November 2001 Blog with Durk and Sandy


On October 30, 2000, the FDA allowed orange juice manufacturers to add a new health claim informing consumers that diets containing foods that are good sources of potassium and are low in sodium may reduce the risk of high blood pressure and stroke.1 Foods that contain (per serving) at least 10% of the daily value for potassium (3500 mg) and less than 140 mg of sodium are eligible to use the claim. Unfortunately, consumers are not told on the label that if a serving contains 10% of the recommended daily amount of potassium, they will need to eat ten of those servings. All they know is that the food is a “good” source of potassium. One of the best food sources is V-8 or tomato juice, but a serving contains only about 15% of the daily value. Our pancake mix is high in protein (whey protein) and whole rye flour (which contains lignans, metabolites of which are a type of phytoestrogen that has been shown in animal studies to reduce the risk of certain cancers) and is also very high in potassium and very low in sodium. In fact, a single serving of the pancakes made from our mix will contain about 80% of the daily value for potassium.

One of the two versions of our pancake mix also contains EPA- and DHA-rich fish oils that are totally undetectable by your taste buds. Since each serving contains about as much as a serving of Chinook salmon, we would expect two servings per week of our heart-healthy pancakes to reduce your risk of sudden death by heart attack dramatically, as has been reported in numerous studies. For example, one serving of coldwater fish oil a week reduced the risk of heart-attack death by 44% in a group of average age 72 years.2 The American Heart Association now recommends two servings of coldwater fish a week because of the cardiovascular benefits of EPA and DHA. The lead editorial of the September 2001 American Journal of Clinical Nutrition2 says, “Japanese, Dutch, and U.S. studies indicate that deaths from coronary artery disease are reduced by ≥50% by the consumption of 1-2 fish meals/week. The most important finding is of a reduction of sudden death from ventricular fibrillation and tachycardia. About 300,000 such deaths occur in the United States each year. Direct clinical trials of fish and fish oil have also shown a striking reduction in sudden death. . . . n-3 Fatty acids from fish and fish oil are natural food substances that prevent coronary artery disease and sudden death. Physicians should become acquainted with the powerful therapeutic potential of these fatty acids.”

If you have tried to take a regular potassium supplement that contains even as much as 50% of the recommended daily value, you may have experienced stomachache or nausea. This won’t happen with our pancake mix, because the potassium is complexed with other food ingredients. A remarkably fun and healthful meal for breakfast, lunch, or even dinner. All proceeds we receive from our pancake mix are donated to the Pearson & Shaw FDA Litigation Fund. You can help yourself while you help us dismantle the FDA’s censorship regime.

New Pancake Variation: Spicy Holiday Pancakes!
If you have tasted our new heart-healthy pancakes, you know how great they are. But we don’t stop there. We are always looking for delicious new variations. Our latest is Spicy Holiday Pancakes. To each cup of dry mix, you add 1 tbsp ground ginger, 1/4 tsp nutmeg, and 1/4 tsp cinnamon, and mix well. Prepare as usual. Wow!


  1. Health-claim notification for potassium-containing foods. (accessed May 31, 2001), as cited in Sowinski et al., “Hyperkalaemia and apple juice” (letter), The Lancet 358:841-2 (2001).
  2. “Dietary fatty fish may reduce heart risk,” Inform 12:500 (2001); Connor, “n-3 Fatty acids from fish and fish oil: panacea or nostrum?” Amer J Clin Nutr 74:415-6 (2001).



A recent study1 reports that the normal drop in blood pressure from day to night, which has emerged as a strong prognostic indicator of cardiovascular morbidity and mortality, is blunted after menopause in both white and African-American women. 112 women (62 premenopausal and 50 postmenopausal) took part in this study. Waking blood pressure did not differ by menopausal status. But the drop (dipping) in both systolic blood pressure and diastolic blood pressure was less during nighttime sleep in postmenopausal as compared to premenopausal women. The authors propose that this reduced blood pressure dipping may contribute to increased cardiovascular risk in postmenopausal women.

One possible way to ameliorate this reduced dipping would be supplementation with arginine just before bedtime. Arginine supplements have been shown in humans to reduce blood pressure by increasing the amount of available arginine, the precursor to the vasodilator nitric oxide. There have been no studies with arginine on this particular (nighttime blood pressure dipping) problem, but it would appear to be a very sensible idea to test. We have been taking arginine, choline, and vitamin B5 (found in our InnerPowerTM) for over 25 years. The mechanism by which nitric oxide dilates arteries (thus reducing blood pressure) involves a cholinergic mechanism.2


  1. Sherwood et al., “Blunted nighttime blood pressure dipping in postmenopausal women,” Amer J Hypertension 14:749-54 (2001).
  2. Dillon and Vita, “Nitric Oxide and Endothelial Dysfunction” (Ch. 13, p. 209), in Nitric Oxide and the Cardiovascular System, ed. by Loscalzo and Vita, Humana Press, 2000.



A paper published in a recent New England Journal of Medicine1 examined various factors in women that affect the risk of developing type 2 diabetes. The findings were similar to those that have been reported before, except that this study involved 89,941 female nurses followed from 1980 to 1996 who were free of diagnosed cardiovascular disease, diabetes, and cancer at baseline. Hence the study had considerable statistical power. The authors report that lack of exercise, a “poor” diet, current smoking, and abstinence from alcohol use were all associated with a significantly increased risk of diabetes.

There were some surprising things in this study, showing once again how difficult it is to cull data from an epidemiological (observational) study, even with large numbers to look at. Excess body fat was the single most important risk factor for type 2 diabetes. No surprise there. Table 2 in the paper shows the relative risk of type 2 diabetes for various lifestyle factors as related to body-mass index. Curiously, while increased weekly exercise did reduce risk in all the body mass index groups (<25, 25.0–29.9, and >30), it showed only slight reductions in risk (relative risks of 0.92, 0.90, and 0.91) in the 25.0–29.9 body mass index group, whether the exercise involved was from 0.5–1.9 hours, 2.0–3.9 hours, or 4.0–6.9 hours per week, respectively. At over 7 hours of exercise per week, the relative risk increased to 1.06. Hence, it would appear that the optimal amount of exercise for the 25.0–29.9 (overweight) group could be a mere 1/2 hour a week.

On the smoking status, the results were even stranger. For the women with a body-mass index of <25 (not overweight), those who were currently smoking 1–14 cigarettes per day had a lower relative risk (0.72) than those who had never smoked (1.0) or who had formerly smoked (0.95). However, smokers in that body mass index group who smoked over 15 cigarettes per day had an elevated risk, as did those in the overweight and obese groups at any level of current smoking.

The largest reduced risk came from daily alcohol consumption. All amounts from 0.1 to >10 grams a day reduced the risk significantly in all body mass index categories. As shown in Table 2, with zero grams a day of alcohol consumption set as a relative risk (RR) of 1, alcohol vs. RR was: for body mass index <25, 0.85 RR for 0.1–5.0 grams alcohol/day, 0.64 for 5.1–10.0 grams alcohol/day, and 0.85 for >10 grams alcohol/day. For body mass index 25.0–29.9 (overweight), RR was 0.70 for 0.1–5.0 grams alcohol/day, 0.62 for 5.1–10.0 grams alcohol/day, and 0.57 for >10 grams alcohol/day. For body mass index >30 (obese), RR was 0.81 for 0.1–5.0 grams alcohol/day, 0.60 for 5.1–10.0 grams alcohol/day, and 0.61 for >10 grams alcohol/day. One glass of wine per day with the largest meal of the day is a reasonable amount of alcohol for a woman.


  1. Hu et al., “Diet, lifestyle, and the risk of type 2 diabetes mellitus in women,” New Engl J Med 345(11):790-7 (2001).



Many of us are using bioelectrical impedance devices, such as those made by Tanita, to measure our body fat. They are convenient and easy to use. A recent study,1 however, indicates that after a meal, the bioelectrical impedance is decreased significantly (resulting in a decrease in the calculated percentage of body fat) and that the effect lasts 2-4 hours. Moreover, the impedance decrease was additive during the day, although it was more pronounced after the first meal, possibly because of the combined effect of rising from the supine position and meal ingestion.

Bioelectrical impedance was measured 18 times during a 24-hour period in 18 healthy subjects (10 women and 8 men, aged 31.5 ± 11.7 years; body mass index 22.2 ± 2.7). Subjects were given an identical meal for breakfast, lunch, and dinner. The percentage of body fat varied by 8.8% from the highest to the lowest measurement in women, and by 9.9% from the highest to the lowest measurement in men. Rodriguez et al.2 suggest that the decrease in impedance may be consistent with a redistribution of extracellular fluids, which would occur as a result of electrolyte intake during a meal and, in the case of the first meal of the day, changing from a supine position to an upright one. The impedance study authors note that because impedance increased 3-4 hours after all three meals, the decrease in postprandial impedance was a direct effect of ingestion and was not due to redistribution of body fluids as a result of a change in body position.

We suggest, therefore, that you use these devices upon arising in the morning and before your first meal.


  1. Slinde and Rossander-Hulthen, “Bioelectrical impedance: effect of 3 identical meals on diurnal impedance variation and calculation of body composition,” Am J Clin Nutr 74:474-8 (2001).
  2. Rodriguez et al., “Diurnal variation in the assessment of body composition using bioelectrical impedance in children” (letter), Eur J Clin Nutr 53:244 (1999).



An interesting study1 reports measurements by the authors of the terminal restriction fragments (TRF), a measure of average telomere size, in leukocyte DNA of ten patients with severe coronary artery disease (CAD), as compared to that in 20 controls without CAD. Although atherosclerotic plaques are focal, there is increasing evidence that systemic processes, such as inflammation and oxidative processes, also take place in patients with atherosclerosis. Hence, the authors of this study hypothesized that the presence of atherosclerosis could be marked by increased cell turnover and increased biological age in cell types other than those directly involved in the plaques.

Telomeres are structures at the ends of chromosomes that maintain the integrity of chromosomes by preventing chemical interactions between chromosome ends and by providing “handles” for the replication enzymes. Telomeres progressively shorten with repeated cell division, and senescence (end of cellular reproductive life) is reached when the telomeres shorten to a critical length. The authors examined whether patients with advanced CAD had systemic evidence of telomeric shortening compared with individuals without CAD.

They found that there was a highly significant effect of age on mean leukocyte TFR, with an average decrease in length equivalent to 35 (standard error = 4) base pairs (bp) per year of life. Adjusting for sex and age, patients with CAD had mean TRF lengths of 303 (standard error = 90) bp shorter than those of controls. On average, mean TRF length of leukocytes from individuals with CAD was similar to those without but who were 8.6 years older. The authors propose that the shorter leukocyte telomeres in patients with CAD reflect increased leukocyte turnover from the inflammation believed to occur in atherosclerosis.


  1. Samani et al., “Telomere shortening in atherosclerosis,” The Lancet 358:472-3 (2001).



A significant body of evidence has been developed linking increased COX-2 activity with cancer growth.1 COX-2 is an inducible form of cyclooxygenase that is expressed at sites of inflammation. A recent paper2 in FASEB Journal identifies vascular endothelial growth factor (VEGF), which stimulates the formation of blood vessels, as an inducer of COX-1 and COX-2. The same authors examined the effect of COX inhibitors in an in vitro angiogenesis model. Blood vessel growth, as measured by microtubule formation, was increased by exogenous VEGF and almost completely inhibited by the COX-1 inhibitor SC560, but was unaffected by the COX-2 inhibitor NS398.

In cultures of VEGF-treated endothelial cells, SC560 when applied alone was partially effective in inhibiting cell proliferation, while NS398 had no effect. However, when the COX-1 and COX-2 inhibitors were applied together, cell proliferation induced by VEGF was inhibited. A similar effect was seen with aspirin.

COX-2 inhibition has been reported to suppress growth in colon cancer cell lines and to induce apoptosis in some tumors. COX-2 is also expressed in the vasculature surrounding colon cancers and some evidence indicates that inhibition of COX-1 and COX-2 suppresses angiogenesis. The paper notes that several reports have shown an increase in cyclooxygenase activity in human endothelial cells treated with VEGF.

Natural COX Inhibitors
There are a large number of natural COX inhibitors. In a paper in the Journal of Medicinal Food,3 herbal expert James A. Duke listed 24 such substances, including melatonin, nordihydroguaiaretic acid (NDGA), resveratrol (inhibits COX-2), salicin, thymol, capsaicin, curcumin (found in turmeric), gingerol, and zingerone (the latter two found in ginger).

COX Inhibition by Vitamin E and Aspirin
The use of aspirin for the treatment of rheumatoid arthritis pain is limited by the gastric toxicity that often occurs at the high aspirin doses that are required. Inhibition of cyclooxygenase (COX) activity and the subsequent prostaglandin synthesis is considered essential to aspirin’s analgesic and antipyretic activities. Aspirin inhibits both COX-2 and COX-1, which is a problem at higher aspirin doses since COX-1 protects the gastric mucosa by generating cytoprotective mediators such as prostacyclin. A recent paper4 reports that the combination of aspirin and vitamin E is more effective in inhibiting COX-2 than either agent by itself. Further study revealed that vitamin E renders COX-2 more sensitive to inhibition by aspirin by unknown mechanisms. Hence, in combination with vitamin E, less aspirin can be used while still effectively inhibiting COX-2 and its inflammatory effects. The study was performed on mouse macrophages stimulated to produce COX-2 by the presence of LPS, lipopolysaccharide, from E. coli.

Clinical evidence indicates a reduced need for nonsteroidal anti-inflammatory drugs in patients who are also taking vitamin E. Moreover, additive anti-inflammatory effects of combined aspirin and vitamin E have also been demonstrated in rat adjuvant arthritis, a good animal model of human rheumatoid arthritis. In this study, simultaneous incubation of cells with vitamin E (300 µM) enhanced the inhibitory action of aspirin (1 µM) and led to virtually complete blockade of LPS-induced PGE2 (59% inhibition in the presence of aspirin alone, 95% inhibition in the presence of aspirin and vitamin E).

The authors show that it is not vitamin E’s antioxidant properties that are responsible for this effect, since the addition of vitamin C (which regenerates vitamin E from its radical form) did not further enhance COX-2 inhibition. (In fact, the vitamin C tended to increase COX-2 in the presence of LPS.)

We take low-dose aspirin, acetylsalicylic acid (Durk, 81 mg; Sandy, 40 mg), 350-700 mg magnesium salicylate, and 800 IU vitamin E per day. (Note: Ringing in the ears indicates excessive intake of salicylate, either as salicylate or acetylsalicylic acid.)


  1. Williams et al., “Host cyclooxygenase-2 modulates carcinoma growth,” J Clin Invest 105(11):1589-94 (2000).
  2. Murphy and Fitzgerald, “Vascular endothelial growth factor induces cyclooxygenase-dependent proliferation of endothelial cells via the VEGF-2 receptor,” FASEB J (May 29, 2001).
  3. Duke, “Clippings from my COX box,” J Medicinal Food 1(4):293-8 (1998/1999).
  4. Abate et al., “Synergistic inhibition of cyclooxygenase-2 expression by vitamin E and aspirin,” Free Rad Biol Med 29(11):1135-42 (2000).



A new paper1 reports finding a possible mechanism for the primary pulmonary hypertension (PPH) that developed in some people using the combination of phentermine and fenfluramine for weight loss. According to the paper, the remodeled pulmonary arteries in PPH show various degrees of medial hypertrophy and intimal thickening that eventually clog the vessels. Hyperplasia of the pulmonary artery smooth muscle cells is the main component of these changes.

The changes leading to PPH were found to be associated with serotonin (5-HT) and the serotonin transporter (5-HTT). Studies were performed on lung specimens obtained during lung transplantation in eight patients with PPH, as well as on control lung tissue. In cultured smooth muscle cells from PPH patients, 5-HT produced a concentration-dependent increase in DNA synthesis, associated with smooth muscle cell hyperplasia. Pretreatment of the cells with fluoxetine (as in Prozac) or citalopram, two 5-HTT inhibitors, completely abolished the increase in DNA synthesis. The authors recently found that discontinuation of chronic dexfenfluramine treatment in rats was followed by increased lung 5-HTT expression, which promoted the development of hypoxic PH. Individuals with a high basal serotonin uptake related to the presence of the long 5-HTT gene promoter variant may be particularly susceptible to one or more of these potential mechanisms of appetite suppressant-related PPH.


  1. Eddahibi et al., “Serotonin transporter overexpression is responsible for pulmonary artery smooth muscle hyperplasia in primary pulmonary hypertension,” J Clin Invest 108(8):1141-50 (2001).



Two experts in the cancer risks of arsenic published a letter in the August 6, 2001 Chemical & Engineering News1 in which they pointed out:

It needs to be realized that all known human cancer risks, such as those associated with tobacco use or certain nutritional customs (for example, excessive salt, carcinogens in meat cooked at high temperatures, and insufficient fiber) have been faithfully reproduced in animal models. This is not true for arsenic compounds, which have not caused tumors in animals despite many attempts for over 40 years.

Yet in parts of Taiwan, Chile, Argentina, India, and Bangladesh, where the available drinking water contains levels of arsenite many times higher than are found in the U.S. (up to 3000 ppb), there is a statistical association with increased cancer risk. People in Taiwan (the best-studied population) have increased risk of skin, lung, bladder, and possibly other cancers. Data from Chile and Argentina also show increased cancer risk at high doses. These reports have given arsenite the reputation of being a human carcinogen.

John H. Weisburger developed the concept that risk assessment of chemicals requires an evaluation as to whether or not they are genotoxic [Toxicol Sciences 57, 4 (2000)]. Genotoxic carcinogens react with DNA and are mutagenic. The conclusion was that virtually all human cancer risks are genotoxic, where there are other chemicals that enhance the risk but do so with a sharp dose-response relationship and a threshold that often is quite high.

Toby G. Rossman has done research on the mechanisms of action of arsenic compounds as found in drinking water [Mutat Res 478, 159 (2001)]. It was demonstrated clearly that arsenite (the likely carcinogenic form of arsenic) does not react with DNA to cause mutations and is not genotoxic in several tests. Rather, it appears to operate by inhibiting DNA repair and increasing cell proliferation (growth). In a model of skin cancer in mice irradiated with ultraviolet light, arsenite alone in drinking water [at a concentration more than 10 times the current allowable level (50 ppb)] caused no tumors at any site, but it enhanced the effect of solar UV.

This means that without a genotoxic carcinogenic partner, arsenite would likely have no effect at concentrations found in U.S. drinking water. In those instances where exposure to high levels of arsenic has led to cancer, the question needs to be asked as to the associated genotoxic carcinogenic partner. For skin cancer, it is likely exposure to UV light. For lung cancer, it is likely exposure to tobacco smoke, and for other types of cancer, the associated genotoxic carcinogens need to be evaluated and, if possible, eliminated.

Based on these concepts, which have a solid scientific foundation, it can be suggested that the risk analysis for arsenic in drinking water should not be based on a linear extrapolation with no threshold. The data suggest that the current level of 50 ppb arsenic in water has not been proven to be a cancer risk. It is not clear that there is need to make great public expenditures to reduce naturally occurring arsenic in water in the U.S. to a level of 10 ppb.

— Toby G. Rossman, New York University School of Medicine, Tuxedo, NY
— John H. Weisburger, American Health Foundation, Valhalla, NY

The report of the National Research Council of the National Academy of Sciences on the cancer risks of arsenic used a linear no-threshold model, that is, they disregarded the evidence cited by Rossman and Weisburger. Even accepting (which we do not) the NRC estimates that the lifetime risk for bladder and lung cancer from drinking water with 3 ppb arsenic is about 1 in 1000, however, the cost of reducing naturally occurring arsenic in small Western public water systems to 10 ppb could run about $6,500,000 per assumed avoided cancer case, which is very expensive compared to other public health and safety measures.2 Taking into account that there is a lag time between the rule’s implementation and the time in which the purported benefits will begin to emerge (the latency period for cancer is several years to a few decades), the cost is even greater, because we have to pay now for benefits we won’t get (if we get them at all) for a long time.3 The EPA did a cost-benefit analysis on the new rule and determined that the cost for the 10 ppb standard would be about $200 million annually, while the benefits would be about $170 million annually. The EPA asserted that nonquantitative benefits of the new standard would outweigh the $30 million net cost.4

There are other scientific questions to be answered here. For example, the Nevada town of Fallon has a naturally occurring level of arsenic of 100 ppb in its drinking water. This is a town where people have been living for 135 years. Though there has been considerable study to date of the cancer incidence in this population, there has been no increased incidence of any of the arsenic-associated cancers. According to the absurd NRC extrapolations, about 2% of the Fallon residents should be dying of additional arsenic-related cancers, an easily detectible increase. It is fraudulent for the NRC bureaucrats to ignore the fact that this is not happening. Finally, there is no constitutional authority under the Commerce Clause or elsewhere for the federals to regulate the amount of arsenic in Fallon’s water, though the Commerce Clause does provide authority to ban the sale of such water to parties in other states, Indian tribes, or foreign nations.

There is a political question as well. It has been the goal of rabid environmentalists to clear humans off the sparsely populated lands of the West – what is sometimes called “rural cleansing.” The practice of increasing environmental costs to small communities to make it difficult or impossible to maintain communities in the rural West is part of this strategy. In this instance, there is the further strategy of making some federal money available to these small communities to “help” them to pay the large costs for the unnecessary reduction of arsenic in the drinking water, with the result that the small communities become dependent upon the federal government and can be intimidated into doing anything desired by the federals, including surrendering the rights of locals.

We live in a small town with 12 ppb of arsenic in its drinking water (obtained from the town’s own wells). We would not be concerned if the level were 100 ppb, as in Fallon. What does concern us is Washington, DC making decisions for us about our own drinking water and doing so for its own political benefit, not for our health.


  1. Rossman and Weisburger, “Arsenic in water,” Chem & Eng News August 6, 2001, p.2.
  2. Hogue, “Arsenic debate: it’s all about cost,” Chem & Eng News Oct. 15, 2001, pp.20-21.
  3. Burnett and Hahn, “A costly benefit,” Regulation 24(3):44-9, Fall 2001.
  4. “The arsenic controversy,” Regulation 24(3):42, Fall 2001.



One thing that has especially struck us about the federal government’s response to the anthrax threat and the subsequent realization of the threat of smallpox is the government’s attempt to monopolize health choices to determine who will and who won’t get access to various vaccines and medicines. The government stockpiles supplies, and then some czar decides who gets them. It was nice, therefore, to hear Senator Arlen Specter say on C-SPAN today (11/2/01) that the government should not interfere with the distribution of smallpox vaccine and should accept that individuals (not the government) will decide whether to buy it and use it.

It’s about time that individuals come into the “war on terrorism” to protect themselves. The government has responded inappropriately to a decentralized threat: bioterrorism. If more security is needed at airports, then those who want it should pay for it. One inexpensive approach is to let crew members carry guns. Passengers will ultimately have to pay for additional security in their air fares. (And, yes, we do expect that fewer people will want to fly, but that is what happens when things cost more, and why should people think that expensive security is free or that companies whose products are not wanted should be bailed out at taxpayer expense? In a free market system, those who want to benefit from goods or services pay for them.)

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