June 2003 Blog with Durk and Sandy

The human brain is not an organ of thinking but an organ of survival, like claw and fangs. It is made in such a way as to make us accept as truth that which is only advantage.

— Albert Szent-Györgi

But how can it be an advantage if it is not true?

— Sandy Shaw

Knowledge will forever govern ignorance. And a people who mean to be their own governors must arm themselves with the power which knowledge gives.

— James Madison



The FDA continues on its collision course with personal freedom. The agency has now released a 547-page proposal for Good Manufacturing Practices (GMPs) for the dietary supplement industry and requested public comments. The proposed rules include registration of every facility that manufactures dietary supplements with the FDA and permits FDA warrantless inspections (whatever happened to the Fourth Amendment?), presumably anytime they want to during regular business hours. They tell you how to design your plant, where to put your toilets, what quality control procedures to use, and how to store your products. There’s more, much more.

As we see it, there are several purposes of these GMPs: (1) to serve the interests of the FDA’s most important “clients,” the pharmaceutical companies, since the GMPs will reduce competition from dietary supplements by drastically increasing the cost of their production and, hence, their sales price; (2) to serve the interests of the few large dietary supplement companies—large companies are defined as those with 500 or more employees—that have pushed for GMPs because, among other things, the costs imposed by the GMPs eliminate competition by small companies (there are thousands of them) by driving many out of business or, at the least, making their products much more expensive; (3) to stop the troublemakers (all affiliated with small dietary supplement companies) who keep suing the FDA and winning for First Amendment violations, by drastically increasing their business expenses or driving them out of business. With the GMPs in place, the FDA will have dietary supplement companies under their thumb, with the constant threat of inspections, harassment, and fines, thus shutting up previously defiant voices. You will be able to read and download the public comments we and others filed on the proposed GMPs at www.emord.com soon after June 11 (the filing deadline).

Most of the myriad proposed rules and regulations in the new GMPs have nothing to do with health and safety, but with reducing competition. Of course, a group of us is once more filing public comments. We cannot stop the institution of GMPs, but we hope to modulate them with our comments. Although there is no overriding constitutional right that we can use to defend ourselves from centralized economic planning (such as federal GMPs), since limitations of federal regulation under the Commerce Clause and the requirements for warrants based upon probable cause under the Fourth Amendment have been drastically narrowed from original constitutional intent, we still have some potentially powerful arguments to use to modify the proposed rules. One is that the statute (the Dietary Supplement Health and Education Act of 1994) under which the FDA was authorized to develop and enforce GMPs required that they be no more onerous than the GMPs for foods. Yet the new GMPs are more like those for prescription drugs than for foods.

We also think the timing for the release of the GMPs is highly suspicious. The DSHEA, passed in 1994, contained a provision whereby Congress authorized the FDA to develop and implement a system of Good Manufacturing Practices. Yet nothing had happened for nine years. Then, suddenly, the FDA releases them. Well, coincidently (or not), just before the FDA released these GMPs, our group had filed an appeal of a federal district court ruling in our new lawsuit in which we challenged the constitutionality (under the First Amendment) of the FDA’s prohibiting “treatment” claims on dietary supplements. The 1994 statute clearly provided for claims for dietary supplements on any nutrient-disease relationship.

But even if the statute didn’t intend to allow for treatment claims and even if the Congress decided to amend the statute to explicitly prohibit “treatment” claims, neither the FDA nor the Congress can prohibit the communication of truthful, nonmisleading information (about treatments or anything else) and be in compliance with the First Amendment. As we see it and as the Courts have interpreted it, that Amendment prohibits the government from reserving the right to communicate certain kinds of information only to people of the government’s choice. Naturally, that has frightened the FDA because, if they lose, it will mean the end of most of their current control paradigm over medicine, and it will also mean the end of pharmaceutical companies being willing to pay them hundreds of millions of dollars a year in exchange for a monopoly on treatment claims. Regardless of what happens with the GMPs, the group of us will do our best to pursue this treatment-claims case to the U.S. Supreme Court, where it is sure to be decided. Our case is strong. The determining factor will probably be whether the Justices are willing to live with the consequences in this case of supporting the First Amendment.

This suit will, however, be our most costly endeavor yet. Our attorney, Jonathan Emord, has estimated the total cost to be about $500,000. We will need to raise money. Follow the suit by visiting www.emord.com. You can help change the world by donating any amount to the Durk Pearson & Sandy Shaw Litigation Fund; send it to Pearson & Shaw Litigation Fund, c/o Emord & Associates, 5282 Lyngate Court, Burke, VA 22015.


Another issue that has taken up much of our time has been our personally researching, writing, and filing public comments on the issue of whether the EPA and the Army Corps of Engineers can regulate bodies of water entirely intrastate with no connection with “navigable waters” (the original basis for being a “water of the United States”) and with only small or no effects upon interstate commerce. In preparation for this, we read several recent U.S. Supreme Court decisions, including especially U.S. v. Lopez (1995), U.S. v. Morrison (2000), and Solid Waste Agency v. Army Corps of Engineers, No. 99-1178.

The problem with the EPA or the Army Corps of Engineers or any federal agency regulating intrastate waters is that, under our federal system, ownership and use of intrastate water is to be regulated by the states. The above U.S. Supreme Court cases clarify under what conditions the federal government may regulate intrastate bodies of water under the Commerce Clause (which authorizes the federal government to regulate trade between the states) and makes it clear that it may do so only when there is a “significant effect” on interstate commerce. That leaves a great deal of water that the feds cannot touch under the Commerce Clause, the supposed justification in Solid Waste Agency for regulating entirely intrastate wetlands, swamps, ponds, puddles, intermittently wet places, and even (in the case of Solid Waste Agency) an abandoned gravel pit. Yes, the federals would like to command and control everybody who owns a creek, spring, pond, or (yes) abandoned gravel pit, but fortunately the Constitution’s Commerce Clause and the U.S. Supreme Court’s rulings on it do provide limitations to how far they can go. Sorry, we have no Web site at present that we can direct you to read and download our 23 pages and one exhibit of comments.

Why bother? As we have mentioned before, when you provide public comments in response to an agency’s Federal Register request for comments on rules and regulations, you can go directly to the federal courts if the agency doesn’t deal with your objections rather than having to “exhaust your administrative remedies” by appearing before the administrative courts (where the “judges” are paid by the agency and any fines these “judges” impose are received by the agency—talk about a conflict of interest!)—you could spend millions and never get anywhere. (Note: no Pearson & Shaw Litigation Fund money was spent on this.)

The constitutionality of federal regulatory agencies

Recently the California Coastal Commission was declared unconstitutional by the California Supreme Court because it was in violation of the separation of powers—the legislature established it and the executive branch was supposed to execute it, but the legislature was controlling the members. We have long thought that the so-called “independent” agencies established by Congress (such as the FDA and EPA) that are supposed to be part of the executive branch are in violation of the separation of powers (and, hence, unconstitutional) because they exercise executive, judiciary, as well as some legislative powers (owing to the wide discretion given them by Congress). This is not the sort of thing that is likely to be overturned anytime soon, but we have read that Justice Scalia believes that federal agencies like the FDA are unconstitutional. We hope to live a long time, and in that time we will be watching vigilantly for any opportunity to bring this issue to the fore and to help make mincemeat of these unconstitutional agencies.


We have long wished that we could take tetrahydrobiopterin (BH4) as a dietary supplement, because it is a cofactor in many important metabolic processes. For example, it has long been known that pteridine in a reduced state is required as a cofactor in the conversion of phenylalanine to tyrosine, of tyrosine to dopamine and noradrenaline, and of tryptophan to serotonin.1 [The closest we could get to adding tetrahydrobiopterin to our phenylalanine-plus-cofactors formulations was to add folic acid, because our intermediary pathways charts suggested to us over 15 years ago that folic acid might increase the amount of tetrahydrobiopterin. As it turns out, we were pretty close.]

Recent studies have revealed that tetrahydrobiopterin (BH4) is also an essential cofactor required for the activation of nitric oxide synthase (NOS, the enzyme that makes nitric oxide from L-arginine). BH4 transfers electrons to arginine bound to the enzyme as well as stabilizing the active form of NOS and increasing the affinity of arginine for the enzyme. In addition—and this is very important—in the presence of inadequate levels of BH4, NOS becomes “uncoupled” from the production of nitric oxide, instead producing superoxide radicals but no nitric oxide! In animal and human studies, acute and chronic supplementation with BH4 has been shown to improve endothelium-dependent vasodilation.2

It has been suggested that in diseases such as diabetes, hypertension, and atherosclerosis, there is a BH4 deficiency that correlates with decreased NO synthesis and with endothelial dysfunction.3,7 Since, at low levels of BH4, more superoxide radicals are released by NOS, this in itself can explain, at least in part, the deficiency of NO, since NO reacts with superoxide to form peroxynitrite, a powerful oxidant. Thus, low levels of BH4 produce a state that is functionally like that of having almost no endothelial NOS at all, since superoxide radicals are produced, but little or no nitric oxide. Knockout mice lacking endothelial NOS develop hypertension, insulin resistance, hyperlipidemia, and augmented ischemia-reperfusion injury.3

Folate may improve vascular function by mimicking BH4 activity3

A recent paper reports evidence that 5-methyltetrahydrofolate (5-MTHF, the physiological form of folate) directly interacts with NOS to promote NO versus superoxide formation, thus improving endothelial function.4 The authors show that the 5-MTHF binds the active site of NOS and mimics the orientation of tetrahydrobiopterin. (Amazingly, however, the paper did not provide chemical structures for the two substances; hence, if you want to compare the structures yourself, you’ll have to get them somewhere else, such as The Merck Index.) They demonstrated that 5-MTHFsupplementation in BH4-deficient fructose-fed rats restored NO-dependent endothelial function.

While folate is converted to 5-MTHF in healthy persons, there is a common mutation of 5,10-methylenetetrahydrofolate reductase, the enzyme that converts 5,10-methylenetetrahydrofolate to 5-MTHF, that has been reported to be a risk factor for vascular disease.5

These results suggest that folic acid supplementation may provide the protective effects of BH4 in the endothelial NOS system. We are currently recommending 800 mcg of folic acid a day. However, if you want to take more (even pregnant women have been given 5 mg/day for months in clinical studies to prevent neural-tube-defect births), just make sure that you are taking B6 and B12 along with it.

Vitamin C increases tetrahydrobiopterin levels in vitro and in vivo

Another paper6 notes that in cultured endothelial cells, L-ascorbic acid increases NOS activity, possibly via chemical stabilization of tetrahydrobiopterin (BH4). The authors conducted experiments in wild-type (C57BL/6J) and apolipoprotein E (apoE)-deficient mice and found that 26 to 28 weeks of dietary supplementation with vitamin C (1%/kg of chow) resulted in a significantly increased ratio of BH4 to 7,8-BH2/biopterin (an oxidized form of BH4) in aortas of both apoE-deficient and wild-type mice (the apoE-deficient mouse is a commonly used model of human atherosclerosis development). Vitamin C significantly decreased 7,8-BH2/biopterin levels in apoE-deficient mice, while the vitamin increased BH4 levels in wild-type mice without affecting 7,8-BH2/biopterin levels.

We have had vitamin C in our phenylalanine-plus-cofactors formulations for over 15 years because the aromatic amino acid hydroxylation requires vitamin C.


  1. Wurtman and Wurtman, eds. Nutrition and the Brain, Vol 3, p 268 (1979).
  2. Verma et al. Novel cardioprotective effects of tetrahydrobiopterin after anoxia and reoxygenation: identifying cellular targets for pharmacologic manipulation. J Thorac Cardiovasc Surg 123(6):1074-83 (2002).
  3. Vasquez-Vivar et al. The role of tetrahydrobiopterin in superoxide generation from eNOS: enzymology and physiological implications. Free Rad Res37(2):121-7 (2003).
  4. Hyndman et al. Interaction of 5-methyltetrahydrofolate and tetrahydrobiopterin on endothelial function. Am J Physiol Heart Circ Physiol 282:H2167-72 (2002).
  5. Verhaar et al. Folates and cardiovascular disease. Arterioscler Throm Vasc Biol22:6-13 (2002).
  6. d’Uscio et al. Long-term vitamin C treatment increases vascular tetrahydrobiopterin levels and nitric oxide synthase activity. Circ Res 92:88-95 (2003).
  7. Landmesser et al. Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in hypertension. J Clin Invest 111(8):1201-9 (2003)


. . . Czeisler found that subjects who fall asleep when their body temperature is low tend to sleep for short periods, whereas those who fall asleep when their temperature is high will sleep for long periods. Moreover, the relationship between sleep duration and sleep-onset time relative to the temperature cycle is discontinuous. Several hours after the body temperature reaches its low point, sleep duration jumps abruptly from very short periods to very long ones, then slowly decreases back to short durations. This gradual descent leads to the surprising effect that if you stay awake longer than usual and go to sleep later in your body’s temperature cycle, you tend to sleep less, even though you may be exhausted from a late-night party.— J. J. Collins, in a review of Steven Strogatz,
Sync: The Emerging Science of Spontaneous Order
Hyperion/Allen Lane, 2003
Nature 422:117-118 (2003)


Lung cancer is the leading cause of cancer death for Taiwanese women, even though fewer than 10% of Taiwanese women smoke. A recent study of nonsmoking women who lived with a smoking husband indicated a 30% higher risk for lung cancer than those with a nonsmoking husband, but the relationship was not significant. However, the researchers found that there was a significant relationship for women who prepared meals in a kitchen without a fume vacuum and who heated oil to a high temperature. A recent paper1 reports that benzo[a]pyrene-7,8-diol-9,10-epoxide N-2 deoxyguanosine (BPDE-N-2-dG) adduct was identified as the major bulky DNA adduct after treatment of human lung adenocarcinoma CL-3 cells with cooking oil fumes (COF) from frying fish and that this adduct has been linked with the p53 (a tumor-suppressor gene) hot-spot mutation in human lung tumors. Thus, the authors propose that BPDE-N-2-dG in cooking oil fumes may play an important role in lung cancer development of nonsmoking Taiwanese women.

The researchers cite a recent epidemiological study that shows a significant inverse relation between lung cancer risk and the flavonoid quercetin found in foods such as onions and apples. Quercetin may reduce DNA damage caused by hydrogen peroxide and benzo[a]pyrene and NFkappaB binding activity. Quercetin was found to effectively suppress COX2 (cyclooxygenase-2) the activation of which has been associated with the development of many cancers) in colon cancer cells. The results of their study demonstrated that quercetin inhibited not only cooking oil fume-induced COX2 expression but also cooking oil fume-induced CYP1A1 (cytochrome P450 1A1) transcription.

Quercetin, like most antioxidants, can become a pro-oxidant and mutagen in excessive quantities.


  1. Lin et al. Protection by quercetin against cooking oil fumes-induced DNA damage in human lung adenocarcinoma CL-3 cells: role of COX2. Nutr Cancer44(1):95-101 (2002).


The Spanish flu epidemic of 1918 killed 20–30,000,000 people (probably a low estimate). The mortality rate was about 2.5%. Of course, nobody really knows whether it was actually a form of influenza or some other virus. Although samples of tissue from Spanish flu victims that were stored have been examined, and cadavers buried in permafrost have even been dug up, nobody has been able to isolate any influenza sequences by PCR. Many viruses have symptoms that can be described as flulike.

A recent paper1 reports, however, that influenza infections are characterized by decreased levels of intracellular glutathione and that people with low levels of this antioxidant are more susceptible to infection. In fact, many viruses cause oxidative stress, with decreases in intracellular glutathione, including, for example, Sendai virus, HIV virus, and herpes simplex virus type 1.

In this study, researchers found that glutathione significantly inhibited production of active influenza virus, both in cell cultures (MDCK cells) and in a normal human small-airway-epithelial cell line. They also added supplemental glutathione (50 mM) to the drinking water of female Balb/c mice inoculated with influenza and found that it inhibited viral titer in trachea and lung.

The dose of influenza used to treat the mice was not lethal; none of the mice died during the experiment. The glutathione was found not to exert its effects on active virus production by preservation of the total lung glutathione content. The authors suggest that the glutathione probably had an effect in the oral, nasal, or upper-airway epithelium.

The limiting factor in the body’s manufacture of glutathione is the amino acid cysteine. In fact, a clinical trial with 262 subjects who were given a continuous supplement of N-acetylcysteine (600 mg twice daily) for six months showed significant protection against flulike symptoms, although (the authors note) N-acetylcysteine may not protect the rate of infection per se.1 The way that N-acetylcysteine is used by the body to make glutathione requires that it be deacetylated to cysteine. We take cysteine supplements ourselves as part of our daily personal regimen. See our discussion in this newsletter (Vol. 5 No. 5, Oct. 2002) on why we use cysteine rather than N-acetylcysteine.

The researchers suggest that glutathione “provides an alternate [to antiviral drugs] strategy to limiting influenza infection.”

Vitamin C helps prevent cysteine from being oxidized to insoluble cystine in your kidneys and urinary bladder.


  1. Cai et al. Inhibition of influenza infection by glutathione. Free Rad Biol Med34(7):928-36 (2003)


As a result of immense expenditures, air pollution has been greatly decreased in the United States. Nevertheless, it is always possible to improve what has already been improved at great additional cost, and there are those who propose to spend lots of other people’s money to do it. We examine here the problems posed by air pollution to a particularly vulnerable population group and how those problems might be solved more cost-effectively with dietary n-3 fatty acids (omega-3 fatty acids, or fish oils).

A recent study1 reports that air pollution episodes have been associated with increased cardiovascular hospital admissions and mortality. The researchers tested the hypothesis that patients with a history of serious arrhythmia who had, as a result, implanted cardioverter defibrillators experience potentially life-threatening arrhythmias after such air pollution episodes. Their results indicated that elevated levels of nitrogen dioxide, carbon monoxide, black carbon, and fine-particle mass are associated with potentially life-threatening arrhythmias, leading to automatic therapeutic interventions by an implanted cardioverter defibrillator.

In a second paper,2 researchers studied the association between ambient pollution levels and cardiovascular function in 21 active Boston residents aged 53 to 87 years, observing each up to 12 times from June to September 1997. The protocol involved 25 minutes per week of continuous Holter ECG monitoring, including 5 minutes of rest, 5 minutes of standing, 5 minutes of exercise outdoors, 5 minutes of recovery, and 20 cycles of slow breathing. Heart-rate variability was assessed. Mean 4-hour PM(2.5) (particles with aerodynamic diameter less than or equal to 2.5 µm) ranged from 3 to 49 µg/m(3); one-hour ozone levels ranged from 1 to 77 ppb. The authors concluded that the particles and ozone exposure may decrease vagal (cholinergic) nerve tone, resulting in reduced heart-rate variability. Reduced heart-rate variability is a strong risk factor for potentially fatal cardiac arrhythmias.

There is a large and growing body of scientific literature showing that n-3 fatty acids (also called omega-3 fatty acids) from fish oils are effective in animal and human studies in combating arrhythmias and improving heart-rate variability.3-11 We would like to see a study similar to the one done in the paragraph above except that the participants would be supplemented with 1–2 g of EPA/DHA daily. It would be particularly interesting to see what the protective effective of EPA/DHA might be during periods of exceptionally bad pollution.


  1. Peters et al. Air pollution and incidence of cardiac arrhythmia. Epidemiology11(1):11-17 (2000).
  2. Gold et al. Ambient pollution and heart rate variability. Circulation 101:1267-73 (2000).
  3. Siscovick et al. Dietary intake and cell membrane levels of long chain n-3 polyunsaturated fatty acids and the risk of primary cardiac arrest J Am Med Assoc 274:1363-7 (1995).
  4. Sellmayer et al. Am J Cardiol 76(12):974-7 (1995).
  5. Riemersma and Sargent. Dietary fish oil and ischaemic arrhythmias. J Int Med225(Suppl 1):111-6 (1989).
  6. Christensen et al. Heart rate variability and fatty acid content of blood cell membranes: a dose-response study with n-3 fatty acids. Am J Clin Nutr 70:331-7 (1999).
  7. Leaf et al. n-3 Fatty acids in the prevention of cardiac arrhythmias. Lipids34:S187-9 (1999).
  8. Christensen et al. n-3 Fatty acids and the risk of sudden cardiac death assessed by 24-hour heart rate variability. Lipids 34:S197 (1999).
  9. Albert et al. Blood levels of long-chain n-3 fatty acids and the risk of sudden death. N Engl J Med 346(15):1113-8 (2002).
  10. Jones and Lau. Effect of n-3 polyunsaturated fatty acids on risk reduction of sudden death. Nutr Rev 60(12):407-9 (2002).
  11. Sheard. Fish consumption and risk of sudden cardiac death. Nutr Rev 56(6):177-9 (1998).


People who want to work from home in Belgium must clean their house every day and are obliged to take a shower after a day’s work, have separate toilets for men and women, and post notices stating that it is forbidden to spit. Alcohol in a house is also strictly prohibited.— Radio Vlaanderen International, as reported in Liberty

Comment: One wonders how the EUcrats enforce all this. Do they send inspectors to check how clean your house is or whether your body smells clean? Do they do DNA analyses for the spit? When regulations seem bad here, we just think about the EU . . . .


Malaria continues to be a very serious health problem in less developed countries where there are large populations of mosquitoes to spread the disease. (Early in the history of the United States, there was a serious problem with malaria, too, until swamps supporting the responsible mosquito populations were drained. We dread to think what will be happening in Florida when and if the restoration of the Everglades swamp system is undertaken. During the nineteenth century, malaria was found as far north as Chicago. As a child in Chicago, Durk read about and saw massive areas of swamps that had been drained and filled with soil to suppress the dangerous mosquito populations. It was a massive public health mega-engineering project, he says; one of the results of the work is that to this day the Chicago River runs backward.)

The most serious complication of malaria is cerebral malaria. A new study1 reports that in children with cerebral malaria, there is low plasma arginine concentration and decreased nitric oxide production. In fact, the same authors earlier showed plasma arginine and nitric oxide production inversely associated with the severity of malaria, with the lowest levels found in cerebral malaria. Low arginine plasma concentration was associated with death in individuals with cerebral malaria.

As the authors note, NO has antiparasitic effects. Apparently, arginine levels are depleted by the large amounts of NO made to fight the parasitic infection. When arginine levels are low, nitric oxide synthase (NOS) is “uncoupled” from the production of nitric oxide, producing superoxide radicals but little or no nitric oxide. Hence, low arginine levels can result in low nitric oxide production and greatly increased oxidative stress through the increase in superoxide and peroxynitrite (the reaction product of nitric oxide and superoxide).

The authors suggest, “Clinical trials are warranted to ascertain whether or not correction of L-arginine deficiency provides adjunctive prophylactic and therapeutic benefit in malaria.” We agree. Since NOS is activated by the neurotransmitter acetylcholine, we would also add choline and B5 to the arginine, as in the formulation we have been using for about 20 years.


  1. Lopansri et al. Low plasma arginine concentrations in children with cerebral malaria and decreased nitric oxide production. Lancet 361:676-8 (2003).

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