In Thompson v. Western States Medical Center, 535 U.S. 357, 371 (2002), the U.S. Supreme Court “made it clear that if the Government could achieve its interests in a manner that does not restrict speech, or restricts less speech, the government must do so.” Ib. 373: “If the First Amendment means anything, it means that regulating speech must be a last—not a first—resort.”1
1. Our group filed an amicus brief in this case (the decision allows compounding pharmacists to advertise what particular compounds they offer), which we believe was important in making possible this
. . . the increase in body weight in the U.S. is not a recent phenomenon. The average body mass index (BMI) value has been increasing for more than 150 years. A large part of the ‘recent’ obesity epidemic is due to a curve-shifting phenomenon. Now that the right tail of the bell-shaped curve for BMI in the U.S. population has crossed the threshold for obesity (BMI of 30 kg/m2), small increases in average BMI and rightward shifts of the curve mean a sharp increase in the number of people considered obese.— From a book review by Samuel Klein
Journal of Clinical Investigation 113(1):2 (2004)
Scientific knowledge is a body of statements of varying degrees of certainty—some most unsure, some nearly unsure, none absolutely certain.The FDA doesn’t like statements on labels about foods, dietary supplements, and drugs that are not absolutely certain (as determined by them), as it suggests that there might be honest differences of scientific opinion, and, worse yet, some such opinions might be different from the FDA’s. The FDA is supported by some scientists (largely academic and government authoritarian types) who think the public an idiot horde that shouldn’t be “confused” by hearing scientific differences of opinion and, hence, should be given a supposed consensus statement or, as it is sometimes put, the scientific community “speaking with one [political] voice.” It is freedom of speech that is our major protection from that one voice backed by government guns.— Richard Feynman
The whole aim of practical politics is to keep the populace alarmed (and hence clamorous to be led to safety) by menacing it with an endless series of hobgoblins, all of them imaginary.— H. L. Mencken
Two important metabolic pathways use the amino acid arginine as the precursor: the enzyme nitric oxide synthase, which converts arginine to nitric oxide, and citrulline and the enzyme arginase, which converts arginine to ornithine and urea. The latter is part of a pathway for detoxifying ammonia. Ornithine is also part of a proliferative pathway that is involved in cell division and tissue regeneration. Arginase II is the form of arginase that is thought to be involved in the synthesis of polyamines, which control cell proliferation and collagen production. It is most highly expressed in the prostate and kidney.1
There has been considerable recent publication of papers on nitric oxide synthase because of the importance of nitric oxide in functions such as (importantly) vasodilation (endothelial function). Scientists have found that an inadequate supply of arginine or too little of the cofactor tetrahydrobiopterin (which one paper reports may be mimicked by folic acid2) results in an “uncoupling” of nitric oxide synthase from the production of nitric oxide, producing superoxide anion instead. Not only is there a reduction in the production of nitric oxide when nitric oxide synthase is uncoupled, but oxidative stress is greatly increased.
Now, another major mechanism of decreased production of nitric oxide has been reported: an increase in the arginase pathway for the use of arginine. Recent studies have reported increases in arginase in conditions including reperfusion injury,3asthma,4,5 psoriasis,6 arthritis,7 and human breast cancer.8 (Since arginase II is highly expressed in the prostate, it would be interesting to see whether there is increased expression in prostate cancer.) The increased arginase decreases arginine availability to be converted to nitric oxide, as well as increasing ornithine that can be converted into polyamines, procellular proliferation factors.6 In psoriasis, for example, there is hyperproliferation of keratinocytes. In the arthritis paper,7 it was reported that arginase II could be induced ex vivo (outside the body) by inflammatory factors such as PGE2 and LPS (lipopolysaccharide, from bacteria). Ornithine, produced by arginase, is necessary for the production of collagen, which occurs in rheumatoid arthritis.7
Arginase in the brain
Not only is arginine in the brain vital for the manufacture of nitric oxide, it is also used in brain protein synthesis and is the substrate for the production of urea (detoxification of ammonia), creatine, agmatine, glutamic acid, ornithine, proline, and polyamines.9 In a new study,9 caffeine was shown, in Wistar rats given “small doses” of caffeine in their drinking water (2 g/l over the first 3 days to 4 g/l over the last 7 days—however, mice drink far less water in proportion to food than humans do), to decrease arginase activity. The results indicated that caffeine’s inhibitory effect on arginase left more arginine available for use by the nitric oxide synthase pathway.
As the authors9 explained, caffeine is an inhibitor of adenosine receptors, decreasing adenosine bound to its receptors and increasing free adenosine. Adenosine, adenine, inosine, and uric acid are competitive inhibitors of arginase.9 Valine, leucine, isoleucine, and ornithine are also reported to have inhibitory effects on arginase activity.
Caffeine and compounds related to caffeine, such as theophylline and theobromine, increase cellular levels of cyclic AMP that are hypothesized9 to possibly be, at least in part, a reason for caffeine’s depression of arginase activity. We wonder, too, whether the prescription drug pentoxifylline, a prescription methylxanthine drug used in the treatment of poor circulation in the extremities (especially legs), might reduce arginase activity (thus increasing arginine’s availability to be converted to nitric oxide), which (if true) might account for some of the drug’s beneficial effects.
A number of scientists have suggested that the cardioprotective effect of wine, and especially red wine, cannot be explained by the antioxidant effects of its phenolic constituents and that other mechanisms need to be examined. A new paper1 reports such an antioxidant-independent beneficial effect of red wine: it increases the expression of nitric oxide synthase by human endothelial cells in culture. The effects were reported using several French red wines, as noted by the authors, who also report finding little or no effect on endothelial nitric oxide synthase with the German wines they used. The authors (all located in Germany) attributed the differences between the two countries’ wines to the French red wines’ “contain[ing] high polyphenol levels compared with wines from other regions.” We have read elsewhere that red wines from Argentina and Chile are particularly rich in polyphenols. As a rough general rule, the darker the (red) wine, the higher the polyphenol content.
If this effect also occurs in human endothelial cells in vivo, it would mean that for any given amount of arginine available in the bloodstream, more arginine would be used by nitric oxide synthase to produce nitric oxide, thus improving endothelial function. Since arginase and nitric oxide synthase compete for the common substrate arginine, there would be less arginine used by the arginase pathway as compared to that which would occur at a lower level of expression of nitric oxide synthase.
Although there have been several studies suggesting greater weight loss from a high-protein, low-fat diet compared to a high-carbohydrate, low-fat diet, the mechanisms remain undetermined. One small recent study1 (10 healthy, normal-weight, nonsmoking women aged 19–22 years) suggests that postprandial (after-meal) thermogenesis is increased, averaging about 2-fold higher at 2.5 hours postmeal, after the high-protein, low fat-meal as compared to the high-carbohydrate, low-fat meal.
In a randomized trial cited in the paper, 65 healthy, overweight, and obese subjects consumed ad libitum (as much as they wanted) a high-protein test diet containing 24% of energy from protein and 29% of energy from fat. The high-carbohydrate diet contained 59% energy from carbohydrate and 29% energy from fat. After 3 months, the subjects consuming the high-protein diet lost more weight (7.5 kg) compared to subjects consuming the high-carbohydrate diet (5.0 kg). After 6 months, the weight loss was 8.7 kg vs. 5.0 kg, respectively; 35% of the high-protein-diet subjects lost greater than 10 kg of weight, whereas only 9% of the high-carbohydrate-consuming subjects did so.
The authors note that the thermic response to protein ingestion is 50% to 100% higher than that for carbohydrate, which is generally attributed to the additional energy costs of metabolizing proteins in, for example, breaking peptide bonds and gluconeogenesis. Moreover, others had reported that following protein consumption, postprandial REE (resting energy expenditure) rises rapidly and is sustained for as long as 4 to 5 hours. Carbohydrate consumption, by contrast, induces REE more modestly, and REE falls rapidly 1 to 2 hours after the meal. The purpose of their study was to determine, with commonly eaten foods and meal plans, the metabolic cost of a high-protein, low-fat diet versus the “currently recommended” high-carbohydrate, low-fat diet. The authors conclude that “Increased diet-induced thermogenesis, in association with the preservation of REE [resting energy expenditure], may contribute to the reported weight-loss success of diets high in protein with moderate levels of carbohydrate and lends credence to the observation that weight loss on high-protein diets is predominantly body fat, not body water.”
One interesting point made by some researchers cited in the paper is that thermogenesis is increased more by more palatable food. They use, as an example, that a palatable meal of Parmesan fondue, spaghetti and meatballs, and a chocolate clair increased diet-induced thermogenesis 50% more than if the same meal ingredients were blended, desiccated, and consumed as a tasteless biscuit! This would suggest that, all other things being equal, if you want to increase thermogenesis, it may not help to eat tasteless food. (But you will have to avoid overeating delicious foods, too! Note that the example is loaded with carbohydrate . . .)
This is interesting information on the thermogenic effects of a high-protein versus high-carbohydrate diet. Still, it is a very small study (10 subjects), and the subjects were very young (19–22 years). We hope there will be more and larger studies of this kind that include middle-aged subjects.
Many neurological disorders are characterized by abnormal, insoluble deposits of protein aggregations, including Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, and others. In the case of Huntington’s, the insoluble deposits are formed from polyglutamine aggregates (an abnormal expansion of CAG repeats in the huntingtin protein). In a new study,1 researchers report that various disaccharides (including the sugar trehalose) reduced the formation of polyglutamine aggregates in vitro and that this correlated with a decrease in cell death in a cellular model of Huntington’s disease. Moreover, oral feeding in vivo of trehalose to a transgenic mouse model of Huntington’s disease inhibited the formation of truncated huntingtin aggregates and improved the associated motor dysfunction. Hence, trehalose is potentially a therapeutic agent in human Huntington’s disease.
Trehalose is a food, available commercially for use in foods and dietary supplements. One would think, therefore, that if there is even a small chance that trehalose would be beneficial in the disastrous Huntington’s disease, human experiments should be begun forthwith. After all, there can be no question of its safety. As the comments on this study2 note, “The extremely low toxicity and high water solubility of this compound make this an attractive therapeutic approach, although the therapeutic effects seem to result from prevention of new aggregate formation, not from reversal of the pathology.”
So what’s the holdup? First, trehalose must be tested in a Phase I human trial,2 which is a test for safety, not for effectiveness in treating disease. Why spend millions on an entirely unnecessary Phase I human trial for a low-toxicity food? Because that is how the FDA’s rules say it must be done in order to be approved for drug use (i.e., to be permitted to put truthful information on the trehalose label concerning its relation to a disease), for example, as a possible treatment for Huntington’s disease. Trehalose can be sold legally as a food or dietary supplement, but only if you do not mention anything about a possible effect on disease. It is the information when placed on the label or labeling, not the substance, that is illegal. We argue in our ongoing suit against the FDA, Whitaker v. Thompson, that the FDA’s prohibition on the communication of truthful, nonmisleading information about a legal dietary supplement or a food (such as trehalose) is a violation of the First Amendment (“Congress shall make no law . . . abridging the freedom of speech . . .”).
Prohibiting the communication of information to the public (and even to doctors) about food substances unless the FDA says you can say it is the basis of the FDA’s approval process, which is biased in favor of drugs. If the First Amendment means anything, it means that you can communicate truthful, nonmisleading information to anyone you like without having to get the government’s permission. That is why Dr. Julian Whitaker and a few others of us are continuing this expensive battle all the way to the U.S. Supreme Court. You can follow this case, read all the briefs and court decisions, laugh and weep, and donate money (any amount will help), at www.emord.com. If you really want to live an extended lifespan (not to speak of living in a free society), this is a battle that we must win.
Ironically, new methods of producing trehalose are being developed commercially to reduce its price and to make it possible to use as a substitute for high-effectiveness carbohydrate sugars in mass-produced food products, especially low-carbohydrate foods. Once again, the FDA prohibits communication on labels of “forbidden” knowledge, at the point of a gun—knowledge that might reduce terrible pain and suffering for thousands.
The ratio of tryptophan to large neutral amino acids (including tyrosine, phenylalanine, and the branched-chain amino acids leucine, isoleucine, and valine, all of which compete with tryptophan to enter the brain) determines tryptophan availability to the brain, where it is used to make serotonin and other biomolecules. Serotonin is known to affect appetite, especially for carbohydrates. Insulin, released as a result of eating carbohydrates, causes the aromatic and branched-chain amino acids to be removed from the bloodstream (taken up largely by muscle), which allows tryptophan to more easily enter the brain. A low ratio of tryptophan to the large neutral amino acids means that there is a low availability of tryptophan to the brain.
A recent paper1 reports on nine obese patients who completed a weight-loss program, which involved taking a commercial very-low-energy liquid diet under medical supervision. At the conclusion of their stringent diet, the obese subjects had lost almost 30% of their initial body weight. The percentage body-fat values decreased almost to that of the controls. The lean body mass (except for one subject who had an unusual increase during weight loss) did not differ significantly before and after weight loss.
The plasma tryptophan concentrations and ratios of tryptophan to large neutral amino acids in the obese subjects were, however, low at all times, with these effects persisting after weight reduction. Before weight loss, the subjects had below-normal plasma tryptophan concentrations, with concentrations of the other LNAAs moderately elevated, with the result being a low ratio of tryptophan to LNAAs. After weight loss, there was some reduction in plasma LNAA concentration, but the tryptophan ratio remained low because of persistently low tryptophan concentrations. They found no difference between the subjects and controls in the response of branched-chain amino acids to insulin infusion (uptake from the bloodstream into peripheral tissues). The authors note that obese subjects are often insulin-resistant and that diminished insulin action may cause low plasma tryptophan ratios. Plasma tryptophan ratios are also reported to be below normal in obese subjects, and the ratios may decrease with dieting—a possible reason, the authors suggest, for relapse after diet-induced weight loss.
The authors note another study in which the acute increase in plasma tryptophan concentration that followed oral tryptophan treatment in obese subjects was less than that observed in normal-weight subjects. In that study, however, the baseline levels of tryptophan in the obese subjects were not below normal.
The obvious conclusion from these data is that obese people probably ought to be taking tryptophan supplements, not necessarily because it would cause them to lose the weight they need to lose, but because low levels of tryptophan (and consequently of serotonin) are conducive to depression, impulsive violence (including suicide), and low self-esteem. The FDA is entirely responsible for the continued, unjustified prohibition of tryptophan as a dietary supplement. Since the banning of tryptophan, there have been a number of multibillion-dollar-per-year selective serotonin reuptake inhibitor (SSRI) drugs (such as Prozac®), expensive drugs that would otherwise have had to compete with much cheaper tryptophan supplements. Tryptophan might have made it possible to use lower doses of SSRIs or even, in some people, made it possible to discontinue the drugs entirely.
One dietary method that may increase tryptophan concentration and the tryptophan/branched-chain amino acids ratio is to take supplements of whey protein, a protein that has an unusually large amount of tryptophan and a higher ratio of tryptophan to branched-chain amino acids as compared to other proteins (such as soy protein or casein). A small amount of carbohydrate (as little as 10 grams may be adequate) taken at the same time to cause a release of insulin will increase the passage of tryptophan into the brain.
New understanding of how fat tissue grows suggests possible new ways to inhibit it. Recent studies suggest that adipose (fat) tissue depends upon its blood supply in order to maintain its mass. Although most blood vessels in an adult are mature and not growing, adipose tissue can expand and contract throughout life, and its blood vessels can grow to meet the needs of larger adipose stores or regress when adipose stores become smaller.1 The growth-stimulatory effect on endothelial cells of adipose blood vessels when cultured with preadipocytes (immature fat cells) appears to affect no other cell type.2
Adipocytes and endothelial cells interact with each other. Adipocytes, for example, produce and release growth factors such as vascular endothelial growth factor (VEGF), monobutyrin, and leptin, all of which promote the proliferation of endothelial cells.2 At the same time, endothelial cells secrete factors that promote and support the proliferation of preadipocytes, such as basic fibroblast growth factor and platelet-derived endothelial-cell growth factor.2 In an animal model, weight regain taking place after weight loss on a food-restricted diet resulted in increased angiogenic activity in the adipose tissue mass, due to the induction of VEGF.2
In a recent paper,1 scientists investigating the sensitivity of adipose tissue (in ob/obmice, which accumulate fat mass rapidly) to antiangiogenic drugs found that the suppression of endothelial cell proliferation by the drugs resulted in a significantly lower adipose tissue mass. In fact, in the ob/ob mice, which lack leptin, the antiangiogenic drugs had similar effects in reducing fat mass as did treatment with leptin. The researchers also found that weight reduction from angiogenesis inhibitors, leptin, or calorie-restricted diets were all associated with adipose endothelial cell apoptosis (programmed cell death). Moreover, they found that endothelial cells in mature tissues (that have reached their adult size and do not continue to grow) were not responsive to antiangiogenic drugs, while the endothelial cells in adipose tissue were responsive. (Interestingly, the vasculature of hair follicles also expands during the growth phase, decreasing during the rest phase.3 There is also vascular growth in inflammatory skin diseases, such as psoriaris.3)
A recent paper even suggests that angiogenesis is associated with Alzheimer’s disease,4 showing vascular basement membranes from Alzheimer’s disease and normal brain that reveal much higher microvascular density in the Alzheimer’s brain. The authors suggest that anti-inflammatory drugs, H2-receptor blockers, antihypertensives, and statins may reduce the risk of Alzheimer’s via their antiangiogenic effects.
There are many natural substances with antiangiogenic properties, for example, green tea and epigallocatechin-3-gallate (EGCG, a constituent of green tea),5 flavonoids found in edible berries,3 curcumin6 (comprising about 40% of the spice turmeric), genistein, fisetin, and luteolin,7 and resveratrol (found in grapes and red wine). While it would appear that nobody has done a weight-control study in humans using dietary increase of antiangiogenic foods (and possibly nobody ever will, because of the high costs of such a study and the unpatentability of natural substances), increasing dietary intakes of substances such as those mentioned here might help and is unlikely to hurt.
The paper that follows was written for and published in Liberty magazine (February 2004, pp. 29-31). We are contributing editors to Liberty and highly recommend it to lovers of freedom. (Published by the Liberty Foundation, 1018 Water St., Suite 201, Port Townsend, WA 98368. Tel 800-854-6991.) If any of you reading this are not lovers of freedom, we would appreciate it if you would discontinue reading our newsletter.
By Sandy Shaw & Durk Pearson
Remarkably, recent theoretical and experimental studies1,2 by two entirely different groups of scientists studying cooperation by humans in collective enterprises (public goods) now provide evidence to support the idea that being able to opt out of public goods games maintains a higher percentage of cooperation (people willing to support the collective enterprise), while not being able to opt out leads to much lower levels of cooperation, along with a rise in the number of defectors (who contribute nothing but take the benefits of the collective enterprise).
The latest work on this development appeared in the 25 September 2003 Nature.1 The authors introduce their paper by explaining that in public goods experiments, initial cooperation usually drops quickly, almost to zero. Mechanisms used to maintain “cooperation” include punishing defectors (Communist/Nazi punishment society model or the Regulatory State or, at a local level, boycotting or shunning) or the need to maintain good reputation. As the authors note, these mechanisms require that defectors be identified. (Defectors are also likely to attempt to deceive others in an attempt to establish a phony “good” reputation, making it more difficult to distinguish the real good reputations.3) Theorists have proposed a different mechanism for maintaining cooperation that works under conditions of anonymity.
The proposed mechanism is to allow optional participation in the public goods game, where people can choose not to participate in the game; those people are called “loners.” The authors staged experiments in which participants could be either cooperators, defectors, or loners and show that on average, cooperation is maintained at a substantial level. The “return” to each individual in the cooperators and defectors groups is calculated based upon the amount of money the cooperators pay into the public goods pool (where multiples of the money contributed by cooperators is added to the pool by the experimenters) divided by the number of individuals in the game, including defectors.
The authors displayed the group decisions (cooperator, defector, or loner) of the group (without identifying who made what decisions). The “decisions” were faked for seven rounds so as to test the predictions of the theory, e.g., how the players would respond to the different levels of cooperators, defectors, and loners. In the eighth round, the prediction was that if you started the round with mostly loners, you would then see more cooperators; if you started the round with mostly defectors, you would see more loners; if you started the round with mostly cooperators, you would see more defectors. This is what the authors call rock-paper-scissors dynamics. They then ran 50 rounds without manipulation to see what sort of oscillations would appear among the three groups. They found that the predicted strategy became most frequent significantly more often than did the alternative strategy (P < 0.001, n = 20, paired t-test, t = 6.588, 2-tailed). As they put it, “As the model predicts, after loners have the highest frequency, cooperators become most frequent, thereafter defectors, and then loners again. After a prevalence of cooperators, defectors become most frequent, followed by loners, and then cooperators again.” An excellent example of this dynamic is how de Tocqueville marveled at what he saw as an America dominated by cooperators. Most of the people arriving in America were opting out of collective impositions in European countries and, hence, were loners. The prediction is that when loners are most frequent, it is followed by a prevalence of cooperators. Moreover, most Americans lived at that time in small towns, which is conducive to cooperation.
The authors stated, “We found that volunteering (the option to choose between joining the public goods group and taking the loner strategy) indeed protected cooperation in the public goods game by inducing small group sizes [that remain in the game]. On average, there was a rather stable frequency of cooperators that was higher than what is usually found in public goods games after several rounds. . . . It is not just the fact that volunteering is possible that induces cooperation, but rather that volunteering reduces public goods groups to small sizes for which the individual cost-to-benefit ratio becomes more favorable. . . . Even though defectors are still better off than are cooperators in each group, cooperators do better when averaged over small groups according to Simpson’s paradox.”
The earlier paper on the same subject2 used a mathematical model of interacting cooperators, defectors, and loners. The researchers made certain assumptions based upon r, the payoff to society (of the public goods); the individual payoff is the societal payoff divided by the number of individuals in the society. The individual investment is normalized to 1 and multiplied by a factor r (an arbitrary number set by the researchers to represent, in theory, the collective benefit of the public good in question if everybody cooperated). In fact, most public goods have an r of less than 1, meaning that it is in the interest of all the players to defect. However, the researchers found that adding an opt-out option (loners) changes the results dramatically. In a game of cooperators and defectors (no loners permitted), the r must be quite large to support cooperation (cooperation increases rapidly from nearly 0 at r ~= 4). In the cooperators/defectors/loners game, cooperators emerge from nearly 0 at r ~= 2, persist at 35–40% of the group to r ~= 3.90, and then rapidly increase at higher r. In fact, the authors report, at r = 4.17 and above, it is not profitable to choose to be a loner, and loners essentially go extinct.
A finding from the earlier paper2 is that cooperation is higher in small, local groups than in nonlocal (what they call “well mixed”) groups. Not only are the benefits of cooperation higher in a small group, but reputation is more easily discerned.
A good, concrete example of how reducing the size of the group results in more benefits to cooperators is how the two of us, living in a small rural town in Nevada, have become involved in much public goods activity by volunteering our time to advisory groups and committees overseeing various public projects. This is something that we never did when living in the Los Angeles beach community from which we escaped 12 years ago; it would have been a total waste of our time. Here, our participation allows us to help steer public activities in the “right” direction (from our point of view), toward more freedom.
When we decided that we had to get out of not only the Los Angeles beach community where we lived, but California itself, we engaged in a systematic search for someplace (limited to the United States) where property rights and personal freedom were high, and regulation and taxation were low. We considered a number of states, such as Wyoming, but Nevada, with no state income tax and, in the rural areas, low population density,4 was also very convenient for moving our many tons of possessions because of its relative nearness to Los Angeles. Durk made telephone calls to all the rural Nevada counties. When he called one of the counties, he asked the courthouse employee “Can I speak to someone in the land-use planning department, please?” The woman answered, “We don’t do that here.” Then Durk asked, “Well, then can I speak with someone in the zoning department?” The woman replied, “We don’t do that here, either.” Durk continued, “Then can I speak to someone in the building-permit department?” She answered, “Young man, before you waste any more of my time, we don’t do that here. You’re supposed to build according to the Uniform Commercial Building Code, but if you don’t and it falls on your head and kills you, that’s your funeral, because we don’t do building inspections either!” “Wow,” Durk said, “that sounds like our kind of place.” “Well,” she replied, “if that is your kind of place, we’d love to have you up here.”
Lonerville is a place where there aren’t many public goods foisted upon residents, so people don’t have to (often) play the game. We drove through the different towns in the winning county, looking for clues telling us that we had reached Lonerville. As we entered the town that is now home, we saw several large piles of rusting junk in people’s yards (right on the main thoroughfare through town and directly across the street from the county courthouse). It could have been trash or it could have been potentially useful pieces of scrap, but it was definitely messy. Sandy said, “Wow, this looks like our kind of place!” A town that doesn’t try to stop people from keeping whatever they like on their own property is a property-respecting town that is unlikely to have many rules and regulations. Yes, we found Lonerville and are doing our very best to keep it that way, even though the best way to do that is to sometimes be cooperators.
The published studies and experiments suggest strongly that if we are to avoid being taken over by defectors (as is surely happening now), opting out is a practical solution. “All” that needs to be done now is to remove the criminal defector class from control of the political process by introducing “opting-out.” The establishment of convincing evidence that permitting opting-out leads to more voluntary cooperation (and, though not mentioned in the paper, less of the highly dangerous war of all against all) is a very important first step.
Vernon Smith won the Nobel Prize for his development of just such game theory experiments as were done in this study. Hence, it is not too much to expect that recognition for these results favoring voluntarism to maintain social cooperation will eventually take place. Just the fact that the two papers on the rock-paper-scissors dynamic cited below appeared in Science and Nature is evidence enough of the acceptance of these findings as solid scientific contributions. (Considering how left-wing these journals are, especially Science, we wonder how well they understand the revolutionary implications of these studies.)
Of course, these experiments are simplified from reality by the fact that, for one thing, they involve a single public good over which people are choosing to cooperate, defect, or (if allowed) opt out. In the real political world, each individual who can make a choice has to consider huge numbers of different public goods, where some will provide gain and others loss. Reflecting the studies, people are not pure cooperators, defectors, or loners, but change in response to what other people do (or what they believe other people do).
Finally, we note that deriving libertarianism from game theory experiments is a totally different approach than that of deriving libertarianism from a noncoercion moral principle. Though the fraction of the population for which a morality of noncoercion or even personal freedom is at the top or near the top of their values is probably fairly small, the number of people who are fearful of societal breakdown because of increasing defectors and decreasing cooperators (and more “command and control” by governments) is probably a great deal larger. Open borders are incompatible with a continuing (and growing) welfare state or progressive taxation, but both have very powerful political support. Allowing loners to opt out of both the costs and benefits may be the most practical way of preventing the rapidly progressing collapse of social cooperation into a Hobbesian war of all against all. The open borders/welfare state conundrum may ultimately make the future brighter for liberty. (That is one reason why it is advisable to extend your lifespan, because this may take quite some time; still, when the tide turns against the public goods games dominated by defectors, it is likely to happen fast.)