April 2003 Blog with Durk and Sandy

It is the purpose of the First Amendment to preserve an uninhibited marketplace of ideas in which truth will ultimately prevail.

— Byron White, U.S. Supreme Court Justice, 1917–2002

The illegal we do immediately. The unconstitutional takes a bit longer.

— Henry Kissinger

Nothing could so completely divest us of . . . liberty as the establishment of the opinion that the state has a perpetual right to the services of all its members.

— Thomas Jefferson


New victory

On December 23, 2002, the U.S. District Court for the District of Columbia ruled that the FDA’s suppression of a health claim that “antioxidant vitamins may reduce the risk of certain kinds of cancer” is unconstitutional. [This is the second time we have won this decision in the courts. Remember, the court of appeals (Jan. 19, 1999) had already ruled that the suppression of this health claim, as well as three others, was unconstitutional.] The judge for the district court ordered the FDA to draft one or more “short, succinct, and accurate” disclaimers from which we might choose, to accompany our antioxidant vitamin claim. The FDA provided three choices. The one that the two of us chose was, “Some scientific evidence suggests that consumption of antioxidant vitamins may reduce the risk of certain forms of cancer. However, the FDA has determined that this evidence is limited and not conclusive.” The great virtue of this disclaimer is that it clearly distinguishes between the statement of scientific fact and the opinion of the FDA.

The defeat

On January 3, 2003, the U.S. District Court for the District of Columbia upheld the FDA’s refusal to process a health claim for saw palmetto [“Consumption of 320 mg daily of saw palmetto extract may improve urine flow, reduce nocturia, and reduce voiding urgency associated with mild benign prostatic hyperplasia (BPH).”] The FDA deems this claim to be a “treatment” claim, not a health claim, and therefore the FDA need not review the claim under the Food Drug and Cosmetic Act’s (FDCA) dietary supplement health claim provision. In order to use this “treatment” claim for saw palmetto, we would have to get the FDA’s drug approval—at a cost of at least $50,000,000 for an unpatentable product. The saw palmetto “treatment” speech is virtually prohibited under these conditions.

We disagree. The FDCA’s dietary supplement health provisions refer to a health claim as one that “characterizes the relationship of any nutrient . . . to a disease or a health-related condition.” This language clearly allows for the saw palmetto claim and other similar “treatment” claims. The district court ruled that the court had to give the FDA “deference” in its decision to exclude claims of an effect of a supplement on an existing disease under the health claims definition. This is incorrect. The U.S. Supreme Court has ruled that an agency cannot be given deference when a constitutional issue is at stake: “Where an administrative interpretation of a statute would raise serious constitutional problems, the court will construe the statute to avoid such problems unless the construction is plainly contrary to Congress’ intent.” Solid Waste Agency of Northern Cook County v. United States Army Corps of Engineers et al., No. 99-1178, decided January 9, 2001.

The district court refused to evaluate the FDA’s suppression of the FDA’s decision under the applicable First Amendment commercial speech standard (the four-pronged Central Hudson test) because, the court held, the claim proposed by the plaintiffs was “illegal” and therefore, since only truthful speech concerning legal products is protected speech under the First Amendment, need not be evaluated under the First Amendment standard. This is an immense legal error. Under this sort of reasoning, all commercial applications of the First Amendment could be eliminated by simply declaring that the speech itself was “illegal.” Moreover, we had entered into evidence a letter from the FDA stating unequivocally that saw palmetto is a legal dietary supplement, so long as no health claims are made. Hence, this is a pure First Amendment issue. You can get a copy of the district court’s decision by contacting Katie Bond at 202-466- 6937.

The appeal

In order to expand the universe of health claims to include “treatment” claims (e.g., where a supplement affects an existing disease), we have filed a notice of appeal concerning this decision to the U.S. Court of Appeals for the District of Columbia. Keep in mind that being able to offer dietary supplements for the treatment of existing diseases is a very serious disruption to the FDA’s current drug monopoly approval process, in which “treatment” speech is reserved only for the use of companies producing certain products (drugs), which requires the payment of immense sums to go through the FDA’s drug approval process and pay the FDA’s “user fees,” which will total about $200,000,000 in 2004. However, under the First Amendment, the government is explicitly denied any authority to “reserve” the communication of certain truthful information only to certain government-preferred people. The prevention of just that sort of government-granted speech privilege was one of the main purposes of the First Amendment.

There can be no doubt that if we win this appeal, the FDA will appeal to the U.S. Supreme Court. They have no choice if they wish to retain their current monopoly-granting power over speech concerning medical therapies. If we lose the appeal, we will appeal to the U.S. Supreme Court. Hence, the next three or four years, until this case is finally decided, will cost us and our coplaintiffs about $500,000. Yet somebody has to do it, and, if not us, who? We’ve got very strong arguments and a brilliant attorney. What else do we need? More money. If there are those of you out there with ideas on how to raise money for this important cause, please contact us c/o this magazine or Web site. If anyone wants to help, you can do so by sending any size donation (small donations add up, you know) to: The Pearson & Shaw FDA Litigation Fund, c/o Emord & Associates, 5282 Lyngate Court, Burke, VA 22015.


Last issue, in our article Why Antioxidants Do Not Necessarily Prevent Aging Due to Free Radicals, we discussed how the generation of free radicals by mitochondria appears to be of much more importance in determining maximum lifespan than tissue antioxidant capacity. In other words, you get more protection from mechanisms that reduce the generation of free radicals in the first place than you do from those that simply sop up the radicals after they have been generated.

This brings us to the topic of this article: preconditioning. Preconditioning is a process in which undergoing a free radical stress at the right time and in the right amount results in a substantial increase in protection against later free radical-initiated damage. Brief periods of heat shock are an example of preconditioning, by upregulating processes that protect against later heat and oxidative stress, and providing cardioprotection. On the other hand, taking a free radical-scavenging supplement at the wrong time can actually reduce or eliminate protection against free radicals that would have occurred otherwise. The reason for these different results is that free radicals are not just bad guys that cause damage. They are important signaling elements in oxidant pathways that change the expression of protective genes and their products.

A new paper1 explains how the protective effects of alcohol are initiated via an oxidant-dependent signaling pathway and how the use of antioxidant supplements at the wrong time can block these protective effects. We have found this paper to be of great practical help in deciding when we drink wine during the day.

The paper starts off by noting that tissues can be preconditioned to resist the deleterious effects (largely free radical-caused) of prolonged ischemia followed by reperfusion (such as occurs during heart attacks and strokes) by short previous exposure to stimuli such as brief periods of vascular occlusion, adenosine, nitric oxide donors, endotoxin derivatives, and oxidants. They note that recent work has shown that consumption of ethanol at low to moderate amounts also causes the inducement of anti-inflammatory preconditioned states that limit both short-term and longer-term ischemia/reperfusion injury. Some of the details of this preconditioning pathway have been discovered, such as the involvement in the protective effects of a single dose on isolated myocytes or intact hearts of protein kinase C-epsilon and ATP-sensitive potassium channels, but not adenosine or oxidants.

Although oxidants seem to play no role in the early phase (one hour after ethanol ingestion in mice) of ethanol preconditioning, they seem to be important signaling elements in the second window of protection (24 hours after ethanol ingestion). Ethanol increases tissue levels of the oxidant-producing enzyme xanthine oxidase. The researchers studied whether this or the oxidant enzyme NAD(P)H oxidase might be the source of the reactive oxygen species that cause the late-phase ethanol preconditioning. In fact, concurrent antioxidant treatment actually completely abolished this late-phase ethanol protection.

The results of these studies showed that oxidants produced as a result of xanthine oxidase and NAD(P)H oxidase that trigger the late ethanol preconditioning are formed during the time frame during which ethanol is elevated in the plasma (i.e., the first 60 minutes after ethanol administration by gavage—stomach tube—in C57BL/6 mice). If antioxidants were given at the same time as alcohol, the effectiveness of late ethanol preconditioning was attenuated, whereas antioxidants given after the first hour following alcohol ingestion had no effect on this later preconditioning. The researchers conclude that the oxidant pathway responsible for this preconditioning occurs during the first hour after alcohol ingestion.

Mice metabolize alcohol much more quickly than humans. Hence, it might be necessary to wait 2 or even 3 hours after drinking alcohol before you take antioxidant supplements in order to get the protective alcohol effects. There was no mouse experiment reported as to when antioxidants could be taken before alcohol ingestion in order to avoid attenuating the alcohol-protective effects. Our guess would be that you should wait about 4 hours after taking antioxidant supplements before drinking alcohol for greatest benefit. For example, Durk takes his allopurinol, a xanthine oxidase inhibitor that protects him from familial gout, at bedtime 3 or 4 hours after drinking wine. Yes, it does require a certain amount of planning when you drink alcohol for best effect.

Resveratrol, a polyphenolic constituent of grapes and, hence, of wine, has also been recently shown to provide pharmacological preconditioning to protect the heart from ischemic-reperfusion injury by upregulating nitric oxide.2


  1. Yamaguchi et al. Late preconditioning by ethanol is initiated via an oxidant-dependent signaling pathway. Free Rad Biol Med 34(3):365-76 (2003).
  2. Hattori et al. Pharmacological preconditioning with resveratrol: role of nitric oxide. Am J Physiol Heart Circ Physiol 282:H1988-95 (2002).


The “French Paradox” is the way some people express the need to explain why the mortality rate for coronary artery disease in France is only about 50% compared with other European countries and the U.S., despite similar intakes of animal fats. It has been argued that higher wine consumption by the French might explain these mortality differences. Researchers now report1 that cellular signals initiated by the platelet-derived growth factor beta receptor (betaPDGFR), which plays a critical role in the pathogenesis of atherosclerosis, are inhibited by red wine, but not white wine.

The authors explain that flavonoids of the catechin family found in red wine potently inhibit the PDGF-dependent tyrosine phosphorylation of the betaPDGFR at concentrations found in wine. They note that the inhibitory effects of each catechin are less potent than red wine, but appear to be additive. White wine did not inhibit betaPDGFR signaling and PDGF-dependent DNA synthesis, but “flavonoid-enriched” white wine (made by incubating white wine in various concentrations of shredded grape seeds for 96 hours) did.

In conclusion, red wine, but not white wine, specifically inhibits betaPDGFR signaling, PDGF-dependent proliferation, and migration of VSMC (vascular smooth muscle cells). The researchers also report that recent studies have shown that catechins are largely bioavailable after red wine intake. Concentrations of red wine catechins shown to inhibit the betaPDGFR in vitro (~400 mcg/l) correlate with the serum levels of catechin after red wine consumption in humans (up to 600 mcg/l). Also, in apolipoprotein E-deficient mice (a model for human atherosclerosis), oral ingestion of red wine, catechin, or a mixture of various catechins led to a reduction of atherosclerotic lesion areas of 48%, 39%, and 23%, respectively.


  1. Rosenkranz et al. Inhibition of the PDGF receptor by red wine flavonoids provides a molecular explanation for the “French paradox.” FASEB J (Oct. 18, 2002)


A new paper1 reports another mechanism that may play an important role in red wine’s cardiovascular protective effects. Researchers report that in human endothelial cells treated with red wine, there was an upregulation of endothelial nitric oxide synthase (eNOS) mRNA and eNOS protein expression. The endothelial cells treated with the red wines produced up to three times more bioactive nitric oxide (NO) than did control cells.

The NO produced by endothelial NOS (eNOS) acts as a vasodilator, allowing arteries to expand in size when necessary to increase blood flow. In fact, the first sign of developing atherosclerosis (even before the development of a fatty streak) is a failure of arterial dilation in response to acetylcholine (which is called endothelial dysfunction), a failure of NO production and/or release. NO also decreases the expression of adhesion molecules and of platelet-derived growth factors that stimulate proliferation of smooth muscle cells, and it inhibits platelet aggregation, among other effects.

P.S. The authors made a point of mentioning that they used red wine from France, so we are passing that along, but we see no reason to suppose that French red wine is superior to, say, Californian, Italian, Argentinean, Chilean, or Australian red wine.


  1. Wallerath et al. Red wine increases the expression of human endothelial nitric oxide synthase. J Am Coll Cardiol 41(3):471-8 (2003). Our thanks to Will Block for sending us this paper.


There is evidence that IGF-1 (insulinlike growth factor 1) signaling may play a role in certain cancers (such as prostate, breast, lung, and colorectal in women) by acting as a mitogen (a substance that increases cell proliferation) and inhibiting apoptosis (programmed cell death). In observational studies, higher levels of IGF-1 are associated with higher risks of these and possibly other cancers.1 Hence, interfering with IGF-1 signaling, especially if such interference can be localized to high-risk tissues sensitive to its mitogenic effects,2 would be very desirable in terms of reducing cancer risk.

A recent paper8 reports that, in mammary cancer cells, growth stimulation by IGF-1 was markedly reduced by lycopene treatment. The researchers note that these effects were not associated with changes in the number or affinity of IGF-1 receptors, but were a result of an increase in membrane-associated IGF-binding proteins, which were shown previously to negatively regulate IGF-1 receptor activation in different cancer cells. Moreover, they report that lycopene inhibited basal and IGF-induced thymidine incorporation into DNA (as a measure of growth) and slowed cell cycle progression, while not causing cell death. These same authors had previously reported that lycopene inhibited mammary, endometrial, and lung cancer cell growth in a dose-dependent manner; the concentration causing 50% inhibition was approximately 2 microM. The latter inhibition was detected after 24 hours of incubation and was maintained for at least three days.


  1. See, e.g., a review by Yu and Rohan, Role of the insulin-like growth factor family in cancer development and progression. J Natl Cancer Inst 92(18):1472-89 (2000).
  2. On the other hand, IGF-1 has shown protective effects in the pathogenesis of diabetic angiopathy,3 in accelerating muscle and motor neuron regeneration,4 in enhancing DNA accretion and growth in skeletal muscle,5 and possibly in enhancing the removal of amyloid-beta from the brain.6 Recently, transgenic mice (which had one gene for the IGF-1 receptor knocked out, while the other gene was normal) had greater resistance to oxidative stress and lived an average of 26% longer than their wild-type littermates (the 16% increase in lifespan for the male mice was not statistically significant, however; the male mice, but not females, also had abnormal blood glucose regulation).7 Hence, the overall picture for the risk/benefit of IGF-1 is decidedly complex.
  3. Janssen and Lamberts. Circulating IGF-1 and its protective role in the pathogenesis of diabetic angiopathy. Clin Endocrinol 52:1-9 (2000).
  4. Rabinovsky et al. Targeted expression of IGF-1 transgene to skeletal muscle accelerates muscle and motor neuron regeneration. FASEB J (Nov. 1, 2002).
  5. Fiorotto et al. Persistent IGF-1 overexpression in skeletal muscle transiently enhances DNA accretion and growth. FASEB J (Nov. 15, 2002).
  6. Carro et al. Serum insulin-like growth factor 1 regulates brain amyloid-beta levels. Nature Med 8(12):1390-7 (2002). See last issue of this newsletter for discussion.
  7. Holzenberger et al. IGF-1 receptor regulates lifespan and resistance to oxidative stress in mice. Nature 421:182-7 (2003).
  8. Karas et al. Lycopene interferes with cell cycle progression and insulin-like growth factor 1 signaling in mammary cancer cells. Nutr Cancer 36(1):101-111 (2000)


As a number of possible “treatment” health claims for dietary supplements line up to wait for a go-ahead court decision, there are now new reports on the potential use of lycopene as an adjunct treatment for prostate and breast cancer, in addition to its prostate cancer preventive effects.

One study1 reports that of 26 men with newly diagnosed prostate cancer, half received a tomato oleoresin extract containing 30 mg of lycopene (while the other half received no supplement) for three weeks before they received radical prostatectomy. Biomarkers of cell proliferation and apoptosis were assessed in benign and cancerous tissues. After intervention, the subjects receiving supplementation had smaller tumors (80% vs. 45% less than 4 ml), less involvement of surgical margins and/or extraprostatic tissues with cancer (73% vs. 18% organ-confined disease), and less diffuse involvement of the prostate by high-grade prostatic intraepithelial neoplasia (33% vs. 0% focal involvement) compared to those who received no supplementation. The mean plasma prostate-specific antigen levels were lower in the intervention group compared with controls. Thus, the authors conclude, “. . . lycopene may have beneficial effects in prostate cancer.” They recommend larger clinical trials.


  1. Kucuk et al. Effects of lycopene supplementation in patients with localized prostate cancer. Exp Biol Med 227:881-5 (2002)


We have been following the development of a diacylglycerol (DAG) oil in scientific papers and in trade and marketing publications as it has been readied for release in the United States during the past couple of years. Diacylglycerol is a form of long-chain fatty acid esters naturally found in edible oils; the big difference is that diacylglycerols have only two fatty acids per fat molecule, as compared to triacylglycerols (TAG), the most commonly found fats, which have three fatty acids per fat molecule. Natural fats are made up of a glycerol backbone, where the three hydroxyl groups of the glycerol are either each bonded to a fatty acid (TAG), or in which two hydroxyl groups are bonded to a fatty acid (DAG), or where only one hydroxyl group is bonded to a fatty acid (monoglycerides). Because DAG has one less fatty acid than TAG, pure DAG has only about 2/3 of the caloric content of pure TAG. Natural edible oils contain various combinations of TAG and DAG.

Moreover, DAG oil is metabolized differently than TAG. For example, postprandial hypertriglyceridemia (elevated fat in the blood following a meal) was reduced by DAG as compared to TAG in a study of a single ingestion of a lipid emulsion by healthy men.1In an animal study2 of C57BL/6J mice fed a high-DAG or high-TAG diet, the researchers analyzed the expression of genes involved in lipid metabolism at an early stage of obesity development in these mice. They found that the differential effects of DAG may be related to its stimulating effects on intestinal lipid metabolism. In another mouse study,3 researchers found that obesity-prone C57BL/6J mice fed a high-TAG diet for five months had significant increases in body weight, visceral fat accumulation, and circulating insulin and leptin levels compared with mice fed the control diet (5% TAG). Compared with the mice fed the high-TAG diet, the mice fed the high-DAG diet had body weight gain and visceral fat weight reduced by 70% and 79%, respectively. Moreover, circulating leptin and insulin levels were reduced to control levels.

Last year, in a randomized, double blind study, overweight or obese men and women were given food products containing either DAG or TAG, having the same overall fatty acid composition and incorporated into a reduced-energy diet, for 24 weeks4. By the end of the trial, body weight had decreased 3.6% (DAG) and 2.5% (TAG), and fat mass decreased 8.3% (DAG) and 5.6% (TAG). In an earlier double-blind, controlled study,5 38 healthy men (aged 27–49) completed the study. After a run-in period, the subjects were divided into two groups. One group consumed test meals containing DAG-rich oil (10 g/d; actual lipid intake was 43 g/d). The other group received TAG oil. Visceral fat and subcutaneous fat in the abdomen decreased significantly from baseline only in the DAG group. Kao Corporation of Japan first discovered this oil about 15 years ago, when the company was looking for an oil that was more easily digested. The weight loss was an unexpected discovery that resulted from this research. The DAG oil was introduced into Japan in 1999 for weight loss and has been extremely successful, now being the top-selling cooking/salad oil in Japan, with over 80,000,000 bottles sold. Kao formed a partnership with ADM, and ADM has now introduced the oil into the United States as ENOVA, debuting in test markets in Chicago and Atlanta in January 2003. Cleverly, they have priced the oil higher than soybean oil but slightly less than olive oil. The oil is being sold here under the slogan, “Don’t change the way you eat, change your oil.”6 The oil has undergone “all kinds of safety tests in adults, children, people with renal problems, and diabetics,” says Tony DeLio, ADM’s corporate vice president for marketing and external affairs.7

The weight-loss claims (lose one or two pounds a year) are being kept conservative, not only to avoid disappointing consumers but also because individuals are different and because use of the oil may be intermittent or inconsistent.

Because diacylglycerol is an important signaling molecule, it is a good idea to keep an eye on ongoing research, as we are, that is being done to uncover the mechanisms for DAG-induced weight loss and to detect any possible undesirable effects. Not surprisingly, much of this research has been and is being done by Japanese scientists.


  1. Matsuo and Tokimitsu. Metabolic characteristics of diacylglycerol. Inform 12:1098-1102 (2001).
  2. Murase et al. Anti-obesity effect of dietary diacylglycerol in C57BL/6J mice: dietary diacylglycerol stimulates intestinal lipid metabolism. J Lipid Res 43:1312-9 (2002).
  3. Murase et al. Dietary diacylglycerol suppresses high fat and high sucrose diet-induced body fat accumulation in C57BL/6J mice. J Lipid Res 42:372-8 (2001).
  4. Maki et al. Consumption of diacylglycerol oil as part of a reduced-energy diet enhances loss of body weight and fat in comparison with consumption of a triacylglycerol control oil. Am J Clin Nutr 76:1230-6 (2002).
  5. Nagao et al. Dietary diacylglycerol suppresses accumulation of body fat compared to triacylglycerol in men in a double-blind controlled trial. J Nutr130:792-7 (2000).
  6. Dahm. When losing is winning: a revolutionary oil from ADM can help consumers lose a few pounds. STAGNITO’S New Products Magazine, January 2003, pp 26-27.
  7. Watkins. Time for an oil change? Inform 14:70 (2003)


“Canada published new nutrition labeling standards on Jan. 1, 2003. One of the provisions of the new rules was the allowance, for the first time in Canada, of health claims. The only health claims allowed, however, are scientifically established relationships between diet and the reduction in risk of chronic disease, such as sodium and its link to high blood pressure; calcium and vitamin D and the link to osteoporosis; saturated fat and trans-fat and the link to heart disease; and underconsumption of vegetables and fruits and the link to some types of cancer. Not much, but it’s a start. Too bad they don’t have a First Amendment in Canada.”

— Inform, Feb 2003, p 59


The statins are a relatively new class of drugs that are effective in the reduction of cholesterol by inhibiting the rate-limiting enzyme in the synthesis of cholesterol, 3-hydroxy-3-methylglutaryl coenzyme A reductase. Statins also have a number of other effects, including increasing endothelial nitric oxide release.

A new study1 found, by screening human umbilical-vein endothelial cells with complementary DNA microarray for the gene expression modified by homocysteine, that 3-hydroxy-3-methylglutary1 coenzyme A reductase is increased by homocysteine. This, then, appears to be yet another mechanism by which homocysteine increases the risk of cardiovascular disease, in this case by increasing the production of cholesterol.

Moreover, some statins have been found to reduce cardiovascular disease risks more than expected by their effects on cholesterol alone. Perhaps their interference with homocysteine signaling has something to do with this.


  1. Li et al. Homocysteine induces 3-hydroxy-3-methylglutaryl coenzyme A reductase in vascular endothelial cells. Circulation 105:1037-43 (2002)


All forms of alcohol taken in moderation seem to have the same protective effects in observational studies in humans. A new study looked at the effects of short-term moderate beer consumption on plasma circulating fibrinogen in patients who already had coronary atherosclerosis.1 Fibrinogen is a plasma protein that plays a role in blood clotting.

The patients were 48 males between ages 46 and 72 years. They were randomly divided into two groups. Twenty-four of them received, in addition to a Mediterranean-type diet rich in vegetables and fruits, a supplement for 30 days of 330 ml of Maccabee beer (about 20 g of alcohol, which is about the same amount of alcohol found in two glasses of wine). The other 24 ate the same diet but received 330 ml of mineral water instead of beer.

After the 30 days of beer (or mineral water) consumption, only the beer-drinking subjects had improvements in lipid metabolism and antioxidant and anticoagulant activities. The researchers concluded that their findings “indicate that one of the positive benefits of moderate beer consumption is to diminish the production of fibrinogen and its stability, which reduces the potential risk exerted by this protein.”


  1. Gorinstein et al. Structural changes in plasma circulating fibrinogen after moderate beer consumption as determined by electrophoresis and spectroscopy. J Agric Food Chem 51:822-7 (2003)


Neither “property” nor the value of property is a physical thing. Property is a set of defined options . . . It is that set of options which has economic value . . . It is the options, and not the physical things, which are the “property”—economically as well as legally . . . But because the public tends to think of property as tangible, physical things, this opens the way politically for government confiscation of property by forcibly taking away options while leaving the physical objects untouched.

— Thomas Sowell, economist

The above is simply the finest and most explanatory definition of property and property rights (“options”) that we have seen. It is extremely useful in understanding the basis for “takings” (forcible taking away of options by government), which, under the Fifth Amendment of the U.S. Constitution, requires “just compensation” (“. . . nor shall private property be taken for public use without just compensation”).

The purpose of the “takings” clause is not to prevent government regulation of private property, but to ensure that such regulations are restricted only to important public uses by requiring that the public be willing to pay. What reason is there to restrain your wish list when it is paid for by somebody else? Current regulatory regimes routinely forcibly take away options, and just compensation is rarely provided. This creates what is called a “moral hazard,” because it creates strong political incentives to rip off people who own property, such as turning over the use of private property to certain species of animals by declaring it “critical habitat,” without cost or consequences to anybody but the targeted victims. The “takings” clause says, in effect, if the public is not willing to pay for a proposed public benefit, then there can be no government taking of private property for that proposed public benefit.

Full implementation (or not) of the Fifth Amendment’s “takings” clause (and the survival—or not—of private property in America) is currently the focus of immense amounts of resources and political battles, as well as much private litigation. For further information, including the important new rulings that have arisen in the course of a “takings” case currently before the United States Court of Federal Claims, Hage v. United States, see www.stewardsoftherange.org


In a letter to the Dec. 14, 2002 Science News, Rich Norwood of Johnson City, Tennessee, writes, “Since consciousness is spread out across the brain, and since those centers of brain activity cannot communicate faster than the speed of light, ‘now’ is not the hard point in time we usually imagine.” Indeed, since neural impulses travel at about 30 m/s, as compared to 300,000,000 m/s for light, “now” is quite indeterminate.

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