September 2008 Blog with Durk and Sandy


According to an article published in the May 2008 inform (published by the American Oil Chemists’ Society), the Swiss government has “developed guidelines for use by grant agencies to determine which research projects could ‘deeply offend’ plant dignity. If a research application was found to be offensive to the dignity of plants, funds for the project would not be granted.”

The article reported further that “though the ethics committee has developed a ‘decision tree’—a metric for the kinds of issues that must be considered when determining the ‘dignity’ of a particular case—specific examples of experiments that violate that dignity are lacking.”

D&S comment: Believe us, folks, we didn’t make this up. We never could have thought of anything like this. Frankly, the idea of having people’s lives controlled by loonies concerned about “plant dignity” is appalling, if not frightening. Watch out, the zealots in white coats may be coming to take you away . . .

. . . if a little knowledge is a dangerous thing, where is
the man who has so much as to be out of danger?

— T. H. Huxley
On Elementary Instruction in Physiology
(Collected Essays, 1903)
Single nations have therefore a natural tendency to
centralization, and confederations to dismemberment.

— de Tocqueville
Democracy in America

This is profound and accurately depicts the consequences of the Civil War, whereby a constitutional republic akin to a confederation (e.g., with sharply limited powers of the national government and largely unlimited powers of state governments) was converted to a single nation [e.g., centralized powers in a national government and greatly decreased state (local) powers]. The risk of dismemberment was thereby converted to the risk of centralization, from which we suffer today.


Half of the secret of resistance to disease
is cleanliness; the other half is dirtiness.

— Anonymous (quoted in
Oxford Dictionary of Scientific Quotations)


We’ve discovered an exercise product that even we use—and we definitely hate to exercise. Called Rock-n-Go™, it is a reasonably affordable (about $300 plus shipping) exercise machine that requires you to do absolutely nothing. There is no work. You just sit passively on the saddle-shaped seat and let the machine rock you back and forth (with three speeds to choose from), while you watch television or listen to music. As you maintain your balance in response to the movements, it works your abdomen, hips, and buttocks. One other nice thing is that it arrives fully assembled, so even that doesn’t require any work (except for putting on the foot pedals, which takes a minute or two). The Rock-n-Go is available from a number of mail-order catalogs (for instance, the Walter Drake’s “Easy Comforts” catalog, 800-308-1384). The contact information on the Rock-n-Go User’s Guide is: e-mail,; phone, 877-261-1570. The device is made in China. This is an unsolicited plug.



In 1943, when Germany had virtually no sources of petroleum to fuel its Luftwaffe, U-boats, and Tiger tanks, its scientists (arguably among the best in the world at that time) didn’t turn to solar and wind power. . . . Hitler’s technical advisers turned to another energy source to keep their Wehrmacht running steadily for several years without petroleum. They used the Fischer-Tropsch process to convert coal into diesel fuel and employed the Bergius hydrogenation (or liquefaction) process to convert coal into aviation gasoline and high-quality truck and automobile gasoline.

— From The New American, June 9, 2008

Durk is very familiar with both processes. The conversion of coal to gasoline, diesel, heating oil, and jet fuel is economically feasible when oil prices are above about $80 per barrel. Each ton of coal produces about two barrels of oil. About 30% of the fuel used by South Africa’s commercial jet fleet is made from coal. Twenty-seven new coal-to-liquid conversion plants are under construction in Germany, and over 40 in Europe as a whole.

Last May, the U.S. Air Force certified jet fuel made from coal for both subsonic and supersonic use; it cost $4.64 per gallon from a small pilot plant. Congressional Democrats passed a bill banning any further purchases. America has enough coal to supply 100% of our current liquid fuel needs at about $2.00 to $2.50 per gallon for over ONE THOUSAND YEARS, but “our” government has prohibited it. We are all victims of the Green Taliban, which is as fanatically opposed to carbon dioxide emissions as the Islamic Taliban is opposed to the public display of women’s ankles. For further information, please see:



A recent news report1 in the Journal of the National Cancer Institute discussed the work of doctors attempting to increase the effectiveness of breast cancer chemotherapy and to reduce the risk of recurrence by including concurrent treatments to reduce insulin levels. One doctor-researcher, Pamela Goodwin, M.D., said, “If you look at the effect of insulin, the women in the highest quartile levels in the studies that have been done all yield the same result. They have a triple risk of death. If we could lower those insulin levels by 25%, we might see a 5%–6% absolute improvement in outcome, and that’s huge.” Goodwin and coworkers published a prospective study in 2002 looking at the outcomes for 512 nondiabetic women with early-stage breast cancer. They reported that the “women with the highest fasting insulin levels had three times the risk of recurrence and death compared with women with the lowest insulin levels.”

In a new paper,2 unrelated researchers did a meta-analysis of 39 studies that reported cancer risk estimates for glycemic index (GI, glucose released from carbohydrate-containing foods compared to pure glucose) and glycemic load (GL, the glucose derived from all carbohydrate-containing foods consumed per day). Overall, both GI and GL were significantly associated with a greater risk of colorectal or endometrial cancer but not (after correcting for publication bias) for breast cancer.

Other studies were reported in Ref 1 to support the hypothesis that higher insulin is associated with increased risk of breast cancer. The NCI-sponsored Health, Eating, Activity, and Lifestyle (HEAL) study found that “higher body mass index and lower physical activity levels are associated with higher insulin levels in breast cancer survivors and that women with invasive disease and the highest insulin levels have three times the risk of death of women with the lowest insulin levels.” These data were reported by Melinda Irwin, Ph.D., an epidemiologist at the Yale School of Public Health in New Haven, Connecticut, at the American Association for Cancer Research’s prevention meeting last year. Michael Pollak, M.D., professor of oncology at McGill University in Montreal, was quoted in the report: “The high-insulin effect is large. The adverse effect of high insulin on outcome of postmenopausal breast cancer is in the same order of magnitude as the beneficial effect of adjuvant chemotherapy. This is nothing subtle.”

The rest of the article reported on attempts of doctors to follow up on this by using metformin as an adjuvant treatment because of its insulin-lowering effects. Metformin is a drug approved for use in the treatment of diabetes. Goodwin was reported to have recently completed a prospective phase II clinical trial of 32 nondiabetic breast cancer patients that found that metformin treatment produced an insulin reduction of 22%.

There are a number of ways to reduce insulin levels, however, which do not involve the use of xenobiotic drugs. One way is to reduce the amount of high-glycemic-index carbohydrates in your diet and increase fiber and resistant starch.3-7 In fact, we developed our Glycemic Control line of low-glycemic-index, high-fiber (beta-glucan) barley products (flour, nuggets, and quick flakes, and cookie, pudding, and cake mixes) and Durk & Sandy’s resistant starch and erythritol for the explicit purpose of reducing blood glucose and insulin for better health and longer life.

Another effective method is exercise. The JNCI article1 reported on a recent study by Melinda Irwin in which 75 overweight, sedentary, postmenopausal breast cancer survivors performed an aerobic exercise regimen for 6 months and had a 6% reduction in their insulin levels, as compared to a 36% increase in insulin levels in the control (not exercised) group.

Incidentally, breast cancer risk is a definite health issue for Sandy. Although she does not have it, her sister did (quite a few years ago), and the risk of breast cancer is increased two-fold for a woman whose sister (or other first-degree relative) has had this cancer.

Insulin Signals Plentiful Nutrient Supplies, which Stimulates Cell Growth and Proliferation

One reason that high insulin levels are a risk factor for cancer is that insulin stimulates a signaling pathway (PI3K-PTEN-Akt-TOR) that promotes cell growth and proliferation.8,9In fact, numerous tumor suppressors act on this pathway, “suggesting that it must be important in cancer since it is kept under such tight negative regulation. . . . Persistent activation [of this pathway] by excess nutrients can lead to insulin resistance and diabetes.”7 Inflammation is also associated with insulin resistance.10 Caloric restriction reduces insulin levels, among its many longevity-inducing effects.


  1. Hede. Doctors seek to prevent breast cancer recurrence by lowering insulin levels. J Natl Cancer Inst 100(8):530-2 (2008).
  2. Gnagnarella et al. Glycemic index, glycemic load, and cancer risk: a meta-analysis. Amer J Clin Nutr 87:1793-801 (2008).
  3. Dumesnil et al. Effect of a low-glycaemic index–low fat-high protein diet on the atherogenic metabolic risk profile of abdominally obese men. Br J Nutr 86:557-68 (2001).
  4. Achour et al. Metabolic effects of digestible and partially indigestible cornstarch: a study in the absorptive and postabsorptive periods in healthy humans. Amer J Clin Nutr 66:1151-9 (1997).
  5. Yamada et al. Effect of bread containing resistant starch on postprandial blood glucose levels in humans. Biosci Biotechnol Biochem 69(3):559-66 (2005).
  6. Robertson et al. Insulin-sensitizing effects of dietary resistant starch and effects on skeletal muscle and adipose tissue metabolism. Amer J Clin Nutr 82:559-67 (2005).
  7. Behall et al. Consumption of both resistant starch and beta-glucan improves postprandial plasma glucose and insulin in women. Diabetes Care 29:976-81 (2006).
  8. Zandonella. Life’s throttle: the PI3K-PTEN-Akt-TOR pathway in cell growth and survival. The New York Academy of Sciences eBriefing, posted Sept. 28, 2007.
  9. Luo et al. Targeting the PI3K-Akt pathway in human cancer: rationale and promise. Cancer Cell 4:257-62 (2003).
  10. Shoelson et al. Inflammation and insulin resistance. J Clin Invest 116(7): 1793 (2006).

Zyvox was released in 2001 as the first member of the
oxazolidinones and is the only new class of antibacterial for 30 years.

— Gibbons. Phytochemicals for bacterial resistance—strengths,
weaknesses and opportunities. Planta Medica 74:594-602 (2008)


D&S comment: Interestingly, this class of compounds has been used in antibacterial cleaners (such as for toilets) for over 30 years. This slooooow development of new antibiotics is one reason we developed and use Self-Defensin™ to increase our resistance to getting infections.



We have explained in earlier newsletters that eating food, especially high-fat meals, results in an inflammatory state.1,1b New reports suggest that at least part of this food-induced inflammation is due to the stimulation of gut bacteria to release bacterial endotoxins (lipopolysaccharide, LPS),1 which result in the release of inflammatory cytokines. LPS is the major component of the cell walls of gram-negative bacteria and is the primary cause of sepsis, a hyperactive inflammatory immune response to LPS. More important for most people is the positive association between LPS-induced inflammation and insulin resistance; a mouse study found that subcutaneous injections of a low dose of LPS led to excessive weight gain and insulin resistance.1c

For most people in Western countries, there is very little time spent in the fasted state (except during sleep); thus, food-induced inflammation could be taking place most of the time and is therefore importantly related to many inflammation-associated diseases, such as cardiovascular disease, obesity, diabetes, and cancer. Indeed, a recent hypothesis2 proposes that “the reduction in lifetime exposure to infectious diseases and other sources of inflammation . . . has . . . made an important contribution to the historical decline in old-age mortality.”

A recent study1 of 12 healthy men (20–58 years of age) reported that blood endotoxin levels increased significantly by about 50% (as compared to no meal) after a high-fat meal. In another recent study3 of 1015 subjects (in which 201 men had their plasma LPS levels measured), it was reported that endotoxemia was correlated with energy (calorie) intake, e.g., the higher the calorie intake, the higher the level of endotoxemia.

As the authors of Ref 3 also noted, it has recently been shown that “abdominal obesity is associated with a low-grade chronic systemic inflammation.” They also pointed out the association between insulin resistance and the proinflammatory cytokines released by fat tissue in models of diet-induced and genetic obesity. The authors of Ref 3 concluded that “these data suggest that a reduction in plasma LPS concentrations might be a potent strategy for the control of metabolic diseases in humans.”

LPS-Induced Inflammation Reduced

While LPS-induced inflammation is an important part of the immune system’s acute protective responses against bacterial invasion, chronic, low-grade, LPS-induced inflammation is undesirable. Certain nutrients and foods can provide protection.

There are plant constituents (phytonutrients) called proanthocyanidins that can bind and neutralize lipopolysaccharides.4 A recent study of cranberry proanthocyanidins4 (where human embryonic kidney cells were incubated with E coli and either with or without added proanthocyanidin-rich concentrate of cranberry juice) found that the cranberry juice proanthocyanidins inhibited the LPS-induced activation of NF-kappaB, a transcription factor that induces release of proinflammatory cytokines. They identified a mechanism in which the proanthocyanidins actually bind directly to and neutralize LPS by blocking its interaction with certain cell receptors. They cite an earlier study in which a proanthocyanidin-rich fraction of cranberry juice concentrate inhibited the LPS-induced production of the proinflammatory cytokines IL-6 and IL-8, as well as the proinflammatory prostaglandin E2.

Though not tested in this study, other foods that are rich in proanthocyanidins include apple, pear, grapes, blueberries, avocado, chocolate, red wine, tea, and pine bark.5,6

Another recent study7 reported on the results of a gamma-tocopherol supplementation experiment involving 16 human volunteers, some of whom had moderate to severe asthma and others of whom were healthy. Subjects initially took 1 capsule (containing 623 mg of gamma-tocopherol, 61.1 mg of d-alpha-tocopherol, 11.1 mg of d-beta-tocopherol, and 231 mg of d-sigma-tocopherol) per day for 8 days, followed by an 8-day washout period, and then took 2 capsules per day for another 8 days. Peripheral blood monocytes (PBMCs) were collected from each subject and tested by incubating with LPS and measuring proinflammatory cytokines IL-1beta, IL-6, and TNF-alpha, as well as chemokines MCP1 and MIP1beta and the anti-inflammatory cytokines IL-1RA and IL-10.

They found that gamma-tocopherol, but not alpha-tocopherol, “moderately inhibited LPS-induced IkappaBalpha degradation [which activates NFkappaB] in recovered PBMCs after LPS stimulation.” They also found that the LPS-induced secretion of IL-1beta, IL-6, and TNF-alpha and the chemokines MCP1 and MIP1alpha was significantly decreased after treatment with the gamma-tocopherol-enriched supplement. (There was no change in lung function in the asthmatics.)


1. Erridge et al. A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation. Am J Clin Nutr 86:1286-92 (2007).
1b. Aljada et al. Increase in intranuclear nuclear factor kappaB and decrease in inhibitor kappaB in mononuclear cells after a mixed meal: evidence for a proinflammatory effect. Am J Clin Nutr 79:682-90 (2004).
1c. Cani et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes 56:1761-72 (2007), as cited in Membrez et al. Gut microbiota modulation with norfloxacin and ampicillin enhances glucose tolerance in mice. FASEB J 22:2416-26 (2008).
2. Finch and Crimmins. Inflammatory exposure and historical changes in human life-spans. Science 305:1236-9 (2004).
3. Amar et al. Energy intake is associated with endotoxemia in apparently healthy men. Am J Clin Nutr 87:1219-23 (2008).
4. Delehanty et al. Binding and neutralization of lipopolysaccharides by plant proanthocyanidins. J Nat Prod 70:1718-24 (2007).
5. Anon. Oligomeric proanthocyanidins. Altern Med Rev 8(4):442-50 (2003).
6. Gu et al. Screening of foods containing proanthocyanidins and their structural characterization using LC-MS/MS and thiolytic degradation. J Agric Food Chem51:7513-21 (2003).
7. Wiser et al. In vivo gamma-tocopherol supplementation decreases systemic oxidative stress and cytokine responses of human monocytes in normal and asthmatic subjects.Free Rad Biol Med 45:40-9 (2008).


As we have reported a few times on the global warming nonconsensus, we thought we would also mention Durk’s own observations on cooling in central Nevada. As we have mentioned before, we own a herd of cattle, now at 174 head (in the top 1% of herd size), that are raised free-grazing on lush, natural pasturelands and sold as natural beef. Durk was recently out at a large ranch where he and other ranchers were branding all the new calves, including our own. (Ranching frequently involves mutual assistance by a number of local cattle ranchers.) The grass had come up late this year, and some of the cattle still had their winter coats (at the end of June!). The owner of the large ranch where the branding was taking place said that he had never seen cattle with their winter coats this late in the year. One nice thing about this sort of data: cattle coats don’t lie.



The ability to measure changes in gene expression through the use of gene microarrays has led to deep insights into the effects of nutrients on physiological functions. In a very interesting recent study,1 researchers exposed adult rat cardiomyocytes (heart muscle cells) to individual fatty acids, including octanoate (the main fatty acid in medium-chain triglycerides), palmitate (long-chain saturated fat), stearate (long-chain saturated fat), oleate (oleic acid, monounsaturated fat), and linoleate (linoleic acid, polyunsaturated fat), and determined their effect on about 22,000 genes, looking for significant differences among the effects of the different fatty acids.

The most important findings were that the long-chain unsaturated fatty acids (oleate and linoleate) induced genes that promote fat oxidation (beta-oxidation, the use of fats as a metabolic fuel), whereas the long-chain saturated fatty acids (palmitate and stearate) induced genes associated with endoplasmic reticulum (ER) stress and oxidative stress. (The endoplasmic reticulum is a cellular structure that, among other things, is responsible for manufacturing and properly folding proteins. ER stress is a state in which there is a pileup of improperly folded proteins, requiring the ER to temporarily stop synthesizing proteins and to attempt to speed up the disposal of misfolded proteins.)

For example, carnitine palmitoyltransferase transfers fatty acids to mitochondria for beta-oxidation. One of the genes upregulated 4.3-fold by oleate was cpt1a (carnitine palmitoyltransferase 1A); the other fatty acids had no significant effect. Uncoupling protein 3 (ucp3) protects heart cells against apoptosis (a form of programmed cell death); a study by another researcher reported here showed that ucp3 is cardioprotective during ischemia/reperfusion. The microarray results showed that, acutely (6 hr), stearate, palmitate, and oleate induced ucp3 to a similar extent, but the response of ucp3 was transient for palmitate and stearate, whereas the effect of oleate persisted chronically (24 hr). Glutathione synthetase (activates synthesis of the major cellular antioxidant glutathione) was induced by palmitate 1.8-fold compared to no significant effects for the other fatty acids, suggesting a response to oxidative stress induced by palmitate.


  1. Lockridge et al. Bioinformatic profiling of the transcriptional response of adult rat cardiomyocytes to distinct fatty acids. J Lipid Res 49:1395-1408 (2008).


In one of the best Supreme Court decisions (written by Scalia) on “privacy” in recent years, the Court ruled in 2001 that “Where . . . the government uses a [‘sense-enhancing technology’] device that is not in general public use, to explore details of the home that would previously have been unknowable without physical intrusion, the surveillance is a ‘search’ and is presumptively unreasonable without a warrant.” Kyllo v. U.S., 533 U.S. 27 (2001).

D&S comment: Durk helped the lead attorney for Kyllo to prepare the arguments in this case.



To change the world into a more libertarian one, it would be helpful to understand how the libertarian brain works as compared to the nonlibertarian brain. This knowledge might lead to methods (such as targeted designer foods and dietary supplements) that nudge the human brain in a more libertarian direction. Marketing such products is a separate problem, but it might be at least partially solved if they made people feel good about themselves and/or improved their cognitive or emotional function.

It is good news, therefore, that there have been several studies published recently that provide insight into the libertarian brain and how people with that kind of brain function in various types of societies. Hopefully, this will lead to a molecular pathways chart to the creation or maintenance of a libertarian brain.

A Model for the Evolution of Libertarian Traits

Tolerance and Nonaltruism

The most remarkable study (The coevolution of parochial altruism and war, by Choi and Bowles) was published in the 26 October 2007 Science. The conclusion these researchers reached, through simulations using a genetic evolution model, was that war drives the coevolution of altruism and hostility to outsiders. The model simulated the evolution of tolerance and altruism (see paper for details) by assuming, for simplicity, that there were two alleles, one representing either tolerance (T) or nontolerance (P, for parochial) and the other representing altruistic behavior (A) or nonaltruistic behavior (N).

The commentary on the paper (“The sharp end of altruism”), published in the same issue of Science, set the scene very nicely in the first sentence, “Which would you prefer, a society of selfish but tolerant freetraders, or a warrior society in which people help one another but are hostile to outsiders?”

In this study, libertarians (not called that in the study) were clearly represented by the TN (tolerant, nonaltruistic) genotype. As the researchers explain, there were two types of selection at work in the model. “Within-group selection favors tolerant nonaltruists and tends to eliminate parochial altruists [intolerant to outsiders, altruist to the in-group] as well as tolerant altruists and parochial nonaltruists. By contrast, the second process, selective collective extinction resulting from intergroup conflict, may favor parochial altruists despite the fact that they risk death even in victorious battles.” (For example, the authors report that in early human societies there was a “. . . markedly higher reproductive success of predominantly parochial altruist groups when interacting with groups with fewer parochial altruists . . .” Under nonhostile conditions, however, tolerant nonaltruists do best because they are able to receive a mutual benefit from tolerant members of outsider groups and also benefit from altruistic contributions to the in-group.

The bottom line was that high levels of parochial altruism promoted frequent conflicts, the victors being those groups with many parochial altruists while, when nonaltruistic tolerant individuals were most prevalent, hostilities were rare. As the authors note, their study explained how Homo sapiens could have become a warlike yet altruistic species, but there is no evidence that the hypothetical alleles used in the simulation actually exist. They carefully note that, “Thus, we have not shown that a warlike genetic predisposition exists, only that should one exist, it might have coevolved with altruism and warfare in the way that we have described.” As the commentary author points out, “Evidence that intergroup violence killed a nontrivial proportion of our ancestors has fueled interest in war as a force for robust group selection.” The commentary sums up by noting that the evolutionary process (as developed in the simulations) showed “war as both the engine of the coevolutionary process and its legacy.”

Using the terminology developed in the model, political liberals would probably mostly fit in the bully category (N–nonaltruistic, P–nontolerant), while many conservatives would fit the P–nontolerant, A–altruistic category. I call political liberals nonaltruistic because, despite their frequent calls for money to be spent on others, it is other people’s money rather than their own that they propose be used for this purpose. “Volunteering” other people’s money to charitable causes is hardly altruistic. In fact, the commentary describes a study in which 15 small-scale societies played a donation game; the “average generosity correlated with the amount of market exchange and economic cooperation typical in the society.”

Resistance to Social Defeat

A second study [Krishnan et al. Cell 131:391-404 (2007)] reports finding molecular adaptations in the brain of mice that lead to resistance to social defeat. This could be important in humans, where similar resiliency has been reported under adverse conditions, by supporting independence of social subordination. I do not propose that libertarians are more resistant to social defeat than nonlibertarians, as I have no data other than my knowledge of libertarian friends and acquaintances, but I would like to see more libertarians who have such resistance in an inherently nonlibertarian, hostile society.

Briefly, the authors found that in an inbred population of mice, where animals were exposed to ten consecutive incidents of social defeat (being put into the cage of a resident stranger), 40–50% of the defeated mice (the unsusceptible group) did not display behavioral effects of defeat (e.g., depression, social avoidance, anhedonia, weight loss), while the others (the susceptible mice) did. As the authors explained, their main goal was to identify genetic differences between the susceptible and unsusceptible mice.

One of their findings was that, after chronic (but not a single) defeat, there was augmented firing of dopaminergic neurons in a particular brain area [the ventral tegmental area (VTA)] in the susceptible mice, whereas in the unsusceptible mice, there was significant upregulation of genes whose proteins would be expected to reduce such neuronal excitation. This finding might suggest (though not discussed by the authors, who were focused on the increased brain-derived neurotrophic factor, BDNF, induced in that brain area in the susceptible mice) that dopamine (an important signal in the reward areas of the brain) was depleted by the chronic defeat. Dopamine levels can be increased in the brain by its amino acid precursors tyrosine or phenylalanine. (In fact, studies by the Army on tyrosine supplements have shown it to be a potent reliever of stress in soldiers under battlefield conditions. Phenylalanine has also been shown to have antidepressant effects in humans.) Hence, the “crash” in dopamine levels from exposure to chronic defeat can be, I believe, modulated by taking appropriate supplements that increase brain dopamine levels.

Compared to the unsusceptible mice, the susceptible mice exhibited a deficit in reward-seeking activity, such as sucrose ingestion, and also showed an increased reward from cocaine (which, among other things, stimulates increased dopamine release in the brain until dopamine supplies are depleted, after which the cocaine “crash” takes place). Hence, chronic social defeat may be a factor leading people to become hooked on cocaine, helping to explain why cocaine users tend to be losers.

The authors propose that there is an increase in dopamine release by neurons in the VTA because “in the context of social defeat, [increased dopamine release] may promote alertness during a potentially harmful situation.” They conclude by noting that resilient humans “display a striking ability to preserve optimism in the face of adverse situations, a characteristic that may reflect reward substrates that are either especially plastic or insensitive to change.”

Response to Inequality

There have also been recent scientific studies published on the negative response (reduced willingness to cooperate) to inequality of reward for equal (perceived) effort in experiments in small groups of humans, chimps, and various monkeys.1,2 As was suggested in one such paper on monkeys,1 when there is a collective effort (say, a group hunt for meat), then a genetic predisposition to carefully examine the distribution of the results of the cooperative effort and to have a negative response to inequality of the distribution (all other things, such as effort expended, being equal) would be an unsurprising evolutionary result. However, what is not discussed in the papers I’ve seen is an explanation of how you can extrapolate such rules from the small groups in which they support cooperation into groups of millions of individuals, where you don’t know what the result of the “group hunt” has produced or how it has been distributed, and where effort expended by individual members is likewise unknown. I am inclined to think that the negative response to inequality, supported by genes that evolved in small groups and helped promote cooperation, has degenerated into an inappropriate pathological response in large human groups that actually hinders cooperation by fostering widespread negative responses to ubiquitous unequal outcomes of individual effort, luck, and natural ability.

In the monkey study,1 animals were studied for the effect of unequal rewards on their willingness to cooperate in activities requiring working together. The monkeys showed a negative reaction (less willingness to cooperate) to receiving a less-favored reward (a piece of cucumber rather than a grape) than their partner. The authors reported that effort expended for a reward had a major effect on the willingness to cooperate, as “by far the lowest level of performance in the entire study occurred in subjects required to expend a large effort while at the same time seeing their partner receive a better reward.” The authors conclude that “These effects are as expected if the inequity response evolved in the context of cooperative survival strategies.” Unlike humans, interestingly, the monkeys did not have a negative response to getting a better reward than their partner.

In a human study,2 researchers used magnetic resonance imaging to detect blood oxygenation-level-dependent (BOLD) responses in the ventral striatum to differences between rewards in subject pairs performing the same work under the same conditions for a money reward. The ventral striatum is an area of the brain engaged in the prediction and registration of reward via dopaminergic projections. As the authors suggest, understanding of how humans respond to unequal rewards has far-reaching economic implications, including the “design of optimal taxation and redistribution schemes” and “the optimal provision of incentives in firms.”

The authors tested the hypothesis that activity in the ventral striatum and the midbrain-prefrontal dopaminergic projections would increase with higher relative payments (e.g., a higher BOLD signal in subjects receiving more than their partner), and, in fact, that was what was observed. Moreover, the subjects reacted with a higher BOLD signal when large amounts of money were unequally paid, regardless of which of the subjects received more.

People are weird animals, and it is important to understand the basis for values that stem from neurobiological mechanisms evolved under conditions that may not reflect current conditions.

Punishment as a Form of Altruism

There have been a number of recent papers on the fact that humans are often willing to punish violators of social norms and defectors in cooperative activities even when they impose costs upon themselves. I think libertarians are less likely to engage in this type of activity, but it is widespread. One paper that reported on this phenomenon3 notes that “Costly punishment seems to be an altruistic act, given that individuals who contribute [to joint enterprises] but do not punish are better off than the punishers.”

They examined the punishment question by looking at a model of situations where individuals can decide whether to take part in a joint enterprise. The participants include defectors (aka free riders, who do not contribute but benefit from the contributions of others), cooperators (who contribute but do not punish), and punishers (who contribute, but also punish the defectors). However, in this model, the authors indicate that “in the absence of the option to abstain from the joint enterprise, punishers are often unable to invade, and the population is dominated by defectors. This means that if participation in the joint enterprise is voluntary, cooperation-enforcing behavior emerges. If participation is obligatory, then the defectors [free riders] are more likely to win.” Hopefully, this result has captured your attention, as it did mine!

One of the most widely studied models of punishment behavior is the ultimatum game, in which a player has the option of keeping an amount of money or offering to a partner player any portion of the money; the partner can then accept or reject the offer. If the partner rejects the offer, both individuals get nothing. Unequal distributions (usually less than a 60:40 split) are considered “unfair,” and most such offers are rejected in Western societies (though not in all societies). Rejecting an offer of money because it is “unfair” is costly to the individual the offer is made to and is a type of punishment behavior. It seems dumb because some money is better than no money, but that is the way most people react to an “unfair” offer. Incidentally, another recent paper4 estimated, using an ultimatum game played for money by pairs of identical twins, that greater than 40% of the variation in subjects’ rejection behavior is explained by additive genetic effects.

Predicting Political Elections from Rapid Exposures to Candidates’ Faces

I finish this edition of “The Search for the Libertarian Brain” by reporting a mind-boggling new paper on decision-making in elections.5

Researchers showed participants (120 Princeton University undergraduates, who were paid $5) faces of candidates for gubernatorial elections. (If any participant recognized a face, that datum was not included.) They were asked to make a rapid decision on which of two individuals (the winner and runner-up) was more competent on the basis of their faces. Predictions were as accurate after a 100-ms exposure to the faces as after 250 ms and even after unlimited exposure. The researchers compared competence judgments collected before the election of 2006 and found that they predicted 68.6% of the outcome of the gubernatorial races and 72.4% of the Senate races! The results were independent of the incumbency status of the candidates.


  1. van Wolkenten et al. Inequity responses of monkeys modified by effort. Proc Natl Acad Sci USA 104(47):18854-9 (2007).
  2. Fliessbach et al. Social comparison affects reward-related brain activity in the human striatum. Science 318:1305-8 (2007).
  3. Hauert et al. Via freedom to coercion: the emergence of costly punishment. Science 316:1905-7 (2007).
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