August 2009 Blog with Durk and Sandy

The first panacea for a mismanaged nation is inflation of the currency; the second is war. Both bring a temporary prosperity; both bring a permanent ruin. But both are the refuge of political and economic opportunists.

— Ernest Hemingway

There is nothing so useless as doing efficiently that which should not be done at all.

— Peter Drucker

There is a zone of liberty … where the individual can tell the government, “Beyond this line you may not go.”

— Justice Anthony M. Kennedy

(D&S Comment: We are not quite sure where the “line” is in Justice Kennedy’s mind and, judging from Justice Kennedy’s Supreme Court opinions, we don’t think he could tell us.)

It is the highest impertinence and presumption, therefore, in kings and ministers to pretend to watch over the economy of private people, and to restrain their expense … They are themselves always, and without any exception, the greatest spendthrifts in the society.

— Adam Smith (1723-1790),
An Inquiry into the Nature and
Causes of the Wealth of Nations,
 1776

SANDY’S WONDERFUL POTATO SALAD

Here’s Sandy’s greatly fat-reduced recipe for lovers of potato salad, but made with sweet potatoes, which have a much lower glycemic index and a much higher fiber content than regular potatoes. This recipe is delicious! Great with corned beef.

1 tbspPrepared mustard (your favorite)
2 tbspGrated fresh horseradish (or prepared horseradish)
2 tbspRice wine vinegar (or, if unavailable, rice vinegar)
2 tspFresh thyme leaves
3 tbspDurk & Sandy’s High Oleic Sunflower Oil™
(or extra virgin olive oil)
Lite salt and freshly ground black pepper, to taste
2 lbSweet potatoes, cooked and diced
1/2 cupCelery, chopped
3 stripsReduced fat bacon, diced
1Hard boiled egg, chopped
2Cloves shallot, chopped finely
3Cloves garlic, minced
6 ozLow fat yogurt
1/2 tspDurk & Sandy’s Ineffable Essence™*

Wash, but do not peel potatoes. Boil sweet potatoes to desired tenderness. Let cool. Then cut into bite sized pieces.

In a medium sized bowl, mix all other ingredients until blended. Gently (so the pieces don’t break up) stir in the cooked bite-sized sweet potatoes. Chill covered overnight in refrigerator for best flavor. Keep leftovers (if you have any!) refrigerated, but best to eat within 3 days.

*Ineffable Essence contains natural flavor molecules (monosodium glutamate and disodium inosinate) that bring back that fresh taste because fresh meats and vegetables naturally contain higher amounts of these molecules. The bad reputation of monosodium glutamate (Chinese Restaurant Syndrome) is due to adverse effects experienced by some sensitive individuals to extremely high amounts (much higher than naturally found in fresh foods) used at some Chinese restaurants — up to 20 grams in a cup of hot soup! Even when it comes to food, the dose makes the poison.

Please ask for this product.

 

CHRONIC STRESS: CURCUMIN PROTECTION IN CHRONICALLY STRESSED RATS

Who isn’t under a lot of stress these days? If you are, it is good to know that the major turmeric constituent curcumin provided major protection in chronically stressed rats, including reversing impaired hippocampal neurogenesis and up-regulating brain-derived neurotrophic factor (BDNF) expression and serotonin (5HT) receptor 1A mRNA.1

The researchers subjected rats to chronic unpredictable stress (shaker stress, cold swim, restraint, tail pinch, water deprivation, and foot shock) once per day for various periods of time between 8 am and 12 am. Meanwhile, during the stressor period, rats were given chronic curcumin treatment (5, 10, and 20 mg/kg orally) or the antidepressant imipramine (10 mg/kg i.p.), or placebo. Curcumin at 10 or 20 mg/kg increased hippocampal neurogenesis in chronically stressed rats, similarly to the effect of imipramine treatment. The new cells were shown to mature and become neurons. Curcumin also significantly prevented the stress-induced decrease in 5-HT1A (serotonin 1A) receptors and BDNF (brain derived neurotrophic factor) protein levels in the hippocampal subfields, two molecules that function as part of hippocampal neurogenesis.

The negative effects of stress on motivation and cognition, including prolonged “learned helplessness” and increased corticosterone levels, have been shown to be reversed in animal models by fluoxetine (Prozac,® a serotonin reuptake inhibitor antidepressant drug) and these effects are thought to be mediated by the serotonin receptor 1A.1 Brain-derived neurotrophic factor has been found to protect against the suppressed neurogenesis and increased neuronal death in the hippocampus that accompanies depression and post-traumatic stress disorder.1 The authors conclude: “These results raise the possibility that increased cell proliferation and neuronal populations may be a mechanism by which curcumin treatment overcomes the stress-induced behavioral abnormalities and hippocampal neuronal damage. Moreover, curcumin treatment, via up-regulation of 5-HT1A receptors and BDNF, may reverse or protect hippocampal neurons from further damage in response to chronic stress, which may underlie the therapeutic actions of curcumin.”

Reference

  1. Xu et al, Curcumin reverses impaired hippocampal neurogenesis and increases serotonin receptor 1A mRNA and brain-derived neurotrophic factor expression in chronically stressed rats. Brain Res1162:9-18 (2007).

 

SLEEP DEPRIVATION: CURCUMIN PROTECTS AGAINST BEHAVIORAL ALTERATIONS AND OXIDATIVE DAMAGE IN 72 HOUR SLEEP-DEPRIVED MICE

Imagine that you were kept awake for 72 hours. You could expect to have symptoms similar to 72 hour sleep-deprived mice: anxiety-like behavior, oxidative damage (such as increased lipid peroxidation and decreased glutathione and catalase activity), impaired locomotor activity, and possibly weight loss. Moreover, persistent sleep deprivation is considered a risk factor for a number of neurological disorders, including depression and memory dysfunction. A new paper1 reports that curcumin protected 72 hour sleep-deprived mice from these symptoms.

As the authors explain, “sleep deprivation stimulates hypothalamic-pituitary-adrenal axis resulting in an increased production of corticosterone that leads to cell damage.” Excess corticosteroids are known to cause neuronal damage and, hence, impair cognitive function. Curcumin is a powerful scavenger of the superoxide anion, the hydroxyl radical, nitrogen dioxide, and protects against singlet-oxygen-induced DNA strand breaks.1

Mice were 72 hour sleep deprived and received 10 and 20 mg/kg, i.p., curcumin extract treatment (begun two days before 72 hour sleep deprivation) or placebo. Some of the curcumin-treated mice also received supplemental L-arginine (50 mg/kg, i.p.) to test the hypothesis that the modulation of nitric oxide release was associated with the symptoms of sleep deprivation. The results showed that the curcumin treatment significantly decreased the sleep-deprived-induced anxiety-like behavior and oxidative stress and improved the impaired locomotor activity compared to control mice. However, interestingly, L-arginine pretreatment combined with the 10 mg/kg curcumin treatment resulted in a significant decrease in the protective effects compared to curcumin alone. The authors consider this to indicate that nitric oxide release is associated with the effects of sleep deprivation.

The study does not report what type of nitric oxide synthase is responsible for the excess nitric oxide release associated with sleep deprivation, that is, whether it is the inducible nitric oxide synthase associated with inflammation or nitric oxide produced by neuronal nitric oxide synthase or that produced by the endothelial nitric oxide synthase.

The results suggest that, if taking curcumin to help overcome the negative effects of sleep deprivation, take separately from an L-arginine supplement. After a poor night’s sleep, we take curcumin the morning after and L-arginine later that day.

The least expensive way to take curcumin (and a method we use) is to take it as whole ground turmeric root (the spice used in cooking, especially heavily in Indian food). One benefit of this source of curcumin (about 40% of ground turmeric is curcumin) is that it contains, in addition to curcumin, chemically related molecules called curcuminoids that are also beneficial.2,3 We generally take 2 capsules of ground turmeric (each containing 600 mg) 3 or 4 times/day in our Turmeric Root Power™ as well as getting more in our brain maintenance formulation GalantaMind Plus™ capsules (no taste!) If you are taking GalantaMind Plus, you are getting 92.8 mg. curcumin (in 2 capsules/day) or 139.2 mg curcumin (in 3 capsules/day) from turmeric root powder.

References

  1. Kumar and Singh. Possible nitric oxide modulation in protective effect of (Curcuma longa, Zingiberaceae) against sleep-deprivation-induced behavioral alterations and oxidative damage in mice. Phytomedicine 15:577-86 (2008).
  2. Niranjan and Prakash. Chemical constituents and biological activities of turmeric (Curcuma longa L.)— A review. J Food Sci Toxicol 45(2):109-16 (2008).
  3. Rastogi et al. Curcuminoids modulates oxidative damage and mitochondrial dysfunction in diabetic rat brain. Free Radic Res42(11-12):999-1005 (2008).

 

LONG-TERM ADMINISTRATION OF GREEN TEA CATECHINS PREVENTS AGE-RELATED DECLINES IN COGNITION IN MICE

More good news for tea drinkers: A new study1 reports that 14 month old (aged) C57BL/6 J mice given 0.05% or 0.1% green tea catechins in their drinking water for six months maintained spatial learning and memory in the Morris Water Maze to levels similar to young controls. Meanwhile, aged controls had significantly longer mean swimming distance (to reach the underwater platform) as compared to the young controls and the treated old mice. When the platform was removed, aged control mice spent considerably less time in the target area (where the platform had been) than the young control mice. The 14 month old mice treated with 0.05% and 0.1% green tea catechins performed similarly to the young control mice.

The authors also investigated possible mechanisms for the beneficial cognitive effects of the green tea catechins. As noted in the paper, BDNF (brain derived neurotrophic factor) and Bcl-2 are targets of CREB (cAMP Response Element Binding Protein) and are key proteins involved in neuronal plasticity and synaptic structure. Levels of both BDNF and Bcl-2 were significantly decreased in the hippocampus of aged control mice compared with young control mice. However, “the reductions of BDNF were prevented by 0.05% and 0.1% GTC [green tea catechins] supplementation … and the reductions of Bcl-2 were prevented by all three doses [0.025%, 0.05%, and 0.1% green tea catechins] …”1 The researchers also found that the phosphorylation of transcription factor CREB at Ser133 (thought to be a pivotal step in long term memory formation) was significantly improved (as compared to aged controls) in the 0.05% and 0.1% green tea catechins treated mice.

Durk drinks our ShapeShifter Teas™ every day, as well as adding our ShapeShifter Teas Booster Caps™. Sandy drinks combinations of various green and black teas daily.

Another great benefit approved by reality (no bureaucrats or “czars” needed)!

Reference

  1. Li et al. Long-term administration of green tea catechins prevents age-related spatial learning and memory decline in C57BL/6 J mice by regulating hippocampal cyclic AMP-response element binding protein signaling cascade. Neuroscience159:1206-15 (2009).

 

NEW PATHWAYS OF INFLUENZA VIRUS REPLICATION AND POSSIBLE INHIBITION BY NATURAL PRODUCTS

Although with the onset of summer, influenza incidence is sure to decline, the next winter it could be back with a vengeance. New research continues to elucidate the various steps in the influenza A virus life cycle, pointing the way to methods to interfere with it. (H1N1 swine flu is a type of influenza A.)

A new paper1 reports that highly pathogenic influenza A virus strains are known to cause hyperactivation of p38MAPK. Influenza A infection has been found to trigger several MAPK (mitogen-activated protein kinase) pathways in host cells, “which reportedly promotes vRNP [viral ribonucleoprotein capsids] traffic and virus production.”1 The paper reports observations of a highly complex interaction between Bcl-2 expression (Bcl-2, when expressed, suppresses apoptosis) and p38MAPK. The bottom line, as summed up by the authors, was that “[t]he fact that a cellular kinase like p38MAPK is involved in both influenza virus replication and virally induced apoptosis has intriguing implications for the development of novel anti-influenza strategies aimed at limiting both the acute respiratory effects of influenza and its potential neurological complications.”

Resveratrol, Vitamin C, and Quercetin Can Inhibit p38MAPK a Possible Mechanism for Their Viral Protective Effects

The authors of the paper reported above described earlier work2 in which they observed that resveratrol reduced nuclear vRNP export by inhibiting, among other signaling pathways, p38 MAPK. Moreover, in another paper,3 researchers reported that vitamin C inhibited p53 induced replicative senescence by suppressing reactive oxygen species and p38MAPK activity. Quercetin has also been reported to inhibit the expression of p38 MAPK in human mast cells.4

We designed and take daily a selection of nutrients as a viral shield that includes (among others) resveratrol, quercetin, and vitamin C, to help protect ourselves against viruses. See our article “Defending Yourself Against Virus Infections.”

References

  1. Nencioni et al. Bcl-2 expression and p38MAPK activity in cells infected with influenza A virus.J Biol Chem 284(23):16004-15 (2009).
  2. Palamara et al. Inhibition of influenza A virus replication by resveratrol.J Infect Dis 191:1719-29 (2005).
  3. Kim et al. Vitamin C inhibits p53-induced replicative senescence through suppression of ROS production and p38MAPK activity. Int J Mol Med22(5):651-5 (2008).
  4. Min et al. Quercetin inhibits expression of inflammatory cytokines through attenuation of NF-kappaB and p38MAPK in HMC-1 human mast cells. Inflamm Res56:210-15 (2007).

 

COULD THE FRENCH PARADOX AND THE BENEFITS OF THE MEDITERRANEAN DIET BE PARTLY DUE TO ACTIVATION OF THE NIACIN RECEPTOR?

It possibly could. Let us explain. GPR109A is the nicotinic acid receptor (also called HM74a/PUMA-G), which is activated by nicotinic acid (niacin), resulting in the suppression of lipolysis (release of fatty acids) by adipocytes (fat cells). Niacin is an extremely effective antilipolytic agent, which is the basis for its beneficial effects in reducing LDL cholesterol and triglycerides. Niacin also increases HDL and acts as an anti-inflammatory agent.

In a recent study,1 researchers hypothesized that many phenolic acids might bind and activate GPR109A, the receptor for the antidyslipidemic effects of niacin. They noted that consumption of products rich in phenolic acids, such as wine and the “Mediterranean Diet” correlates with a reduced risk of cardiovascular disease. They explain that “both phenolic acids and nicotinic acid are small carboxylic acids with close structural similarity. We also note that application of certain phenolic acids, such as benzoic acid, also induces a flushing response and prostaglandin D2 release in a manner similar to that of nicotinic acid treatment. We thus asked whether phenolic acids could act as GPR109A agonists [activators].”

They, indeed, found that phenolic acids could activate GPR109A, with a potency (in the cinnamic acid class) in the order of trans-cinnamic acid > p-coumaric acid > 0-coumaric acid > sinapic acid > ferulic acid > caffeic acid. In the benzoic acid class, the order of potency was benzoic acid > protocatechuic acid > salicylic acid > p-hydroxybenzene acid.

Part of this study used membranes from Chinese Hamster Ovary cells stably expressing GPR109A, GPR109B, GPR81, or PUMA-G to assess the binding of the test phenolic acids. Human adipocytes were used to test for the anti-lipolytic effect of the tested compounds. Also, mice with knockouts of the PUMA-G receptor were generated to study the effect of the phenolic acids on epididymal fat pad lipolysis.

The IC50 (concentration that inhibited human adipocyte lipolysis by 50%) was, for nicotinic acid, 0.2 μm. The IC50 for trans-cinnamic acid was 160 μm for o-Coumaric acid was 470 μm and for p-Coumaric acid was 130 μm. As the authors note: “Interestingly, the apparent potency of caffeic, gallic and protocatechuic acids observed from the adipocyte lipolysis assay appeared much higher than that found in the 35S-GTPgammaS [*] binding assay, suggesting that a mechanism independent of GPR109A may contribute to an antilipolytic activity of these phenolic compounds as well.” Importantly, the authors noted synergistic antilipolytic effects of a combination of trans-cinnamic acid, p-coumaric acid, or benzoic acid, which alone suppressed lipolysis by 17, 26, and 3%, respectively. A combination of the three at the same concentrations, however, resulted in a reduction of lipolysis by 53%. “These data suggest that while individually an antilipolytic effect of these phenolic compounds may be weak, together they could potentially achieve a functional significance.”

* Phenolic acids stimulate 35S-GTPgammaS binding to membranes from cells transfected with GPR109A.

Within 15 minutes of oral administration of 0.15 mg of cinnamic acid per mouse, there was a significant reduction of plasma free fatty acids in the wild-type mice, but not in the PUMA-G (niacin receptor) knockout mice.

So, the next time somebody asks you whether you think that GPR109A (or HM74A/PUMA-G) could be an important factor in the French Paradox or the benefits of the Mediterranean Diet, you will know what to tell them. On the other hand, if nobody asks you this rather unlikely question, you will still have this very useful knowledge to help guide your own and your family and friends’ eating and drinking. Live long & prosper!

We recommend both eating diets enriched in phenolic acids and taking supplemental niacin (such as our Niacin Easy™). Some people (like ourselves) actually like the niacin flush. Durk always takes it just before sex so that he is flushing during orgasm.

Reference

  1. Ren et al. Phenolic acids suppress adipocyte lipolysis via activation of the nicotinic acid receptor GPR109A (HM74a/PUMA- G). J Lipid Res50:908-14 (2009).

 

EMERGING MEDICINE/SPECULATION:

THE NIACIN FLUSH: COULD IT SIGNAL A HEART PROTECTIVE PATHWAY?

One new research paper1 reports efforts to separate the mechanisms that control niacin flushing from the beneficial antilipolytic effects of niacin in order to get rid of that pesky flushing that some people find annoying or even intolerable. But, not so fast. It may be that the flushing is part of something important that niacin is doing and that you wouldn’t want to get rid of it.

Prostaglandin D2 has been identified as the molecule that naturally causes niacin flushing.1 “Nicotinic acid-mediated stimulation of GPR109A receptors expressed on Langerhans cells in the skin leads to activation of cytosolic phospholipase A2 (cPLA2) and subsequent production and secretion of prostaglandin D (PGD2), which through activation of its own 7TMR [7 transmembrane receptors], leads to cutaneous flushing.”1The title of a new paper published subsequently2 caught our eye when it implied that prostaglandin D2 produced and released in the heart, where the enzyme responsible for its synthesis is reported to be highly expressed, could be responsible for major heart protective effects. The study reported that glucocorticoids protected rodent hearts from ischemia/reperfusion injury, the protection being a result of increased synthesis of PGD2. Moreover, the “the activation of L-PGDS-mediated production of PGD2 was crucial for the cardioprotection against ischemia/reperfusion conferred by glucorticoid-GR [glucorticoid receptor] signaling.” “Indeed, L-PGDS-knockout mice are prone to develop atherosclerosis when fed a high-fat diet.”2

As the authors2 explain, glucocorticoids are anti-inflammatory and generally repress prostaglandin biosynthesis in most cells. However, in rat heart cells glucocorticoids upregulated the enzyme that synthesizes PGD2 and, in fact, they report, “PGD2 was the most prominently induced prostaglandin in vivo in mouse hearts and in vitro in cultured rat cardiomyocytes after exposure to GR [glucocorticoid receptor]-selective agonists.” Glucocorticoids are released as a natural part of the body’s protective response to a heart attack.

Although the authors of this paper2 did not mention niacin or the fact that the niacin flush is caused as a result of the release in the skin of PGD2, it is hard not to speculate that there may be a connection between the niacin flush and the very substantial (and not entirely explained) cardiovascular benefits of niacin. If PGD2 in skin is released in response to the same signals as that in heart cells, then the skin flush could be a part of a much more important process than the mere sensation of hot and itching skin. Perhaps we shouldn’t get rid of the niacin flush.

Aspirin has been reported to be a possible way to mitigate or eliminate the niacin flush. (It is a known anti-prostaglandin compound.) However, we personally have not noticed any interference between taking a daily 81 mg low dose aspirin and the occurrence of niacin flushing.

References

  1. Walters et al. Beta-arrestin 1 mediates nicotinic acid-induced flushing, but not its anti-lipolytic effect, in mice. J Clin Invest119(5):1312-21 (2009).
  2. Tokudome et al. Glucocorticoid protects rodent hearts from ischemia/reperfusion injury by activating lipocalin-type prostaglandin D synthase-derived PGD2 biosynthesis. J Clin Invest119(6):1477-88 (2009).

 

QUACK “ECONOMICS” IN A MAJOR SCIENCE JOURNAL

Robert Costanza, director of the Gund Institute for Ecological Economics at the University of Vermont, Burlington, Vermont, wrote the following as part of his comments in a book review (“Could climate change capitalism,” Nature, pp. 1107-8 (April 2009):

There is evidence in developed countries that economic growth beyond a certain point does not improve well-being, owing to the hidden, external costs of that growth, including climate impacts. For example, an oil spill increases gross domestic product (GDP) as someone must pay to clean it up, yet it detracts from well-being. Increased crime, sickness, war, pollution, fires, storms and pestilence are all positive for GDP because they increase economic activity.

D&S Respond: This is totally spurious, yet has unbelievably passed the editors of Nature. It is a horrible reminder that so few understand economics, including those who apparently understand complex scientific issues (though not necessarily without bias when politics and government grants are involved). This purported “ecological economist” (as well as the editors of Nature) do not understand one of the basic elements of economics concerning the creation and destruction of wealth. This was explained masterfully by the 19th century economist Frederic Bastiat (1801–1850) in the fallacy of the broken window in his 1850 essay “That Which is Seen and That Which Is Unseen.”

The Fallacy of the Broken Window

Bastiat described the fallacy that, by breaking a window, a vandal could create increasing economic activity because the owner of the broken window would have to hire somebody to fix it. The glazier who fixes the window would then have money to spend on something else, the recipients of that money would be able to spend it on other things, and so on and so on, resulting in a spiral of increasing economic activity. This is a fallacy, Bastiat explained, resulting from the failure to distinguish the seen from the unseen. What you see is the economic activity resulting in the fixing of the window, but what you don’t see is the economic activity that would have taken place in the absence of the broken window. The overall wealth in the economy would have been greater if the window hadn’t been broken because there would not only be the value of an unbroken window but that which would have accrued from the spending of money for other values rather than fixing a broken window.

It is horrifying that Nature would publish an article by a purported economist who actually believes that war, sickness, pestilence, pollution, fires, storms and, by analogy, broken windows, are a source of increased economic activity (wealth) in a society. ThatNature’s editors would accept and publish this insane assertion without any documentation, as if it were simply self-evident, is itself extremely frightening.

The economic know-nothings live in a different world than you do and they are positioning themselves to impose their vision on your world.

There is an excellent write-up on the “Parable of the broken window” in Wikipedia. (We read Bastiat’s arguments—in English translation—on the broken window fallacy 40 years or so ago, but it is nice to know that the argument is now so readily available. You can read it at: https://en.wikipedia.org/wiki/Parable_of_the_broken_window.) Another source of information on the parable is found in economist Henry Hazlitt’s classic “Economics in One Lesson.” A discussion of the parable would make a wonderful lesson for a junior high or high school class. Even kindergarten kids could understand it: https://www.amazon.com/Economics-One-Lesson-Shortest-Understand/dp/0517548232/

Even the latest Nobel Prize winning economist appears to have made the broken window error! According to the Wikipedia write-up on the “Parable of the broken window,” Economist Walter E. Williams and commentators Jonah Goldberg and Robert Tracinski accused economist Paul Krugman of committing the broken-window fallacy soon after the September 11, 2001 attacks. Krugman wrote: “Ghastly as it may seem to say this, the terror attack—like the original ‘day of infamy’ which brought an end to the Great Depression—could even do some economic good. […] the driving force behind the economic slowdowns has been a plunge in business investment. Now, all of a sudden, we need some new office buildings. As I’ve already indicated, the destruction isn’t big compared with the economy, but rebuilding will generate at least some increase in business spending.”1 Here a Nobel Prize winning economist appears to be suggesting that blowing up the Twin Towers was a benefit to the economy and, by logical inference, if there had been even greater destruction (a few more buildings, say), it would have been an even bigger boost to the economy! Why not just blow up the entirety of New York City!! Think of all the building projects and job openings you would “create”!!!

Reference

  1. This was discussed in Walter E. Williams’ syndicated newspaper column “There’s no free lunch,” https://www.jewishworldreview.com/cols/williams100401.asp

 

IS A PREFERENCE FOR INFLATION HARD-WIRED IN HUMANS?

A recent paper1 suggests that people respond positively to an increase in income, even when prices go up by the same amount (e.g., real purchasing power stays the same). Economists have traditionally been skeptical of this “money illusion,” the authors say, but recent evidence is providing support for the notion. For example, a study cited by the authors found that, when asked to rate the happiness of two otherwise identical persons who received either a 2% wage increase without inflation or a 5% wage increase with 4% inflation, the majority of subjects thought the 5% wage increase with 4% inflation would result in more happiness, despite the fact that it would result in a lower nominal income gain compared to the 2% wage increase without inflation. Their new paper1 reported evidence of a brain preference for money illusion.

The researchers “compared blood oxygen level dependent (BOLD) activity in response to earned incomes that differed in nominal terms, but that were identical in real terms.” Subjects earned money in a “simple estimation task” and then, later, spent their earnings on items in a catalog. The situation set up by the experimental conditions resulted in subjects being in one of two conditions: in the high price condition incomes and catalog prices were 50% higher than in the second (low price) condition. Real purchasing power was the same in both conditions, despite the 50% difference in nominal incomes. Subjects were aware of whether they were earning/buying in the high price or low price condition and also knew what the catalog prices were in both conditions.

The authors hypothesized that “areas of the brain that are engaged in the experiencing of rewards, such as the ventromedial prefrontal cortex, would exhibit money illusion in the sense of exhibiting a stronger BOLD response for incomes that were higher in nominal terms, but had an identical real value.”

That is just what they found. There was significantly increased BOLD activity in the ventromedial prefrontal cortex during the high price trials. “This result means that reward activation generally increased with income, but was significantly higher in situations where nominal incomes and prices were both 50% higher, which supports the hypothesis that activity in the ventromedial prefrontal cortex is subject to money illusion.”

A political result of a human money illusion bias might be an actual preference for money inflation, where incomes increase but prices do, too as compared to lower nominal incomes with lower prices that have similar purchasing power. Of course, in the real world, income and prices in an inflationary period are unlikely to increase by the same amount for any particular individual, so this study is a simplification compared to an economy, but it still makes you wonder whether money illusion explains (at least in part) why people like inflation and why it is therefore so politically easy for governments to tax covertly by inflating the money supply, thereby reducing the value of currency, allowing the government to inflate away its debts.

Reference

  1. Weber et al. The medial prefrontal cortex exhibits money illusion. Proc Natl Acad Sci U S A 106(13):5025-8 (2009)

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