The Durk Pearson & Sandy Shaw®
Life Extension News™
|Vol. 8 No. 3
"It is a commonplace that the history of civilisation is largely the history of weapons... And though I have no doubt exceptions can be brought forward, I think the following rule would be found generally true: that ages in which the dominant weapon is expensive or difficult to make will tend to be ages of despotism, whereas when the dominant weapon is cheap and simple, the common people have a chance. Thus, for example, tanks, battle- ships and bombing planes are inherently tyrannical weapons, while rifles, muskets, long-bows and hand-grenades are inherently democratic weapons. A complex weapon makes the strong stronger, while a simple weapon -- so long as there is no answer to it -- gives claws to the weak."
-- George Orwell, "You and the Atomic Bomb," published in the British Labour Party journal Tribune (Oct. 19, 1945)
"Wherever the real power in a Government lies, there is the danger of oppression. In our Governments the real power lies in the major- ity of the Community, and the invasion of private rights is chiefly to be appre- hended, not from acts of Government contrary to the sense of its constituents, but from the acts in which the Government is the mere instrument of the major number of the constit- uents."
-- James Madison, in a letter to Thomas Jefferson, Oct. 17, 1788
"Madison did not see that minorities could exploit majorities when the benefits of government action to those minorities were huge and the costs to each individual in the majority were small."
-- John Samples, Cato Policy Report, Mar./Apr. 2001
"A standing military force, with an overgrown Executive will not long be safe companions to liberty. The means of defence against foreign danger, have been always the instru- ments of tyranny at home."
-- James Madison, speech at the Constitutional Convention, June 29, 1787
"Our peculiar security is in the possession of a written Constitution. Let us not make it a blank paper by construction."
-- Thomas Jefferson
Table of Contents This Issue
Restless Legs: the Iron Connection
Before you rush out to buy the latest expensive prescription drug for "restless legs," you might consider that one cause of this condition is iron deficiency1. The prescripion drugs used to treat restless legs stimulate the function of dopaminergic neurons. Iron deficiency is known to cause a reduction in dopaminergic activity (as well as a rise in serum prolactin).2
Many people these days have reduced their intake of red meat, the best dietary source of iron. White meat (such as poultry) contains much less. Moreover, those who eat a diet rich in polyphenols as are found in fruits, vegetables, green, black and oolong tea, etc., may be absorbing much less than the quantity of iron they ingest because of the potent iron- chelating properties of many polyphenols (such as quercetin). If you are eating a diet like this and have developed restless legs, it is quite possibly due to iron deficiency.
In a recent study1, rats were fed diets either deficient in iron (ID) or iron adequate (CN). Another group of ID rats were given iron supplements (IR). Studies were done on the dopamine, serotonin, and noradrenaline transporter binding in various brain areas. The results showed that ID male rats (but not ID females) had a decrease of 20-40% in dopamine transporter binding in the nucleus accumbens, caudate putamen and substantia nigra. ID males also had a 20-30% reduction in serotonin transporter binding in the nucleus accumbens, olfactory tubercle, and colliculus, while ID females had 15-25% increased serotonin transporter binding in the olfactory tubercle, zona incerta, anteroventreal thalamic nucleus and vestibular nucleus. (It is possible that this increased serotonin transporter binding is linked to increased sensitivity to depression in females, at least in those who are iron deficient, since the serotonin reuptake inhibitors such as fluoxetine (ProzacR) inhibit the serotonin transporter.) Iron deficiency reduced binding to the noradrenaline transporter in locus ceruleus and anteroventral thalamic nucleus in ID and IR males but not females. Some, but not all, of the changes induced by iron deficiency were reversed by iron supplementation.
The authors state: "This experiment extends our knowledge to include the olfactory tubercle as a tissue sensitive to iron deficiency. This might implicate iron deficiency in endocrinological difficulties such as hyperprolactinemia." Prolactin is regulated by dopamine. High levels of prolactin stimulates the growth of breast and prostate tissue and, thus, may be a risk factor for developing breast and prostate cancers and would certainly stimulate the growth of such cancers.
We became interested in the connection between iron deficiency and restless legs when Sandy developed the latter condition. It has been completely eradicated with daily RDA level iron supplementation. Iron supplements should be taken at separate times from other supplements because of the possibility of chemical interactions with vitamin C resulting in free radical generation or with irreversible binding to polyphenols, especially quercetin. We suggest using ferrous gluconate; iron EDTA chelates produce hydroxyl radicals very efficiently in the presence of vitamin C and ferrous sulfate can be quite irritating.
1 Burhans et al, "Iron deficiency: Differential effects on monoamine transporters," Nutritional Neuroscience 8(1):31-38 (2005)
2 Barkey et al, "Characterization of the hepatic prolactin receptors induced by chronic iron deficiency and neuroleptics," European Journal of Pharmacology 122:259-267 (1986)
Tocopherol Radical Regeneration by Antioxidants
A recent paper1 reports on the ability of various antioxidants to regenerate vitamin E from the vitamin E radical (tocopheroxyl radical). Though vitamin C is a well known regenerater of the vitamin E radical to its normal non-radical form, there are other antioxidants that can do so and in some cases even more powerfully than vitamin C. This paper focused on catechins (found in tea): epicatechin (EC), epicatechin gallate (ECG), epigallocatechin (EGC), and epigallocatechin gallate (EGCG). The researchers found that EC, ECG, EGC, and EGCG "have activity similar to or higher than that of vitamin C in vitamin E regeneration at pH 7-12 in micellar solution."
They also looked at the regeneration capability of other antioxidants. They found that the rate of regeneration reaction of the tocopheroxyl radical with the natural antioxidants examined increases in the order of: methyl linoleate << rutin < EC < ECG < EGC ~ vitamin C (ascorbate anion) < EGCG < quercetin (pH 8) << CoQ10. The authors suggest that "catechins may function as antioxidants in biological systems."
It is interesting to note that in studies of the effect of vitamin E on the course of cardiovascular disease in patients with that condition, most included no regeneraters of vitamin E from its radical, leaving excess vitamin E radicals in the circulation. This may have accounted, in full or in part, for the negative impact of vitamin E in those studies. A few studies have used both vitamin E and vitamin C; however, there were no measurements made of the redox state in the circulation, so we don't know whether the doses of E and C used were adequate to reduce oxidative stress in cardiovascular disease patients.
Moreover, many of the studies of vitamin E and cardiovascular disease with negative results were done on patients with pre-existing cardiovascular disease; most of those patients would have been taking statins. Statins powerfully inhibit the production of both cholesterol and CoQ10, the latter being the most powerful regenerater of the tocopheroxyl radical (see above). All users of statins should take 120-240 mg./day of supplemental CoQ10.
1 Mukai et al, "Structure-activity relationship of the tocopherol-regeneration reaction by catechins," Free Radical Biology & Medicine 38:1243-1256 (2005)
Arginine Improves Endothelial Function in Healthy Individuals Older Than 70 Years
As we explained in our last issue, mortality from cancer now exceeds mortality from heart disease except in those over 85.1 A new study2 found oral L-arginine to "partially correct severely depressed endothelial function in healthy individuals older than 70 years. This suggests a novel therapeutic strategy all the more because neither pravastatin nor vitamin E were effective in correcting endothelial function in asymptomatic men older than 70 years with moderate hypercholesterolaemia."
The 12 subjects (eight men and four women) in the study were healthy, lifelong nonsmokers, with no signs of cardiovascular disease and with a mean age of 73.8 years (70-78). The subjects were studied for the effects of oral arginine (8 grams twice daily) or placebo on endothelium-dependent NO-mediated vasodilation, as indicated by flow-induced vasodilation in the brachial artery. "Flow-induced, NO-mediated vasodilation of the brachial artery was 2.65+-1.15% before L-arginine intake and 0.64 +-0.89% before placebo intake [not significant] as compared with 11.00 +-3.4% in healthy young subjects (p<0.01). Supplementation with oral l-arginine significantly enhanced endothelium-dependent vasodilation (to 5.73 +- 1.19%, p<0.05 versus baseline and p<0.0001 versus placebo); whereas placebo had no significant effect ... " As the authors pointed out, the decline (from youthful levels) in endothelial-dependent vasodilation measured in this study is compatible with data from an earlier study3 showing a "gradual decline in FMD [flow mediated vasodilation] with increasing age in 238 asymptomatic subjects aged 15-72 years without known atherosclerotic risk factors."
The points to note are: 1. The endothelial function was severely depressed in these 12 healthy nonsmoking subjects over 70 who were examined for and found to have no signs of cardiovascular disease. Hence, "healthy" is a relative term, as the endothelial function (as explained in the previous paragraph) in the healthy 70+ year olds would be considered seriously dysfunctional in the healthy young. 2. Oral L-arginine (8 grams twice a day) was effective in partially and significantly improving endothelial function.
We have been using an arginine + choline + vitamin B5 formulation (Inner Power™, Power Maker™, which contain 6 grams of arginine per serving) for almost 30 years. We include choline and vitamin B5 in our formulation, though we haven't seen these nutrients in other arginine formulas, because the vasodilatory response is mediated through acetylcholine as well as nitric oxide.4
In a separate paper5, four weeks of oral supplemental L- arginine (7 grams three times a day) in 27 young hypercholesterolemic subjects aged 29 +- 5 years (19-40) significantly improved (compared to placebo) endothelium- dependent vasodilation (which improved from 1.7 +- 1.3 to 5.6 +- 3.0%).
1 Twombly, "News: Cancer surpasses heart disease as leading cause of death for all but the very elderly," Journal of the National Cancer Institute 97(5):330-331 (2005)
2 Bode-Boger et al, "Oral l-arginine improves endothelial function in healthy individuals older than 70 years," Vascular Medicine 8:77-81 (2003)
3 Celermajer et al, "Aging is associated with endothelial dysfunction in healthy men years before the age-related decline in women," J Am Coll Cardiol. 24:471-76 (1994)
4 Ignarro et al, "Endothelium-derived relaxing factor from pulmonary artery and vein possesses pharmacologic and chemical properties identifical to those of nitric oxide radical," Circulation Research 61:866-879 (1987)
5 Clarkson et al, "Oral L-arginine improves endothelium-dependent dilation in hypercholesterolemic young adults," Journal of Clinical Investigation 97:1989-1994 (1996)
Arginine and Protective Ischemic Preconditioning
Preconditioning is the term for the protective effect induced in tissues exposed to brief periods of reduced oxygen availability against later (within a certain time period) exposure to more severe reduced oxygen availability. It is believed to be due to the induced expression of protective substances such as antioxidant enzymes and heat shock proteins. An example of preconditioning is that the brief periods of ischemia followed by reperfusion that occur during angina provide protection to the heart against damage from ischemia/reperfusion events during the following day or so.
A recent study1 reports that the amino acid L-arginine induces a protective effect like preconditioning in the liver by stimulating the production of nitric oxide which, the authors suggest, might inhibit the downregulation of eNOS (endothelial nitric oxide synthase, which makes nitric oxide in the lining of blood vessel walls) during reperfusion following ischemia (reduced oxygen availability).
Ischemia-reperfusion is a source of considerable damage during a heart attack. While the reduced oxygen availability of ischemia causes damage (for example, by reducing the ability of heart cells to produce ATP, for which oxygen is required), the reperfusion following ischemia also causes damage via increased free radical activity. Liver suffers similar damage in response to ischemia-reperfusion (IR). In this study of preconditioning in the rat liver, IR was associated with a decline in L-arginine levels and decreased eNOS activity in the affected tissue. (An excessively low level of L-arginine is associated with decreased production of nitric oxide and also with "uncoupling" of nitric oxide synthase, where the enzyme produces superoxide radicals rather than nitric oxide, with resulting increased production of the potent oxidant peroxynitrite.) The researchers also found increased ornithine levels in the IR group, which suggests that there was an increase in liver arginase activity. Arginase is an enzyme that metabolizes L-arginine to ornithine, which is then converted to polyamines. Many cancers are associated with upregulated arginase, which reduces the availability of L-arginine for conversion to nitric oxide by nitric oxide synthase.
The authors induced preconditioning in the rat livers by causing 5 minutes of lobar ischemia and 10 minutes of reperfusion; this was followed by the more severe treatment of 45 minutes ischemia and 2 hours of reperfusion. The authors report: "The major finding of the study is that cytoprotective nitric oxide is produced by eNOS during ischemic preconditioning of the liver... The results also demonstrate that IPC [ischemic preconditioning] was associated with an increased availability of the l-arginine substrate." "Arginine is degraded by arginase to ornithine and sufficient quantities of arginase can limit the availability of arginine for NO synthesis and hepatic [liver] ischemia reperfusion has been shown to be associated with an increased arginase 1 activity. The low ornithine levels in the preconditioned [by exposure to short term ischemia followed by reperfusion] livers could suggest the possibility that the effect of IPC may involve modulation of arginase to increase substrate availability for NO biosynthesis."
"The effects of L-arginine administration were similar to those evident following IPC." "L-arginine supplementation modulates the NO-dependent vascular functions and clinical studies have reported that l-arginine administration reduces the symptoms of coronary heart disease in patients." However, "the administration of exogenous l-arginine not only significantly increased plasma level but also led to increased ornithine levels. The higher production of ornithine would indicate arginase activity. This raises the possibility that some of the NO generation after l-arginine administration may be independent of the l-arginine/NOS pathway."
In conclusion, arginine may provide protection similar to preconditioning in tissues subject to ischemia and reperfusion. This is one reason that both of us take L-arginine supplements in the form of our Inner Power™ (also called Power Maker™) formulation which contains L-arginine plus choline, B5 and other nutrients.
1 Koti et al, "Nitric oxide synthase distribution and expression with ischemic preconditioning of the rat liver," The FASEB Journal 19:1155-1157 (2005)
Cholinergic Agonists Improve Survival in Experimental Sepsis; Link to Arthritis
We have written previously on protective strategies against out-of-control bacterial infections (sepsis), an increasing risk due to antibiotic resistant bacteria. We have also written about the cholinergic vagus nerve anti-inflammatory pathway. Here, a recent study1,2 reports that cholinergic agonists protected mice against sepsis induced by lipopolysaccharide and by cecal (part of the large intestine) ligation and puncture.
The authors of the study note that they recently identified high mobility group box 1 (HMGB1) protein as a late mediator of lethal systemic inflammation in sepsis. In another paper3, the researchers identify HMGB1 as a "mediator of interest" in human and experimental arthritis; they note that HMGB1 can either be actively secreted by macrophages or passively released by necrotic cells of all kinds and that macrophages and unprogrammed cell death caused by ischemia or activated complement are prominent features of the persistent synovial inflammation of chronic arthritis. The authors3 also note that elevated levels of HMGB1 are present in synovial fluid samples from rheumatoid arthritis patients. Inhibition of HMGB1 (with either neutralizing antibodies or the antagonistic A box domain of HMGB1) was reported to ameliorate collagen-induced arthritis in both mice and rats and inhibits local overexpression of the inflammatory cytokine IL-1beta in the joints.
The researchers3 note that serum HMGB1 levels are below 5 ng/mL in the serum of healthy animals and normal humans, but that much higher circulating levels (up to 150 ng./mL) were observed in human patients with severe sepsis, with the highest levels in those who died.
The researchers of paper 1 report that they discovered that acetylcholine release through the vagus nerve can modulate circulating tumor necrosis factor alpha (TNFalpha) levels induced by endotoxin. In this paper, they find that acetylcholine suppresses HMGB1 release from macrophages through a nicotinic cholinergic receptor. Nicotinic cholinergic receptors are stimulated by acetylcholine (which also stimulates muscarinic cholinergic receptors); selective nicotinic cholinergic receptor stimulators include nicotine, but unfortunately for many reasons nicotine is not recommended. However, nicotine was used to treat the experimental mice in this study. Their results indicated that nicotine could rescue animals from established severe sepsis.
Our choline supplement (Memory Upgrade™ or Choline Cooler™) includes choline and vitamin B5, as well as other nutrients. Vitamin B5 is required to convert choline to acetylcholine. We take it daily for its cognition enhancing effects, but would take more if we became infected with an antibiotic-resistant strain of bacteria. It may also help with arthritis, though it is hard to separate the effects from everything else we take.
1 Wang et al, "Cholinergic agonists inhibit HMGB1 release and improve survival in experimental sepsis," Nature Medicine 10(11):1216-1221 (2004)
2 Matrthay & Ware, "Can nicotine treat sepsis?" Nature Medicine 10(11):1161-1162 (2004)
3 Andersson and Erlandsson-Harris, "HMGB1 is a potent trigger of arthritis," Journal of Internal Medicine 255:344-350 (2004)
Urinary Tract Infections Nicotinic Acid Prevents Candida Adherence
Most of you have probably read about the effects of certain constituents of cranberry juice that inhibit the adhesion of microbes to the epithelial lining of the bladder and urinary tract, thus helping to prevent and eliminate urinary tract infections. According to a new study1, nicotinic acid (niacin) can also help.
The study examined the effect of nicotinic acid on urinary tract infection caused by Candida glabrata. The paper reports that Candida accounts for about 25% of all urinary tract infections relating to indwelling catheters, with C. glabrata accounting for about 15% of the Candida isolates. Adherence to the urinary tract cells is necessary for infection and, in C. glabrata, is mediated by a lectin encoded by the EPA1 gene family. In this organism, EPA6 and EPA7 are normally silenced, but their expression (unsilencing) leads to adhesion in the urinary tract. The authors found that nicotinic acid deficiency in the urinary tract was the cause of the re-initiation of expression of these genes. The way this works is that Sir2p (a silencing gene that is also implicated in longevity) is modulated by cellular levels of nicotinamide adenine dinucleotide (NAD), for which nicotinic acid is a precursor. The authors say that "Here we provide data suggesting that cellular NAD+ levels, which in C. glabrata are tied to environmental NA [nicotinic acid] levels, modulate Sir2p-mediated silencing of subtelomeric EPA genes in response to the host environment."
To sum it up: Relatively low nicotinic acid levels in the urinary tract result in increased adhesion of Candida. Hence, supplementation with nicotinic acid ought to help prevent or to eliminate Candida urinary tract infections.
1 Domergue et al, "Nicotinic acid limitation regulates silencing of Candida adhesins during UT1," Science 308:866-870 (2005)
More on Glycogen Synthase Kinase-3, Inhibited by Lithium: Alzheimer's, Neurotoxicity, and Cellular Senescence
Glycogen synthase kinase-3beta is a central figure in many intracellular signaling pathways and is inhibited by lithium.1 We wrote earlier about this in our discussion of Galantamind Plus™, our brain maintenance formulation that includes low-dose lithium for the purpose of partially inhibiting glycogen synthase kinase-3beta.*
As glycogen synthase kinase-3 is importantly involved in cell survival and proliferation, many new findings are being reported on its effects. Here we report on four of the latest papers we've found: inhibition of glycogen synthase kinase-3 as a potential protectant against the development of Alzheimer's disease2,3, how the inactivation of glycogen synthase kinase-3 beta protects against kainic acid-induced excitotoxicity in brain cells4, and how glycogen synthase kinase-3 accumulates in the nucleus of replicatively senescent human fibroblasts.5
Alzheimer's: A new paper2 reports that inhibition of glycogen synthase kinase-3 by lithium correlates with reduced levels of aggregated, insoluble tau. Tau is a normal protein found in the brain but its abnormal aggregated and insoluble form is found in neurofibrillary tangles such as are found in aging and in larger quantities in Alzheimer's disease. This study found that levels of aggregated tau correlated strongly with the degree of axonal degeneration, while lithium treated mice showed less degeneration when begun during the early stages of tangle development.2
In the next paper3, researchers found that glycogen synthase kinase-3 protein was increased in white blood cells in both Alzheimer's patients and those with mild cognitive impairment relative to elderly controls. The authors explain: "These data are in line with previous studies suggesting an altered response to insulin in AD [Alzheimer's disease]. Glucose regulation is aberrant in AD and fasting plasma insulin levels are higher; features of insulin resistance indicative of a failure of the normal inhibitory effects of insulin on GSK-3 [glycogen synthase kinase-3]. They are also in line with neuroimaging studies pointing to altered glucose utilization in brain in AD." (citations omitted). The authors suggest, therefore, that "...inhibition of GSK-3 [glycogen synthase kinase-3] might be a useful therapeutic strategy." Moreover, "Our findings raise the possibility that measures of GSK-3 in circulating white cells might be useful in the diagnosis of AD."
Excitotoxicity: In another paper4, scientists found that lithium was protective against kainic acid-induced excitotoxicity in hippocampal slice cultures.
Cellular Senescence" In the final paper5, an interesting interaction of glycogen synthase kinase-3 with p53 (an important tumor suppressor protein), in which the activity of p53 was enhanced was reported. When cells are damaged, p53 is induced; p53 suppresses cell division and, hence, permits damage repair (or apoptosis if the damage is too great to repair) to take place. Senescent cells do not divide and, hence, having a large percentage of senescent cells can promote aging by limiting repair by cell division to replace damaged and defective cells. The researchers found that compared with young and middle-aged human WI-38 fibroblasts, senescent cells contained increased levels of glycogen synthase kinase-3beta in the nucleus (and also tended to contain increased levels of the other isoform, glycogen synthase kinase-3alpha). Upon inhibition of glycogen synthase kinase-3beta with lithium, the senescence associated accumulation of p53 was reduced. The treated cells exhibited changes (lithium blocked the increases in beta glucosidase, p53, and p21 normally associated with senescence) suggesting a reversal of senescence into a reversible state of quiescence. These effects were seen for lithium at a dose of 10mM, but not at 1 mM or 3 mM. It is not clear from this study, as it is a cell culture study, what would be an appropriate and effective, yet nontoxic dose of lithium in a whole organism, let alone a human, for the purpose of "treating" cell senescence. Nevertheless, we consider safe low-dose lithium supplementation to possibly have a beneficial effect on such senescence, since even small doses may inhibit glycogen synthase kinase-3beta to some extent. It is certainly worth studying further.
* See "Maintain Your Brain the Durk Pearson and Sandy Shaw Way" in the May 2004 Life Enhancement (issue free from Life Enhancement Products, Inc., PO Box 751390, Petaluma, CA 94975- 1390)
1 Jope and Bijur, "Mood stabilizers, glycogen synthase kinase- 3beta and cell survival," Molecular Psychiatry 7:S35-S45 (2002)
2 Noble et al, "Inhibition of glycogen synthase kinase-3 by lithium correlates with reduced tauopathy and degeneration in vivo," Proceedings of the National Academy of Sciences USA 102(19):6990-6995 (2005)
3 Hye et al, "Glycogen synthase kinase-3 is increased in white cells early in Alzheimer's disease," Neuroscience Letters 373:1-4 (2005)
4 Goodenough et al, "Inactivation of glycogen synthase kinase- 3beta protects against kainic acid-induced neuirotoxicity in vivo," Brain Research 1026:116-125 (2004)
5 Zmijewski and Jope, "Nuclear accumulation of glycogen synthase kinase-3 during replicative senescence of human fibroblasts," Aging Cell 3:309-317 (2004)
Serotonin Transporter Found in B-Cell Malignancies Inhibition of Cancer Growth by Inhibiting Transporter
The serotonin transporter (SERT) has recently1 been reported to be present in a large number of B-cell malignancies, including B cell precursor acute lymphoblastic leukemia, multiple myeloma, Burkitt's lymphoma, pro-lymphocytic leukemia, mantle cell lymphoma, diffuse large B cell lymphoma, and primary mediastinal B cell lymphoma. Normal tonsilar B cells, however, contained no detectable SERT. Mitogenic stimulation (causing cells to divide) by phorbol ester, a known cancer promoter, and a calcium ionophore led to the induction of readily detectable SERT in resting B cells that otherwise had no detectable SERT.
The researchers then tested drugs that are known to target SERT, which includes selective serotonin uptake inhibitors (SSRI fluoxetine), tricyclic antidepressant clomipramine, and the amphetamine derivatives MDMA ("Ecstasy"), and fenfluramine, to see whether they could arrest the growth of the model Burkitt's lymphoma cell line. Twelve of the 17 derived B cell lines showed an antiproliferative response to the tested psychotropics. Thus, as the authors note, this study establishes SERT expression as a phenotype common to neoplastic B cell clones of widely distinct tumor origin.
The concentrations required for MDMA and fenfluramine to elicit an anti-tumor response were high. However, the effects of fluoxetine and clomipramine occurred at concentrations known to be reached in the serum of patients on standard dosing regimes for anxiety-related disorders; as these two agents pass the blood-brain barrier, the authors suggest that they be studied for the possible treatment of CNS lymphomas.
It is also interesting to note that the potent proinflammatory cytokine tumor necrosis factor alpha enhances the function of the serotonin transporter2, pointing out a possible mechanism for the depression associated with inflammation and/or cancer.
1 Meredith et al, "The serotonin transporter (SLC6A4) is present in B-cell clones of diverse malignant origin: probing a potential anti-tumor target for psychotropics," The FASEB Journal 19:1187- 1189 (2005)
2 Mossner et al, "Enhancement of serotonin transporter function by tumor necrosis factor alpha but not by interleukin-6," Neurochemistry International 33:251-254 (1998)
Search Studies Show Airline Baggage Inspections a Waste of Time and Resources
A short report in Nature1 found that in searches for rare targets, the more infrequently the target is actually there, the greater the risk that human inspectors will miss it. The researchers compared the performance of searchers in an artificial baggage-screening task in which people were to look for "tools" among objects in other categories. The number of objects shown in a display was 3, 6, 12, or 18 and target prevelance was 1%, 10%, or 50%.
In the 1% prevelance condition, 12 paid volunteers searched in 2,000 trials (broken into 250 trial blocks) that included 12 target-present trials. Each observer was also tested separately in over 200 trials of the 10% and 50% target-present trials. The 50% prevelance trials resulted in 7% miss errors (failing to notice a target), which (the authors say) is typical for laboratory search tasks of this sort. However, at 10% prevelance, the miss error was 16% and errors were 30% at 1% prevelance.
These data suggest that the federal government is wasting everybody's tax money on these searches, while wasting the time of those "inspected." Where is the supposed safety these inspections are supposed to foster when, supposing the appearance of actual important forbidden objects (such as knives, guns, etc.) is even as high as 1% (though this seems unlikely to us), then 30% of these objects are likely to be missed. Add on to that the fact that there is little or no accountability for searchers who habitually miss items and you have to wonder whether these monopoly unionized federal inspectors are even doing so "well" as a 30% error rate.
Next time you or your baggage are searched at an airline, you might think of this. Of course, you mustn't say anything to the nice inspector about these data because your First Amendment rights to criticize "your" government do not apply when talking to federal airline inspectors and you might get thrown off your flight (or fined or imprisoned) for "harrassing" the government.
1 Wolfe et al, "Rare items often missed in visual searches," Nature 435:439 (2005)
© 2005 by Durk Pearson & Sandy Shaw