October 2010 Blog with Durk and Sandy

A few good laughs from late night TV humor:

The liberals are asking us to give Obama time. We agree … and think 25 to life would be appropriate.— Jay Leno

Q: Have you heard about McDonald’s new Obama Value Meal?
A: Order anything you like and the guy behind you has to pay for it.
— Conan O’Brien

Q: What’s the difference between Obama and his dog, Bo?
A: Bo has papers.
— Jimmy Kimmel

Other gems of wisdom or humor:

Whenever the legislators endeavor to take away and destroy the property of the people, or to reduce them to slavery under arbitrary power, they put themselves into a state of war with the people, who are thereupon absolved from any further obedience.— John Locke (1632–1704)He who dares not offend cannot be honest.— Thomas PaineIf there had been any formidable body of cannibals in the country he would have promised to provide them with free missionaries fattened at the taxpayer’s expense.— H. L. Mencken (Baltimore Sun, 7 Nov. 1948)
[of Truman’s success in the 1948 presidential election]



Sleep Disordered Breathing (Such as Sleep Apnea)
May Increase the Risk of Coronary Artery Disease
by Increasing Protein Carbonylation—How to
Reduce the Risk

Although it is known that sleep apnea, whether obstructive sleep apnea or central sleep apnea, is correlated with an increased risk of cardiovascular disease, the mechanisms are not well understood. During sleep apnea, there is a diminished or transiently discontinued breathing, which results in intermittent hypoxia (reduced oxygen supply) and generation of ROS, reactive oxygen species. A 2010 paper1 reports that this increased cardiovascular risk may be due to the production of higher levels of carbonyl compounds (which cause oxidative damage to proteins). Fortunately, there are natural substances that, taken as a supplement, can substantially reduce damage by carbonyl compounds.

The new paper1 did a study on 14 individuals with sleep disordered breathing as well as cardiovascular disease and 33 controls with less than 50% coronary artery narrowing. They tested the hypothesis that carbonyl compounds are causative factors in the increased risk cardiovascular disease in sleep disordered breathing. The results included that the coronary artery disease patients had higher erythrocyte (red blood cell) carbonyl concentrations. There was a positive correlation between the apnea-hypopnea index (AHI, a measure of the severity of apnea (no breathing) and hypopnea (diminished breathing)) and erythrocyte carbonyl concentrations. Then, to predict coronary artery disease, the researchers examined a multiple regression between AHI, erythrocyte carbonyl, gender, age, and body mass index; the significant variables in this Poisson multiple regression model were AHI and erythrocytes carbonyl. Their model (based on the data from the patients and controls) predicts that an increase of 1 pmol/gHb (Hb is hemoglobin) in erythrocyte carbonyl levels increases by 1.8% the risk of coronary artery disease and one unit of AHI increases by 3.8% the risk of coronary artery disease.

These data represent newly emerging information on the relationship of carbonyl compounds and the risk of cardiovascular disease. The authors of paper #1 say that in humans, “only one study was reported showing evidence of augmented carbonylation of intercostal muscle proteins in OSA [obstructive sleep apnea] patients.” (This was in 12 male patients with severe obstructive sleep apnea as compared to 6 controls without obstructive sleep apnea.) Though erythrocyte carbonyl content was predictive of coronary artery disease, the researchers1 did not observe a correlation between PLASMA carbonyl and coronary artery disease or AHI. Interestingly, plasma carbonyl showed a negative correlation with vitamin C and, the authors note, “vitamin C levels is lower in group 1 (sleep disordered breathing plus coronary artery disease) as compared to group 2 (controls with coronary artery narrowing of less than 50%).

The authors conclude: “The evidence here obtained supports our initial hypothesis that repeated episodes of hypoxia encountered in sleep apnea increase the oxidative damage to erythrocyte proteins, suggesting, therefore, involvement of sleep apnea in CAD [coronary artery disease] pathogenesis through oxidative stress mechanisms. Vitamin C may assist in preventing plasmatic protein damage in patients with sleep apnea.”1

Reducing the Risk

Carbonyl compounds that result in protein and lipid oxidation processes can act as powerful inducers of the formation of AGEs (advanced glycation endproducts, which are markers of carbonyl stress), implicated as causative factors in cancer, cardiovascular disease, complications of diabetes, and even aging. We developed a formulation called AGEless™ specifically for the purpose of inhibiting formation of or reducing the damage caused by AGEs and/or to scavenge carbonyl compounds that includes benfotiamine (a lipid soluble form of thiamine), carnosine, histidine, alpha-lipoic acid, and rutin. [For more on these nutrients and their effects on AGEs, as well as references, see “Reducing Glycation Reactions for Better Health and Longer Life” in the February, 2008 issue of Life Enhancement.]


  1. Klein et al. Carbonyl groups: bridging the gap between sleep disordered breathing and coronary artery disease. Free Radical Research 44(8):907-12 (2010).


Three papers1,2,3 focus on the very interesting relationship between increased white blood cell numbers and the morbidity and mortality of acute and chronic vascular disease.

One of these papers1 reports that in the oldest old (age 85 and older), white blood cell (WBC) count and CRP (C-reactive protein, a strong marker of systemic inflammation and a good predictor of vascular events and mortality1), were both independently predictive of mortality. A total of 599 85-year old women and men were followed for five years in the Leiden-85-plus Study. Blood samples were taken at age 85 and then yearly; after age 90, remaining subjects were followed up for mortality. The results showed that for every increase of 1 SD (standard deviation) in WBC count, there was a 1.26 (95% confidence interval [CI]=1.15-1.38) increased risk for all-cause mortality, with similar increased mortality risks for both vascular mortality and nonvascular mortality. An increase of 1 SD in CRP level was associated with a 1.22 (95% CI=1.10-1.35) increased risk for all-cause mortality, with similar increases in mortality risk for nonvascular mortality. There was a tendency for an increased risk of vascular mortality (that is, it didn’t quite reach statistical significance).

A second paper2 reviews the association between leukocytosis (increased white blood cell numbers) and increased morbidity and mortality of ischemic vascular disease. The author refers to the discussion in Dr. Paul Dudley White’s 1949 edition of his text on heart disease, in which Dr. White wrote (without a reference) that severe and sustained leukocytosis after myocardial infarction was associated with poor prognosis. In 1954, it was reported by Cole et al4 that more than 32% of patients with an acute heart attack having a white blood cell count of greater than 15,000/uL died within the first two months after the attack, whereas less than 9% of patients with a WBC count less than 10,000/uL died within the first two months. Studies involving over 350,000 patients treated with “more modern therapies” have been published to date and “in nearly all of these studies, a significant relationship between leukocyte count and vascular disease morbidity and mortality was observed.”2 The paper2 summarized the results of selected studies assessing the association between WBC count and morbidity and mortality of ischemic vascular diseases from 1999–2004. The author2 states that “regardless of the mechanism underlying the association between leukocytosis and mortality after acute myocardial infarction, it appears that modern reperfusion and early revascularization strategies mitigate or eliminate the association between WBC count and mortality during the first 6 months after a myocardial infarction.”

The third paper3 reports that in cholesterol-fed rabbits (either a 0.25% or a 0.1% cholesterol-enriched diet), circulating WBC were elevated by one week of feeding and these higher levels were sustained for at least 30 weeks. But switching the cholesterol-fed rabbits to a regular rabbit chow diet resulted in a reversal to pre-treatment levels of WBC.

Aspirin May Lower WBC Counts

Paper #2 reports that in four separate studies of leukocytosis and cardiovascular risk involving a total of greater than 160,000 patients, “aspirin use was associated with significantly lower WBC counts.” However, the author cautions “[b]ecause these studies were not randomized, many confounding factors may have influenced the apparent association between aspirin use and lower leukocyte counts.”2 Here, again, is a relatively simple and potentially important hypothesis to test in a randomized trial: whether aspirin can be used to reduce excessive WBC counts.


  1. Willems et al. White blood cell count and C-Reactive protein are independent predictors of mortality in the oldest old. J Gerontol A Biol Sci Med Sci 65(7):764-8 (2010).
  2. Coller. Leukocytosis and ischemic vascular disease morbidity and mortality: is it time to intervene? Arterioscler Thromb Vasc Biol 25:658-670 (2005)
  3. Feldman et al. Leukocytosis in rabbits with diet-induced atherosclerosis. Arterioscler Thromb Vasc Biol 11:985-94 (1991).
  4. Cole et al. The long-term prognosis following myocardial infarction, and some factors which affect it. Circulation 9:321-34 (1954).


A 2010 paper1 reports on the “controversial clinical finding that reduced sodium intake or reduced urine output inversely correlates with cardiac mortality in patients.” This is not something being widely discussed in public media.

The authors of this new paper say that “… an interesting series of clinical studies by Alderman over the past 20 years call into question the wisdom of this approach [following a low salt diet], lacking a strong mechanistic scientific basis such as reduced NO bioavailability in the heart. For instance, patients on a LS [low salt] diet have an increase in coronary events compared to those on normal salt (NS) intake.” “The controversy around the potential detrimental effects of a LS diet has been discussed by Aviv, proposing the hypothesis that there is a U-shaped function curve governing salt intake. Furthermore, the effect responsible for mortality at both high and LS intake is proposed to be NO-superoxide.”

The authors cite a paper supporting their statement that “during restriction of salt intake, it is already established that there is an increase in plasma angiotensin II.” “The ability of NO [nitric oxide] to reduce oxygen consumption in vitro in the normal mouse heart is almost abolished during incubation with angiotensin II via an AT1 [angiotensin II type 1] receptor-dependent mechanism.” Increased superoxide production stimulated by angiotensin II results in decreased availability of NO due to the interaction of superoxide and NO that creates the potent oxidant peroxynitrite. Interestingly, gamma tocopherol is a potent scavenger of peroxynitrite (more effective than alpha tocopherol) and protects against peroxynitrite-induced lipid oxidation.2

The researchers performed experiments on adult male mongrel dogs that were placed on a low salt (LS) diet (0.05% sodium chloride) for two weeks. They found that NO-mediated vasodilation was inhibited by 44% in the LS as compared to controls. However, importantly they found that intravenous infusion of ascorbic acid or apocynin at the same time as the LS diet “acutely and completely reversed this inhibition.” As apocynin is a powerful inhibitor of NADPH oxidase, which generates superoxide, it shows how important superoxide is to the inhibitory effect of LS on NO-mediated vasodilation.

Moreover, LS induced increases in two subunits of NADPH oxidase, p47phox (121% increase) and gp91phox (44% increase) and also increased gene expression in the LS heart tissue of p47phox by 1.6 fold and gp91phox by 2.0 fold. The authors conclude: “LS diet induces the activation of the renin-angiotensin system, which increases oxidative stress via the NADPH oxidase and attenuates NO bioavailability in the heart.”

“… our studies have defined a potential mechanism, the reduction in NO bioactivity, which may contribute to the detrimental effects of LS in patients.”1 The authors caution, however, that “[t]he clinical relevance of our study still remains to be determined.”1

Lower Ratio of Potassium/Sodium in Modern Diet As Compared to Paleolithic Diet

Evidence indicates that it is not high sodium that is the basic problem in hypertension, but the low ratio of potassium to sodium in the modern diet.3 In a study of patients selected for essential hypertension, potassium bicarbonate significantly reduced high blood pressure by 8 weeks compared with placebo, while potassium chloride did not,3 suggesting the possibility that excess chloride rather than sodium may be the pathogenic agent in salt-induced hypertension. In another study, this one performed by the authors of paper #3, they showed in 41 metabolically controlled studies of 38 healthy normotensive men (24 black men and 14 white men) “that in most of the blacks but not the whites, salt sensitivity occurred when dietary potassium was even marginally deficient, 30 mmol/day, but not attended by hypokalemia [clinically apparent potassium deficiency], as judged by a fasting serum concentration of potassium of 4.0 mmol/L. However, the pressor [blood pressure increasing] effect of NaCl loading was dose-dependently suppressed when dietary potassium was increased to 70 and 120 mmol/L per day by supplemental KHCO3 [potassium bicarbonate].” Moreover, the authors3 report that with aging, plasma bicarbonate decreases, while the serum concentration of chloride increases. Hence, if excess chloride is a problem and decreasing bicarbonate certainly is, it gets worse with age.

We each take a potassium bicarbonate supplement (Potassium Basics™) for reduced blood pressure, as well as reduced dietary acid load, increased muscle mass, decreased bone loss, reduced risk of stroke, and improved endothelial function. [See “Potassium Bicarbonate Supplementation” and “Potassium Bicarbonate for Reduced Blood Pressure and Increased Muscle Mass” in the April 2009 issue.]


1. Suematsu et al. Potential mechanisms of low sodium diet induced cardiac disease: superoxide-NO in the heart,” Circ Res 106:593-600 (2010).
2. Christen et al. Gamma tocopherol traps mutagenic electrophiles such as [reactive nitrogen oxide species] and complements alpha-tocopherol: physiological implications. Proc Natl Acad Sci USA 94:3217-22 (1997).
3. Morris et al. Differing effects of supplemental KCl and KHCO3: pathophysiological and clinical implications. Semin Nephrol 19(5):487-93 (1999).


You are probably already familiar with the fact that if you have symptoms of a heart attack, you should chew and swallow a 325 mg aspirin (this is a full size aspirin, not the low dose kind) to interfere with ongoing platelet aggregation and increase your chances of both surviving and of preserving more of your myocytes (heart cells). A new paper1 reports a simple and very cheap new technique for improving the outcome if you have a heart attack.

A newly reported study1 tested the hypothesis that remote ischemic conditioning (induced by repeated brief periods of limb ischemia—reductions in and then restoration of blood flow) after the onset of a heart attack but before reperfusion, reduces the size of the infarct (killed heart tissue). This technique had already been shown to reduce infarct size in a pig heart attack model. The remote ischemic conditioning was applied during the ride in the ambulance and consisted of four cycles of 5 minute inflation and 5 minute deflation of a blood-pressure cuff around the arm.

The researchers report on a group of 333 consecutive adult patients with a suspected first acute heart attack who received this remote ischemic conditioning treatment (82 were excluded on arrival at the hospital because they did not meet inclusion criteria, while another 77 did not complete followup, leaving 174 patients in the analysis of results). The median salvage index (calculated as the difference between area at risk and final infarct size as a percentage of the left ventricular mass volume) was 0.75 in the remote conditioning group versus 0.55 in the control group. The authors conclude: “Remote ischaemic conditioning before hospital admission increases myocardial salvage and has a favourable safety profile.”

A question unanswered by this study is whether chewing and swallowing an aspirin along with remote ischemic conditioning would have greater (additive or synergistic) beneficial effects over an aspirin alone or (though we consider it unlikely) a lower amount of protection than an aspirin alone. Only new research will answer this question.

In the meantime, the hell with Medicare. Paramedics are not likely to charge you much (we certainly hope!) to pump up and release a blood pressure cuff for four cycles of 5 minutes of inflation and 5 minutes of deflation. If it was us, we’d do it to ourselves but we can make NO recommendation concerning anyone else—we mean it. Show your doctor the paper and discuss it with him/her.

How Remote Ischemic Conditioning Works

There was a short review in the July 2010 Nature Medicine2 on the current understanding of how remote conditioning works. The author cites a 1986 study3 of induced heart attacks in dogs that introduced the term and the concept of “ischemic conditioning.” The researchers used the technique of four intermittent periods of occlusion and reperfusion for five minutes—accomplished in this case by constricting and then releasing a coronary artery with a silk suture. The result was a reduction in the size of myocardial infarction. Since then it has been found that the brief episodes of ischemia-reperfusion that comprises the conditioning doesn’t even have to be performed in the myocardium, but can provide heart protection even when done in a tissue far from the heart such as the lower limb muscle, as was shown in a rabbit study.4In another study cited in the Nature Medicine review,2 remote conditioning administered to patients undergoing coronary stenting (the insertion of a device to hold open a blood vessel) experienced lower procedure-related ischemic chest discomfort, cardiac troponin I release, and subsequent cardiovascular events.5

The actual mechanisms that are responsible for the protective effects of remote conditioning are still in early stages of investigation. The author2 of the review notes that autocoids, biological factors locally released from the preconditioned tissue, which includes bradykinin, adenosine, or opioids, are hypothesized to be involved. In percutaneous interventions such as angioplasty, it has been found that cardioprotection is enhanced by combining conditioning with the opioid morphine, as was shown in one study6 cited in the review where the combination of conditioning and morphine was monitored by ST-segment deviation resolution and lower-peak troponin I levels. Moreover, “exogenous activation of delta- and kappa-opioid receptors confers protection against myocardial stunning in mouse heart, such as improved recovery from contractile dysfunction after ischemia.”2 The review continues with further discussion of possible effects of various opioid receptors on chemokines involved in inflammatory reactions that might be involved in ischemia-reperfusion injury.

Clearly the mechanistic basis for remote conditioning is not very well understood, but it is something that ought to be thoroughly investigated as it could potentially save large numbers of lives. It is a technique that (based on the available data) might be safe and beneficial, though the author2 of the review cautions that “[a]lthough this noninvasive and inexpensive intervention is simple and safe to apply and was even beneficial in patients with an occluded coronary artery, large-scale trials are necessary to confirm these results.” Though nobody is going to make any money investing in clinical research on blood pressure cuffs, the good news is that this sort of large clinical trial would be much less expensive and produce results much more quickly than drug studies. Hence, it is likely that there will eventually be a large trial funded by grants from government, foundations, or cardiovascular disease charities (such as the American Heart Association).


  1. Betker et al. Remote ischaemic conditioning before hospital admission, as a complement to angioplasty, and effect on myocardial salvage in patients with acute myocardial infarction: a randomised trial. The Lancet 375:727-4 (2010).
  2. Weber. Bedside to bench: Receptor cross-talk in remote conditioning. Nature Medicine 16(7):760-2 (2010).
  3. Murry et al. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation 74:1124-36 (1986).
  4. Birnbaum et al. Ischemic preconditioning at a distance: reduction of myocardial infarct size by partial reduction of blood supply combined with rapid stimulation of the gastrocnemius muscle in the rabbit. Circulation 96:1641-6 (1997).
  5. Hoole et al. Cardiac Remote Ischemic Preconditioning in Coronary Stenting (CRISP Stent) Study: a prospective, randomized control trial. Circulation 119:820-7 (2009).
  6. Rentoukas et al. Cardioprotective role of remote ischemic periconditioning in primary percutaneous coronary intervention: enhancement by opioid action. JACC Cardiovasc Interv 3:49-55 (2010).


Cognitive dissonance is a state of lingering uncertainty about a decision that has been made where one had to choose one of two or more choices. This has been studied extensively in the context of experimental setups where people are given the choice of two similarly attractive options, such as say a vacation to two places you’d love to visit where you have to choose one. The result of a decision is cognitive dissonance as there is generally some lingering doubt about whether you should have made the other attractive choice. Studies have shown that the way people handle this cognitive dissonance is to downgrade the desirability of the rejected choice following the decision not to choose it.1 This mental manipulation justifies the choice made and eliminates the unpleasant lingering uncertainty.

Researchers studied the possibility that hand washing could reduce cognitive dissonance in the subjects of their experiment.1 The participants were 40 undergraduates who thought they were involved in a consumer survey. They were asked to pick out 10 CD covers that they would like to own out of a selection of 30. Then they were asked to rank order the CDs they chose as to preference. The subjects were next given the opportunity to choose either of their choice number 5 or 6 as a gift for participating in the “survey.” That was followed by having the subjects “evaluate” a liquid soap, either by examining it or by washing their hands with it. After all this, the researchers had the subjects again rank the top 10 CDs, “allegedly because the sponsor wanted to know what people think about the CDs after leaving the store.”1 The results showed that the people who just examined the soap increased their preference for the chosen CD over the rejected alternative whereas the people who washed their hands did not, suggesting that cognitive dissonance had been reduced by hand washing. The authors1 then describe another choice experiment in the literature that included hand washing with an antiseptic wipe and which replicated the findings of the first described experiment.

The authors ponder these results. They suggest that “the psychological impact of physical cleansing extends beyond the moral domain. Much as washing can cleanse us from traces of past immoral behavior, it can also cleanse us from traces of past decisions, reducing the need to justify them.” However, they admit that there is a need for an understanding of the processes that mediate this purported mental “cleansing” (the psychological impact) of physical cleansing.

Sounds like something your marketing department would like to know!


  1. Lee and Schwartz. Washing away postdecisional dissonance. Science 328:709 (2010).


A key problem in diabetes is the failure of the liver to stop generating glucose, a process called gluconeogenesis. When blood sugar is low (such as when fasting during sleep), the liver is supposed to create glucose (either by breaking down glycogen or synthesizing glucose from amino acids), but when blood sugar is increased (as it is following a meal), gluconeogenesis by the liver is supposed to be inhibited by the insulin released following the meal. But, as diabetics typically are insulin resistant, the insulin signal is ineffective in stopping the liver from continuing to churn out glucose.

Hence, natural substances that attenuate gluconeogenesis can be highly beneficial for people who are insulin resistant. A recent paper1 describes a study of the effect of L-carnitine on gluconeogenesis in rats. Male Wistar rats were divided into four groups of six rats each. One group was fed a control diet, a second group was fed a high fructose* diet, the third group was fed the high fructose diet plus L-carnitine (CA) (300 mg of CA/kg body weight/day i.p.), and the fourth group received the control diet plus the same dose of supplemental CA. The diet and supplementation regimen ran 30 days.

* 60 g fructose/100 g diet is a very high fructose diet.

The results showed that the fructose-fed rats had significant increases of the circulating gluconeogenic substrates such as glycerol, lactate, and pyruvate as compared to the control rats. The L-carnitine (CA) supplementation to fructose-fed rats significantly reduced those levels as compared to the untreated fructose-fed rats. Liver cells from the fructose-diet fed rats produced significantly more glucose from pyruvate, lactate, glycerol, fructose, and alanine as compared to the liver cells from rats on the control diet. But the liver cells from the fructose-fed rats also supplemented with CA produced normal levels of glucose similar to the levels of the control animals.

The authors state: “The abnormalities associated with fructose feeding such as increased gluconeogenesis, reduced glycogen content and other parameters were brought back to near normal levels by CA.” “The benefits observed could be attributed to the effect of CA on fatty acyl-CoA transport.” The latter refers to the fact that CA transports fatty acids into the mitochondria for oxidation. Under conditions of CA deficiency, there is an excess of free fatty acids in the bloodstream, which inhibits the uptake and metabolism of glucose in skeletal muscle and the heart.1

As the authors explain, “[f]atty acid supply to the liver plays an important role in determining both the ability of insulin to suppress glucose production and the rate of gluconeogenesis.”1

It is also interesting to note the suggestion made recently2 that increased fructose intake may be a risk factor for dementia. The authors cite an animal study showing that a high fat/refined sugar diet even for a short duration (in this case, 2 months) was found to be associated with reduced hippocampal levels of brain-derived neurotrophic factor (BDNF), an important molecule in learning and memory) and impaired spatial memory. Another recent study they cite found that in overweight and obese women, high fructose intake was associated with increased de novo lipogenesis (the synthesis of triglycerides), lipid peroxidation, and gluconeogenesis. They also describe two animal studies suggesting that “insulin resistance status induced by high fructose intake and/or the insulin resistance syndrome (i.e., metabolic syndrome) is linked to cognitive decline and neurodegeneration, namely AD [Alzheimer disease] type pathology.” However, they note that no human studies have been performed on the short-term and long-term effects of fructose on cognition and dementia risk, although there has been preliminary evidence from subjects with type 2 diabetes of an association between insulin resistance and brain structural changes along with deficits in cognitive performance.3

We both take CA, in the form of acetyl-L-carnitine, 2 grams per day, to improve our insulin sensitivity and also for possible protection against cognitive decline.3,4


  1. Rajasekar and Anuradha. Fructose-induced hepatic gluconeogenesis: effect of L-carnitine. Life Sci 80:1176-83 (2007).
  2. Stephan et al. Perspective: Increased fructose intake as a risk factor for dementia. J Gerontol A Biol Sci Med Sci 65(8):809-14 (2010).
  3. Juliet et al. Carnitine: a neuromodulator in aged rats. J Gerontol A Biol Sci Med Sci 58(11):970-4 (2003).
  4. Ames and Liu. Delaying the mitochondrial decay of aging with acetylcarnitine. In: Alesci S et al, eds. Carnitine: the Science Behind a Conditionally Essential Nutrient. New York, NY: Ann N Y Acad Sci;1033:108-16 (2004).


A remarkable suggestion was made by Australian scientists writing in a recent Nature.1 They noted the lack of funds for expanding protected areas for conservation purposes in Australia and proposed (we can still hardly believe it) that the Australian government sell off some of the poorly performing protected areas (which are not providing cost-effective outcomes for public spending) and reinvest the money obtained from the sales into protecting different areas that would provide better conservation outcomes. The researchers estimate that “by selling off 70 of Australia’s nearly 7,000 protected areas, the government could raise Aus$20.6 billion (US$17.4 billion) …”

The areas protected for conservation in Australia are said to comprise about 8% of Australia’s landmass. (Compare this to the U.S., where about one third of the land area of the United States has been nationalized and is controlled by various agencies of the Federal government (e.g., U.S. Forest Service, Bureau of Land Management) and most uses are strictly regulated, mostly in the name of conservation.) As is noted in the accompanying commentary,2 “growth in global spending on protected areas has stagnated in recent decades. …” Hence, the suggestion has been made that money be raised by selling poorly performing conservation areas to protect “the best places.” As is noted in the commentary,2 however, “the idea of applying a return on investment approach to the design of networks of protected areas has yet to gain traction in the messy world of non-governmental organizations involved in conservation, or that of national governments.” “The idea that a protected area might not be secured in perpetuity will be unsettling, as such a precedent may make it too easy for governments to revoke systems of protected areas in times of economic stress. Also, those 70 protected areas in Australia—the bottom 1%—tend to be in locations where land prices are high, which means that they are near urban centres.” “… their public accessibility and visibility could be essential in maintaining public support for conservation.” As the commentary surprisingly notes, however, that protected areas established as rigid “do not touch” ever again resources with little or no regard to cost-benefit may strike the general public as “monuments to one special-interest group—conservationists.”

Wow! This is a wonderful idea! Nice to see it in Nature. It is about time that the Federal government of the USA started selling off much of the huge land estate they now mismanage to pay for their unfunded promises (e.g., Social Security, Medicare, Obamacare, etc., etc.). Most of this land (such as that controlled by the Bureau of Land Management) is nothing special, of no great conservation value, like Australia’s lowest 1%. How can the Feds justify hoarding in perpetuity this hugely valuable estate that, at least in the West (such as in Nevada, where over 90% of the state is controlled by the Feds), often restricts people to small and diminishing areas of private property—while limiting public access to and usage of the so-called public lands—and while they are squeezing the public with higher and higher taxes to pay for more and more spending? Sell it off and pay your bills!!!!


  1. Fuller et al. Replacing underperforming protected areas achieves better conservation outcomes. Nature 466:365-367 (2010).
  2. Kareiva. Trade-in to trade-up. Nature 466:322-3 (2010).

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