. However, these researchers had earlier found in an animal study that curcumin was rapidly biotransformed to dihydrocurcumin and tetrahydrocurcumin and that these compounds were later converted to monoglucuronide conjugates. They suggest that some of the metabolites may retain the pharmacologic properties of curcumin, so the relatively low serum concentrations in the patients in this trial may not reflect the entire beneficial activity of the oral curcumin.

After 3 months in this study, they found histologic improvement in 7 out of 25 patients with these various high-risk and premalignant lesions. They note the need for further phase IIb studies with placebo control for individual lesions to confirm the findings of this study. The authors recommend an oral dose of 6000–8000 mg/day of curcumin in the phase II study. However, since this would be a study of high-risk individuals, 6000–8000 mg/day of curcumin would be an excessive dose for a healthy individual taking curcumin as a supplement; we suggest 200 mg/day.

Experiments on mice genetically engineered to express human amyloid-beta protein (and that develop a condition resembling Alzheimer’s) show a delayed onset with curcumin supplementation, but an accelerated onset if they take too much. Curcumin, like most antioxidants, becomes a pro-oxidant if taken at excessive levels. More is not always better, and it is the dose that makes the poison.

  1. Cheng et al. Phase I clinical trial of curcumin, a chemopreventive agent, in patients with high-risk or premalignant lesions. Anticancer Res 21:2895-2900 (2001).

Xanthine Oxidase and Endothelial Dysfunction in Heavy Smokers

Xanthine oxidase (XO) is one of the major free radical-producing enzymes (others are NADPH oxidase, myeloperoxidase, and endotoxin). XO, present in high concentrations in endothelial cells of capillaries and sinusoids, can produce superoxide, as well as other oxygen free radicals. The XO-derived superoxide radicals generate hydrogen peroxide, which can then produce hydroxyl radicals. XO activity is increased in ischemia-reperfusion injuries, anoxia, and inflammation.

An interesting, single-blinded, randomized, 2-phase crossover study of endothelial function in heavy smokers1 was recently reported. The authors hypothesized that xanthine oxidase contributed to endothelial dysfunction (failure of arteries to dilate in response to acetylcholine) in cigarette smokers. They inhibited XO by giving subjects 600 mg of allopurinol. Earlier studies had shown that oxypurinol, an active metabolite of allopurinol, improved resistance vessel endothelial vasodilator function in hypercholesterolemic, but not hypertensive, patients.

The 14 smokers included in this study were chosen to have no other risk factors for atherosclerosis. Blood vessel dilation produced by acetylcholine was significantly less in smokers (254; +57%) than in healthy controls (390; +55%). Allopurinol reversed the endothelial dysfunction in smokers (acetylcholine, 463; +78%) without affecting responses in nonsmokers (401; +80%).

Few if any people reading this newsletter are likely to be smokers, but you may have a friend or relative who smokes and who may find it useful to take allopurinol, a readily available and inexpensive prescription drug. Durk takes 200 mg/day for gout. Allopurinol can cause liver problems in some people, especially at high doses. Uric acid, a potent destroyer of the strong oxidant peroxynitrite, is made by xanthine oxidase, so we do not recommend that you lower your uric acid levels below the normal human range.

  1. Guthikonda et al. Xanthine oxidase inhibition reverses endothelial dysfunction in heavy smokers. Circulation 107:416-21 (2003).

Xanthine Oxidase Mediates Cytokine-Induced but Not Hormone-Induced Bone Resorption

Loss of estrogen in postmenopausal women is not the only aging mechanism that increases bone loss (resorption). Bone resorption can also be caused by increased amounts of calcitropic hormones, prostaglandins, and the proinflammatory cytokines TNF-alpha (tumor necrosis factor-alpha) and IL-1-beta (interleukin-1-beta).1

Osteoclasts are cells that cause bone resorption, while osteoblasts increase bone. The balance between them, determined by many factors, is responsible for whether bone is being removed or added. In response to stimulation by cytokines, osteoblasts induce osteoclastic bone resorption. Reactive oxygen species are involved as well; hydrogen peroxide, for example, has been shown to directly induce osteoclastogenesis (creation of osteoclasts) and to induce osteoclast activity. As noted above, however, xanthine oxidase (XO) generated superoxide radicals and hydrogen peroxide. In this study,1 researchers examined the potential of XO to mediate in part, via the production of reactive oxygen species (hydrogen peroxide), TNF-alpha-, IL-1-beta-, parathyroid hormone-, and 1,25-(OH)2 vitamin D3-induced mouse calvarial bone resorption.

The authors found, by using allopurinol to block xanthine oxidase activity, that the osteoclast bone resorption produced by the elevation of proinflammatory cytokines resulted from the hydrogen peroxide produced by XO. They did not observe any inhibitory effects of allopurinol on parathyroid hormone and 1,25-(OH)2 vitamin D3-induced bone resorption, but catalase did have an inhibitory effect, indicating that hydrogen peroxide (but not from XO) is part of this process.

The authors propose that the elevation of proinflammatory cytokines in bone-destructive diseases such as rheumatoid arthritis mediates their proresorptive effects via the generation of reactive oxygen species from XO.

  1. Kanczler et al. Xanthine oxidase mediates cytokine-induced, but not hormone-induced, bone resorption. Free Rad Res 37(2):179-87 (2003).

Xanthine Oxidase Inhibition by Flavonoids

There are currently some 4000 flavonoids known, of which many have a high potential for xanthine oxidase (XO) inhibition.1 Black cherries and black cherry juice have been traditionally used to treat gout. They are high in flavonoids, and this may explain why the treatment often works. The authors of a recent paper1 report the results of a structure-function analysis for flavonoids to find those with the most XO-inhibitory properties. They describe a method for predicting IC50 (50% inhibitory concentration) values of xanthine oxidase very accurately by calculating the contribution of each hydroxyl moiety toward inhibition of XO.

The flavonoids listed by Van Hoorn et al. that have the lowest IC50 values include: chrysin (2.5 µM), apigenin (1.0 µM), luteolin (0.75 µM), kaempferol (2.5 µM), quercetin (1.5 µM), and myricetin (1.5 µM). The IC50 for allopurinol was given as 6.2 µM.

  1. Van Hoorn et al. Accurate prediction of xanthine oxidase inhibition based on the structure of flavonoids. Eur J Pharmacol 451:111-8 (2002).

Quercetin and Kaempferol Inhibit in Vitro Osteoclastic Bone Resorption

As noted above, quercetin and kaempferol are flavonoids that inhibit xanthine oxidase, which is associated with cytokine-induced osteoclastic bone resorption. A recent paper1 examined the effects of quercetin and kaempferol on in vitro osteoclastic bone resorption and found both not only to inhibit bone resorption, but also to directly induce apoptosis of mature osteoclasts in the same dose range. When osteoclasts were treated with 50-µM quercetin and kaempferol, intracellular reactive oxygen species levels decreased significantly, by 75% and 25%, and apoptotic osteoclasts in cultures were increased about 3-fold compared with control cultures. At concentrations below 50 µM, however, neither flavonoid had antiradical action, suggesting, the authors say, that antioxidant properties cannot fully explain the inhibitory effect on bone resorption, because at lower doses (0.1 µM, 1 µM, and 10 µM), the flavonoids had pro-oxidant effects (particularly for kaempferol) and still had apoptotic effects on the osteoclasts in culture.

The authors show here that quercetin and kaempferol directly promoted spontaneous apoptosis of osteoclasts in a dose range that correlated well with those for inhibition of bone resorption. Kaempferol was observed to stimulate apoptosis at lower concentrations (0.1 µM and 1 µM) than quercetin (where effects were first noted at 10 µM), but quercetin effects were observed earlier.

The researchers examined whether estrogenic effects of the flavonoids were part of their anti-bone-resorption effects. They used ICI 182780, a pure antagonist that can block the estrogen receptor, and found that it partially reversed the inhibitory effect on resorption by kaempferol, but not by quercetin. Estrogens and bisphosphonates (a class of drug used to treat bone loss) act at least in part by inducing osteoclast apoptosis.

The authors also report a study that showed that several vegetables, especially onion extracts (a relatively rich source of quercetin), can significantly inhibit bone resorption in the rat. Another recent study reported that, among elderly women in Britain, tea (another source of quercetin) drinkers had significantly greater bone mineral density than non-tea drinkers. The authors note that possible candidates as bioactive molecules in onion and tea are flavonols. A further study found that rutin, a quercetin glycoside, can preserve bone mass in ovariectomized rats by slowing down bone resorption.

  1. Wattel et al. Potent inhibitory effect of naturally occurring flavonoids quercetin and kaempferol on in vitro osteoclastic bone resorption. Biochem Pharmacol 65:35-42 (2003).

When Shopping for High-Polyphenol Cocoa, All Cocoas Are Not Alike

Most, but not all, cocoa powders these days are alkali treated at some stage in their manufacture to improve color, flavor (reduces bitterness), and dispersibility.1 Unalkalized cocoa powders have a pH of about 5.5, whereas alkalized cocoa powder is about 7.1. One reason that alkali (also called Dutch) treatment improves the flavor is that it destroys many polyphenols, which are bitter, thus “improving” the cocoa by making it less bitter. However, the polyphenols in cocoa have been found to have many beneficial properties, just as the polyphenols in red wine and in green tea have. For example, flavonoids, including cocoa flavanols, are thought to decrease certain risk factors for cardiovascular disease by reducing LDL oxidation, improving endothelial-dependent vasodilation, and modulating eicosanoids and cytokines involved in inflammatory processes.2 A recent study2 of 32 healthy men and women reported that cocoa flavanols and procyanidin supplementation (234 mg of cocoa flavanols and procyanidins/day in a tablet) for 28 days resulted in significantly decreased platelet function, as well as significantly increased plasma epicatechin and catechin, as compared to placebo (6 mg or less of cocoa flavanols and procyanidins/day).

Therefore, when selecting cocoa powder, find one that is not labeled as being Dutch or alkali-treated.

  1. Kirk-Othmer Encyclopedia of Chemical Technology, 2nd ed, Vol 5, pp 383-4.
  2. Murphy et al. Dietary flavanols and procyanidin oligomers from cocoa (Theobroma cacao) inhibit platelet function. Am J Clin Nutr 77:1466-73 (2003).

Ecology and Bias in Scientific Media: Is It 300 Years or 50 Years of Deformed Frogs? Neither Multilegged Frogs Nor Biased Reporting Is New

Science published a news story in its 15 August 2003 issue entitled “Fifty Years of Deformed Frogs.” In the text of the story, however, they mention that “Reports of multilegged amphibians aren’t new; they go back to the early 1700s.” Then why should we be worried about something going on for nearly 300 years, in fact to well before the Industrial Revolution and the dreaded “anthropogenic” effects? It is obviously something to worry about because, as the news story says, “The scientists have found 50 hot spots for malformed amphibians in the past five years, far more than the nine historical accounts they dug up.” This all assumes that, in the past all the way to the early 1700s, people were as likely to write accounts of malformed frogs as recently as, say, in the past 50 years. Also, it assumes that accounts written by naturalists without long lists of alphabet-soup credentials after their names would be as likely to attract attention to their observations as recent stuff written by their credentialed “betters.” And just how hard did these guys search the available literature, such as reports not published in scientific journals? In the early 1700s and even the early 1800s, much of America was not settled. Who would be reporting on multilegged frogs then?


Ain’t FDA Regulations Fun?

The 29 August 2003 Science reports, in their “Random Samples” section, an article entitled “A Painful Separation,” which reflects poorly on the FDA’s approval process. The article reports that two scientists, Raymond Goodwin and Craig Smith, cloned the primary receptor for the inflammatory cytokine tumor necrosis factor (TNF) that led to the development of a blockbuster arthritis drug, Enbrel. But when the company at which they had worked (Immunex) was bought out by biotech “behemoth” Amgen, the two scientists had resigned, “victims of the merger.” Although Smith hopes to launch his own biotech company, Goodwin (at 52) has retired, “saying he no longer has the desire to push another compound all the way to market: ‘I don’t know if I want to work that hard.’”


Reforming the FDA

Nobel Prize-winning economist Gary Becker has said, “Eliminating all requirements except a reasonable safety standard would vastly reduce drug prices in the U.S., as companies would be encouraged to develop additional compounds to compete for customers.” The 1962 Kefauver Amendments to the Food, Drug, and Cosmetic Act that required proof of efficacy as well as safety of new drugs have had a dramatically negative effect on the number of new drugs developed, the time it takes to develop them, and the affordability of those drugs. Unfortunately, this isn’t just a matter of economics and science, but of politics. There are many special interests and those who represent them (e.g., Henry Waxman, Ted Kennedy, Center for “Science” in the Public Interest, FDA, and many others) who would fight tooth and nail the repeal of the Kefauver Amendments.

That is why it is so important to fight for the freedom we have now in the dietary supplement industry. It is one of the few comparatively free markets in medicine left in the U.S. (in fact, the only other one we can think of is compounding pharmacy, which is exempted from FDA’s Good Manufacturing Practices for drugs. See our first [in last months issue of Life Enhancement] and second sets of comments to the FDA on proposed CGMPs (Current Good Manufacturing Practices) for dietary supplements that follow this newsletter for our take on the destructive effects of drug CGMPs, after which the FDA modeled their proposed rule on dietary supplement CGMPs. (The latter is a violation of the law, as the DSHEA authorized the FDA to put CGMPs “modeled after food CGMPs” in place for dietary supplements.)


Bioengineering Healthier Corn

The September 2003 issue of Nature Biotechnology reports1 a scientific group that has determined the sequence of an enzyme specific for tocotrienol synthesis. Expression of the cDNAs for HGGT (homogentisic acid geranylgeranyl transferase), the enzyme unique to the tocotrienol biosynthetic pathway in plants, results in transgenic plants that generate large increases in the amounts of vitamin E and tocotrienols in their leaves and seeds. The researchers found a 10-to-15-fold increase in the tocotrienol and tocopherol content of Arabidopsis thaliana leaves in response to overexpression of the barley HGGT. Overexpression of the same cDNA resulted in up to a six-fold increase in tocotrienol and tocopherol content in corn seeds.

Currently tocotrienols are nutraceuticals extracted from rice and palm oils. Using genetic engineering, tocotrienols will become dirt cheap and readily available in the everyday vegetables you eat. It is one thing for those who are anti-GMO foods to reject foods that were crops engineered to be resistant to herbicides, but another entirely to reject healthier GMO versions of regular food. Hey, they can call high-tocotrienol and -tocopherol versions of corn Frankenfoods if they like, but they’ll just look like Frankenfools . . . .

  1. Cahoon et al. Metabolic redesign of vitamin E biosynthesis in plants for tocotrienol production and increased antioxidant content. Nature Biotech 21(9):1082-7 (2003). Dormann. Corn with enhanced antioxidant potential. Nature Biotech 21(9):1015-6 (2003).

© 2005 by Durk Pearson & Sandy Shaw