Life Enhancement News with Durk Pearson and Sandy Shaw

June 2009 Blog with Durk and Sandy

by Jamie Riedeman on Jun 27, 2009

June 2009 Blog with Durk and Sandy

“Organized Science” Going to the Dogs (or, as in This Case, to the Frogs)

Even the very best and most reputable scientific journals are now being run by the “big government is good, bigger government is better” crowd . . . and they’re proud of being part of it. A particularly disgusting example of the political editorials now coming out of scientific journals is the one in the March 2009 FASEB Journal. Gerald Weissmann, the journal’s editor-in-chief opines that “[i]n the current debate over the future of medical care in the United States, we could do worse than to consult two authorities in the field, Prof. Pierre C. A. Louis, the father of medical statistics, and Michael Moore, ‘the angry filmmaker.’ Moore’s [movie] SiCKO suggests that we have a lot to learn from France; Prof. Louis reminds us that it wouldn’t be the first time.” “More and more Americans also agree with Michael Moore and SiCKO that universal health coverage should be as much a part of ordinary existence for Americans as it has been for Parisians for over a decade.”

Michael Moore is an authority in the field of medical care? Universal health coverage should be (whether you like it or not) a part of ordinary existence for Americans? The U.S. should pattern its health care delivery after that of France?? Lest you forget (or perhaps never knew), the French state is (unlike the mostly common law-based United States) an administrative state, where nearly all laws are determined and administered by public agencies akin to the FDA, EPA, OSHA, ad nauseum, agencies whose rules and regulations are determined and violators judged and punished internally largely by unelected bureaucrats. When you are accused of wrongdoing, you are guilty until you prove yourself innocent (no presumption of innocence as under the common law of the United States). The French government health care system is very similar to the British National Health Service, but with a lot of pork built in (for example, you can complain of being under stress and get a taxpayer paid vacation for a week at a spa; wonderful if you like paying high taxes for other people’s vacations).

“Organized science” continues to progress in the direction of top-down dogma and lies maintained by an elite that act as agents of the government by virtue of being in control of huge amounts of government money. The arrogance of these people knows no bounds now that the new Administration has handed them huge additional amounts of printing press money (e.g., by inflating the money supply). The FASEB Journal rarely published politically-oriented editorials before the one cited above and has never before published editorials containing such outrageous personal opinions best left unexpressed (lest your biases and foolishness be revealed) such as endorsing Michael Moore as an expert on health care.


Climate Change Treaty Negotiations: Oil Exporting Nations Want Bailout

Maybe they should be serving fish at the climate talks. But then again that would probably only result in a heated battle over what fish would be politically correct to eat. In any event, the potential costs of an international agreement on regulation of carbon emissions keep increasing (thank goodness, as this reduces the likelihood that any such agreement may ever happen). On March 29th, the first day of an international preparatory meeting for the December Copenhagan meeting, reports Nature (pg. 815, 16 April 2009), “[o]il-exporting nations, led by Saudi Arabia, are also interested in a transfer of funds, saying they will demand compensation if a climate agreement cuts oil revenue. ‘We share the concern for climate change but at the same time we don’t want to be a victim,’ Mohammad Al Sabban, an adviser to Saudi Arabia’s Ministry for Petroleum and Mineral Resources, told reporters in Bonn.”


No bird soars too high, if he soars with his own wings. 
— William BlakeA desire not to butt into other people’s business is eighty percent of all human wisdom. 
— Robert A. HeinleinEvery election is a sort of advance auction sale of stolen goods. 
— H. L. MenckenNever underestimate the power of very stupid people in large groups. 
— John Kenneth GalbraithI think we have more machinery of government than is necessary, too many parasites living on the labor of the industrious. 
— Thomas Jefferson 
(in a letter to Charles Yancey, 1816)
To contract new debts is not the way to pay old ones. 
— George Washington 
(to James Welch, Apr. 7, 1799)
We must not let our rulers load us with perpetual debt. 
— Thomas Jefferson 
(in a letter to Samuel Kercheval, July 12, 1816)

Effects of Potassium on Blood Pressure via Reduction of Endothelial "Stiffness" and Increased NO Release

The April 2009 issue of the Life Enhancement magazine contained an interview with us as well as a review of some of the scientific literature on important effects of potassium bicarbonate supplements, including beneficial effects on blood pressure and the risk of stroke.

A new study1 now reports that potassium controls endothelial deformability (by preventing the stiffness that results from small physiological changes in extracellular sodium concentration2) and increases nitric oxide (NO) release. The authors speculate that “… soft endothelial cells have a larger degree of physical compliance compared with stiff ones, and more easily undergo rapid morphological changes that occur during cardiac pulsations and thus generate more NO.” The authors propose that a submembrane compartment of endothelial cells may “rapidly switch between solation (a change toward a fluid-like state) and gelation (a change to a more solid state) depending on ambient sodium and potassium.”

The researchers found that when the endothelial cells were cultured in high-sodium medium in the presence of aldosterone (an adrenal hormone that regulates sodium and potassium homeostasis, in part by modulating sodium resorption in the kidney), the cells did not respond anymore to changes in extracellar potassium between 2 and 8 mM. The authors suggest that these findings indicate that high potassium level can stimulate NO release as long as ambient sodium concentration is low, with aldosterone’s effects on the entry of sodium into the cell playing the role of a key modulator.

It is also interesting that a very recent clinical trial3 reported that in 29 overweight and obese normotensive men and women, a low salt diet (50 mmol sodium/day) as compared to a usual-salt diet (150 mmol sodium/day) for 2 weeks resulted in improved endothelium dependent vasodilation independently of the changes in the measured resting blood pressure. In that paper, the authors note that “A high salt intake has been shown to be a determinant of arterial stiffness, and a low salt intake has been associated with reduced arterial stiffness in normotensive adults, both epidemiologically and in an intervention.” Moreover, they continue, increased arterial stiffness “predicts the development of CVD [cardiovascular disease] and is an independent predictor of mortality in hypertensive patients.”

Our new Potassium Basics™ is now available from Life Enhancement Products. Recommended dosage is two capsules containing 1,053 mg. of potassium as potassium bicarbonate taken 2-4 times daily.


  1. Oberleithner et al. Potassium softens vascular endothelium and increases nitric oxide release. Proc Natl Acad Sci U S A. 106(8):2829-34 (2009).
  2. Oberleithner et al. Plasma sodium stiffens vascular endothelium and reduces nitric oxide release. Proc Natl Acad Sci U S A. 104(41):16281-6 (2007).
  3. Dickinson et al. Effects of a low-salt diet on flow-mediated dilatation in humans. Am J Clin Nutr 89:485-90 (2009).

Protective Effect of the Inhibition of the Renin-Angiotensin System on Aging

Although recent economic events may have focused decision-making and planning attention on the short term, in the longer term there is still life extension. Evidence is mounting that inhibiting the renin-angiotensin system may be a way to prevent many deleterious effects of aging. As the authors of one recent paper note: “Experimental studies indicate that long-term inhibition of the renin-angiotensin system (RAS) can prevent most of the deleterious effects due to aging in the cardiovascular system and in the kidney of the normal mouse and rat.”1

Angiotensin converting enzyme (ACE) inhibitors and angiotensin II nonpeptide type 1 receptor (AT1) blockers are currently used widely to treat hypertension, which induces cardiovascular changes (enhanced stiffness, hyperplasia, and collagen accumulation) that are also observed in aging. “The similarities between aging and hypertension added to the fact that increased BP [blood pressure] is usually observed in aged humans and rats, suggest the possibility that hypertension could be a form of accelerated aging.”

Kidney failure is a frequent cause of death in rodents and decline of the kidney’s filtering ability is a usual feature in human aging. Glomerulosclerosis, a process that commonly occurs in the aging kidney and in various models of kidney injury can be effectively treated with ACE inhibitors as well as by AngII antagonists. (AngII binds to the AT1 receptor.) In one study reported by the authors of ref 1, chronic ACE inhibitor treatment during the entire lifespan of the rat reduced proteinuria and albumin accumulation in podocytes (a type of epithelial cell in the kidney), delayed the progression of glomerulosclerosis and prevented the age-related hypertrophy of the mesangial domain [thickening of the basement membrane, as also occurs normally in human kidney aging] of the glomeruli.2 Similarly, treatment with ACE inhibitors or AngII antagonists abolished the increase in blood pressure seem in untreated rats and also delayed cardiac and left ventricular hypertrophy/hyperplasia and aortic growth.1 Moreover, other animal studies have shown that these drugs can increase the production of nitric oxide by preserving NOS (nitric oxide synthase) activity in endothelial cells of elastic arteries. The treatments have even been shown to reduce anxiety, and improve learning, memory and motor performance in the aged rat.3

Improvement in Endothelial Function in Penile Tissue of Mice

Another recent paper3A even reported improvement of penile endothelial function of the corpus cavernosum in apolipoprotein E knockout mice (a widely used animal model of the development of human atherosclerosis) treated with an angiotensin receptor blocker drug, irbesartan. “The local synthesis of angiotensin II in the corpus cavernosum initiating the detumescence phase in humans could be responsible.”3A This suggests that angiotensin II might be a cause of human erectile dysfunction.

Life Extension in Mice with Disrupted Angiotensin Receptor

A new study4 now reports that targeted disruption of the gene that encodes AT1A results in a 26% increase in lifespan in mice compared to wild-type mice. The treated animals developed less cardiac and vascular injury, and multiple organs showed less oxidative damage as compared to the untreated (wild-type) animals. The authors report that the treated mice had more mitochondria and upregulation of two longevity associated genes, nicotinamide phosphoribosyltransferase (Nampt) and sirtuin 3 (Sirt3) in the kidney. The mice with the disrupted AT1A gene substantially outlived the wild type mice. “At 29 months, when all wild-type animals [had] died, 17 AT1A-deficient mice (85%) were still alive These remaining mice lived for an additional 7 months.”4

Renin-Angiotensin System and Muscle Function

As we have written before in this newsletter, studies in humans suggest that ACE inhibitors may halt or slow decline in muscle strength in elderly persons.5,6,6A In another study,6B British army recruits were subjected to an 11 week mostly aerobic physical training regimen; there was enhanced anabolic effect of the training in those with a form of the ACE gene with lower ACE activity.

Improved Vascular Function In Rheumatoid Arthritis Patients

A recent paper7 also reports that ACE inhibition improved vascular function in rheumatoid arthritis patients (who are at increased risk of cardiovascular disease), despite the fact that systolic blood pressure and heart rate were unchanged in the study and diastolic blood pressure decreased only slightly. There was, however, an increase in flow-mediated dilation, indicating improved endothelial function.

Vitamin D as a Possible Modulator of the Renin-Angiotensin System

Finally, an interesting recent paper8 reports that 1,25(OH)2D3 (Vitamin D) suppresses the transcription of the renin gene in mouse cell culture (that is, it prevents the production of renin, the renin gene product; renin is the first and rate-limiting component of the renin-angiotensin system). Interestingly, renin inhibition has been reported to reduce hypercholesterolemia-induced atherosclerosis in mice.9 We get our Vitamin D from our high potency SunPower Vitamin D™ capsules. ACE activity has been reported to be inhibited by flavanol-rich foods, such as nuts, cranberries, apples, red wine, tea, and cocoa or chocolate10 and also by pomegranate juice.11 Taurine has been reported to attenuate the effects of angiotensin II on calcium transport, protein synthesis, and angiotensin II signaling.12


1. Basso et al. Protective effect of the inhibition of the renin-angiotensin system on aging. Regul Pept 128:247-52 (2005). 
2. Hendes et al. Effect of chronic ANG I-converting enzyme inhibition on aging processes: I. Kidney structure and function. Am J Physiol 266:R1038-51 (1994). 
3. Basso et al. Long-term inhibition of the renin-angiotensin system improves spatial working memory in the rat. J Hypertens 18(Suppl. 4):S77 (2000). 
3A. Baumhäkel et al. Improvement of endothelial function of the corpus cavernosum in apolipoprotein E knockout mice treated with irbesartan. J Pharmacol Exp Ther327(3):692-8 (2008). 
4. Benigni et al. Disruption of the Ang II type 1 receptor promotes longevity in mice. J Clin Invest 119(3):524-30 (2009). 
5. Carter et al. Angiotensin-converting enzyme inhibition intervention in elderly persons: effects on body composition and physical performance. J Gerontol A Biol Sci Med Sci 60A(11):1437-46 (2005). 
6. Onder et al. Relation between use of angiotensin-converting enzyume inhibitors and muscle strength and physical function in older women: an observational study. Lancet 359:926-30 (2002). 
6A. Di Bari et al. Antihypertensive medications and differences in muscle mass in older persons: the Health. Aging and Body Composition Study. J Am Geriatr Soc 52:961-6 (2004). 
6B. Williams et al. The ACE gene and muscle performance. Nature 403:614 (2000). 
7. Flammer et al. Angiotensin-converting enzyme inhibition improves vascular function in rheumatoid arthritis. Circulation 117:2262-9 (2008). 
8. Yuan et al. 1.25-dihydroxyvitamin D3 suppresses renin gene transcription by blocking the activity of the cyclic AMP response element in the renin gene promoter. J Biol Chem282(41):29821-30 (2007) 
9. Renin inhibition reduces hypercholesterolemia-induced atherosclerosis in mice. J Clin Invest 118(3):984-92 (2008). 
10. Actis-Goretta et al. Inhibition of angiotensin converting enzyme (ACE) activity by flavan-3-ols and procyanidins. FEBS Lett 555:597-600 (2003). 
11. Aviram and Dornfeld. Pomegranate juice consumption inhibits serum angiotensin converting enzyme activity and reduces systolic blood pressure. Atherosclerosis 158:195-8 (2001). 
12. Schaffer et al. Interaction between the actions of taurine and angiotensin II. Amino Acids 18:305-18 (2000).


Hydrogen Sulfide as a Mediator of Erection via Corpus Cavernosum Smooth-Muscle Relaxation

We have written before on some of the interesting new findings concerning hydrogen sulfide, another endogenously produced gas (other gases important in physiological signaling include nitric oxide and carbon monoxide). In the case of hydrogen sulfide, it has been found to mediate vascular relaxation. Early work with animals has indicated that hydrogen sulfide facilitates erectile function.1

A new study1 reports further to extend the data to humans. Using human corpus cavernosum (obtained during a surgical procedure), the researchers demonstrate that human penile tissues contain both enzymes required for conversion of L-cysteine to hydrogen sulfide, cystathione beta-synthase (CBS) and cystathione gamma-lyase (CSE). Providing human corpus cavernosum strips with sodium hydrogen sulfide (an exogenous source of hydrogen sulfide) or L-cysteine (converted by CBS and CSE to hydrogen sulfide) caused the strips to relax in a concentration-related manner.

The authors found that an “intracavernous administration of L-cysteine (30 ug per rat) caused a significant increase in intracavernous pressure. Intravenous administration of [the CSE inhibitor] PAG (50 mg/kg. at 30 and 60 minutes significantly reduced L-cysteine-elicited rat penile erections.” The investigators did not examine how much L-cysteine would need to be taken orally to get a similar effect.

As the authors note, “[t]o what extent this pathway complements the L-Arg/NO signaling pathway in promoting erectile function is presently unknown.”

If you take a cysteine supplement, be sure to take 2–3 times as much vitamin C as cysteine to help prevent the formation of cystine stones. Eggs are a good food source of cysteine; each egg contains about 250 mg. We supplement our diet with the cysteine in Root Food™.


  1. d’Emmanuele di Villa Bianca et al. Hydrogen sulfide as a mediator of human corpus cavernosum smooth-muscle relaxation. Proc Natl Acad Sci USA106(11):4513-8 (2009).


Leptin, a Hormone Important in Satiety and Food Intake, Decreases After Meals Cooked at High Temperatures

Leptin was discovered not too long ago to be an important hormone released by adipocytes (fat cells) that regulates satiety and food intake, as well as aspects of immunity and inflammation. The hormone is synthesized and released in response to increased energy storage in fat.1 Obesity and diabetes are both associated with high leptin levels combined with leptin resistance. Hence, leptin signaling is impaired. Both hyperinsulinemia and hyperglycemia are responsible (but mainly the latter) for the modulation of leptin secretion.2 The authors of a new study2 hypothesized that not only meal composition, but the temperature at which it is cooked, would modulate postprandial leptin levels.

The study reports on the results of feeding type 2 diabetic patients with the same meal either cooked at high temperatures or at low temperatures. The high temperature meal (but not the low temperature meal) was associated with higher blood AGE (advanced glycation end-products) and TBARS (a measure of lipid peroxidation) levels. The meal prepared at a high temperature (but not at a low temperature) was also associated with a significant decrease in leptin levels. The reduced leptin levels may result in an impairment of the anorectic effect of leptin in type 2 diabetics.

Interestingly, short sleep was also associated with reduced leptin as well as elevated ghrelin (stimulates appetite).3 The authors suggest that this might explain the increased BMI (body mass index) observed in people with short sleep duration.


  1. Wang et al. A nutrient-sensing pathway regulates leptin gene expression in muscle and fat. Nature 393:684-8 (1998)
  2. Stirban et al. Leptin decreases postprandially in people with type 2 diabetes, an effect reduced by the cooking method. Horm Metab Res 40:896-900 (2008)
  3. Taheri et al. Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS Medicine 1(3):e62 (Dec. 2004) (


Upregulation of Aldose Reductase During Foam Cell Formation: Possible Link Among Diabetes, Hyperlipidemia, and Atherosclerosis

The enzyme aldose reductase is the rate-limiting enzyme in the polyol pathway, whereby aldehydes as well as sugars such as glucose and galactose are metabolized to produce sorbitol. Sorbitol is then metabolized by the enzyme sorbitol dehydrogenase to fructose. Increased fructose is a source of AGE production and oxidative stress. Various pathological conditions have been found to be improved by inhibitors of aldose reductase, including impaired nerve conduction velocity and symptoms of neuropathy, as are found in diabetes. Recent research using LDL receptor-deficient diabetic mice was reported to find increased atherosclerotic lesions in the transgenic animals overexpressing human aldose reductase.1

A study1 using gene chips to identify differences in gene expression during foam cell formation reported that there was “a significant increase of aldose reductase mRNA expression after treatment of primary human blood monocyte-derived macrophages with oxidized low-density lipoprotein (oxLDL).” The authors therefore hypothesized that increased aldose reductase expression in human foam cell formation may represent a novel proinflammatory pathway leading to increased oxidative stress and to an increased risk of atherosclerosis.

The authors report in their new study2 that there was a significant increase of aldose reductase expression in human macrophages under hyperglycemic as compared to normoglycemic conditions. Moreover, “[e]xposure of macrophages to oxLDL resulted in a 10-fold increase of AR [aldose reductase] activity under hyperglycemic, but not normoglycemic conditions.” Pretreatment of macrophages with an aldose reductase inhibitor (the drug epalrestat) before and throughout exposure to oxLDL resulted in a significantly reduced formation of reactive oxygen species (ROS) under hyperglycemic conditions. The authors interpret their findings to suggest that “under hyperglycemic conditions ~20% to 30% of the oxidative stress in macrophage foam cells is attributable to AR activity.”

Interestingly, there are a number of readily available, relatively inexpensive natural products that inhibit aldose reductase. For example, a recent paper3 reports that a hot water extract of Matricaria chamomilla (chamomile tea) showed potent inhibition against aldose reductase and that its components umbelliferone, esculetin, luteolin, and quercetin “could significantly inhibit the accumulation of sorbitol in human erythrocytes.” The authors report that the major flavonoid components of chamomile are apigenin, luteolin, and quercetin, which comprise 16.8%, 1.9%, and 9.9%, respectively, of total flavonoids. The authors conclude: “These results clearly suggested that daily consumption of chamomile tea with meals could contribute to the prevention of the progress of hyperglycemia and diabetic complications.”


  1. Cho et al. “Induction of dendritic cell-like phenotype in macrophages during foam cell formation,” Physiol Genomics 29:149-160 (2007).
  2. Gleissner et al. “Upregulation of aldose reductase during foam cell formation as possible link among diabetes, hyperlipidemia, and atherosclerosis,” Arterioscler Thromb Vasc Biol 28:1137-43 (2008).
  3. Kato et al. “Protective effects of dietary chamomile tea on diabetic complications,” J Agric Food Chem 56:8206-11 (2008).


A Secret for Successful Negotiation: Fish

No, we don’t propose negotiating with fish, but treating a person or persons with whom you are negotiating to a leisurely cold water fatty fish meal beforehand to increase your chances of getting them to accept your offer. Here’s how it worked as described in a recent study.1

Researchers doing the study hypothesized that low serum levels of omega-3 fatty acids, having been associated with increased hostility and decreased impulse control, might have a measurable effect on the willingness of people to accept offers made to them in the ultimatum bargaining game. You may recall our discussion (or have read about it elsewhere) that, in the ultimatum bargaining game, two players negotiate over the division of a given amount of money. The proposer (who initially has the money) offers a split with a responder. If the responder accepts the offer, they make the division and keep the proceeds. If the responder rejects the offer (as “unfair”), neither proposer or responder gets any money.

The ultimatum game has been a popular method of assessing how people make economic decisions, including fuzzy modulating concepts such as “fair” and “unfair.” A 50:50 split in the ultimatum game would be (as reflected in results of studies) considered “fair,” while most would reject a 10:90 split as “unfair.”

In this particular study, the researchers measured fasting serum alpha-linolenic acid (ALA, an omega-3 fatty acid), eicosapentaenoic acid (EPA, an omega-3 fatty acid), docosahexaenoic acid (DHA, another omega-3 fatty acid), as well as linoleic acid (an omega-6 fatty acid) and arachidonic acid (a product of omega-6 fatty acids) in sixty undergraduate economics students. The results showed that the ratio of serum omega-3/omega-6 fatty acids was significantly lower in individuals who rejected “unfair” offers as compared to those who did not. There was a significant depletion of ALA, EPA, and DHA in the rejectors of “unfair” offers.

We make no guarantees concerning the outcome of your negotiation, but it would appear that you can reduce the likelihood of irrational rejections of perfectly reasonable offers on the basis of biases concerning “fair” and “unfair” by feeding those with whom you are negotiating a cold water fatty fish meal (rich in EPA and DHA) — wine along with it would probably improve the absorption of the omega-3 fatty acids — at a good restaurant before you get down to business.


  1. Emanuele et al. “Serum omega-3 fatty acids are associated with ultimatum bargaining behavior,” Physiol Behav 96:180-183 (2009)


When Money Dies

BOOK REVIEW: When Money Dies: The Nightmare of the Weimar Collapse (107 pp., available without charge from

The Approaching Inflation

For those who are concerned about the severe inflation (possibly hyperinflation) to come as the trillions of new printing press dollars continue to flow and will soon drive down the value of the dollar, we give our highest recommendation to this book. Unlike conventional books on economic subjects, this one paints a portrait of life in the Weimar Republic as the mark became worth less and less, eventually resulting in the legendary “wheelbarrow” full of marks needed to buy a loaf of bread. It describes, often in their own words, how the lives of ordinary people were changed as this appalling inflation developed. “We haven’t had any fun since 1914. If you made any money it gets no good, and there is only to spend it. Last year I had enough money saved up to buy a Gasthaus at Hernberg,” says one man, a waiter, “now that money wouldn’t buy four bottles of Champagne.” (This was recorded by Ernest Hemingway, who was in Germany at the time, 1923.)

In another example, Lady Listowel (Judith, Countess of Listowel), whose father held a senior post in the Hungarian diplomatic service, commented on distress among the circle of her family’s friends in Budapest during their hyperinflationary period at about the same time as it occurred in Germany: “One used to see the appearance of their flats gradually changing. One remembered where there used to be a picture, or a carpet, or a secretaire. Eventually their rooms would be almost empty and on paper some people were reduced to nothing. In practice, people didn’t just die. They were terribly hungry, and relations and friends would help with a little food from time to time. . . . And some of them begged—not in the streets—but by making casual visits (one knew only too well what they had come for) . . . Everyone still tried to keep up appearances at first, early on, people looked around to see what economies they could make, what clubs to resign from, what luxuries to do without. Later it was a question of considering what necessities to do without.”

Paying Off Public Debt by Depreciating the Currency

Inflation is a way that government can pay off their debts (albeit with depreciated currency) without outright default or overt tax increases. In Weimar Germany, the initiating factor underlying the government’s unleashing of the printing presses was the required payment to the Allies of immense war reparations.

In the U.S., government debt has grown to impossible-to-pay levels. Yet the spending is accelerating. The immensely costly new programs being created on an almost daily basis by the Obama Administration and the Democrats (mostly) in Congress come at a huge price, most of which (along with the continuing burden of Medicare and Social Security, etc.) can only be paid for by continually increasing the money supply into hyperinflationary territory.

What It Is Like to Live Through Hyperinflation

This book is an incredible eye-opener! It reads almost like a thriller; you can’t stop turning the pages as money loses its value, people’s savings are destroyed, people buy tangible goods (almost anything) rather than hold marks when they do have them, the decline of social cohesion, widespread corruption, and it sucks you into the action so that you, too, experience what it is like living in a hyperinflation.

Hyperinflation is NOT Uncharted Territory

There is much that is eerily familiar about the current course of the U.S. economy, particularly the immense, endless expansion of the money supply accompanied by the falling value of the dollar and the decreasing willingness (both foreign and domestic) to hold U.S. debt instruments (IOUs), and the development of hyperinflation in the Weimar Republic and in Austria, Hungary, and Poland and, of course, we all know one end result of the ensuing economic chaos in Germany: Hitler.

Another of the eerily familiar processes reported in the book concerned taxes. As of August 1923 in Weimar Germany, the book reports, “[s]tatute books on taxation formed a mountain several feet high, and none could tell who was liable to pay what, when or to whom. . . . in human terms, the imposition of unpayable taxes to settle an impossible debt had at last destroyed tax morals at every level of society.”

What Lies Ahead for the U.S.?

Last summer, the U.S. monetary base was $800 billion. Last fall, the Federal Reserve more than doubled the U.S. monetary base to $2.1 trillion. This March, the Fed announced that they are more than redoubling the U.S. monetary base by adding an additional $2.55 trillion dollars. Because we have a fractional reserve banking system, the U.S. money supply is about 10 times the monetary base. It usually takes about 18 months for newly created money to work its way through the banking system to Main Street where consumer prices are bid up.

Historically, it has taken about 20 years to quadruple the U.S. monetary base, which has resulted in slow inflation. Back in 1968, for example, you could buy a new luxury car for $1,695. Quintupling the money supply in 6 months is not unprecedented—as shown in the case of Weimar Germany. Read this free (download it from the Website given above) book—it might help you to save your wealth and even your life.

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